DeLee, Drez and Miller’s Orthopaedic Sports Medicine [2-Volume Set] [5th Edition] 9780323544740, 9780323544757

Table of contents :
Cover......Page 1
DeLee Drez & Miller's Orthopaedic Sports Medicine......Page 2
Copyright Page......Page 4
Dedication......Page 5
Section Editors......Page 6
Preface......Page 7
Contributors......Page 8
Video Table of Contents......Page 20
Structure......Page 24
Keywords......Page 25
Injury......Page 26
Inflammatory Phase......Page 27
Methods for Augmentation of Tendon and Ligament Healing......Page 28
Structure......Page 30
Injury......Page 31
Articular Cartilage......Page 32
Transitional zone.......Page 33
Joint Loading......Page 34
Types of Bone......Page 35
Tissue Surrounding Bone......Page 36
Fracture Repair......Page 37
Summary:......Page 38
References......Page 39
Degrees of Freedom......Page 44
Keywords......Page 45
Newton’s Second Law (Acceleration)......Page 46
Statics......Page 48
Ligament and Joint Contact Forces......Page 50
Joint Motions......Page 51
Fluid Mechanics......Page 52
Structural Properties......Page 53
Mechanical Properties......Page 54
Practical Application......Page 56
Functional Tissue Engineering......Page 57
Summary:......Page 58
References......Page 59
Augmented Autograft......Page 60
Allograft......Page 61
Healing of Autograft Versus Allograft......Page 62
Summary:......Page 63
Summary:......Page 64
References......Page 65
Implants for Tendon Repair......Page 67
Keywords......Page 68
Implants for Ligament Reconstruction......Page 71
Implants for Meniscus Repair......Page 74
Implants for Cartilage and Osteochondral Repair......Page 75
Sutures......Page 78
Suture Anchors......Page 79
Summary......Page 80
Summary:......Page 81
Summary:......Page 82
References......Page 83
Preparation and Composition......Page 91
Keywords......Page 92
Tendon and Ligament Injuries......Page 95
Anterior Cruciate Ligament Surgery......Page 96
Platelet-Rich Plasma in Meniscal Repair......Page 97
Definitions and Preparations of Stem Cell Therapy......Page 98
Cell-Based Therapy in Tendon and Ligament Healing and Repair......Page 100
Cell-Based Therapy in Cartilage Repair......Page 101
Summary:......Page 102
Summary:......Page 103
References......Page 104
Physiology of Skeletal Muscle Contractions......Page 108
Keywords......Page 109
Force Production of Muscle......Page 111
Glycolytic Energy System......Page 112
Muscular Response to Training......Page 113
Neuromuscular Adaptation to Exercise......Page 114
Effects of Aging on Skeletal Muscle......Page 115
Pituitary......Page 116
Gonadal Hormones......Page 117
Exercise Capacity......Page 118
Respiratory Response......Page 119
Summary:......Page 120
References......Page 121
Technical Considerations......Page 125
Keywords......Page 126
Fluoroscopy......Page 127
Arthrography......Page 128
Disadvantages......Page 129
Technical Considerations......Page 130
Musculoskeletal Ultrasound: Appearance of Normal and Pathologic Structures......Page 131
Ultrasound Elastography......Page 135
Disadvantages......Page 136
Technical Considerations......Page 137
Disadvantages......Page 139
Bone Scans......Page 140
Labeled White Blood Cell Scans......Page 141
Disadvantages......Page 142
Magnetic Resonance Imaging......Page 144
Imaging protocols.......Page 145
Image formation.......Page 146
Pulse sequences.......Page 147
Gradient echo.......Page 148
Inversion recovery.......Page 149
Magnetic resonance artifacts.......Page 150
Coils.......Page 151
Ultrashort Time to Echo Sequence......Page 152
Dynamic Contrast Enhancement......Page 153
Contraindications to Magnetic Resonance Imaging......Page 154
Radiation Exposure in Medical Imaging......Page 155
Summary:......Page 156
References......Page 157
Arthroscope......Page 160
Keywords......Page 161
Basket Forceps......Page 163
Electrocautery and Radiofrequency Instruments......Page 164
Patient Positioning and Preparation......Page 165
Arthroscopic Complications......Page 166
Postoperative Complications......Page 167
Citation:......Page 168
Summary:......Page 169
References......Page 170
Shoulder Injuries......Page 172
Keywords......Page 173
Knee Injuries......Page 174
Facial Injuries......Page 175
Ankle Injuries......Page 176
Lower Extremity......Page 177
Elbow/Forearm Injuries......Page 178
Back and Pelvis Injuries......Page 179
Team Handball......Page 180
Concussions......Page 181
Rugby......Page 182
Upper Extremity Injuries......Page 183
Concussions......Page 184
Lower Extremity Injuries......Page 185
Finger/Wrist Injuries......Page 186
Musculoskeletal Injuries......Page 187
Citation:......Page 188
Summary:......Page 189
References......Page 190
Biomechanical Factors......Page 195
Keywords......Page 196
Femoral Neck Stress Fractures......Page 197
Tibia Stress Fractures......Page 198
Proximal Fifth Metatarsal Stress Fractures......Page 199
Other Metatarsal Stress Fractures......Page 200
Pars Stress Fractures......Page 201
Rib Fractures......Page 202
Return to Sport......Page 204
Summary:......Page 207
References......Page 208
Timing, Setting, and Organization......Page 212
Keywords......Page 213
Cardiovascular System......Page 214
Pulmonary System......Page 216
Hematologic and Infectious Disease......Page 217
Heat Illness......Page 218
Emergency Action Plan......Page 219
General Approach to the Collapsed Athlete......Page 220
Cervical Spine Injury......Page 221
Anaphylaxis......Page 222
Conclusion......Page 223
Professional Athletics......Page 224
Case 3......Page 225
Summary:......Page 226
References......Page 227
Historical Perspective......Page 230
Keywords......Page 231
Preparticipation Screening......Page 232
Atria......Page 233
Gender, Genetics, and Race......Page 234
Cardiovascular Screening of the Athlete......Page 235
Electrocardiogram Screening in Athletes......Page 236
Transthoracic Echocardiography Screening in Athletes......Page 237
Structural/Congenital Disease States in Elite Athletes......Page 239
Acquired Cardiovascular Conditions in the Athlete......Page 242
Arrhythmias......Page 245
Conclusions and an Optimistic View of the Future......Page 246
Summary:......Page 247
References......Page 248
Clinical Presentation......Page 253
Keywords......Page 254
Objective Testing......Page 255
Nonpharmacologic Therapy......Page 256
Potential Complications......Page 257
Summary:......Page 258
References......Page 259
Preoperative Thromboembolic Risk Factors......Page 261
Keywords......Page 262
Diagnosis and Clinical Manifestations: Imaging and Laboratory Findings......Page 264
Thromboembolic Disease Treatment......Page 266
Sports Issues, Return to Play, and Travel......Page 267
Level of Evidence:......Page 268
Summary:......Page 270
References......Page 271
Upper Gastrointestinal Tract Conditions......Page 273
Keywords......Page 274
Gastroesophageal Reflux Disease Treatment......Page 275
Impact of Aspirin and Nonsteroidal Antiinflammatory Drugs......Page 276
Diarrhea......Page 277
Diarrhea Management......Page 278
Celiac Disease......Page 279
Selected Readings......Page 280
References......Page 281
Pathophysiology......Page 283
Keywords......Page 284
Diagnosis......Page 285
Definition......Page 286
Diagnosis......Page 287
Summary:......Page 288
References......Page 289
Exercise and the Immune System......Page 290
Keywords......Page 291
Return-to-Play Guidelines......Page 292
Diagnosis......Page 293
Return-to-Play Guidelines......Page 294
Definition......Page 295
Pathobiology......Page 296
Diagnosis......Page 297
Pathobiology......Page 298
Treatment......Page 299
Waterborne Diseases and Recreational Water-Related Illness......Page 300
Diagnosis......Page 301
Other Fecally-Derived Waterborne Diseases......Page 302
Treatment......Page 303
Diagnosis......Page 304
Definition and Epidemiology......Page 305
Citation:......Page 306
Summary:......Page 307
References......Page 308
Diagnosis......Page 310
Keywords......Page 311
Medical Nutrition Therapy......Page 312
Insulin and Insulin Analogs......Page 313
Glucose Regulation During Exercise in Athletes With Type 1 Diabetes Mellitus......Page 314
Pathophysiologic Responses to Exercise in Persons With Diabetes Mellitus......Page 315
Training Versus Competition......Page 316
Management of Type 1 Diabetes......Page 317
Summary......Page 318
Summary:......Page 319
References......Page 320
Diagnosis......Page 322
Keywords......Page 323
Treatment......Page 324
Summary:......Page 325
References......Page 326
Diagnosis and Evaluation......Page 327
Keywords......Page 328
Exercise and Seizures......Page 329
Safety Considerations Regarding Participation in Sports......Page 330
Summary:......Page 332
References......Page 333
Return to Play......Page 335
Keywords......Page 336
Pathophysiology......Page 337
Pathophysiology......Page 338
Laboratory Findings......Page 339
Prevention......Page 340
Laboratory Findings......Page 341
Treatment......Page 342
Laboratory Tests......Page 343
Diagnosis......Page 344
Advice for the Team Physician Traveling to Altitude......Page 345
Summary:......Page 346
Exertional Heat Illness......Page 347
Cold Injury......Page 348
High Altitude Illness......Page 349
Impetigo......Page 352
Keywords......Page 353
Cellulitis/Erysipelas......Page 354
Erythrasma......Page 355
Dermatophytoses......Page 356
Herpes Simplex......Page 357
Verruca vulgaris (Common Warts)......Page 358
Pediculosis Capitis......Page 359
Abrasions/Lacerations......Page 360
Acne Mechanica......Page 361
Hidradenitis Suppurativa......Page 362
Irritant Contact Dermatitis......Page 363
Exercise-Induced Anaphylaxis......Page 364
Citation:......Page 365
Summary:......Page 366
References......Page 367
Cleaning......Page 368
Postclosure Wound Care......Page 369
Complex Lacerations......Page 370
Periorbital Lacerations......Page 371
Evaluation......Page 372
Nasal Fractures......Page 374
Midface Fractures......Page 375
Orbital Fractures......Page 376
Differentiating Between Primary and Permanent Teeth......Page 377
Citation:......Page 378
Summary:......Page 379
References......Page 380
Historical Perspective and Evolution......Page 381
Keywords......Page 382
Decision-Making Principles......Page 383
Level of Evidence:......Page 385
Summary:......Page 386
References......Page 387
Macronutrients: Carbohydrate, Protein, and Fat......Page 389
Keywords......Page 390
Monitoring Hydration......Page 391
Vitamin D......Page 392
Sports Supplementation......Page 393
Summary:......Page 394
Summary:......Page 395
References......Page 396
Testosterone: Historical Perspectives......Page 397
Keywords......Page 398
Physiologic Considerations......Page 399
Adverse Effects......Page 400
Psychiatric.......Page 401
Erythropoietin......Page 402
Physiology......Page 403
Adverse Effects......Page 404
Epidemiology......Page 405
Other Considerations......Page 406
Effects on Athletic Performance......Page 407
Summary:......Page 408
References......Page 409
Conditioning......Page 412
Keywords......Page 413
Nutrition and Hydration......Page 415
Female Athlete Triad......Page 417
Osteoporosis and Osteopenia......Page 418
Pregnancy......Page 420
Psychological Issues in the Female Athlete......Page 421
Concussions......Page 422
Epidemiology of Sports Injuries......Page 423
Foot and Ankle Injuries......Page 424
Patellofemoral Pain Syndrome......Page 425
Risk Factors for Noncontact Anterior Cruciate Ligament Injury......Page 426
Prevention of Noncontact Anterior Cruciate Ligament Injury......Page 428
Frozen Shoulder/Adhesive Capsulitis......Page 429
Shoulder Instability......Page 431
Idiopathic Scoliosis......Page 432
Stress Fractures......Page 433
References......Page 434
Classification......Page 445
Keywords......Page 446
Dermatologic Conditions......Page 447
Exercise Physiology......Page 448
Musculoskeletal Injuries......Page 449
Autonomic Dysreflexia......Page 450
Exercise Physiology......Page 451
Intellectually Disabled Athletes......Page 452
Cardiac Abnormalities......Page 453
Acknowledgment......Page 454
Summary:......Page 455
References......Page 456
Obstructive Sleep Apnea......Page 460
Keywords......Page 461
Hypertrophic Cardiomyopathy......Page 462
Patient Characteristics......Page 463
Tourniquets......Page 464
Overview......Page 465
Supraclavicular Block......Page 466
Femoral Nerve Block......Page 468
Ankle Block......Page 469
Local Anesthetic Systemic Toxicity......Page 470
Perioperative Pain Management......Page 471
Buprenorphine......Page 473
Dexmedetomidine......Page 474
Parsonage-Turner Syndrome......Page 475
Summary:......Page 476
References......Page 477
Education......Page 481
Keywords......Page 482
Regulation......Page 483
Immediate and Emergent Care......Page 484
Psychosocial Strategies and Referral......Page 485
Summary:......Page 486
References......Page 487
Acute: Chronic Workload Ratio......Page 488
Keywords......Page 489
Tissue Healing Considerations......Page 490
Range of Motion......Page 491
Hypertrophy Versus Motor Learning......Page 492
Muscle Performance......Page 493
Role of Preoperative Rehabilitation......Page 494
Timing of Communication and Follow-Up......Page 495
References......Page 496
Manual Therapy......Page 499
Keywords......Page 500
Impairment-Based Rehabilitation Programs......Page 501
Manual Therapy......Page 503
Cryotherapy......Page 504
Ultrasound......Page 505
Iontophoresis......Page 506
Laser......Page 507
Superficial Heat......Page 508
Mobilizations With Movement......Page 509
Muscle Dysfunction......Page 511
Muscle Energy Technique......Page 512
Conclusion......Page 513
References......Page 514
Plantar Fascia/Arch Taping......Page 518
Keywords......Page 519
Knee Stability......Page 520
Length of Wear/Length of Effectiveness......Page 521
Criticisms of Taping Techniques......Page 522
Evaluating the Foot......Page 523
Outcomes for Common Overuse Issues......Page 524
Summary:......Page 525
Summary:......Page 526
References......Page 527
Risk Factors......Page 529
Keywords......Page 530
Prevention of Anterior Cruciate Ligament Tears in the Female Athlete......Page 531
Taping and Bracing......Page 534
Education of Risk......Page 535
Summary:......Page 538
References......Page 539
35 Return to Activity and Sport After Injury......Page 542
Keywords......Page 543
Citation:......Page 547
Summary:......Page 549
References......Page 550
Pertinent Bony Anatomy......Page 553
Keywords......Page 554
Glenohumeral Joint......Page 556
Glenohumeral Joint Capsule......Page 557
Sternoclavicular Joint......Page 558
Rotator Cuff......Page 559
Other Muscles of the Shoulder Complex......Page 560
Level of Evidence:......Page 561
Summary:......Page 562
References......Page 563
History......Page 566
Keywords......Page 567
Physical Examination......Page 568
Cervical Disc Herniation......Page 570
Shoulder instability.......Page 571
Summary:......Page 572
References......Page 573
Scapular Y View......Page 574
Keywords......Page 575
Stryker Notch View......Page 576
Arthrography Technique......Page 577
Ultrasonography......Page 578
Magnetic Resonance Imaging......Page 579
Osseous Outlet and Acromion......Page 581
Magnetic Resonance Imaging of the Osseous Outlet and Acromion......Page 582
Rotator Cuff......Page 584
Magnetic Resonance Evaluation of the Rotator Cuff......Page 586
Rotator Interval, Biceps, and the Biceps Pulley......Page 589
Long Head of the Biceps Tendon......Page 591
Anatomy......Page 594
Anterior......Page 595
Posterior......Page 596
Superior Labrum, Anterior, and Posterior Tears......Page 597
Articular Surfaces......Page 598
Summary:......Page 599
References......Page 600
Preoperative Imaging......Page 603
Keywords......Page 604
Patient Positioning......Page 605
Anatomy and Portal Placement......Page 606
Diagnostic Examination......Page 607
Complications......Page 609
Summary:......Page 610
References......Page 611
Anatomy......Page 612
Pathoanatomy......Page 613
Physical Examination......Page 619
Imaging......Page 620
Decision-Making Principles......Page 622
First-Time Versus Recurrent Instability......Page 624
Associated Injuries......Page 625
On-Field Management......Page 626
Surgical Management......Page 627
Future Considerations......Page 633
Summary:......Page 634
References......Page 635
Pathogenesis......Page 640
Keywords......Page 641
Physical Examination......Page 643
Imaging......Page 645
Treatment Options......Page 646
Postoperative Management......Page 647
Results......Page 651
Complications......Page 652
Summary:......Page 653
References......Page 654
42 Multidirectional Instability of the Shoulder......Page 657
Keywords......Page 658
Physical Examination......Page 659
Decision-Making Principles......Page 661
Open Inferior Capsular Shift......Page 662
Postoperative Management......Page 663
Results......Page 665
Return to Sport......Page 667
Complications......Page 668
Summary:......Page 669
Summary:......Page 670
References......Page 671
Physical Exam......Page 675
Keywords......Page 676
Imaging......Page 677
Decision-Making Principles......Page 680
Treatment Options......Page 681
Preferred Surgical Technique......Page 682
Postoperative Management......Page 685
Complications......Page 686
Future Considerations......Page 687
Summary:......Page 688
References......Page 689
Physical Examination......Page 693
Keywords......Page 694
Imaging......Page 695
Decision-Making Principals......Page 697
Treatment Options......Page 698
Results......Page 700
Summary:......Page 701
Summary:......Page 702
References......Page 703
Adaptations to the Throwing Shoulder......Page 705
Keywords......Page 706
Biomechanics of Throwing......Page 707
Dynamic Shoulder and Scapular Stability......Page 708
Physical Examination......Page 709
Imaging......Page 710
Decision-Making Principles......Page 711
Superior Labral From Anterior to Posterior Tears......Page 712
Posterior Capsular Contracture and Glenohumeral Internal Rotation Deficit......Page 713
Results......Page 716
Rotator Cuff Débridement......Page 717
Rotator Cuff Repair......Page 718
Summary and Future Considerations......Page 719
Summary:......Page 720
References......Page 721
Physical Examination......Page 724
Keywords......Page 725
Imaging......Page 727
Decision-Making Principles......Page 728
Indications......Page 729
Diagnostic Arthroscopy and Biceps Tenotomy......Page 730
Other Techniques......Page 731
Biceps Tenodesis Rehabilitation Protocol......Page 733
Phase II: Moderate Protection Phase (Weeks 7 to 12)......Page 734
Summary:......Page 737
Summary:......Page 738
References......Page 739
Anatomy......Page 742
Keywords......Page 743
Static Stabilizers......Page 745
Physical Examination......Page 746
Impingement Test......Page 749
Decision-Making Principles......Page 750
Preventive Treatment......Page 751
Stretching, strengthening, and conditioning.......Page 752
Subacromial decompression and rotator cuff repair.......Page 753
Arthroscopic techniques.......Page 756
Level of Evidence:......Page 757
Summary:......Page 758
References......Page 759
Anatomy......Page 765
Keywords......Page 766
Mechanism of Injury......Page 767
History and Physical Exam......Page 768
Decision-Making Principles......Page 769
Treatment Options......Page 770
Postoperative Rehab......Page 772
Results......Page 774
Future Considerations......Page 775
Selected Readings......Page 776
References......Page 777
Technical Factors......Page 779
Keywords......Page 780
Decision-Making Principles......Page 781
Revision Repair......Page 782
Results and Complications......Page 784
Future Considerations......Page 786
References......Page 787
Classification......Page 790
Keywords......Page 791
Treatment......Page 792
Treatment......Page 793
Selected Readings......Page 795
References......Page 796
Pain......Page 798
Keywords......Page 799
Exacerbating and Relieving Factors......Page 800
Primary/Idiopathic Adhesive Capsulitis......Page 801
Secondary/Acquired Causes of Shoulder Stiffness......Page 802
Palpation......Page 803
Imaging......Page 804
Treatment Options......Page 805
Postoperative Managment......Page 806
Complications......Page 809
Summary:......Page 810
Summary:......Page 811
References......Page 812
Instability Arthropathy......Page 814
Keywords......Page 815
Chondrolysis......Page 816
Rheumatoid Arthritis......Page 817
Physical Examination......Page 818
Treatment Options......Page 819
Nonoperative Treatment......Page 820
Microfracture.......Page 821
Humeral head resurfacing, biologic resurfacing, and osteochondral grafting.......Page 822
Glenohumeral arthroplasty.......Page 824
Arthroplasty for instability arthropathy.......Page 825
Decision-Making Principles......Page 826
Rehabilitation After Arthroplasty......Page 828
Complications......Page 829
Level of Evidence:......Page 830
Summary:......Page 831
References......Page 832
History......Page 837
Keywords......Page 838
Inspection......Page 840
Palpation......Page 841
Wall Push-Up......Page 842
Pain and/or Crepitus......Page 843
Nonoperative......Page 844
Open technique.......Page 845
Results......Page 848
Recommended Viewing......Page 849
References......Page 850
Anatomy and Biomechanics......Page 851
Keywords......Page 852
Clinical Evaluation......Page 853
Diagnostic Studies......Page 854
Nonoperative......Page 855
Clinical Evaluation......Page 856
Anatomy and Biomechanics......Page 858
Clinical Evaluation......Page 859
Clinical Evaluation......Page 860
Level of Evidence:......Page 861
Summary:......Page 862
References......Page 863
Classification......Page 866
Keywords......Page 867
Anatomy......Page 869
Physical Examination......Page 871
Imaging......Page 873
Decision-Making Principles......Page 874
Treatment Options......Page 875
Results......Page 876
Postoperative Management......Page 877
Summary:......Page 878
Summary:......Page 879
References......Page 880
56 Injury to the Acromioclavicular and Sternoclavicular Joints......Page 883
Keywords......Page 884
History......Page 886
Physical Examination......Page 887
Imaging......Page 890
Decision-Making Principles......Page 892
Treatment Options......Page 894
Postoperative Management/Return to Play......Page 902
Physical Examination......Page 903
Imaging......Page 906
Decision-Making Principles......Page 907
Dislocations (Type III Injuries)......Page 912
Medial Clavicle Excision......Page 914
Level of Evidence:......Page 916
Summary:......Page 917
References......Page 918
Capsuloligamentous Restraints......Page 922
Keywords......Page 923
Pronation-Supination......Page 924
Radial head.......Page 926
Muscular contributions and joint reactive forces.......Page 927
Level of Evidence:......Page 928
Summary:......Page 929
References......Page 930
Lateral Elbow......Page 932
Keywords......Page 933
Posterior Elbow......Page 934
Medial Elbow......Page 935
Neurologic Assessment......Page 936
Ulnar Nerve Compression (Cubital Tunnel Syndrome)......Page 937
Radial Tunnel Syndrome......Page 938
Pronator Syndrome......Page 939
Medial (Ulnar) Collateral Ligament......Page 940
Citation:......Page 941
Summary:......Page 942
References......Page 943
Computed Tomography......Page 944
Keywords......Page 945
Magnetic Resonance Imaging......Page 946
Occult Fracture......Page 947
Collateral Ligament Injury......Page 948
Ulnar Collateral Ligament Injury......Page 949
Lateral and Medial Epicondylitis......Page 950
Distal Biceps Tendon......Page 951
Acknowledgment......Page 952
Level of Evidence:......Page 953
Summary:......Page 954
References......Page 955
Decision-Making Principles and Treatment Options......Page 957
Keywords......Page 958
Fluid Management and Instrumentation......Page 959
Standard Anteromedial Portal......Page 960
Proximal Anteromedial Portal......Page 961
Accessory Portals......Page 962
Order of Portal Placement......Page 963
Summary:......Page 969
Summary:......Page 970
References......Page 971
Physical Examination......Page 973
Keywords......Page 974
Imaging......Page 975
Therapy......Page 976
Surgical Treatment......Page 977
Surgical Treatment of Medial Epicondylitis......Page 978
Decision-Making Principles......Page 979
Operative......Page 980
Future Considerations......Page 981
Decision-Making Principles......Page 982
Treatment Options......Page 983
Summary:......Page 984
References......Page 985
Biomechanics......Page 988
Keywords......Page 989
History......Page 990
Imaging......Page 991
Treatment Options......Page 992
Results......Page 993
Complications......Page 994
Classification......Page 995
Nonoperative Treatment......Page 996
Operative Treatment......Page 997
Future Considerations......Page 998
Summary:......Page 999
References......Page 1000
Electrophysiologic Testing......Page 1002
Median Nerve......Page 1003
Postoperative Management and Return to Play......Page 1005
Treatment Options......Page 1006
Cubital Tunnel Syndrome......Page 1007
In Situ Decompression (Fig. 63.4)......Page 1009
Anterior Nerve Transposition: Submuscular (Fig. 63.7)......Page 1010
Preferred Technique......Page 1011
Radial Tunnel Syndrome......Page 1012
Preferred Technique......Page 1014
Results......Page 1015
Summary:......Page 1016
References......Page 1017
History......Page 1021
Keywords......Page 1022
Physical Examination......Page 1023
Decision-Making Principles......Page 1025
Tendinopathy......Page 1026
Ulnar Collateral Ligament Injuries......Page 1027
Valgus Extension Overload and Loose Bodies......Page 1028
Olecranon Stress Fracture......Page 1029
Ulnar Neuritis......Page 1030
Ulnar Collateral Ligament Injury......Page 1033
Future Considerations......Page 1035
Summary:......Page 1036
References......Page 1037
Assessing Impairment......Page 1040
Keywords......Page 1041
Physical Examination......Page 1042
Decision-Making Principles and Treatment Options......Page 1043
Anesthesia and Positioning......Page 1045
Anteromedial portal.......Page 1046
Anterolateral portal.......Page 1047
Anterior release.......Page 1048
Posterior release.......Page 1049
Open Release......Page 1050
Complications......Page 1051
Citation:......Page 1052
Summary:......Page 1053
References......Page 1054
Muscles and Tendons......Page 1055
Keywords......Page 1056
Metacarpophalangeal Joint of the Fingers......Page 1058
Proximal Interphalangeal Joint......Page 1059
Wrist Anatomy and Biomechanics......Page 1060
Extensor Tendons of the Wrist and Hand......Page 1061
Vascular Anatomy......Page 1062
Summary:......Page 1063
References......Page 1064
History and Physical Exam......Page 1065
Keywords......Page 1066
Radial Quadrant......Page 1067
Dorsal Quadrant......Page 1069
Ulnar Quadrant......Page 1071
Volar Quadrant......Page 1073
Distal Interphalangeal Joint......Page 1074
Proximal Interphalangeal Joint......Page 1075
Metacarpophalangeal Joint......Page 1076
Summary......Page 1077
Summary:......Page 1078
References......Page 1079
Distal Radius Fractures......Page 1081
Scaphoid Fracture......Page 1082
Trapezium Fracture......Page 1083
Perilunate Dislocation......Page 1084
Intrinsic Carpal Ligament Injury......Page 1085
Tendon Injuries......Page 1087
Triangular Fibrocartilage Complex Injury......Page 1088
Metacarpal Fracture......Page 1089
Level of Evidence:......Page 1090
Summary:......Page 1091
References......Page 1092
Portal Placement......Page 1094
Keywords......Page 1095
Arthroscopic Anatomy......Page 1097
Distal Radioulnar Joint Arthroscopy......Page 1098
Carpal Instability......Page 1099
Arthroscopic Reduction of Selected Scaphoid Nonunions......Page 1102
Transscaphoid Perilunate Fracture-Dislocations......Page 1103
Fractures of the Distal Radius......Page 1104
Operative Technique......Page 1105
Clinical Features......Page 1106
Arthroscopic Management of Traumatic Class I Injuries......Page 1107
Kienböck Disease......Page 1110
Summary:......Page 1111
Summary:......Page 1112
References......Page 1113
History......Page 1115
Keywords......Page 1116
Physical Exam......Page 1117
Decision-Making Principles......Page 1118
Physical Exam......Page 1119
Postoperative Management......Page 1120
Physical Exam......Page 1121
Postoperative Management......Page 1122
Imaging......Page 1124
Postoperative Management......Page 1125
Physical Exam......Page 1126
Results......Page 1127
Postoperative Management......Page 1128
Imaging......Page 1129
Treatment Options......Page 1130
Imaging......Page 1132
Treatment Options......Page 1133
Results......Page 1134
Future Considerations......Page 1135
Summary:......Page 1136
Summary:......Page 1137
References......Page 1138
History......Page 1142
Keywords......Page 1143
Imaging......Page 1144
Treatment Options......Page 1145
Treatment Options......Page 1146
Criteria for Return to Sports......Page 1147
Flexor Carpi Ulnaris Tendinopathy......Page 1148
Future Considerations......Page 1149
Summary:......Page 1150
References......Page 1151
Anatomy......Page 1152
Keywords......Page 1153
Class II Tears (Degenerative)......Page 1154
Physical Examination......Page 1155
Treatment......Page 1156
Complications......Page 1158
Citation:......Page 1159
Summary:......Page 1160
References......Page 1161
Mallet Finger......Page 1162
Keywords......Page 1163
Closed Boutonnière (Central Slip Rupture)......Page 1165
Sagittal Band Rupture......Page 1167
Jersey Finger......Page 1168
Pulley Injury......Page 1170
Tendon Injury Complications......Page 1171
Level of Evidence:......Page 1172
References......Page 1173
Metacarpophalangeal Joint......Page 1176
Keywords......Page 1177
Proximal Interphalangeal Joint......Page 1179
Distal Interphalangeal Joint or Thumb Interphalangeal Joint......Page 1182
Phalangeal Fractures......Page 1184
Metacarpophalangeal Dislocation......Page 1186
Collateral Ligament Injuries of the Metacarpophalangeal Joint......Page 1188
Citation:......Page 1190
Level of Evidence:......Page 1191
References......Page 1192
Physical Examination......Page 1194
Keywords......Page 1195
Imaging......Page 1197
Treatment Options......Page 1198
Postoperative Management and Return to Play......Page 1199
Results......Page 1200
Summary:......Page 1201
Summary:......Page 1202
References......Page 1203
Acetabular Version......Page 1205
Keywords......Page 1206
Proximal Femoral Development......Page 1207
Femoral Head-Neck Junction......Page 1208
Greater Trochanter......Page 1209
Blood Supply......Page 1210
Blood Supply......Page 1211
Articular Cartilage......Page 1212
Capsular Innervation......Page 1213
Muscles Around the Hip Joint......Page 1215
Iliopsoas......Page 1216
Hamstrings......Page 1218
Trochanteric Bursae......Page 1219
Gait Cycle......Page 1220
In Vitro Studies......Page 1221
Hip-Spine Relationship......Page 1222
Summary:......Page 1223
References......Page 1224
Bone Injuries......Page 1228
Keywords......Page 1229
Degenerative Joint Disease......Page 1230
Intra-Articular Pathology......Page 1231
History......Page 1232
Symptom Localization......Page 1233
Measurements and Range of Motion......Page 1234
Supine......Page 1236
Summary:......Page 1237
Summary:......Page 1238
References......Page 1239
Frog-Leg Lateral View......Page 1241
Keywords......Page 1242
Neck Shaft Angle......Page 1243
Anterior Center Edge Angles......Page 1244
Computed Tomography Evaluation of the Hip......Page 1245
Labral Variant......Page 1246
Labrum Tear......Page 1248
Stress Injuries......Page 1249
Summary:......Page 1253
References......Page 1254
Contraindications......Page 1256
Keywords......Page 1257
Traction......Page 1258
Preparation and Draping......Page 1259
Anterolateral......Page 1260
Posterolateral......Page 1261
Central Compartment......Page 1262
Peripheral Compartment......Page 1264
Citation:......Page 1265
Summary:......Page 1266
References......Page 1267
80 Femoroacetabular Impingement in Athletes......Page 1270
Keywords......Page 1271
Clinical Presentation......Page 1272
Physical Examination......Page 1273
Plain Radiographs......Page 1274
Magnetic Resonance Imaging......Page 1277
Ultrasonography......Page 1278
Hip Arthroscopy......Page 1279
Rehabilitation......Page 1281
Summary:......Page 1283
Summary:......Page 1284
References......Page 1285
Hip Dysplasia......Page 1288
Keywords......Page 1289
Physical Examination......Page 1291
Imaging......Page 1292
Hip Dysplasia......Page 1293
Atraumatic Hip Microinstability......Page 1295
References......Page 1297
Iliopsoas Anatomy and Function......Page 1299
Keywords......Page 1300
Iliopsoas Impingement......Page 1301
Iliopsoas Snapping......Page 1303
Imaging......Page 1304
Iliopsoas Snapping......Page 1305
Iliopsoas Impingement......Page 1307
Complications......Page 1308
Citation:......Page 1309
Summary:......Page 1310
References......Page 1311
Treatment Options......Page 1313
Keywords......Page 1314
Results......Page 1319
Imaging......Page 1320
Complications......Page 1321
Treatment Options......Page 1323
Future Considerations......Page 1324
History......Page 1325
Physical Examination......Page 1326
History......Page 1327
Treatment Options......Page 1328
Summary:......Page 1330
References......Page 1331
Anatomy......Page 1334
Keywords......Page 1335
Historical Background......Page 1336
Diagnostic Injections......Page 1337
Dynamic Ultrasonography......Page 1338
Operative Management......Page 1339
Operative Management......Page 1340
Nonoperative Management......Page 1342
Operative Treatment......Page 1343
Summary:......Page 1344
Summary:......Page 1345
References......Page 1346
Sciatic Nerve Characteristics......Page 1348
Keywords......Page 1349
Anatomy......Page 1351
Etiology......Page 1352
Physical Examination......Page 1355
Endoscopic Decompression......Page 1358
Pudendal Nerve Entrapment......Page 1361
Superior and Inferior Gluteal Nerves......Page 1363
Conclusion......Page 1364
References......Page 1365
History......Page 1368
Keywords......Page 1369
Physical Examination......Page 1370
Imaging......Page 1371
Endoscopic......Page 1372
Rehabilitation......Page 1374
Results......Page 1375
Complications......Page 1376
Summary:......Page 1377
References......Page 1378
Treatment Options......Page 1380
Keywords......Page 1381
History......Page 1382
Operative treatment.......Page 1383
Myositis Ossificans......Page 1384
Quadriceps Strains......Page 1385
Treatment Options......Page 1386
Complications......Page 1387
Nonoperative.......Page 1388
Future Considerations......Page 1389
Summary:......Page 1390
References......Page 1391
Physical Exam......Page 1393
Keywords......Page 1394
Imaging......Page 1396
Nonsurgical Measures......Page 1398
Hip Resurfacing......Page 1399
Results......Page 1400
Future Directions......Page 1401
References......Page 1402
Superficial Anatomy......Page 1404
Keywords......Page 1405
Osseous Anatomy......Page 1406
Femur......Page 1407
Muscular Anatomy......Page 1408
Posterior......Page 1409
Medial......Page 1410
Medial Meniscus......Page 1411
Medial Collateral Ligament......Page 1412
Anterolateral Ligament......Page 1413
Joint Capsule and Synovial Membrane......Page 1414
Biomechanics of the Knee......Page 1415
Description of Biomechanical Techniques......Page 1416
Force Measurement of Ligaments......Page 1417
Ligament Biomechanics......Page 1418
Function of the Cruciate Ligaments in Controlling Joint Biomechanics......Page 1420
Medial and Lateral Collateral Ligaments and Their Function in Controlling Joint Biomechanics......Page 1422
Function of the Meniscus in Load Transmission......Page 1423
Function of the Meniscus in Joint Stability......Page 1424
Patellofemoral Contact Area......Page 1425
Patellofemoral Force Transmission......Page 1427
Citation:......Page 1430
Summary:......Page 1431
References......Page 1432
History......Page 1438
Keywords......Page 1439
Inspection......Page 1441
Palpation......Page 1442
Range of Motion and Strength Testing......Page 1444
Patella......Page 1445
Meniscus......Page 1446
Ligamentous Stability......Page 1447
Synthesis and Decision-Making......Page 1451
Conclusion......Page 1452
Summary:......Page 1453
References......Page 1454
Imaging......Page 1456
Keywords......Page 1457
Magnetic Resonance Imaging......Page 1458
Menisci......Page 1459
Pitfalls......Page 1462
Ligaments......Page 1463
Extensor Mechanism......Page 1466
Osseous Structures and Cartilage......Page 1469
Postoperative Imaging......Page 1471
Summary:......Page 1473
References......Page 1474
Portal Placement......Page 1475
Keywords......Page 1476
Diagnostic Arthroscopy......Page 1478
Complications......Page 1480
Summary:......Page 1481
References......Page 1482
Imaging......Page 1483
Keywords......Page 1484
Treatment Options......Page 1485
Posterior Compartments......Page 1486
Future Directions......Page 1487
Summary:......Page 1488
References......Page 1489
Meniscus Anatomy and Structure......Page 1490
Keywords......Page 1491
Meniscus Biomechanics and Function......Page 1493
Epidemiology......Page 1494
Meniscal Injury: Classification......Page 1495
Physical Examination......Page 1496
Imaging......Page 1497
Surgical Indications......Page 1498
Discoid meniscus and meniscal variants.......Page 1499
Decision-Making Principles......Page 1501
Meniscectomy......Page 1502
Meniscal Repair: Inside-Out......Page 1503
Meniscal Repair: Outside-In......Page 1505
Trephination......Page 1506
Platelet Rich Plasma......Page 1507
Meniscal Scaffolds......Page 1508
Postoperative Management......Page 1509
Complications......Page 1510
Level of Evidence:......Page 1511
Summary:......Page 1512
References......Page 1513
Physical Examination......Page 1519
Keywords......Page 1520
Pathophysiology......Page 1521
Operative Management......Page 1522
Medial......Page 1523
Single Bone Plug and Trough......Page 1524
Complications......Page 1525
Conclusion/Future Considerations......Page 1526
References......Page 1527
Relevant Anatomy and Biomechanics......Page 1528
Keywords......Page 1529
History......Page 1530
Contraindications......Page 1531
Marrow Stimulation......Page 1532
Particulated Juvenile Cartilage Allograft......Page 1533
Postoperative Management......Page 1534
Return to Play......Page 1535
Marrow Stimulation......Page 1542
Autologous Chondrocyte Implantation......Page 1543
Future Considerations......Page 1544
Conclusion......Page 1545
References......Page 1546
Surgical Management......Page 1550
Keywords......Page 1551
Reparative......Page 1552
Mesenchymal Stem Cells With Three-Dimensional Matrices......Page 1554
Off-the-Shelf Surface Allograft Transplantation......Page 1555
Summary:......Page 1557
References......Page 1558
Anatomy and Biomechanics......Page 1560
Keywords......Page 1561
Microanatomy......Page 1562
Ligamentous Laxity......Page 1563
Age......Page 1564
Revision Anterior Cruciate Ligament......Page 1565
Graft Selection......Page 1566
Graft Tension and Fixation......Page 1567
Rehabilitation......Page 1568
Muscle Training (Open and Closed Kinetic Chain)......Page 1571
Functional Training......Page 1572
Complications......Page 1573
Summary:......Page 1574
References......Page 1575
History......Page 1582
Keywords......Page 1583
Radiographic Tunnel Positioning......Page 1584
Causes of Failure of Anterior Cruciate Ligament Reconstruction......Page 1586
Articular Cartilage Injury......Page 1587
Tunnel Grafting......Page 1588
Femoral Tunnel......Page 1589
Double-Bundle Reconstruction in Revision Setting......Page 1590
Principles of Rehabilitation......Page 1591
Phase 3: Neuromuscular Conditioning (6 Weeks to 8 Months)......Page 1592
Summary:......Page 1593
Summary:......Page 1594
References......Page 1595
History......Page 1600
Keywords......Page 1601
Posterior Sag Test (Godfrey Test) and Quadriceps Active Test......Page 1602
Collateral Ligament Assessment......Page 1603
Decision-Making......Page 1604
Nonoperative Treatment......Page 1605
Operative Treatment......Page 1606
Transtibial Tunnel Versus Tibial Inlay Techniques......Page 1607
Single-Bundle Versus Double-Bundle Reconstruction......Page 1608
High Tibial Osteotomy for Chronic PCL Injuries......Page 1609
Isolated Posterior Cruciate Ligament Injuries......Page 1614
Single Versus Double Bundle......Page 1615
Summary:......Page 1619
Summary:......Page 1620
References......Page 1621
Physical Exam......Page 1625
Keywords......Page 1626
Imaging......Page 1627
Decision-Making Principles......Page 1629
Treatment Options......Page 1630
Postoperative Management......Page 1634
Results......Page 1635
Complications......Page 1637
Summary:......Page 1638
References......Page 1639
Fibular Collateral Ligament......Page 1642
Keywords......Page 1643
Long head.......Page 1644
Role of Posterolateral Corner Structures to Varus Motion......Page 1645
Role of the Posterolateral Corner Structures in Preventing Anterior/Posterior Tibial Translation......Page 1646
History......Page 1647
Physical Examination......Page 1648
Magnetic Resonance Imaging......Page 1650
Nonoperative Management......Page 1652
Biceps tenodesis.......Page 1653
Isolated structure reconstruction.......Page 1654
Postoperative Management......Page 1655
Complications......Page 1659
Summary:......Page 1661
Summary:......Page 1662
References......Page 1663
Physical Examination......Page 1667
Keywords......Page 1668
Imaging......Page 1669
Surgical Timing......Page 1670
Anterior Cruciate Ligament......Page 1671
Medial/Posteromedial Structures......Page 1672
Lateral/Posterolateral Structures......Page 1673
Postoperative Management......Page 1677
Future Considerations......Page 1678
Summary:......Page 1680
References......Page 1681
Imaging......Page 1684
Keywords......Page 1685
Braces......Page 1687
Arthroscopy......Page 1688
Other techniques.......Page 1689
Combined instability and pain.......Page 1690
Medial Compartment Osteoarthritis......Page 1691
Chronic Anterior Cruciate Ligamentous Insufficiency......Page 1692
Complications......Page 1697
Summary......Page 1698
Summary:......Page 1699
Summary:......Page 1700
References......Page 1701
History......Page 1705
Keywords......Page 1706
Pertinent Soft Tissue Anatomy......Page 1707
Acute Patellar Instability Episode......Page 1708
Supine Examination: Muscle Balance and Special Tests......Page 1709
Radiographs......Page 1710
Magnetic Resonance Imaging......Page 1711
Acute Patellar Instability Episode......Page 1712
Procedures for bone realignment.......Page 1713
Postoperative Management......Page 1717
Summary:......Page 1719
Summary:......Page 1720
References......Page 1721
Anatomy......Page 1726
Keywords......Page 1727
History......Page 1728
Inspection......Page 1729
Range of Motion and Strength......Page 1730
Provocative Tests......Page 1731
Diagnostic Studies......Page 1732
Idiopathic Anterior Knee Pain/Patellofemoral Pain Syndrome......Page 1733
Synovial Impingement Syndromes......Page 1734
Complex Regional Pain Syndrome......Page 1735
Summary:......Page 1736
References......Page 1737
Anatomy......Page 1741
Keywords......Page 1742
Biomechanics......Page 1743
Patellar and Quadriceps Tendinopathy......Page 1744
Patellar and Quadriceps Tendon Ruptures......Page 1745
Patellar and Quadriceps Tendinopathy......Page 1746
Patellar and Quadriceps Tendinopathy......Page 1747
Patellar and Quadriceps Tendinopathy......Page 1748
Patellar and Quadriceps Tendon Ruptures......Page 1749
Patellar Fractures......Page 1750
Nonoperative Treatment of Patellar Fractures......Page 1751
Operative Treatment of Tendon Ruptures......Page 1752
Operative Treatment of Patellar Fractures......Page 1753
Patellar and Quadriceps Tendon Ruptures......Page 1754
Patellar and Quadriceps Tendinopathy......Page 1755
Patellar Fractures......Page 1756
Level of Evidence:......Page 1757
Summary:......Page 1758
References......Page 1759
History......Page 1764
Keywords......Page 1765
Imaging......Page 1766
Decision-Making Principles......Page 1767
Treatment Options......Page 1768
Postoperative Management......Page 1770
Complications......Page 1772
Summary:......Page 1773
Summary:......Page 1774
References......Page 1775
Posterior Dislocation of the Knee......Page 1776
Keywords......Page 1777
Clinical Presentation......Page 1778
Physical Examination and Testing......Page 1779
Treatment Options......Page 1780
Popliteal Artery Entrapment Syndrome......Page 1781
Classification......Page 1782
Physical Examination and Testing......Page 1783
Magnetic Resonance Imaging and Magnetic Resonance Angiography......Page 1784
Angiography......Page 1785
Treatment Options......Page 1786
Summary:......Page 1788
Summary:......Page 1789
References......Page 1790
Kinetics of Gait......Page 1792
Keywords......Page 1793
Kinematics and Biomechanics of the Ankle Joint......Page 1794
Kinematics and Biomechanics of the Subtalar Joint......Page 1797
Windlass Mechanism, Metatarsal Break, and First Metatarsophalangeal Joint......Page 1799
Summary......Page 1801
Summary:......Page 1802
Summary:......Page 1803
References......Page 1804
Overview of Pathologies......Page 1806
Keywords......Page 1807
History......Page 1808
Physical Examination......Page 1809
Magnetic Resonance Imaging......Page 1817
Keywords......Page 1818
Achilles Tendon......Page 1819
Indirect Magnetic Resonance Imaging Signs of Disease......Page 1820
Indirect magnetic resonance imaging signs.......Page 1821
Indirect magnetic resonance imaging signs.......Page 1822
Indirect magnetic resonance imaging signs.......Page 1823
Pitfalls......Page 1824
Direct Magnetic Resonance Imaging Signs......Page 1825
Normal Appearance......Page 1826
Direct Magnetic Resonance Imaging Signs......Page 1827
Normal Appearance......Page 1828
Summary:......Page 1829
Summary:......Page 1830
References......Page 1831
Anatomy......Page 1832
Keywords......Page 1833
Classification......Page 1834
Diagnostics/Imaging......Page 1835
Decision-Making Principles......Page 1836
Compartment Testing......Page 1837
Postoperative Care......Page 1838
Summary Points......Page 1840
Summary:......Page 1841
References......Page 1842
Physical Examination......Page 1845
Keywords......Page 1846
Imaging......Page 1847
Surgical Treatment......Page 1848
Physical Examination......Page 1849
Results......Page 1850
Etiologies......Page 1851
Conservative Treatment......Page 1852
Surgical Treatment......Page 1853
Results......Page 1854
Conservative Treatment......Page 1855
Physical Examination......Page 1856
Physical Examination......Page 1857
Conservative Treatment......Page 1858
Physical Examination......Page 1859
Introduction......Page 1860
Imaging......Page 1861
Complications......Page 1862
Summary:......Page 1863
Summary:......Page 1864
References......Page 1865
Soft Tissue Conditions Amenable to Arthroscopy......Page 1869
Keywords......Page 1870
Imaging......Page 1872
Distraction......Page 1873
Tourniquet......Page 1874
Arthroscopic Examination......Page 1875
Results......Page 1876
Subtalar Arthroscopy......Page 1877
Decision-Making Principles......Page 1878
Results......Page 1880
Complications......Page 1881
Decision-Making Principles......Page 1882
Results......Page 1883
Summary:......Page 1884
References......Page 1885
Research......Page 1888
Keywords......Page 1889
Clinical Applications......Page 1890
Sports Shoes......Page 1892
Midsole......Page 1893
Upper......Page 1894
Selection and Fitting of Sports Shoes......Page 1895
Summary:......Page 1896
References......Page 1897
History and Physical Examination......Page 1899
Keywords......Page 1900
Imaging......Page 1902
Conservative......Page 1903
Surgical Treatment......Page 1904
History and Physical Examination......Page 1906
Decision-Making Principles......Page 1907
Complications......Page 1908
History and Examination......Page 1909
Treatment......Page 1910
Bifurcate Ligament Sprain/Fracture of the Anterior Process of Calcaneum......Page 1912
Results......Page 1913
Imaging......Page 1914
Postoperative Management......Page 1915
Complications......Page 1916
Summary:......Page 1917
References......Page 1918
Treatment Options......Page 1922
Keywords......Page 1923
Results......Page 1924
Posterior Tibial Tendon......Page 1925
Imaging......Page 1926
Treatment Options......Page 1927
Results......Page 1929
Imaging......Page 1930
Treatment Options......Page 1931
Complications......Page 1932
Physical Examination......Page 1933
Decision-Making Principles......Page 1934
Treatment Options......Page 1935
Results......Page 1936
History......Page 1937
Imaging......Page 1938
Decision-Making Principles......Page 1939
Treatment Options......Page 1940
Postoperative Management......Page 1941
Results......Page 1942
Summary:......Page 1943
Summary:......Page 1944
References......Page 1945
Imaging and Diagnosis......Page 1950
Keywords......Page 1951
Nonoperative......Page 1953
Lavage, débridement, and excision and bone marrow stimulation (curettage, drilling, and microfracture).......Page 1954
Osteochondral autograft and allograft.......Page 1955
Newer orthobiologic or synthetic therapies.......Page 1956
Conservative or Nonoperative Management......Page 1957
Osteochondral autografts (osteochondral autologous transplantation system, mosaicplasty).......Page 1958
Autologous chondrocyte implantation or transplantation.......Page 1959
Newer Orthobiologics, Adjuncts, and Future Considerations......Page 1960
Osteochondral Lesions of the Distal Tibial Plafond......Page 1967
Complications......Page 1968
Summary:......Page 1969
Summary:......Page 1970
References......Page 1971
Imaging......Page 1975
Keywords......Page 1976
Decision-Making Principles......Page 1977
Nonoperative Therapy......Page 1978
Operative Therapy......Page 1979
Future Considerations......Page 1980
Imaging......Page 1981
Nonoperative Therapy......Page 1982
Results......Page 1983
Citation:......Page 1985
Summary:......Page 1986
References......Page 1987
Decision-Making Principles......Page 1989
Keywords......Page 1990
Sesamoid Dysfunction......Page 1991
Nonoperative......Page 1992
Postoperative Management......Page 1993
Physical Examination......Page 1994
Nonoperative......Page 1995
Postoperative Management......Page 1996
Future Considerations......Page 1997
Decision-Making Principles......Page 1998
Osteotomy.......Page 1999
Results......Page 2000
Summary:......Page 2001
References......Page 2002
Brain......Page 2005
Keywords......Page 2006
Head Injuries......Page 2007
Concussion......Page 2008
Spine......Page 2009
Neurologic Tissues......Page 2012
Normal/Physiologic Biomechanics......Page 2013
Integration of Biomechanical Considerations for Treatment......Page 2014
Summary:......Page 2015
References......Page 2016
Pathophysiology......Page 2018
Keywords......Page 2019
Imaging......Page 2020
Postconcussion Syndrome......Page 2021
Imaging......Page 2022
Treatment Options......Page 2023
Summary:......Page 2024
References......Page 2025
Radiographs......Page 2027
Keywords......Page 2028
EOS 2D/3D X-Ray Imaging System......Page 2029
Computed Tomography......Page 2030
Magnetic Resonance Imaging......Page 2031
Nuclear Scintigraphy......Page 2032
Single Photon Emission Computed Tomography......Page 2033
Imaging of the Degenerative Spine......Page 2034
Future Considerations......Page 2035
Summary:......Page 2036
References......Page 2037
Pre-Event Planning......Page 2039
Keywords......Page 2040
Approaching the Injured Athlete on the Field......Page 2041
Preparing for Transport......Page 2043
Emergency Department Evaluation......Page 2045
Common Acute Spinal Injuries......Page 2046
Conclusion......Page 2047
Summary:......Page 2048
References......Page 2049
Definition of Concussion......Page 2051
Keywords......Page 2052
Clinical Presentation......Page 2053
Baseline (Preseason) Assessment......Page 2054
Sideline Assessment......Page 2055
Management......Page 2056
Interventions......Page 2057
Summary:......Page 2058
Summary:......Page 2059
References......Page 2060
Physical Examination......Page 2063
Keywords......Page 2064
Imaging......Page 2065
Classification and Decision-Making Principles......Page 2067
Treatment Options......Page 2068
Level of Evidence:......Page 2070
Summary:......Page 2071
References......Page 2072
Imaging......Page 2074
Keywords......Page 2075
Decision-Making Principles of Diagnosis and Treatment......Page 2076
Return to Play......Page 2077
Conclusions......Page 2078
References......Page 2079
Physical Examination......Page 2081
Keywords......Page 2082
Compression Fractures......Page 2083
Stress Fractures......Page 2084
Strains, Sprains, and Contusions......Page 2085
Spondylolisthesis......Page 2088
Posterior Element Overuse Syndrome......Page 2090
Fractures......Page 2091
Summary:......Page 2092
References......Page 2093
Facets......Page 2095
Keywords......Page 2096
Discogenic Pain......Page 2097
Central Stenosis and Cervical Myelopathy......Page 2098
Rheumatoid Cervical Spondylitis......Page 2099
Degenerative Thoracic Spine......Page 2100
Discogenic Low Back Pain......Page 2101
Lumbar Disc Herniation and Radiculopathy......Page 2102
Synovial Facet Cysts......Page 2104
Degenerative Lumbar Spinal Stenosis......Page 2105
Degenerative Spondylolisthesis......Page 2106
References......Page 2108
Pediatric Sports Injury......Page 2110
Keywords......Page 2111
Endurance Training......Page 2112
Strength Training......Page 2113
Readiness for Sport......Page 2114
Nutrition......Page 2115
Regulation of Performance-Enhancing Substances......Page 2116
Arthroscopy in Children......Page 2117
Conclusions......Page 2119
References......Page 2121
Development......Page 2124
Keywords......Page 2125
Acute Injuries......Page 2126
Overuse Injuries......Page 2127
Overuse Injuries......Page 2128
Little Leaguer Elbow......Page 2130
Acute Injuries......Page 2132
Overuse Injuries......Page 2133
Acute Injuries......Page 2134
Overuse Injuries......Page 2135
Acute Injuries......Page 2137
Overuse Injuries......Page 2139
Overuse Injuries......Page 2142
Spine......Page 2144
Miscellaneous......Page 2145
References......Page 2146
Midshaft Clavicle Fractures......Page 2147
Keywords......Page 2148
Nonoperative treatment.......Page 2149
Complications......Page 2150
Physical Examination......Page 2151
Operative treatment.......Page 2152
Medial Clavicle Physeal Fractures......Page 2153
Treatment Options......Page 2154
Imaging......Page 2155
Treatment......Page 2156
Operative Treatment......Page 2157
Glenohumeral Instability......Page 2158
Imaging......Page 2159
Nonoperative Treatment......Page 2160
History......Page 2162
Imaging......Page 2163
Operative Treatment......Page 2164
Physical Examination......Page 2165
Proximal Humerus Epiphysiolysis (Little League Shoulder)......Page 2166
Physical Examination......Page 2167
Nonoperative treatment.......Page 2168
Nonoperative treatment.......Page 2169
Level of Evidence:......Page 2170
Summary:......Page 2171
References......Page 2172
Ligaments and Soft Tissue......Page 2177
Keywords......Page 2178
Throwing Motion......Page 2180
Forces around the elbow during throwing.......Page 2181
History......Page 2182
Physical Examination......Page 2183
Treatment Options......Page 2184
Imaging......Page 2185
Treatment......Page 2186
History......Page 2187
Results......Page 2188
Treatment......Page 2189
Posterior Elbow Pathologic Conditions (Posteromedial Impingement and Olecranon Osteochondrosis)......Page 2190
Medial/Lateral Epicondylitis......Page 2191
Results......Page 2192
Summary:......Page 2193
References......Page 2194
Physical Examination......Page 2199
Keywords......Page 2200
Treatment Options......Page 2201
Complications......Page 2203
Physical Examination......Page 2204
Treatment Options......Page 2205
Imaging......Page 2206
Imaging......Page 2207
Complications......Page 2208
Summary:......Page 2209
Summary:......Page 2210
References......Page 2211
Stress Fractures......Page 2213
Dislocation......Page 2215
Muscle Injury......Page 2216
Snapping Hip (Coxa Saltans)......Page 2217
Legg-Calve-Perthes......Page 2218
Conclusion......Page 2219
Level of Evidence:......Page 2220
Summary:......Page 2221
References......Page 2222
Imaging......Page 2227
Keywords......Page 2228
Treatment Algorithm for Anterior Cruciate Ligament Reconstruction Based on Skeletal Maturity......Page 2229
Anterior Cruciate Ligament Reconstruction Techniques......Page 2231
Postoperative Management and Rehabilitation......Page 2232
Complications......Page 2233
Imaging......Page 2234
Postoperative Management......Page 2235
Classification......Page 2236
Treatment Options......Page 2237
Future Considerations......Page 2238
History and Physical Examination......Page 2239
Nonoperative Management......Page 2240
Operative Treatment......Page 2241
Results......Page 2242
History and Physical Examination......Page 2243
Radiographs......Page 2244
Decision-Making Principles......Page 2245
Results......Page 2246
Complications......Page 2247
Osgood-Schlatter Disease......Page 2248
Physeal Fractures in the Area of the Knee......Page 2249
Treatment Options......Page 2250
Complications......Page 2251
Summary:......Page 2252
Summary:......Page 2253
Citation:......Page 2254
Summary:......Page 2255
References......Page 2256
Tarsal Coalition......Page 2263
Keywords......Page 2264
Accessory Navicular......Page 2266
Soft Tissue Injuries......Page 2267
Clinical Evaluation......Page 2268
Salter-Harris Type IV......Page 2269
Prediction of Outcome......Page 2270
Fractures in the Foot......Page 2272
Osteochondral Lesions of the Talus......Page 2273
Osteochondroses in the Foot......Page 2276
Citation:......Page 2278
Citation:......Page 2279
References......Page 2280
Epidemiology......Page 2282
Keywords......Page 2283
Physical Examination......Page 2285
Imaging......Page 2286
Treatment Options......Page 2287
Complications......Page 2288
Level of Evidence:......Page 2289
Summary:......Page 2290
References......Page 2291
General History and Physical Examination for Evaluation of the Pediatric Spine......Page 2293
Keywords......Page 2294
Spondylolysis/Spondylolisthesis......Page 2295
History and Physical Examination......Page 2296
Treatment......Page 2297
History and Physical Examination......Page 2298
Treatment......Page 2299
History and Physical Examination......Page 2300
Scoliosis and Sports Participation......Page 2302
Decision-Making Principles......Page 2303
History and Physical Examination......Page 2304
Treatment......Page 2305
Imaging......Page 2306
Treatment......Page 2307
Summary:......Page 2308
Summary:......Page 2309
References......Page 2310

Citation preview

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DeLee, Drez, & Miller’s

Orthopaedic Sports Medicine Principles and Practice

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FIFTH EDITION

DeLee, Drez, & Miller’s

Orthopaedic Sports Medicine Principles and Practice

Mark D. Miller, MD S. Ward Casscells Professor of Orthopaedic Surgery Head, Division of Sports Medicine University of Virginia Charlottesville, Virginia Adjunctive Clinical Professor and Team Physician James Madison University Harrisonburg, Virginia

Stephen R. Thompson, MD, MEd, FRCSC Associate Professor of Sports Medicine Eastern Maine Medical Center University of Maine Bangor, Maine

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DELEE, DREZ, & MILLER’S ORTHOPAEDIC SPORTS MEDICINE, FIFTH EDITION

ISBN: 978-0-323-54473-3

Copyright © 2020 by Elsevier, Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2015, 2010, 2003, 1994. International Standard Book Number: 978-0-323-54473-3

Senior Content Strategist: Kristine Jones Senior Content Development Specialist: Joan Ryan Publishing Services Manager: Catherine Jackson Senior Project Manager: Amanda Mincher Design Direction: Ryan Cook Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

1600 John F. Kennedy Blvd. Ste 1600 Philadelphia, PA 19103-2899

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To sports medicine professionals in every discipline and to athletes at every level and every sport. Without them there would be no sports medicine. And to Drs. Jesse DeLee and David Drez. Thank you for entrusting us to keep your vision alive. MARK D. MILLER For Linden Ellis: You are too young to read this now, and you may choose never to read this later, but it is nonetheless still for you. And, for Shannon. As always, thank you for everything you do, including enabling me to do what I do. STEPHEN R. THOMPSON

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SECTION EDITORS Amiethab A. Aiyer, MD Assistant Professor, Chief Foot and Ankle Service Department of Orthopaedics University of Miami, Miller School of Medicine Miami, Florida Leg, Ankle, and Foot Asheesh Bedi, MD Chief, Sports Medicine and Shoulder Surgery Professor of Orthopaedics Head Orthopaedic Team Physician University of Michigan Ann Arbor, Michigan Basic Principles Stephen F. Brockmeier, MD Associate Professor Department of Orthopaedic Surgery Fellowship Director, University of Virginia Sports Medicine Fellowship University of Virginia School of Medicine Charlottesville, Virginia Shoulder Rajwinder Deu, MD Assistant Professor Department of Orthopaedics Johns Hopkins University Baltimore, Maryland Medical F. Winston Gwathmey, Jr., MD Associate Professor of Orthopaedic Surgery University of Virginia School of Medicine Charlottesville, Virginia Pelvis, Hip, and Thigh Joe M. Hart, PhD, ATC Associate Professor Department of Kinesiology University of Virginia Charlottesville, Virginia Rehabilitation and Injury Prevention Anish R. Kadakia, MD Associate Professor of Orthopaedic Surgery Northwestern Memorial Hospital Northwestern University Feinberg School of Medicine Chicago, Illinois Leg, Ankle, and Foot

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Sanjeev Kakar, MD, FAOA Professor of Orthopaedic Surgery Mayo Clinic Rochester, Minnesota Elbow, Wrist, and Hand Morteza Khodaee, MD, MPH, FACSM, FAAFP Associate Professor University of Colorado School of Medicine Department of Family Medicine and Orthopaedics Denver, Colorado Medical Bryson Lesniak, MD Associate Professor University of Pittsburgh Medical Center Rooney Sports Complex Pittsburgh, Pennsylvania Basic Principles Eric C. McCarty, MD Chief, Sports Medicine and Shoulder Surgery Associate Professor Department of Orthopaedics University of Colorado School of Medicine Director Sports Medicine, Head Team Physician University of Colorado Department of Athletics Associate Professor, Adjunct Department of Integrative Physiology University of Colorado Boulder, Colorado Knee Matthew D. Milewski, MD Assistant Professor Division of Sports Medicine Department of Orthopaedic Surgery Boston Children’s Hospital Boston, Massachusetts Pediatric Sports Medicine Francis H. Shen, MD Warren G. Stamp Endowed Professor Division Head, Spine Division Co-Director, Spine Center Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia Spine and Head

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P R E FA C E What’s in a name? In developing and editing the fifth edition of DeLee, Drez, & Miller’s Orthopaedic Sports Medicine: Principles and Practices, we considered removing “orthopaedic” from the title. In an effort to keep pace with the rapidly growing specialty of sports medicine that includes internal medicine, pediatrics, rehabilitation medicine, athletic training, as well as orthopedics and many other disciplines, it is essential to expand the book’s focus beyond orthopedics and address a more all-inclusive vision of sports medicine. Regardless of how sports medicine touches your individual practice, this updated version of this classic textbook remains the most comprehensive in the field. As sports medicine continues to evolve, the need to include additional topics is essential. For this fifth edition, one focus is addressing problems of revision surgery. Important new chapters have been added on revision shoulder instability, revision rotator cuff, and revision anterior cruciate ligament surgery. Additionally, we have fine-tuned the organization of chapters under the dutiful watch of section editors. The hand section has been revised to include more comprehensive chapters on sports-related injuries. The hip section has been updated to reflect the current thinking on the hottest new topics in sports medicine, including new chapters on posterior hip pain and peritrochanteric lesions.

And the non-operative sections have been extensively edited and expanded, to include new information on sports nutrition, psychological adjustment to athletic injury and genitourinary trauma in the athlete. Incredibly, there are over 300 contributors to this new edition, many of whom are widely regarded as the foremost experts in their fields. To each of them, we extend heartfelt gratitude for their willingness to participate and share their knowledge. Similarly, we would be remiss if we did not thank our outstanding section editors: Drs. Bedi, Lesniak, Khodaee, Deu, Hart, Brockmeier, Kakar, Gwathmey, McCarty, Kadakia, Aiyer, Shen, and Milewski. They did the heavy lifting in the publishing process and we are deeply appreciative of their efforts. It remains a distinct honor and pleasure to continue the tradition of Drs. Jesse DeLee and David Drez, who first produced this text in 1994. We hope it enables practitioners to remain on the cutting edge of sports medicine to the benefit of the widest possible spectrum of athletes and patients under our collective care. Mark D. Miller Stephen R. Thompson

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CONTRIBUTORS Kathleen C. Abalos, MD

Christian N. Anderson, MD

Derek P. Axibal, MD

Department of Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts

Orthopaedic Surgeon Tennessee Orthopaedic Alliance/The Lipscomb Clinic Nashville, Tennessee

Department of Orthopedics University of Colorado School of Medicine Aurora, Colorado

Jeffrey S. Abrams, MD Clinical Professor School of Graduate Medicine Seton Hall University South Orange, New Jersey Clinical Associate Professor Penn Medicine Princeton Medical Center Princeton, New Jersey

Julie E. Adams, MD Professor of Orthopedic Surgery Mayo Clinic Health System Austin, Minnesota and Rochester, Minnesota

Bernard R. Bach Jr., MD Lindsay M. Andras, MD Assistant Professor of Orthopaedic Surgery Children’s Orthopedic Center Children’s Hospital Los Angeles Los Angeles, California

Aaron L. Baggish, MD James R. Andrews, MD Medical Director The Andrews Institute Gulf Breeze, Florida Medical Director The American Sports Medicine Institute Birmingham, Alabama

Bayan Aghdasi, MD Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Amiethab A. Aiyer, MD Assistant Professor, Chief Foot and Ankle Service Department of Orthopaedics University of Miami, Miller School of Medicine Miami, Florida

Michael Antonis, DO, RDMS, FACEP, CAQSM Emergency Medicine & Sports Medicine Georgetown University Washington, District of Columbia

Chad A. Asplund, MD, MPH Director, Athletic Medicine Associate Professor, Health and Kinesiology Georgia Southern University Statesboro, Georgia

Nourbakhsh Ali, MD

Rachid Assina, MD, RPH

Spine Surgeon Wellstar Atlanta Medical Center Atlanta, Georgia

Assistant Professor Department of Neurological Surgery Rutgers–New Jersey Medical School Newark, New Jersey

David W. Altchek, MD Co-Chief Emeritus Sports Medicine and Shoulder Service Hospital for Special Surgery New York, New York

Raj M. Amin, MD Resident Physician Department of Orthopaedic Surgery The Johns Hopkins Hospital Baltimore, Maryland

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Director, Cardiovascular Performance Program Massachusetts General Hospital Boston, Massachusetts

Wajeeh Bakhsh, MD Surgical Resident, Department of Orthopaedics University of Rochester Medical Center Rochester, New York

Christopher P. Bankhead, MD Resident, Orthopaedic Surgery University of New Mexico Albuquerque, New Mexico

Michael G. Baraga, MD Assistant Professor of Orthopaedics UHealth Sports Medicine Institute University of Miami, Miller School of Medicine Miami, Florida

Jonathan Barlow, MD, MS Mayo Clinic Rochester, Minnesota

Ashley V. Austin, MD Resident Family Medicine and Physical Medicine and Rehabilitation University of Virginia Charlottesville, Virginia

Luke S. Austin, MD Associate Professor of Orthopaedics Rothman Institute Egg Harbor Township, New Jersey

Kimberly K. Amrami, MD Professor of Radiology Chair, Division of Musculoskeletal Radiology Mayo Clinic Rochester, Minnesota

The Claude Lambert-Helen Thompson Professor of Orthopedic Surgery Rush University Medical Center Chicago, Illinois

John T. Awowale, MD Orthopedic Surgery University of Wisconsin Hospitals and Clinics University of Wisconsin Madison, Wisconsin

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Robert W. Battle, MD Team Cardiologist Associate Professor of Medicine and Pediatrics Department of Cardiology University of Virginia Medical Center Charlottesville, Virginia

Matthew Bessette, MD Sports Medicine Fellow The Cleveland Clinic Foundation Cleveland, Ohio

Thomas M. Best, MD, PhD Professor of Orthopaedics Research Director of Sports Performance and Wellness Institute University of Miami Sports Medicine Institute Miami, Florida

CONTRIBUTORS

Bruce Beynnon, PhD

Stephen F. Brockmeier, MD

Jon-Michael E. Caldwell, MD

McClure Professor of Musculoskeletal Research Director of Research Department of Orthopaedics and Rehabilitation University of Vermont College of Medicine McClure Musculoskeletal Research Center Burlington, Vermont

Associate Professor Department of Orthopaedic Surgery Fellowship Director, University of Virginia Sports Medicine Fellowship University of Virginia School of Medicine Charlottesville, Virginia

Resident, Department of Orthopedic Surgery Columbia University Medical Center New York Presbyterian Hospital New York, New York

Kieran Bhattacharya, BS Research Assistant Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Mary E. Caldwell, DO Jeffrey Brunelli, MD Assistant Professor of Orthopaedic Surgery and Rehabilitation Chief, Sports Medicine and Shoulder Surgery University of Florida-Jacksonville College of Medicine Jacksonville, Florida

Debdut Biswas, MD Hinsdale Orthopaedics Chicago, Illinois

Matthew H. Blake, MD Assistant Director, Sports Medicine Orthopaedic Sports Medicine Avera McKennan Hospital and University Health Center Sioux Falls, South Dakota

Jackie Buell, PhD, RD, CSSD, LD, ATC Assistant Professor, Clinical Health Sciences and Medical Dietetics The Ohio State University Columbus, Ohio

Margaret Boushell, PhD Department of Biomedical Engineering Biomaterials and Interface Tissue Engineering Laboratory Columbia University Medical Center New York Presbyterian Hospital New York, New York

Assistant Professor of Radiology Weill Cornell Medicine New York, New York

Jessica L. Buschmann, MS, RD, CSSD, LD

Ryan P. Calfee, MD, MSc Associate Professor of Orthopedics Washington University School of Medicine St. Louis, Missouri

Christopher L. Camp, MD Assistant Professor of Orthopedics Mayo Clinic Rochester, Minnesota

John T. Campbell, MD Attending Orthopaedic Surgeon Institute for Foot and Ankle Reconstruction Mercy Medical Center Baltimore, Maryland

Clinical Dietician—Board Certified Specialist in Sports Dietetics Sports Medicine Nationwide Children’s Hospital Columbus, Ohio

Kevin Caperton, MD

Brian Busconi, MD

Robert M. Carlisle, MD

Associate Professor of Orthopaedic Surgery Sports Medicine University of Massachusetts Worcester, Massachusetts

Resident, Orthopaedic Surgery Greenville Health System Greenville, South Carolina

James P. Bradley, MD Clinical Professor Orthopaedic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

Assistant Professor of Physical Medicine and Rehabilitation and Sports Medicine Medical College of Virginia Virginia Commonwealth University Richmond, Virginia

Alissa J. Burge, MD

Liljiana Bogunovic Assistant Professor Department of Orthopaedic Surgery Washington University School of Medicine St. Louis, Missouri

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Department of Orthopedics and Sports Medicine Georgetown Orthopedics Georgetown, Texas

Rebecca A. Cerrato, MD Charles A. Bush-Joseph, MD Professor of Orthopaedic Surgery Division of Sports Medicine Rush University Medical Center Chicago, Illinois

William Brady, MD, FAAEM, FACEP

Attending Orthopaedic Surgeon Institute for Foot and Ankle Reconstruction Baltimore, Maryland

Courtney Chaaban, PT, DPT, SCS

Professor of Medicine and Emergency Medicine University of Virginia Charlottesville, Virginia

Kadir Buyukdogan, MD Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Doctoral Student Sports Medicine Research Laboratory Department of Exercise and Sport Science University of North Carolina at Chapel Hill Chapel Hill, North Carolina

Jonathan T. Bravman, MD

E. Lyle Cain Jr., MD

Jorge Chahla, MD

Assistant Professor Director of Sports Medicine Research CU Sports Medicine Division of Sports Medicine and Shoulder Surgery University of Colorado Denver, Colorado

Founding Partner Andrews Sports Medicine and Orthopaedic Center Fellowship Director American Sports Medicine Institute Birmingham, Alabama

Regenerative Sports Medicine Fellow Center for Regenerative Sports Medicine Steadman Philippon Research Institute Vail, Colorado

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CONTRIBUTORS

Peter N. Chalmers, MD

Philip Chuang, PhD

Shannon David, PhD, ATC

Assistant Professor University of Utah Department of Orthopaedic Surgery Salt Lake City, Utah

Department of Biomedical Engineering Biomaterials and Interface Tissue Engineering Laboratory Columbia University Medical Center New York Presbyterian Hospital New York, New York

Assistant Professor Coordinator of Clinical Education North Dakota State University Fargo, North Dakota

Angela K. Chang, MD Center for Outcomes-Based Orthopaedic Research Steadman Philippon Research Institute Vail, Colorado

Nicholas J. Clark, MD Orthopedic Surgeon Mayo Clinic Rochester, Minnesota

Sonia Chaudhry, MD Assistant Professor of Orthopaedic Surgery University of Connecticut School of Medicine Pediatric Orthopaedic, Hand, and Microvascular Surgery Connecticut Children’s Medical Center Hartford, Connecticut

Austin W. Chen, MD Hip Preservation and Sports Medicine BoulderCentre for Orthopedics Boulder, Colorado Academic Faculty American Hip Institute Chicago, Illinois

John C. Clohisy, MD Professor of Orthopaedic Surgery Washington University School of Medicine St. Louis, Missouri

Christopher Coleman, MD Department of Radiology University of Colorado Aurora, Colorado

Francisco Contreras, MD Department of Radiology Jackson Memorial Hospital University of Miami Hospital Miami, Florida

Thomas M. DeBerardino, MD Orthopaedic Surgeon The Orthopaedic Institute Medical Director Burkhart Research Institute for Orthopaedics The San Antonio Orthopaedic Group Co-Director, Combined Baylor College of Medicine and The San Antonio Orthopaedic Group, Texas Sports Medicine Fellowship Professor of Orthopaedic Surgery Baylor College of Medicine San Antonio, Texas

Richard E. Debski, PhD Professor Departments of Bioengineering and Orthopaedic Surgery University of Pittsburgh Pittsburgh, Pennsylvania

Marc M. DeHart, MD Edward C. Cheung, MD

Joseph D. Cooper, MD

Resident Physician Orthopaedic Surgery University of California, Los Angeles Medical Center Los Angeles, California

Resident, Orthopaedic Surgery University of Southern California Los Angeles, California

Associate Professor of Orthopaedic Surgery Chief of Adult Reconstruction UT Health San Antonio San Antonio, Texas

Chris A. Cornett, MD, MPT

Arthur Jason De Luigi, DO, MHSA

Associate Professor of Orthopaedic Surgery University of Nebraska Medical Center Department of Orthopaedic Surgery and Rehabilitation Medical Director Physical/Occupational Therapy Co-Medical Director, Spine Program Nebraska Medicine Omaha, Nebraska

Professor of Rehabilitation Medicine and Sports Medicine Georgetown University School of Medicine Washington, District of Columbia

A. Bobby Chhabra, MD Lillian T. Pratt Distinguished Professor and Chair Orthopaedic Surgery University of Virginia Health System Charlottesville, Virginia

Woojin Cho, MD, PhD Assistant Professor, Orthopaedic Surgery Albert Einstein College of Medicine Chief of Spine Surgery Orthopaedic Surgery Research Director Multidisciplinary Spine Center Montefiore Medical Center New York, New York

Joseph N. Chorley, MD Associate Professor of Pediatrics Baylor College of Medicine Houston, Texas

John Jared Christophel, MD, MPH Assistant Professor of Otolaryngology— Head and Neck Surgery University of Virginia Charlottesville, Virginia

Paul S. Corotto, MD Chief Fellow Department of Cardiology University of Virginia Medical Center Charlottesville, Virginia

Ryan P. Coughlin, MD, FRCSC Department of Orthopaedic Surgery Duke University Durham, North Carolina

Jared A. Crasto, MD Resident, Department of Orthopaedic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

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Elizabeth R. Dennis, MD, MS Resident, Department of Orthopedic Surgery Columbia University Medical Center New York Presbyterian Hospital New York, New York

John J. Densmore, MD, PhD Associate Professor of Clinical Medicine Division of Hematology/Oncology University of Virginia Charlottesville, Virginia

Joshua S. Dines, MD Sports Medicine and Shoulder Service Hospital for Special Surgery New York, New York

Benjamin G. Domb, MD Founder American Hip Institute Chicago, Illinois

CONTRIBUTORS

Jason Dragoo, MD

Anthony Essilfie, MD

J. Craig Garrison, PhD, PT, ATC, SCS

Associate Professor of Orthopaedic Surgery Stanford University Stanford, California

Resident Physician Orthopaedic Surgery University of Southern California Los Angeles, California

Director, Sports Medicine Research Texas Health Sports Medicine Texas Health Fort Worth, Texas

Jack Farr, MD

R. Glenn Gaston, MD

Professor of Orthopedics Indiana University School of Medicine OrthoIndy Knee Preservation and Cartilage Restoration Center Indianapolis, Indiana

Hand and Upper Extremity Surgeon OrthoCarolina Chief of Hand Surgery Division of Orthopedics Carolinas Medical Center Charlotte, North Carolina

Jeffrey R. Dugas, MD Surgeon Andrews Sports Medicine and Orthopaedic Center American Sports Medicine Institute Birmingham, Alabama

Guillaume D. Dumont, MD Assistant Professor of Orthopaedic Surgery University of South Carolina School of Medicine Columbia, South Carolina

Eric W. Edmonds, MD Associate Professor of Clinical Orthopedic Surgery University of California, San Diego Director of Orthopedic Research and Sports Medicine Division of Orthopedic Surgery Rady Children’s Hospital San Diego San Diego, California

Derek M. Fine, MD Associate Professor of Medicine Fellowship Director Division of Nephrology The Johns Hopkins University School of Medicine Baltimore, Maryland

Jake A. Fox, BS Research Assistant Center for Outcomes-Based Orthopaedic Research Steadman Philippon Research Institute Vail, Colorado

Karen P. Egan, PhD

Salvatore Frangiamore, MD, MS

Associate Sport Psychologist Department of Athletics University of Virginia Charlottesville, Virginia

Summa Health Orthopaedic and Sports Medicine Akron, Ohio

Orthopedic Surgeon Mayo Clinic Rochester, Minnesota

Department of Orthopaedic Surgery Rush University Chicago, Illinois

Resident, Orthopaedic Surgery Hospital for Special Surgery New York, New York

Physical Therapist Assistant Research Coordinator University of Indianapolis, Krannert School of Physical Therapy Indianapolis, Indiana

Fatih Ertem, MSc Department of Biomechanics Dokuz Eylul University Health Science Institute Inciralti, Izmir, Turkey Visiting Graduate Researcher Department of Orthopaedics and Rehabilitation McClure Musculoskeletal Research Center Burlington, Vermont

Jason Freeman, PhD Sport Psychologist Department of Athletics University of Virginia Charlottesville, Virginia

Nikhita Gadi, MD, MScBR Internal Medicine Resident, PGY-1 Hackensack University Medical Center Hackensack, New Jersey

Norman Espinosa Jr., MD Head of Foot and Ankle Surgery Institute for Foot and Ankle Reconstruction FussInsitut Zurich Zurich, Switzerland

Brandee Gentile, MS, ATC Athletic Trainer Department of Neurosurgery Rutgers–New Jersey Medical School Newark, New Jersey

Professor of Orthopedic Surgery Western University London, Ontario, Canada

Todd M. Gilbert, MD Heather Freeman, PT, DHS

Claire D. Eliasberg, MD

Alan E. Freeland Chair of Hand Surgery Professor and Chief Division of Hand and Upper Extremity Surgery Chief, Arthroscopic Surgery and Sports Medicine Department of Orthopaedic Surgery and Rehabilitation University of Mississippi Health Care Jackson, Mississippi

J. Robert Giffin, MD, FRCSC, MBA Rachel M. Frank, MD

Bassem T. Elhassan, MD

William B. Geissler, MD

Seth C. Gamradt, MD Associate Clinical Professor Director of Orthopaedic Athletic Medicine Orthopaedic Surgery University of Southern California Los Angeles, California

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Department of Orthopaedic Surgery and Rehabilitation University of Nebraska Medical Center Omaha, Nebraska

G. Keith Gill, MD Department of Orthopaedics University of New Mexico Health Sciences Center Albuquerque, New Mexico

Thomas J. Gill, MD Professor of Orthopedic Surgery Tufts Medical School Chairman, Department of Orthopedic Surgery St. Elizabeth’s Medical Center/Steward Healthcare Network Boston, Massachusetts

Jacob D. Gire, MD Department of Orthopaedic Surgery Stanford University Palo Alto, California

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CONTRIBUTORS

Pau Golanó, MD

Letha Y. Griffin, MD, PhD

Hamid Hassanzadeh, MD

Professor of Human Anatomy Laboratory of Arthroscopic and Surgical Anatomy Human Anatomy and Embryology Unit Department of Pathology and Experimental Therapeutics University of Barcelona–Spain Department of Orthopaedic Surgery University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania

Team Physician Georgia State University Atlanta, Georgia Staff Peachtree Orthopedics Atlanta, Georgia

Assistant Professor Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Jorge E. Gómez, MD, MS Associate Professor of Adolescent Medicine and Sports Medicine Baylor College of Medicine Houston, Texas

Warren C. Hammert, MD Professor of Orthopaedic Surgery and Plastic Surgery Chief, Hand Surgery Department of Orthopaedics and Rehabilitation University of Rochester Medical Center Rochester, New York

Michael R. Hausman, MD Professor of Orthopaedic Surgery Mount Sinai Medical Center New York, New York

Stefan Hemmings, MBBS Post-Doctorate Fellow Division of Nephrology The Johns Hopkins University School of Medicine Baltimore, Maryland

Kyle E. Hammond, MD Juan Gomez-Hoyos, MD Baylor University Medical Center at Dallas Hip Preservation Center Dallas, Texas

Howard P. Goodkin, MD, PhD The Shure Professor of Pediatric Neurology Director Division of Pediatric Neurology Departments of Neurology and Pediatrics University of Virginia Charlottesville, Virginia

Assistant Professor, Department of Orthopaedic Surgery Emory Sports Medicine Center Atlanta, Georgia

R. Frank Henn III, MD

Joseph Hannon, PhD, PT, DPT, SCS, CSCS

Daniel Herman, MD, PhD

Research Physical Therapist Texas Health Sports Medicine Texas Health Fort Worth, Texas

Colin B. Harris, MD Gregory Grabowski, MD, FAOA Associate Professor University of South Carolina School of Medicine Department of Orthopedic Surgery Co-Medical Director Palmetto Health USC Spine Center Residency Program Director Palmetto Health USC Orthopedic Center Columbia, South Carolina

Tinker Gray, MA The Shelbourne Knee Center at Community East Hospital Indianapolis, Indiana

Assistant Professor Department of Orthopaedics Rutgers–New Jersey Medical School Newark, New Jersey

Joshua D. Harris, MD Orthopedic Surgeon Associate Professor, Institute for Academic Medicine Houston Methodist Orthopedics and Sports Medicine Houston, Texas Assistant Professor of Clinical Orthopedic Surgery Weill Cornell Medical College New York, New York

Associate Professor of Orthopaedics University of Maryland School of Medicine Baltimore, Maryland

Assistant Professor Department of Orthopedics and Rehabilitation Divisions of Physical Medicine and Rehabilitation, Sports Medicine, and Research University of Florida Gainesville, Florida

Jay Hertel, PhD, ATC, FNATA Joe H. Gieck Professor of Sports Medicine Departments of Kinesiology and Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Daniel E. Hess, MD Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Carolyn M. Hettrich, MD University of Iowa Iowa City, Iowa

James R. Gregory, MD Assistant Professor of Pediatric Orthopedic Surgery Department of Orthopedic Surgery University of Oklahoma College of Medicine Oklahoma City, Oklahoma

Phillip Gribble, PhD Professor of Rehabilitation Sciences University of Kentucky Lexington, Kentucky

Andrew Haskell, MD

Benton E. Heyworth, MD

Chair, Department of Orthopedics Geographic Medical Director for Surgical Services Palo Alto Medical Foundation Palo Alto, California Associate Clinical Professor Department of Orthopaedic Surgery University of California, San Francisco San Francisco, California

Assistant Professor of Orthopedic Surgery Harvard Medical School Attending Orthopedic Surgeon Department of Orthopedic Surgery Division of Sports Medicine Boston Children’s Hospital Boston, Massachusetts

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CONTRIBUTORS

Ben Hickey, BM, MRCS, MSc, FRCS (Tr & Orth), MD

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John V. Ingari, MD

Robin N. Kamal, MD

Division Chair, Hand Surgery Department of Orthopaedic Surgery The Johns Hopkins Hospital Baltimore, Maryland

Assistant Professor of Orthopaedic Surgery Chase Hand and Upper Limb Center Stanford University Palo Alto, California

Mary Lloyd Ireland, MD

Thomas Kaminski, PhD, ATC, FNATA

Professor, Kinesiology University of Virginia Charlottesville, Virginia

Professor Department of Orthopaedics University of Kentucky Lexington, Kentucky

Professor of Kinesiology and Applied Physiology University of Delaware Newark, Delaware

Betina B. Hinckel, MD, PhD

Todd A. Irwin, MD

Abdurrahman Kandil, MD

Department of Orthopaedic Surgery Brigham and Women’s Hospital Harvard Medical School Boston, Massachusetts

Director of Research OrthoCarolina Foot and Ankle Institute Associate Professor Carolinas Medical Center Charlotte, North Carolina

Stanford University Stanford, California

Consultant Orthopaedic Foot and Ankle Surgeon Wrexham Maelor Hospital Wrexham, Wales, United Kingdom

Michael Higgins, PhD, ATC, PT, CSCS

Gwendolyn Hoben, MD, PhD Instructor Plastic and Reconstructive Surgery Medical College of Wisconsin Milwaukee, Wisconsin

Nona M. Jiang, MD

Christopher Hogrefe, MD, FACEP

Darren L. Johnson, MD

Assistant Professor Departments of Emergency Medicine, Medicine—Sports Medicine, and Orthopaedic Surgery—Sports Medicine Northwestern Medicine Northwestern University Feinberg School of Medicine Chicago, Illinois

Director of Sports Medicine University of Kentucky Lexington, Kentucky

Department of Medicine University of Virginia Charlottesville, Virginia

Research Fellow Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Attending Orthopaedic Surgeon Orthopaedic Specialty Institute Orange, California

Christopher A. Keen, MD Citrus Orthopedic and Joint Institute Lecanto, Florida

Mick P. Kelly, MD

Jared S. Johnson, MD

Resident, Department of Orthopaedic Surgery Rush University Medical Center Chicago, Illinois

St. Luke’s Clinic–Sports Medicine: Boise Boise, Idaho

A. Jay Khanna, MD, MBA

Grant L. Jones, MD Jason A. Horowitz, BA

Jonathan R. Kaplan, MD

Associate Professor of Orthopaedic Surgery The Ohio State University Columbus, Ohio

Professor and Vice Chair of Orthopaedic Surgery Department of Orthopaedic Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Jean Jose, DO, MS Associate Chief of Musculoskeletal Radiology Associate Professor of Clinical Radiology Division of Diagnostic Radiology University of Miami Hospital Miami, Florida

Anthony Nicholas Khoury

Associate Professor of Emergency Medicine Team Physician, Department of Athletics Georgetown University Washington, District of Columbia

Scott G. Kaar, MD

Christopher Kim, MD

Associate Professor of Orthopaedic Surgery Saint Louis University St. Louis, Missouri

Instructor of Orthopaedic Surgery Saint Louis University St. Louis, Missouri

Catherine Hui, MD, FRCSC

Anish R. Kadakia, MD

Lucas R. King, MD, BS

Associate Clinical Professor Division of Orthopaedic Surgery University of Alberta Edmonton, Alberta, Canada

Associate Professor of Orthopaedic Surgery Northwestern Memorial Hospital Northwestern University Feinberg School of Medicine Chicago, Illinois

Sports Orthopedic Surgeon Department of Orthopedic Surgery Parkview Medical Center Pueblo, Colorado

Benjamin M. Howe, MD Associate Professor of Radiology Mayo Clinic Rochester, Minnesota

Baylor University Medical Center at Dallas Hip Preservation Center University of Texas at Arlington Bioengineering Department Dallas, Texas

Korin Hudson, MD, FACEP, CAQSM

R. Tyler Huish, DO First Choice Physician Partners La Quinta, California

Samantha L. Kallenbach, BS Steadman Philippon Research Institute The Steadman Clinic Vail, Colorado

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CONTRIBUTORS

Susan E. Kirk, MD

Marshall A. Kuremsky, MD

Peter Lawrence, MD

Associate Professor of Internal Medicine and Obstetrics and Gynecology Division of Endocrinology and Metabolism, Maternal–Fetal Medicine Associate Dean, Graduate Medical Education University of Virginia Health System Charlottesville, Virginia

Orthopaedic Surgeon Hand and Upper Extremity Surgeon Sports Medicine and Arthroscopic Surgeon EmergeOrtho Raleigh, North Carolina

Wiley Barker Professor of Surgery Chief, Division of Vascular and Endovascular Surgery University of California, Los Angeles Los Angeles, California

Shawn M. Kutnik, MD

Adrian D.K. Le, MD

Orthopedic Surgeon Archway Orthopedics and Hand Surgery St. Louis, Missouri

Department of Orthopedic Surgery Stanford University Stanford, California

Michael S. Laidlaw, MD

Nicholas LeCursi, CO

Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Certified Orthotist Vice President, Services Chief Technology Officer Becker Orthopedic Troy, Michigan

Georg Klammer, MD Consultant Institute for Foot and Ankle Reconstruction FussInsitut Zurich Zurich, Switzerland

Derrick M. Knapik, MD Orthopaedic Surgery University Hospitals Cleveland Medical Center Cleveland, Ohio

Joseph D. Lamplot Chief Resident Department of Orthopaedic Surgery Washington University School of Medicine St. Louis, Missouri

Lee M. Kneer, MD, CAQSM Assistant Professor, Department of Orthopaedic Surgery Assistant Professor, Department of Physical Medicine and Rehabilitation Emory Sports Medicine Center Atlanta, Georgia

Drew Lansdown, MD Section of Young Adult Hip Surgery Division of Sports Medicine Department of Orthopedic Surgery Rush Medical College Rush University Medical Center Chicago, Illinois

Mininder S. Kocher, MD, MPH Professor of Orthopaedic Surgery Harvard Medical School Associate Director Division of Sports Medicine Department of Orthopaedic Surgery Boston Children’s Hospital Boston, Massachusetts

Gabrielle P. Konin, MD Assistant Professor of Radiology Weill Cornell Medicine New York, New York

Matthew J. Kraeutler, MD Department of Orthopaedic Surgery Seton Hall-Hackensack Meridian School of Medicine South Orange, New Jersey

Alexander B. Kreines, DO Resident, Orthopaedic Surgery Rowan University Stratford, New Jersey

Sonya B. Levine, BA Department of Orthopedic Surgery Columbia University Medical Center New York Presbyterian Hospital New York, New York

William N. Levine, MD, FAOA Frank E. Stinchfield Professor and Chairman of Orthopedic Surgery Columbia University Medical Center New York Presbyterian Hospital New York, New York

Matthew D. LaPrade, BS Steadman Philippon Research Institute The Steadman Clinic Vail, Colorado

Robert F. LaPrade, MD, PhD Chief Medical Research Officer Steadman Philippon Research Institute The Steadman Clinic Vail, Colorado

Christopher M. Larson, MD Minnesota Orthopedic Sports Medicine Institute Twin Cities Orthopedics Edina, Minnesota

Xudong Joshua Li, MD, PhD Associate Professor of Orthopaedic Surgery and Biomedical Engineering University of Virginia Charlottesville, Virginia

Gregory T. Lichtman, DO Department of Orthopedic Surgery Rowan University School of Osteopathic Medicine Stratford, New Jersey

Christopher A. Looze, MD Orthopaedic Surgeon MedStar Franklin Square Baltimore, Maryland

Evan P. Larson, MD University of Nebraska Medical Center Department of Orthopaedic Surgery and Rehabilitation Omaha, Nebraska

Gary M. Lourie, MD Hand Surgeon The Hand and Upper Extremity Center of Georgia Atlanta, Georgia

Samuel J. Laurencin, MD, PhD Vignesh Prasad Krishnamoorthy, MD Section of Young Adult Hip Surgery Division of Sports Medicine Department of Orthopedic Surgery Rush Medical College Rush University Medical Center Chicago, Illinois

Department of Orthopaedic Surgery University of Connecticut School of Medicine Farmington, Connecticut

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Helen H. Lu, PhD Professor of Biomedical Engineering Vice Chair, Department of Biomedical Engineering Columbia University Medical Center New York Presbyterian Hospital New York, New York

CONTRIBUTORS

Timothy J. Luchetti, MD

Scott D. Martin, MD

Heather Menzer, MD

Resident, Orthopedic Surgery Rush University Medical Center Chicago, Illinois

Director, MGH Joint Preservation Service Director, Harvard/MGH Sports Medicine Fellowship Program Associate Professor of Orthopaedic Surgery Harvard Medical School Department of Orthopaedic Surgery Massachusetts General Hospital Boston, Massachusetts

Fellow, Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Jessica A. Lundgren, MD Lecturer Department of Internal Medicine Division of Endocrinology and Metabolism University of Virginia Health System Charlottesville, Virginia

Travis G. Maak, MD Associate Professor of Orthopaedic Surgery University of Utah Salt Lake City, Utah

John M. MacKnight, MD Professor of Internal Medicine and Orthopaedic Surgery Team Physician and Medical Director UVA Sports Medicine University of Virginia Health System Charlottesville, Virginia

Nancy Major, MD Department of Radiology University of Colorado School of Medicine Aurora, Colorado

Francesc Malagelada, MD Foot and Ankle Unit Department of Trauma and Orthopaedic Surgery Royal London Hospital Barts Health National Health Service Trust London, England, United Kingdom

Michael A. Marchetti, MD Assistant Attending, Dermatology Service Department of Medicine Memorial Sloan Kettering Cancer Center New York, New York

Patrick G. Marinello, MD Hand and Upper Extremity Surgeon Capital Region Orthopaedic Group Bone and Joint Center Albany, New York

Hal David Martin, DO Medical Director Baylor University Medical Center at Dallas Hip Preservation Center Dallas, Texas

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Sean J. Meredith, MD Resident Physician Department of Orthopaedics University of Maryland School of Medicine Baltimore, Maryland

Rebecca Martinie, MD Assistant Professor of Pediatrics Baylor College of Medicine Houston, Texas

Lyndon Mason, MB BCh, MRCS (Eng), FRCS (Tr & Orth) Trauma and Orthopaedic Consultant Aintree University Hospital Liverpool, England, United Kingdom

Dayne T. Mickelson, MD Department of Orthopaedic Surgery Duke University Durham, North Carolina

Michael R. Mijares, MD Department of Orthopaedics Jackson Memorial Hospital Jackson Health System Miami, Florida

Augustus D. Mazzocca, MD Department of Orthopaedic Surgery University of Connecticut School of Medicine Farmington, Connecticut

David R. McAllister, MD Chief, Sports Medicine Service Professor and Vice Chair Department of Orthopaedic Surgery David Geffen School of Medicine University of California, Los Angeles Los Angeles, California

Meagan McCarthy, MD Fellowship Trained Orthopaedic Sports Medicine Surgeon Reno Orthopaedic Clinic Reno, Nevada

Matthew D. Milewski, MD Assistant Professor Division of Sports Medicine Department of Orthopaedic Surgery Boston Children’s Hospital Boston, Massachusetts

Mark D. Miller, MD S. Ward Casscells Professor of Orthopaedic Surgery Head, Division of Sports Medicine University of Virginia Charlottesville, Virginia Adjunctive Clinical Professor and Team Physician James Madison University Harrisonburg, Virginia

Dilaawar J. Mistry, MD Eric C. McCarty, MD Chief, Sports Medicine and Shoulder Surgery Associate Professor Department of Orthopaedics University of Colorado School of Medicine Director Sports Medicine, Head Team Physician University of Colorado Department of Athletics Associate Professor, Adjunct Department of Integrative Physiology University of Colorado Boulder, Colorado

Sean McMillan, DO Chief of Orthopedics Director of Orthopedic Sports Medicine and Arthroscopy Lourdes Medical Associates Lourdes Medical Center at Burlington Burlington, New Jersey

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Team Physician Primary Care Sports Medicine Western Orthopedics and Sports Medicine Grand Junction, Colorado

Erik Mitchell, DO Valley Health Orthopaedics Front Royal Front Royal, Virginia

Andrew Molloy, MBChB, MRCS Consultant Orthopaedic Surgeon Trauma and Orthopaedics University Hospital Aintree Honorary Clinical Senior Lecturer Department of Musculoskeletal Biology University of Liverpool Consultant Orthopaedic Surgeon Spire Liverpool Liverpool, England, United Kingdom

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CONTRIBUTORS

Timothy S. Mologne, MD

Carl W. Nissen, MD

Evan Peck, MD

Sports Medicine Center Appleton, Wisconsin

Franciscan Orthopedic Associates at St. Joseph Tacoma, Washington

Professor Department of Orthopaedics University of Connecticut Elite Sports Medicine Connecticut Children’s Medical Center Farmington, Connecticut

Amy M. Moore, MD, FACS

Blake R. Obrock, DO

Associate Professor of Surgery Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

Sports Medicine Fellow Department of Orthopaedics University of New Mexico Albuquerque, New Mexico

Section of Sports Health Department of Orthopaedic Surgery Cleveland Clinic Florida Weston, Florida Affiliate Assistant Professor of Clinical Biomedical Science Charles E. Schmidt College of Medicine Florida Atlantic University Boca Raton, Florida

Claude T. Moorman III, MD

James Onate, PhD, ATC, FNATA

Professor of Orthopaedic Surgery Duke Center for Integrated Medicine Durham, North Carolina

Associate Professor School of Health and Rehabilitation Sciences The Ohio State University Columbus, Ohio

Scott R. Montgomery, MD

Gina M. Mosich, MD Resident Physician Orthopaedic Surgery University of California, Los Angeles Los Angeles, California

Scott I. Otallah, MD Carilion Children’s Pediatric Neurology Roanoke, Virginia

Michael R. Moynagh, MBBCh

Brett D. Owens, MD

Assistant Professor of Radiology Mayo Clinic Rochester, Minnesota

Professor of Orthopedics Brown Alpert Medical School Providence, Rhode Island

Andrew C. Mundy, MD

Gabrielle M. Paci, MD

Department of Orthopaedic Surgery The Ohio State University Columbus, Ohio

Physician Orthopaedic Surgery Stanford University Palo Alto, California

Colin P. Murphy, BA Research Assistant Center for Outcomes-Based Orthopaedic Research Steadman Philippon Research Institute Vail, Colorado

Richard D. Parker, MD Department of Orthopaedic Surgery The Cleveland Clinic Foundation Cleveland, Ohio

Jonathan P. Parsons, MD Volker Musahl, MD Assistant Professor Department of Orthopaedic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

Professor of Internal Medicine Department of Pulmonary, Critical Care, and Sleep Medicine Wexner Medical Center The Ohio State University Columbus, Ohio

Jeffrey J. Nepple, MD Assistant Professor of Orthopaedic Surgery Director Young Athlete Center Washington University School of Medicine St. Louis, Missouri

Neel K. Patel, MD Department of Orthopaedic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

Thierry Pauyo, MD Shane J. Nho, MD, MS Assistant Professor Head, Section of Young Adult Hip Surgery Division of Sports Medicine Department of Orthopedic Surgery Rush Medical College Rush University Medical Center Chicago, Illinois

Fellow Department of Orthopaedic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

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Liam Peebles, BA Research Assistant Center for Outcomes-Based Orthopaedic Research Steadman Philippon Research Institute Vail, Colorado

Andrew T. Pennock, MD Associate Clinical Professor Orthopedic Surgery University of California, San Diego San Diego, California

Anthony Perera, MBChB, MRCS, MFSEM, PGDip Med Law, FRCS (Tr & Orth) Consultant, Orthopaedic Foot and Ankle Surgeon University Hospital of Wales Cardiff, Wales, United Kingdom

Jose Perez, BS Research Fellow Department of Orthopedics Sports Medicine Miami, Florida

William A. Petri Jr., MD, PhD Chief, Division of Infectious Disease and International Health Wade Hampton Frost Professor of Epidemiology University of Virginia Charlottesville, Virginia

Frank A. Petrigliano, MD Assistant Professor of Orthopaedic Surgery David Geffen School of Medicine University of California, Los Angeles Los Angeles, California

Adam M. Pickett, MD Faculty, West Point Sports Medicine Fellowship Department of Orthopaedic Surgery United States Military Academy West Point, New York

CONTRIBUTORS

Matthew A. Posner, MD

Eliott P. Robinson, MD

Susan Saliba, PhD, ATC, MPT

Director, West Point Sports Medicine Fellowship Department of Orthopaedic Surgery United States Military Academy West Point, New York

Orthopedic Surgeon OrthoGeorgia Orthopaedic Specialists Macon, Georgia

Professor, Kinesiology University of Virginia Charlottesville, Virginia

Scott A. Rodeo, MD

Adil Samad, MD

Professor of Orthopaedic Surgery Weill Cornell Medical College Co-Chief Emeritus, Sports Medicine and Shoulder Service Attending Orthopaedic Surgeon Hospital for Special Surgery New York, New York

Florida Orthopaedic Institute Tampa, Florida

Tricia R. Prokop, PT, EdD, MS, CSCS Assistant Professor of Physical Therapy Department of Rehabilitation Sciences University of Hartford West Hartford, Connecticut

Matthew T. Provencher, MD, CAPT, MC, USNR

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Anthony Sanchez, BS Medical Doctor Candidate Oregon Health and Science University Portland, Oregon

Anthony A. Romeo, MD

Laura W. Scordino, MD

Professor of Surgery and Orthopaedics Uniformed Services University of the Health Services Complex Shoulder, Knee, and Sports Surgeon The Steadman Clinic Vail, Colorado

Department of Orthopaedic Surgery Rush University Chicago, Illinois

Orthopaedic Surgeon OrthoNY Albany, New York

Kyle Rosen, MD

Virgil P. Secasanu, MD

Dartmouth College Hanover, New Hampshire

Rabia Qureshi, MD

William H. Rossy, MD

Research Fellow Department of Orthopedic Surgery University of Virginia Charlottesville, Virginia

Clinical Associate Professor Penn Medicine Princeton Medical Center Princeton, New Jersey

Clinical Instructor, Housestaff Department of Pulmonary, Critical Care, and Sleep Medicine Wexner Medical Center The Ohio State University Columbus, Ohio

Terrance Sgroi, PT Paul Rothenberg, MD

Fred Reifsteck, MD Head Team Physician University Health Center University of Georgia Athens, Georgia

Resident Physician Department of Orthopaedics University of Miami Miami, Florida

Todd A. Rubin, MD David R. Richardson, MD Associate Professor of Orthopaedic Surgery University of Tennessee–Campbell Clinic Memphis, Tennessee

Orthopaedic Surgeon Hughston Clinic Orthopaedics Nashville, Tennessee

Assistant Professor, Sports Medicine Sports Medicine Fellowship Assistant Director Director of Orthopaedics Sports Medicine Research University of New Mexico Albuquerque, New Mexico

Jason T. Shearn, MD Associate Professor Department of Biomedical Engineering University of Cincinnati Cincinnati, Ohio

K. Donald Shelbourne, MD Robert D. Russell, MD

Dustin Richter, MD

Sports Medicine and Shoulder Service Hospital for Special Surgery New York, New York

Orthopaedic Surgeon OrthoTexas Frisco, Texas

The Shelbourne Knee Center at Community East Hospital Indianapolis, Indiana

Seth L. Sherman, MD David A. Rush, MD Department of Orthopaedic Surgery and Rehabilitation University of Mississippi Medical Center Jackson, Mississippi

Andrew J. Riff, MD Assistant Professor of Clinical Orthopaedic Surgery Indiana University Health Orthopedics and Sports Medicine Indianapolis, Indiana

Joseph J. Ruzbarsky, MD

Christopher J. Roach, MD

Marc Safran, MD

Chairman, Orthopaedic Surgery San Antonio Military Medical Center San Antonio, Texas

Professor of Orthopedic Surgery Associate Director Department of Sports Medicine Stanford University Redwood City, California

Resident, Orthopedic Surgery Department of Orthopaedics Hospital for Special Surgery New York, New York

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Department of Orthopaedic Surgery University of Missouri, Columbia Columbia, Missouri

Ashley Matthews Shilling, MD Associate Professor of Anesthesiology University of Virginia Medical Center Charlottesville, Virginia

Adam L. Shimer, MD Assistant Professor of Orthopaedic Surgery University of Virginia Charlottesville, Virginia

Anuj Singla, MD Instructor, Orthopaedics University of Virginia Charlottesville, Virginia

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CONTRIBUTORS

David L. Skaggs, MD, MMM

Eric Swanton, MBChB, FRACS (Orth)

Jason Thompson, MD

Professor of Orthopaedic Surgery Keck School of Medicine of USC University of Southern California Chief, Orthopaedic Surgery Children’s Hospital Los Angeles Los Angeles, California

Orthopaedic Consultant Department of Orthopaedics North Shore Hospital, Waitemata District Health Board Auckland, New Zealand

Orthopedic Surgery Resident, UT Health San Antonio Adult Reconstructive Surgery Fellow University of Western Ontario London Health Sciences Centre London, Ontario, Canada

Matthew A. Tao, MD Mia Smucny, MD University of Washington Seattle, Washington

Assistant Professor Orthopaedic Surgery University of Nebraska Medical Center Omaha, Nebraska

Niall A. Smyth, MD Resident, Orthopaedic Surgery University of Miami, Miller School of Medicine Miami, Florida

Sandip P. Tarpada, BS Department of Orthopaedic Surgery Montefiore Medical Center Albert Einstein College of Medicine New York, New York

Frederick S. Song, MD Clinical Associate Professor Penn Medicine Princeton Medical Center Princeton, New Jersey

Kurt Spindler, MD Cleveland Clinic Foundation Cleveland, Ohio

Kenneth F. Taylor, MD Department of Orthopaedics and Rehabilitation The Pennsylvania State University Milton S. Hershey Medical Center Hershey, Pennsylvania

Stephen R. Thompson, MD, MEd, FRCSC Associate Professor of Sports Medicine Eastern Maine Medical Center University of Maine Bangor, Maine

Fotios P. Tjoumakaris, MD Associate Professor Department of Orthopedic Surgery Sidney Kimmel College of Medicine Thomas Jefferson University Philadelphia, Pennsylvania

Drew Toftoy, MD Sports Medicine Fellow University of Colorado Aurora, Colorado

Michael Terry, MD Chad Starkey, PhD, AT, FNATA Professor Division of Athletic Training Ohio University Athens, Ohio

Professor Department of Orthopaedic Surgery Northwestern Medicine Northwestern University Feinberg School of Medicine Chicago, Illinois

Siobhan M. Statuta, MD Associate Professor of Family Medicine and Physical Medicine and Rehabilitation University of Virginia Charlottesville, Virginia

Samuel R. H. Steiner, MD Orthopedic Surgery Orthopaedic Associates of Wisconsin Pewaukee, Wisconsin

John W. Stelzer, MD, MS Research Fellow Department of Orthopaedic Surgery Harvard Medical School Massachusetts General Hospital Boston, Massachusetts

Christopher L. Stockburger, MD Department of Orthopedic Surgery Washington University School of Medicine St. Louis, Missouri

J. Andy Sullivan, MD Clinical Professor of Pediatric Orthopedic Surgery Department of Orthopedic Surgery University of Oklahoma College of Medicine Oklahoma City, Oklahoma

John M. Tokish, MD, USAF MC Orthopedic Surgery Residency Program Director Tripler Army Medical Center Honolulu, Hawaii

Gehron Treme, MD Charles A. Thigpen, PhD, PT, ATC Senior Director of Practice Innovation and Analytics ATI Physical Therapy Director, Program in Observational Clinical Research in Orthopedics Center for Effectiveness in Orthopedic Research Arnold School of Public Health University of South Carolina Greenville, South Carolina

Stavros Thomopoulos, PhD Director, Carroll Laboratories for Orthopedic Surgery Vice Chair, Basic Research in Orthopedic Surgery Robert E. Carroll and Jane Chace Carroll Professor of Biomechanics (in Orthopedic Surgery and Biomedical Engineering) Columbia University Medical Center New York Presbyterian Hospital New York, New York

Associate Professor, Orthopaedics University of New Mexico Albuquerque, New Mexico

Rachel Triche, MD Attending Orthopaedic Surgeon Santa Monica Orthopaedic and Sports Medicine Group Santa Monica, California

David P. Trofa, MD Resident, Department of Orthopaedic Surgery Columbia University Medical Center New York, New York

Gift Ukwuani, MD Section of Young Adult Hip Surgery Division of Sports Medicine Department of Orthopedic Surgery Rush Medical College Rush University Medical Center Chicago, Illinois

M. Farooq Usmani, MSc Department of Orthopaedic Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

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CONTRIBUTORS

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Ravi S. Vaswani, MD

Benjamin R. Wilson, MD

Yi-Meng Yen, MD, PhD

Resident, Department of Orthopaedic Surgery University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

Resident Physician Orthopaedic Surgery and Sports Medicine University of Kentucky Lexington, Kentucky

Assistant Professor, Harvard Medical School Boston Children’s Hospital Department of Orthopaedic Surgery Division of Sports Medicine Boston, Massachusetts

Aaron J. Vaughan, MD

Brian F. Wilson, MD

Family Physician Sports Medicine Director Mountain Area Health Education Center Asheville, North Carolina

Director of Orthopaedic Surgery Stormont Vail Health Washburn University Orthopaedic Sports Medicine Topeka, Kansas

Jordi Vega, MD Orthopaedic Surgeon Etzelclinic Pfäffikon, Schwyz, Switzerland

Evan E. Vellios, MD Resident Physician Department of Orthopedic Surgery David Geffen School of Medicine University of California, Los Angeles Los Angeles, California

Armando F. Vidal, MD Associate Professor Department of Orthopedics University of Colorado School of Medicine Aurora, Colorado

Michael J. Vives, MD Professor and Chief of Spine Surgery Department of Orthopedics Rutgers–New Jersey Medical School Newark, New Jersey

James E. Voos, MD Associate Professor of Orthopaedic Surgery Division Chief, Sports Medicine Medical Director, Sports Medicine Institute University Hospitals Cleveland Medical Center Cleveland, Ohio

Dean Wang, MD Fellow in Sports Medicine and Shoulder Surgery Hospital for Special Surgery New York, New York

Jennifer Moriatis Wolf, MD Professor Department of Orthopaedic Surgery and Rehabilitation University of Chicago Hospitals Chicago, Illinois

Rick W. Wright, MD Jerome J. Gilden Distinguished Professor Executive Vice Chairman Department of Orthopaedic Surgery Washington University School of Medicine St. Louis, Missouri

Vancouver, British Columbia, Canada

M. Christopher Yonz, MD Summit Orthopaedics Southeast Georgia Health System St. Marys, Georgia

Tracy Zaslow, MD, FAAP, CAQSM Assistant Professor University of Southern California, Los Angeles Children’s Orthopaedic Center (COC) at Children’s Hospital–Los Angeles Medical Director COC Sports Medicine and Concussion Program Team Physician, LA Galaxy Los Angeles, California

Frank B. Wydra, MD Department of Orthopedics University of Colorado School of Medicine Aurora, Colorado

James Wylie, MD, MHS Director of Orthopedic Research Intermountain Healthcare The Orthopedic Specialty Hospital Murray, Utah

Andrew M. Zbojniewicz, MD Department of Radiology Michigan State University College of Human Medicine Advanced Radiology Services Grand Rapids, Michigan Division of Pediatric Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio

Robert W. Wysocki, MD Rush University Medical Center Chicago, Illinois

Connor G. Ziegler, MD New England Orthopedic Surgeons Springfield, Massachusetts

Haoming Xu, MD Dermatology Service Department of Medicine Memorial Sloan Kettering Cancer Center New York, New York

Kent T. Yamaguchi, MD

University of Iowa Iowa City, Iowa

Resident Physician Orthopaedic Surgery University of California, Los Angeles Los Angeles, California

Barbara B. Wilson, MD

Jeffrey Yao, MD

Associate Professor of Dermatology University of Virginia Charlottesville, Virginia

Associate Professor of Orthopedic Surgery Stanford University Medical Center Palo Alto, California

Robert Westermann, MD

Jane C. Yeoh, MD, FRCSC

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Mary L. Zupanc, MD Professor and Division Chief Neurology and Pediatrics University of California, Irvine Children’s Hospital of Orange County Orange, California

V I D E O TA B L E O F C O N T E N T S Chapter 1 Video 1.1 Physiology and Pathophysiology of Musculoskeletal Tissues—Dean Wang, Claire D. Eliasberg, and Scott A. Rodeo Chapter 2 Video 2.1 Basic Concepts in Biomechanics—Richard E. Debski, Neel K. Patel, and Jason T. Shearn Chapter 4 Video 4.1 Basic Science of Implants in Sports Medicine— Elizabeth R. Dennis, Jon-Michael Caldwell, Sonya B. Levine, Philip Chuang, Margaret Boushell, Stavros Thomopoulos, Helen H. Lu, and William N. Levine Chapter 5 Video 5.1 Orthobiologics: Clinical Application of PlateletRich Plasma and Stem Cell Therapy—Adrian D.K. Le and Jason Dragoo Chapter 7 Video 7.1 Imaging Overview—Francisco Contreras, Jose Perez, and Jean Jose Chapter 8 Video 8.1 Basic Arthroscopic Principles—Michael R. Mijares and Michael G. Baraga Chapter 9 Video 9.1 Overview of Sport-Specific Injuries—Jared A. Crasto, Ravi S. Vaswani, Thierry Pauyo, and Volker Musahl Chapter 10 Video 10.1 Commonly Encountered Fractures in Sports Medicine—Christopher Kim and Scott G. Kaar Chapter 11 Video 11.1 Team Medical Coverage—Daniel Herman, Nikhita Gadi, and Evan Peck

Chapter 15 Video 15.1 Gastrointestinal Medicine in the Athlete—John M. MacKnight Chapter 16 Video 16.1 Hematologic Medicine in the Athlete—John J. Densmore Chapter 17 Video 17.1 Infectious Diseases in the Athlete—Nona M. Jiang, Kathleen C. Abalos, and William A. Petri Jr. Chapter 18 Video 18.1 The Athlete with Diabetes—Jessica A. Lundgren and Susan E. Kirk Chapter 19 Video 19.1 Renal Medicine and Genitourinary Trauma in the Athlete—Stefan Hemmings and Derek M. Fine Chapter 22 Video 22.1 Dermatologic Conditions—Haoming Xu, Barbara B. Wilson, and Michael A. Marchetti Chapter 23 Video 23.1 Facial, Eye, Nasal, and Dental Injuries—John Jared Christophel Chapter 25 Video 25.1 Sports Nutrition—Jessica L. Buschmann and Jackie Buell Chapter 26 Video 26.1 Doping and Ergogenic Aids—Siobhan M. Statuta, Aaron J. Vaughan, and Ashley V. Austin

Chapter 12 Video 12.1 Comprehensive Cardiovascular Care and Evaluation of the Elite Athlete—Paul S. Corotto, Robert W. Battle, Dilaawar J. Mistry, and Aaron L. Baggish

Chapter 27 Video 27.1 The Female Athlete—Letha Lloyd Ireland, Fred Reifsteck, and Benjamin R. Wilson Video 27.2 The Female Athlete—Letha Lloyd Ireland, Fred Reifsteck, and Benjamin R. Wilson

Chapter 13 Video 13.1 Exercise-Induced Bronchoconstriction—Virgil P. Secasanu and Jonathan P. Parsons

Chapter 28 Video 28.1 The Para-Athlete—Daniel Herman, Mary E. Caldwell, and Arthur Jason De Luigi

Chapter 14 Video 14.1 Deep Venous Thrombosis and Pulmonary Embolism—Marc M. DeHart and Jason Thompson

Chapter 30 Video 30.1 The Athletic Trainer—Chad Starkey and Shannon David

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Y. Griffin, Mary Matthew H. Blake, Y. Griffin, Mary Matthew H. Blake,

VIDEO TABLE OF CONTENTS

Chapter 31 Video 31.1 Principles of Orthopaedic Rehabilitation—Courtney Chaaban and Charles A. Thigpen Chapter 32 Video 32.1 Modalities and Manual Techniques in Sports Medicine Rehabilitation—Susan Saliba and Michael Higgins Chapter 38 Video 38.1 Glenohumeral Joint Imaging—Alissa J. Burge and Gabrielle P. Konin

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Chapter 55 Video 55.1 Vascular Problems and Thoracic Outlet Syndrome— Matthew A. Posner, Christopher J. Roach, Adam M. Pickett, and Brett D. Owens Chapter 56 Video 56.1 Injury to the Acromioclavicular and Sternoclavicular Joints—Connor G. Ziegler, Samuel J. Laurencin, Rachel M. Frank, Matthew T. Provencher, Anthony A. Romeo, and Augustus D. Mazzocca

Chapter 41 Video 41.1 Posterior Shoulder Instability—James Bradley and Fotios P. Tjoumakaris

Chapter 57 Video 57.1 Elbow Anatomy and Biomechanics—Marshall A. Kuremsky, E. Lyle Cain Jr., Jeffrey R. Dugas, James R. Andrews, and Lucas R. King

Chapter 42 Video 42.1 Multidirectional Instability of the Shoulder—Robert M. Carlisle and John M. Tokish

Chapter 58 Video 58.1 Elbow Diagnosis and Decision-Making—Nicholas J. Clark and Bassem Elhassan

Chapter 44 Video 44.1 SLAP Tears—Sean Meredith and R. Frank Henn III

Chapter 59 Video 59.1 Elbow Imaging—Benjamin M. Howe and Michael R. Moynagh

Chapter 45 Video 45.1 The Thrower’s Shoulder—Matthew A. Tao, Christopher L. Camp, Terrance Sgroi, Joshua S. Dines, and David W. Altchek

Chapter 61 Video 61.1 Elbow Tendinopathies and Bursitis—Jennifer Moriatis Wolf

Chapter 46 Video 46.1 Proximal Biceps Tendon Pathology—Samuel R.H. Steiner, John T. Awowale, and Stephen F. Brockmeier

Chapter 62 Video 62.1 Distal Biceps and Triceps Tendon Ruptures— James Bradley, Fotios P. Tjoumakaris, Gregory T. Lichtman, and Luke S. Austin

Chapter 47 Video 47.1 Rotator Cuff and Impingement Lesions—Gina M. Mosich, Kent T. Yamaguchi, and Frank A. Petrigliano

Chapter 63 Video 63.1 Entrapment Neuropathies of the Arm, Elbow, and Forearm—Wajeeh Bakhsh and Warren C. Hammert

Chapter 48 Video 48.1 Subscapularis Injury—William H. Rossy, Frederick S. Song, and Jeffrey S. Abrams

Chapter 64 Video 64.1 Elbow Throwing Injuries—Marshall A. Kuremsky, E. Lyle Cain Jr, Jeffrey R. Dugas, James R. Andrews, and Christopher A. Looze

Chapter 49 Video 49.1 Revision Rotator Cuff Repair—Joseph D. Cooper, Anthony Essilfie, and Seth C. Gamradt Chapter 52 Video 52.1 Glenohumeral Arthritis in the Athlete—Jeffrey Brunelli, Jonathan T. Bravman, Kevin Caperton, and Eric C. McCarty Chapter 53 Video 53.1 Scapulothoracic Disorders—G. Keith Gill, Gehron Treme, and Dustin Richter Chapter 54 Video 54.1 Nerve Entrapment—Daniel E. Hess, Kenneth F. Taylor, and A. Bobby Chhabra

Chapter 65 Video 65.1 Loss of Elbow Motion—Timothy J. Luchetti, Debdut Biswas, and Robert W. Wysocki Chapter 66 Video 66.1 Anatomy and Biomechanics of the Hand and Wrist—Raj M. Amin and John V. Ingari Chapter 67 Video 67.1 Hand and Wrist Diagnosis and Decision-Making— Patrick G. Marinello, R. Glenn Gaston, Eliott P. Robinson, and Gary M. Lourie Chapter 68 Video 68.1 Imaging of the Wrist and Hand—Kimberly K. Amrami

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VIDEO TABLE OF CONTENTS

Chapter 69 Video 69.1 Wrist Arthroscopy—William B. Geissler, David A. Rush, and Christopher A. Keen

Chapter 87 Video 87.1 Hip and Thigh Contusions and Strains—Blake R. Obrock, Christopher P. Bankhead, and Dustin Richter

Chapter 71 Video 71.1 Wrist Tendinopathies—Raj M. Amin and John V. Ingari

Chapter 89 Video 89.1 Knee Anatomy and Biomechanics of the Knee— Matthew J. Kraeutler, Jorge Chahla, Francesc Malagelada, Jordi Vega, Pau Golanó, Bruce Beynnon, Fatih Ertem, and Eric C. McCarty

Chapter 72 Video 72.1 Disorders of the Distal Radioulnar Joint—Julie E. Adams Chapter 73 Video 73.1 Tendon Injuries in the Hand—Robin N. Kamal and Jacob D. Gire Chapter 74 Video 74.1 Digit Fractures and Dislocations—Christopher L. Stockburger amd Ryan P. Calfee Chapter 75 Video 75.1 Neuropathies of the Wrist and Hand—Gwendolyn Hoben and Amy M. Moore Chapter 76 Video 76.1 Hip Anatomy and Biomechanics—Marc Safran and Abdurrahman Kandil Chapter 77 Video 77.1 Hip Diagnosis and Decision-Making—Benjamin G. Domb and Austin W. Chen Chapter 78 Video 78.1 Hip Imaging—Brian Busconi, R. Tyler Huish, Erik Mitchell, and Sean McMillan Chapter 79 Video 79.1 Hip Arthroscopy—Joshua D. Harris Chapter 80 Video 80.1 Femoroacetabular Impingement in Athletes—Shane J. Nho, Vignesh Prasad Krishnamoorthy, Drew Lansdown, Gift Ukwuani Chapter 82 Video 82.1 Iliopsoas Pathology—Christian N. Anderson Chapter 83 Video 83.1 Peritrochanteric Disorders—John W. Stelzer and Scott D. Martin Video 83.2 Peritrochanteric Disorders—John W. Stelzer and Scott D. Martin Video 83.3 Peritrochanteric Disorders—John W. Stelzer and Scott D. Martin Chapter 85 Video 85.1 Posterior Hip Pain—Hal David Martin, Anthony Nicholas Khoury, and Juan Gomez-Hoyos

Chapter 90 Video 90.1 Knee Diagnosis and Decision-Making—Andrew J. Riff, Peter N. Chalmers, and Bernard R. Bach Jr. Chapter 92 Video 92.1 Basics of Knee Arthroscopy—Stephen R. Thompson and Mark D. Miller Chapter 94 Video 94.1 Meniscal Injuries—Joseph J. Ruzbarsky, Travis G. Maak, and Scott A. Rodeo Chapter 96 Video 96.1 Articular Cartilage Lesions—Michael S. Laidlaw, Kadir Buyukdogan, and Mark D. Miller Chapter 98 Video 98.1 Anterior Cruciate Ligament Injuries—Edward C. Cheung, David R. McAllister, and Frank A. Petrigliano Chapter 99 Video 99.1 Revision Anterior Cruciate Ligament Injuries— Joseph D. Lamplot, Liljiana Bogunovic, and Rick W. Wright Chapter 100 Video 100.1 Posterior Cruciate Ligament Injuries—Frank A. Petrigliano, Evan E. Vellios, Scott R. Montgomery, Jared S. Johnson, and David R. McAllister Chapter 101 Video 101.1 Medial Collateral Ligament and Posterior Medial Corner Injuries—M. Christopher Yonz, Brian F. Wilson, Matthew H. Blake, and Darren L. Johnson Chapter 102 Video 102.1 Lateral and Posterolateral Corner Injuries of the Knee—Ryan P. Coughlin, Dayne T. Mickelson, and Claude T. Moorman III Chapter 103 Video 103.1 Multiligament Knee Injuries—Samantha L. Kallenbach, Matthew D. LaPrade, and Robert F. LaPrade Chapter 108 Video 108.1 Loss of Knee Motion—K. Donald Shelbourne, Heather Freeman, and Tinker Gray

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VIDEO TABLE OF CONTENTS

Chapter 110 Video 110.1 Foot and Ankle Biomechanics—Andrew Haskell Chapter 115 Video 115.1 Ankle Arthroscopy—Niall A. Smyth, Jonathan R. Kaplan, Amiethab A. Aiyer, John T. Campbell, Rachel Triche, and Rebecca A. Cerrato Chapter 117 Video 117.1 Ligamentous Injuries of the Foot and Ankle—Paul Rothenberg, Eric Swanton, Andrew Molloy, Amiethab A. Aiyer, and Jonathan R. Kaplan

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Chapter 124 Video 124.1 Imaging of the Spine—Adil Samad, M. Farooq Usmani, and A. Jay Khanna Chapter 125 Video 125.1 Emergency and Field-Side Management of the Spine-Injured Athlete—Korin Hudson, Michael Antonis, and William Brady Chapter 132 Video 132.1 Imaging Considerations in Skeletally Immature Athletes—Andrew M. Zbojniewicz

Chapter 118 Video 118.1 Tendon Injuries of the Foot and Ankle—Todd A. Irwin

Chapter 133 Video 133.1 Shoulder Injuries in the Young Athlete—Andrew T. Pennock and Eric W. Edmonds

Chapter 119 Video 119.1 Articular Cartilage Injuries and Defects—David R. Richardson and Jane C. Yeoh

Chapter 134 Video 134.1 Elbow Injuries in Pediatric and Adolescent Athletes— James P. Bradley, Luke S. Austin, Alexander B. Kreines, and Fotios P. Tjoumakaris

Chapter 121 Video 121.1 Forefoot Problems in Sport—Ben Hickey, Lyndon Mason, and Anthony Perera Chapter 122 Video 122.1 Head and Spine Anatomy and Biomechanics—Colin B. Harris, Rachid Assina, Brandee Gentile, and Michael J. Vives Chapter 123 Video 123.1 Head and Spine Diagnosis and Decision-Making— Rabia Qureshi, Jason A. Horowtiz, Kieran Bhattacharya, and Hamid Hassanzadeh

Chapter 137 Video 137.1 Knee Injuries in Skeletally Immature Athletes— Matthew D. Milewski, James Wylie, Carl W. Nissen, and Tricia R. Prokop Chapter 138 Video 138.1 Foot and Ankle Injuries in the Adolescent Athlete—J. Andy Sullivan and James R. Gregory Chapter 139 Video 139.1 Head Injuries in Skeletally Immature Athletes— Tracy Zaslow

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1  Physiology and Pathophysiology of Musculoskeletal Tissues Dean Wang, Claire D. Eliasberg, Scott A. Rodeo

TENDON AND LIGAMENT Structure Tendons and ligaments are both dense, regularly arranged connective tissues. The surface of the tendon is enveloped in a white, glistening, synovial-like membrane, called the epitenon, which is continuous on its inner surface with the endotenon, a thin layer of connective tissue that binds collagen fibers and contains lymphatics, blood vessels, and nerves. In some tendons, the epitenon is surrounded by a loose areolar tissue called the paratenon, which functions as an elastic sheath through which the tendon can slide. In some tendons, the paratenon is replaced by a true synovial sheath or bursa consisting of two layers lined by synovial cells, called the tenosynovium, within which the mesotendon carries important blood vessels to the tendon.1 In the absence of a synovial lining, the paratenon often is called a tenovagina. Together the epitenon and the paratenon compose the peritenon (Fig. 1.1). The blood supply to tendons has several sources, including the perimysium, periosteal attachments, and surrounding tissues. Blood supplied through the surrounding tissues reaches the tendon through the paratenon, mesotenon, or vincula. Vascular tendons are surrounded by a paratenon and receive vessels along their borders; these vessels then coalesce within the tendon. The relatively avascular tendons are contained within tendinous sheaths, and the mesotenons within these sheaths function as vascularized conduits called vincula. The muscletendon and tendon-bone junctions, along with the mesotenon, are the three types of vascular supply to the tendon inside the sheath. Other sources of nutrition2 include diffusional pathways from the synovial fluid, which provide an important supply of nutrients for the flexor tendons of the hand, for example. The nervous supply to a tendon involves mechanoreceptors located near the musculotendinous junction, which provide proprioceptive feedback to the central nervous system. Ligaments grossly appear as firm, white fibrous bands, sheets, or thickened strips of joint capsule securely anchored to bone. They consist of a proximal bone insertion, the substance of the ligament or the capsule, and a distal bone insertion. Because most insertions are no more than 1 mm thick, they contribute only a small amount to the volume and the length of the ligament. Bundles of collagen fibrils form the bulk of the ligament substance.3–5 Some ligaments consist of more than one band of collagen fibril bundles. For example, the anterior cruciate ligament (ACL) has a continuum of fiber lengths; different fibers 2

become taut throughout the range of motion.6 The alignment of collagen fiber bundles within the ligament substance generally follows the lines of tension applied to the ligament. This is in contrast to the alignment of collagen fiber bundles within the tendon, which is generally parallel to its longitudinal axis. In addition, thinner collagen fibrils extend the entire length of the tendon. Light microscopic examination has shown that the collagen bundles have a wave or crimp pattern. The crimp pattern of matrix organization may allow slight elongation of the ligament without incurring damage to the tissue.6 In some regions, the ligament cells align themselves in rows between collagen fiber bundles, but in other regions, the cells lack apparent orientation relative to the alignment of the matrix collagen fibers. Scattered blood vessels penetrate the ligament substance, forming small-diameter, longitudinal vascular channels that lie parallel to the collagen bundles. Nerve fibers lie next to some vessels, and, like tendon, nerve endings with the structure of mechanoreceptors have been found in some ligaments.4,7,8 Tendon and ligament insertions vary in size, strength, angle of the ligament collagen fiber bundles relative to the bone, and proportion of ligament collagen fibers that penetrate directly into bone.4,5,9 Based on the angle between the collagen fibrils and the bone and the proportion of the collagen fibers that penetrate directly into bone, investigators group tendon and ligament insertions into two types: direct and indirect. Direction insertions typically occur at the apophysis or epiphysis of bone, often within or around a synovial joint, and consist of sharply defined regions where the collagen fibers appear to pass directly into the cortex of the bone.9,10 Although the thin layer of superficial collagen fibers of direct insertions joins the fibrous layer of the periosteum, most of the tendon or ligament insertions consist of deeper fibers that directly penetrate the cortex, often at a right angle to the bone surface. The deeper collagen fibers pass through four zones with increasing stiffness: ligament substance, fibrocartilage, mineralized fibrocartilage, and bone.9,10 This four-zone interface is known as the fibrocartilaginous enthesis.11 Dissipation of force is achieved effectively through this gradual transition from tendon to fibrocartilage to bone. A larger area of fibrocartilage can be found on one side of the insertion, which is thought to be an adaptation to the compressive forces experienced by the tendon or ligament on that side.12 Conversely, indirect or oblique insertions, such as the tibial insertion of the medial collateral ligament of the knee or the femoral insertion of the lateral collateral ligament, typically occur at the metaphysis

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CHAPTER 1  Physiology and Pathophysiology of Musculoskeletal Tissues

Abstract

Keywords

Musculoskeletal structures contain tissue-specific cells, extracellular matrix, and fiber arrangements which impart their unique biologic and mechanical properties. Tendon, ligament, meniscus, articular cartilage, and bone all have different structures that determine their specific function. Furthermore, the healing potential and response to injury of these tissues is highly variable and dependent on a number of factors, including the presence of a surrounding vasculature and the ability of intrinsic cells to replicate and remodel the injured matrix. In this chapter, we review the structure, biology, healing response to injury, and potential augmentative therapies of tendon, ligament, meniscus, articular cartilage, and bone.

tendon ligament meniscus cartilage articular bone physiology

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CHAPTER 1  Physiology and Pathophysiology of Musculoskeletal Tissues

Tendon

Peritendon Paratenon Epitenon Endotenon Fibroblast Primary bundle Fibril Microfibril Collagen fibril Tropocollagen Fig. 1.1  Structural organization of tendon.

or diaphysis of bone without an intervening fibrocartilage zone. They usually cover more bone surface area than do direct insertions, and their boundaries cannot be easily defined because the collagen fibers pass obliquely along the bone surface rather than directly into the cortex.

Extracellular Matrix Tendons and ligaments consist of relatively few cells and an abundant extracellular matrix primarily containing collagen, proteoglycans, and water. Tenocytes (tendon-specialized fibroblasts) are the dominant cell of tendons, whereas fibroblasts are the dominant cells of ligaments. Tenocytes and fibroblasts form and maintain the extracellular matrix. Within ligaments, fibroblasts vary in shape, activity, and density among regions of the same tissue and with the age of the tissue.4,5,9,13 Both tenocytes and fibroblasts are spindle shaped, with fibroblasts being rounder, and extend between the collagen fibrils.14 Endothelial cells of small vessels and nerve cell processes are also present.4,5,9,13 Studies have shown that tendon and ligament contain a small population of resident stem cells which function to maintain tissue homeostasis during growth and repair.15–17 Type I collagen, which is the major component of the molecular framework, composes more than 90% of the collagen content of ligaments. Type III collagen constitutes approximately 10% of the collagen, and small amounts of other collagen types also may be present. Ligaments have a higher content of type III collagen than do tendons.18 All types of collagen have in common a triple helical domain, which is combined differently with globular and nonhelical structural elements. The triple helix conformation of collagen is stabilized mainly by hydrogen bonds between glycine residues and between hydroxyl groups of hydroxyproline. This helical conformation is reinforced by hydroxyproline-forming and proline-forming hydrogen bonds to the other two chains. The physical properties of collagen and its resistance to enzymatic and chemical breakdown rely on covalent cross-links within and between the molecules. Elastin is a protein that allows connective tissues to undergo large changes in geometry while expending little energy in the

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process. Tendons of the extremities possess small amounts of this structural protein, whereas most ligaments have little elastin (usually less than 5%), although a few, such as the nuchal ligament and the ligamentum flavum, have high concentrations (up to 75%). In most tendons, elastin is found primarily at the fascicle surface,19 comprising less than 1% of the tendon by dry weight, and it is responsible for the crimp pattern of the tendon when viewed by a light microscope. Elastin forms protein fibrils or sheets, but elastin fibrils lack the cross-banding pattern of fibrillar collagen and differ in amino acid composition, including two amino acids not found in collagen (desmosine and isodesmosine). In addition, unlike collagen, elastin amino acid chains form random coils when the molecules are unloaded. This conformation of the amino acid chains makes it possible for elastin to undergo some deformation without rupturing or tearing and then, when the load is removed, to return to its original size and shape. Approximately 1% of the total dry weight of tendon and ligament is composed of ground substance, which consists of proteoglycans, glycosaminoglycans, structural glycoproteins, plasma proteins, and a variety of small molecules. Most ligaments have a higher concentration of glycosaminoglycans than do tendons, due to the functional need for more rapid adaptation.18 Proteoglycans and glycosaminoglycans both have important roles in organizing the extracellular matrix and control the water content of the tissue.4,20–23 Tendon and ligaments contain two known classes of proteoglycans. Larger proteoglycans contain long negatively charged chains of chondroitin and keratan sulfate. Smaller proteoglycans contain dermatan sulfate. Because of their long chains of negative charges, the large articular cartilage-type proteoglycans tend to expand to their maximal domain in solution until restrained by the collagen fibril network. As a result, they maintain water within the tissue and exert a swelling pressure, thereby contributing to the mechanical properties of the tissue and filling the regions between the collagen fibrils. The small leucine-rich proteoglycans usually lie directly on the surface of collagen fibrils and appear to affect formation, organization, and stability of the extracellular matrix, including collagen fibril formation and diameter. They may also control the activity of growth factors by direct association.21,24 Although noncollagenous proteins contribute only a small percentage of the dry weight of dense fibrous tissues, they appear to help organize and maintain the macromolecular framework of the collagen matrix, aid in the adherence of cells to the framework, and possibly influence cell function. One noncollagenous protein, fibronectin, has been identified in the extracellular matrix of ligaments and may be associated with several matrix component molecules and with blood vessels. Other noncollagenous proteins undoubtedly exist within the matrix, but their identity and their functions have not yet been defined. Many of the noncollagenous proteins also contain a few monosaccharides and oligosaccharides.4,5

Injury Acute strains and tears to tendons and ligaments disrupt the matrix, damage blood vessels, and injure or kill cells. Damage to cells, matrices, and blood vessels and the resulting hemorrhage

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start a response that leads to a sequential process of inflammation, repair, and remodeling.25,26 These events form a continuous sequence of cell, matrix, and vascular changes that begins with the release of inflammatory mediators and ends when remodeling ceases.25 As with any injury to biologic tissue, acute inflammation lasts 48 to 72 hours after the injury and then gradually resolves as repair progresses. Some of the events that occur during inflammation, including the release of cytokines or growth factors, may help to stimulate tissue repair.25 These mediators promote vascular dilation and increase vascular permeability, leading to exudation of fluid from vessels in the injured region, which causes tissue edema. Blood escaping from the damaged vessels forms a hematoma that temporarily fills the injured site. Fibrin accumulates within the hematoma, and platelets bind to fibrillar collagen, thereby achieving hemostasis and forming a clot consisting of fibrin, platelets, red cells, and cell and matrix debris. The clot provides a framework for vascular and fibroblast cell invasion. As they participate in clot formation, platelets release vasoactive mediators and various cytokines or growth factors (e.g., transforming growth factor-β [TGF-β] and platelet-derived growth factor). Polymorphonuclear leukocytes appear in the damaged tissue and the clot. Shortly thereafter, monocytes arrive and increase in number until they become the predominant cell type. Enzymes released from the inflammatory cells help to digest necrotic tissue, and monocytes phagocytose small particles of necrotic tissue and cell debris. Endothelial cells near the injury site begin to proliferate, creating new capillaries that grow toward the region of tissue damage. Release of chemotactic factors and cytokines from endothelial cells, monocytes, and other inflammatory cells helps to stimulate migration and proliferation of the fibroblasts that begin the repair process.25 Overuse tendon injury is one of the more common forms of musculoskeletal injury and clinical causes of pain, although controversy exists in the literature about a universal classification and the responsible pathologic entities. A classification of Achilles tendon disorders27 provides a guide to the structural manifestations of overuse injury as follows: (1) peritendinitis, or inflammation of the peritenon; (2) tendinosis with peritendinitis; (3) tendinosis without peritendinitis; (4) partial rupture; and (5) total rupture. Other classifiers have added a sixth category, tendinitis, in which the primary site of injury is the tendon, with an associated reactive peritendinitis.28 The classification is not universal because some tendons lack a paratenon and instead have synovial sheaths; furthermore, it is unclear if certain histopathologic conditions are actually separate entities. For instance, human biopsy studies have been unable to show histologic evidence of acute inflammation within the tendon substance.29 Because of uncertainty regarding the histologic features of these conditions, several authors have suggested use of the term tendinopathy rather than tendinitis.30,31 Studies have shown that in cases of chronic tendinosis, the pathologic lesion is typical of a degenerative process rather than an inflammatory one and that this degeneration occurs in areas of diminished blood flow. Several authors have documented the existence of areas of marked degeneration without acute or chronic inflammatory cell accumulation in most of these cases.32–34 These changes are separate and distinct from the site of rupture.

A review of patients with chronic tendinitis syndrome revealed similar findings of tendon degeneration.27,35 Nirschl35 described the pathology of chronic tendinitis as “angiofibroblastic hyperplasia.” A characteristic pattern of fibroblasts and vascular, atypical, granulation-like tissue can be seen microscopically.35,36 Cells characteristic of acute inflammation are virtually absent. These observations suggest that factors other than mechanical overuse play an important role in the pathogenesis of these tendon lesions. In several studies, a correlation between age and the incidence of chronic tendinopathy has been identified.37,38 In vitro studies have shown decreased proliferative and metabolic responses of aging tendon tissue.39 Other causative factors include the lack of blood flow in certain areas (e.g., supraspinatus and Achilles tendon) that may predispose a tendon to rupture or may result in chronic tendinopathy.40 Biopsy specimens of young patients with symptoms of chronic tendinopathy have revealed a change in the morphology of tenocytes adjacent to areas of collagen degeneration.28

Repair Tendons and ligaments may possess both intrinsic and extrinsic capabilities for healing, and the contribution of each of these two mechanisms probably depends on the location, extent, and mechanism of injury and the rehabilitation program used after the injury. Several studies2,41–46 have suggested that the inflammatory response is not essential to the healing process and that these tissues possess an intrinsic capacity for repair. Recent research has isolated intrinsic stem cells within tendon and ligament, although their in vivo identities, niche, and role in healing remain controversial.17,47 Lindsay and Thomson43 were the first to show that an experimental tendon suture zone can be isolated from the perisheath tissues and that healing progressed at the same rate as when the perisheath tissues were intact. Later, in isolated segments of profundus tendon in rabbits, these researchers found anabolic and catabolic enzymes, which showed that an active metabolic process existed in the isolated tendon segments.44 As in other areas in the body, tendon healing proceeds in three phases: (1) an inflammatory stage, (2) a reparative or collagen-producing stage, and (3) a remodeling phase.

Inflammatory Phase Tendon and ligament healing begins with hematoma formation and an inflammatory reaction that includes an accumulation of fibrin and inflammatory cells. A clot forms between the two ends and is invaded by cells resembling fibroblasts and migratory capillary buds. Within 2 to 3 days of the injury, fibroblasts within the wound begin to proliferate rapidly and synthesize new matrix. They replace the clot and the necrotic tissue with a soft, loose fibrous matrix containing high concentrations of water, glycosaminoglycans, and type III collagen. Inflammatory cells and fibroblasts fill this initial repair tissue. Within 3 to 4 days, vascular buds from the surrounding tissue grow into the repair tissue and then canalize to allow blood flow to the injured tissue and across small tissue defects. This vascular granulation tissue fills the tissue defect and extends for a short distance into the surrounding tissue but has little tensile strength. The inflammatory phase is evident until the 8th to 10th day after injury.

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Reparative Phase As the repair progresses during the next several weeks, proliferating fibroblasts continue to produce fibrous tissue containing a high proportion of type III collagen. Collagen synthesis reaches its maximal level after approximately 4 weeks, and at 3 months, collagen synthesis continues at a rate 3 to 4 times that of normal tissue. Over time, water, glycosaminoglycan, and type III collagen concentrations decline, the inflammatory cells disappear, and the concentration of type I collagen increases. Newly synthesized collagen fibrils increase in size and begin to form tightly packed bundles, and the density of fibroblasts decreases. Matrix organization increases48–51 as the fibrils begin to align along the lines of stress, the number of blood vessels decreases, and small amounts of elastin may appear within the site of injury. The tensile strength of the repair tissue increases as the collagen concentration increases. Remodeling Phase Repair of many tendon and ligament injuries results in an excessive volume of highly cellular tissue with limited mechanical properties and a poorly organized matrix. Remodeling reshapes and strengthens this tissue by removing, reorganizing, and replacing cells and matrix.25 In most tendon and ligament injuries, evidence of remodeling appears within several weeks of injury as fibroblasts and macrophages decrease, fibroblast synthetic activity decreases, and fibroblasts and collagen fibrils assume a more organized appearance. As these changes occur in the repair tissue, collagen fibrils grow in diameter, the concentration of collagen and the ratio of type I to type III collagen increase, and the water and proteoglycan concentrations decline. During the months after the injury occurs, the matrix continues to align, presumably in response to loads applied to the repair tissue. The most apparent signs of remodeling disappear within 4 to 6 months of injury. However, removal, replacement, and reorganization of repair tissue continue to some extent for years.50,52,53 The mechanical strength of the healing tendon and ligament increases as the collagen becomes stabilized by cross-links and the fibrils assemble into fibers.

Factors Affecting Healing Among the most important variables that affect healing of tendon and ligament are the type of tendon or ligament, the size of the tissue defect, and the amount of load applied to the repair tissue. For example, injuries to capsular and extra-articular ligaments stimulate production of repair tissue that will fill most defects, but injuries to intra-articular ligaments, such as the ACL, often fail to produce a successful repair response. Treatments that achieve or maintain apposition of torn tissue and that stabilize the injury site decrease the volume of repair tissue necessary to heal the injury, which can benefit the healing process. Such treatments may also minimize scarring and help to provide near-normal tissue length. For these reasons, avoidance of wide separation of ruptured tendon or ligament ends and selection of treatments that maintain some stability at the injured site during the initial stages of repair are generally desirable. Early excessive loading in the immediate postoperative period may have a deleterious effect on tendon and ligament healing

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by disrupting the repair tissue, leading to gap formation and ischemia, adverse changes in tendon matrix, and possible rupture.4,25,54–56 However, controlled loading of tendon and ligament repair tissue can promote healing and enhance the mechanical and biologic characteristics of tendon-to-bone healing.57 The optimal amount of tension necessary to promote an acceptable clinical response is currently not well understood and depends on the type of tissue and healing environment, but it is clear that remodeling of collagen scar tissue into mature tendon tissue depends on the presence of tensile forces.58,59 The concept of immediate passive mobilization after flexor tendon repair in the hand was introduced by Kleinert and coworkers,60 who showed that, during limited active extension, reciprocal relaxation of the flexor tendons occurs, allowing passive extension of the repaired tendon. This controlled passive motion was found to be effective experimentally and clinically in decreasing the tethering effect of adhesions and in improving the rates of tendon repair, gliding function, and strength of the tendon.

Methods for Augmentation of Tendon and Ligament Healing A large body of research has demonstrated the potential for growth factors to improve tendon and ligament tissue healing by stimulation of cell proliferation, chemotaxis, matrix synthesis, and cell differentiation (summarized in Table 1.1). In addition to multifunctional cytokines such as TGF-β and platelet-derived growth factor, work has focused on recapitulating the cellular and molecular signals that are expressed during embryonic tendon development, such as scleraxis and TGF-β3.61 However, challenges in the delivery of these growth factors, specifically regarding the optimal carrier vehicles and proper dosing regimen, to the desired site still remain. Platelet-rich plasma (PRP), an autologous blood concentrate, can be used to locally deliver a high concentration “cocktail” of cytokines and has gained popularity as a treatment modality for tendon and ligament injuries. Recent studies have reported potentially promising results with the use of PRP to augment healing of rotator cuff repair62–64 and patellar tendinopathy.65 However, the results of PRP for augmentation of tendon and ligament healing have been variable, which can partially be attributed to the lack of understanding of the optimal PRP formulation for different tissues and pathologies, as well as the tremendous variability in the methods of PRP production among commercial systems.66,67 To complicate matters further, within a given separation technique, there is a high degree of intersubject and intrasubject variability in the composition of PRP produced.68 Cell-based approaches appear promising for tendon and ligament tissue engineering and improvement of healing. Therapies using mesenchymal stem cells (MSCs) derived from adipose and bone marrow to augment tendon and ligament healing have garnered the most attention due to their multipotent potential and ability to exert a paracrine effect to modulate and control inflammation, stimulate endogenous cell repair and proliferation, inhibit apoptosis, and improve blood flow.14,69 However, like PRP augmentation therapy, continued research is needed to identify the optimal cell source and the ideal treatment protocol needed to drive differentiation of these or neighboring

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TABLE 1.1  Growth Factors in Soft Tissue Repair Biologic Factor

Functions

Reference

TGF-β

Influx of mononuclear cells and fibroblasts Enhanced collagen deposition

GDF 5/6/7

Influx of mononuclear cells and fibroblasts Enhanced collagen deposition

IGF-1

Proliferation of fibroblasts Enhanced collagen deposition

PDGF-B

Influx of mononuclear cells and fibroblasts Enhanced angiogenesis Enhanced collagen deposition

bFGF

Proliferation of fibroblasts Enhanced collagen deposition

HGF

Enhanced angiogenesis Enhanced collagen deposition Enhanced angiogenesis Enhanced collagen deposition

Lee J et al: Iowa Orthop J 1998 Spindler KP et al: J Orthop Res 2002 Spindler KP et al: J Orthop Res 2003 Kashiwagi K et al: Scand J Plast Reconstr Surg Hand Surg 2004 Kim HJ et al: Connect Tissue Res 2007 Kim HM et al: Connect Tissue Res 2011 Manning CN et al: J Orthop Res 2011 Kovacevic D et al: Am J Sports Med 2011 Wolfman NM et al: J Clin Invest 1997 Aspenberg P et al: Acta Orthop Scand 1999 Rickert M et al: Growth Factors 2001 Forslund C et al: J Orthop Res 2003 Virchenko O et al: Scand J Med Sci Sports 2005 Fealy S et al: Am J Sports Med 2006 Dines JS et al: J Shoulder Elbow Surg 2007 Saiga K et al: Biochem Biophys Res Commun 2010 Date H et al: J Orthop Res 2010 Abrahamsson SO et al: J Orthop Res 1991 Abrahamsson SO et al: J Orthop Res 1996 Kurtz CA et al: Am J Sports Med 1999 Dahlgren LA et al: J Orthop Res 2002 Dahlgren LA et al: J Orthop Res 2005 Provenzano PP et al: BMC Physiol 2007 Lee J et al: Iowa Orthop J 1998 Hildebrand KA et al: Am J Sports Med 1998 Nakamura N et al: Gene Ther 1998 Kobayashi M et al: J Shoulder Elbow Surg 2006 Uggen C et al: Arthroscopy 2010 Hee CK et al: Am J Sports Med 2011 Lee J et al: Iowa Orthop J 1998 Cool SM et al: Knee Surg Sports Traumatol Arthrosc 2004 Saiga K et al: Biochem Biophys Res Commun 2010 Date H et al: J Orthop Res 2010 Ueshima K et al: J Orthop Sci 2011

PRP

VEGF BMP-12

Enhanced angiogenesis Enhanced collagen deposition Enhanced ossification Enhanced angiogenesis Enhanced collagen deposition

Murray MM et al: J Orthop Res 2006 Murray MM et al: J Orthop Res 2007 Joshi SM et al: Am J Sports Med 2009 Boyer MI et al: J Orthop Res 2001 Petersen W et al: Arch Orthop Trauma Surg 2003 Aspenberg P et al: Scand J Med Sci Sports 2000 Lou J et al: J Orthop Res 2001 Seeherman HJ et al: J Bone Joint Surg Am 2008

bFGF, Basic fibroblast growth factor; BMP-12, bone morphogenetic protein-12; GDF, growth/differentiation factor; HGF, human growth factor; IGF-1, insulin-like growth factor-1; PDGF-β, platelet-derived growth factor-β; PRP, plasma-rich protein; TGF-β, transforming growth factor-β; VEGF, vascular endothelial growth factor.

cells into mature tenocytes and fibroblasts. Recent studies have identified resident tissue-specific stem cells in the perivascular regions of native tendon and ligament that detach from vessels in response to injury, migrate into the interstitial space, and deposit extracellular matrix,70,71 although their precise potential for use in augmenting tendon and ligament healing remains to be elucidated. Research has also investigated scaffold materials to augment tendon repair and ligament reconstruction. Porcine-derived small intestine submucosa has been used as a collagen scaffold

to augment Achilles tendon and rotator cuff tendon repair. However, negative clinical results have been reported, including inflammatory/immunologic response to the small intestine submucosa material believed to be due to residual porcine DNA in the implant.72,73 Various other allografts and xenografts, such as collagen allograft matrices and porcine dermal xenografts, are commercially available and differ from porcine small intestine submucosa in both biologic and mechanical composition.74,75 Nanomaterials are promising for tendon and ligament tissue engineering because the microstructure of the material mimics

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CHAPTER 1  Physiology and Pathophysiology of Musculoskeletal Tissues Superficial layer of random collagen fibers

Deep layer of circumferential collagen fibers

B

A

Fig. 1.2  (A) Diagram of collagen fiber architecture throughout the meniscus. Collagen fibers of the thin superficial sheet are randomly distributed in the plane of the surface and are predominantly arranged in a circumferential fashion deep in the substance of the tissue. (B) Macrophotograph of bovine medial meniscus with the surface layer removed, showing the large circumferentially arranged collagen bundles of the deep zone. ([A] Modified from Bullough PG, Munuera L, Murphy J, et al. The strength of the menisci of the knee as it relates to their fine structure. J Bone Joint Surg Br. 1970;52:564–570. [B] From Proctor CS, Schmidt MB, Whipple RR, et al. Material properties of the normal medial bovine meniscus. J Orthop Res. 1989;7:771–782.)

native extracellular matrix. Multiphasic scaffolds are being used to create bone-ligament composites.76 In addition to various scaffold materials and cell types, it has become clear that mechanical stimulation of the neotissue is also critical to optimize the structure and composition of the tissue.77 The specific scaffold can be modified in vitro by seeding marrow stromal cells on the scaffold and applying cyclic stretching to increase the alignment of cells, as well as to improve the production and orientation of collagen. When applied in vivo, such a tissue-engineered scaffold could serve to accelerate the healing process, ultimately helping to make a better neoligament or tendon.

Anterior 30°

30°

60° 120° 60°

90°

120° 90°

150°

150°

MENISCUS

Posterior

Structure 78

Human menisci are semilunar in shape and consist of a sparse distribution of cells surrounded by an abundant extracellular matrix.79–81 The meniscus functions to optimize force transmission and provide stability to the knee. The medial meniscus is the dominant secondary stabilizer in an ACL-deficient knee during the Lachman maneuver,82 whereas the lateral meniscus is the dominant secondary stabilizer in an ACL-deficient knee during the pivot shift maneuver.83 Within the meniscus lies an anisotropic, inhomogeneous, and highly ordered arrangement of collagen fibrils. The meniscal surface is composed of a randomly woven mesh of fine collagen type II fibrils that lie parallel to the surface. Below this surface layer, large, circumferentially arranged collagen fiber bundles (mostly type I) spread through the body of the tissue (Fig. 1.2).84,85 These circumferential collagen bundles give menisci great tensile stiffness and strength parallel to their orientation.85 The collagen bundles insert into the anterior and the posterior meniscal attachment sites on the tibial plateau, providing for rigid and strong attachment sites. Fig. 1.2A illustrates these large fiber bundles and the thin superficial surface layer. Fig. 1.2B is a photograph of a bovine medial meniscus with the surface layer removed, showing the large collagen bundles of the deep zone.

Fig. 1.3  Radial collagen fiber bundles of the meniscus. Radial tie fibers consisting of branching bundles of collagen fibrils extend from the periphery of the meniscus to the inner rim in every radial section throughout the meniscus. They are more abundant in the posterior sections and gradually diminish in number as the sections progress toward the anterior region of the meniscus. (Modified from Kelly MA, Fithian DC, Chern KY, et al. Structure and function of meniscus: basic and clinical implications. In: Mow VC, Ratcliffe A, Woo SL, eds. Biomechanics of Diarthrodial Joints. Vol 1. New York: Springer-Verlag; 1990.)

Radial sections of meniscus (Fig. 1.3) show radially oriented bundles of collagen fibrils, or “radial tie fibers,” among the circumferential collagen fibril bundles, weaving from the periphery of the meniscus to the inner region.85,86 These tie fibers help to increase the stiffness and the strength of the tissue in a radial direction, thereby resisting longitudinal splitting of the collagen framework. In cross section, these radial tie fibers appear to be more abundant in the posterior sections than in the anterior sections of the meniscus.87 Unlike articular cartilage, the peripheral 25% to 30% of the lateral meniscus and the peripheral 30% of the medial meniscus78,88–90 have a blood supply, and the peripheral regions of the meniscus, especially the meniscal horns,91,92 have a nerve supply as well. Branches from the geniculate arteries form a capillary

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SECTION 1  Basic Principles

plexus along the peripheral borders of the menisci, with the medial inferior geniculate artery supplying the peripheral medial meniscus and the lateral inferior geniculate artery supplying the peripheral lateral meniscus.88,89 Small radial branches project from these circumferential parameniscal vessels into the meniscal substance.90 The central aspects of the meniscus do not have a direct arterial supply and instead receive nutrients primarily through synovial fluid diffusion.

Extracellular Matrix The mechanical functions of the menisci depend on a highly organized extracellular matrix consisting of fluid and a macromolecular framework formed of collagen (types I, II, III, V, and VI), proteoglycans, elastin, and noncollagenous proteins, along with the cells that maintain this matrix. Based on morphologic characteristics, two major types of meniscal cells exist.80,93 Near the surface, the cells have flattened ellipsoid or fusiform shapes and are considered more fibroblastic; in the deep zone, the cells are spherical or polygonal and considered more chondrocytic. The superficial and the deep meniscal cells appear to have different metabolic functions and perhaps different responses to loading.94 Like most other mesenchymal cells, these cells lack cell-to-cell contacts. Because most of the cells lie at a distance from blood vessels, they rely on diffusion through the matrix for transport of nutrients and metabolites. The membranes of meniscal cells attach to matrix macromolecules through adhesion proteins (e.g., fibronectin, thrombospondin, and type VI collagen).80 The matrix, particularly the pericellular region, protects the cells from damage due to physiologic loading of the tissue. Deformation of the macromolecular framework of the matrix causes fluid flow through the matrix94,95 and influences meniscal cell function. Because meniscal tissue is more fibrous than is hyaline cartilage, some authors have proposed that meniscal cells be called fibrochondrocytes.80,96 Water comprises 65% to 75% of the total weight of the meniscus.94,95,97 Some portion of this water may reside within the intrafibrillar space of the collagen fibers.98,99 Most of the water is retained within the tissue in the solvent domains of the proteoglycans due to both their strong hydrophilic tendencies and the Donnan osmotic pressure exerted by the counter ions associated with the negative charge groups on the proteoglycans.94,100,101 Because the pore size of the tissue is extremely small (160/100 mm Hg in adults) should initially be restricted from all participation pending a thorough workup and control of blood pressure.20 Special attention should be directed at excluding MFS (and related connective tissue disorders, such as Ehlers-Danlos and Loeys-Dietz syndromes), which all manifest genetic deficiencies of connective tissue proteins and thereby increase risk of dissection of the aorta and other smaller arteries. Clinical manifestations of MFS may also include the ocular, musculoskeletal, respiratory, neurologic, and integumentary systems (Box 11.2). For the diagnosis of MFS, revised Ghent criteria were published

Musculoskeletal • Tall stature (males taller than 183 cm [6 feet] and females taller than 178 cm [5 feet, 10 inches]); Note: Tall stature is not formally considered a criterion of the revised Ghent nosology • Increased upper segment to lower segment ratio; increased arm span relative to height • Arachnodactyly (wrist and thumb sign) • Pectus carinatum/excavatum • Hindfoot deformity or plain pes planus • Protrusio acetabuli • Scoliosis, kyphosis • Reduced elbow extension Facial Features • Dolichocephaly • Enophthalmos • Downslanting palpebral fissures • Malar hypoplasia, retrognathia Other Systemic Features • Pneumothorax • Dural ectasia • Skin striae Modified from Loeys BL, Dietz HC, Braverman AC, et al. The revised Ghent nosology for the Marfan syndrome. J Med Genet. 2010;47(7):476–485; Giese EA, O’Connor FG, Brennan FH, Depenbrock PJ, Oriscello RG. The athletic preparticipation evaluation: cardiovascular assessment. Am Fam Physician. 2007;75(7):1008–1014.

in 2010 and consequently are not referenced in the PPE-4.21 The revised Ghent criteria have placed more weight on the three cardinal features of MFS17: aortic root enlargement,18 ectopia lentis,19 and FBN1 mutation to differentiate the manifestations of the cardiovascular, ocular, and skeletal organ systems. In the absence of family history, the presence of both aortic root changes and ectopia lentis19 are sufficient to make the diagnosis. However, these two features are not easily assessed in the PPE setting, and thus clinicians should be vigilant to identify any possible physical stigmata of MFS, particularly in male athletes taller than 183 cm (6 feet) and female athletes taller than 178 cm (5 feet, 10 inches). Athletes with a family history of MFS or two or more of the aforementioned physical examination findings should be referred for cardiology consultation to comprehensively assess aortic morphology.22 Given the greater emphasis on ectopia lentis in the revised criteria, a referral to ophthalmology for slit-lamp testing is also prudent.21 Significant debate exists regarding noninvasive cardiac screening during the PPE, and although comprehensive coverage of this

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subject is beyond the scope of this chapter, related controversies are discussed in detail elsewhere in this book. The current AHA guidelines limit the use of electrocardiography (ECG) screening to small cohorts of young people aged 12 to 25 years with suspected cardiovascular pathology based on history and physical examination, provided that close physician supervision and quality control are achieved.16 The guidelines suggest that limitations of using a 12-lead ECG, including poor sensitivity and specificity, should be anticipated. Otherwise, current guidelines do not agree on systematic inclusion of ECG in preparticipation screening of athletes and nonathletes to identify congenital or other cardiovascular abnormalities.16,23 These guidelines are in contradistinction with recommendations of the International Olympic Committee24 and the European Society of Cardiology (ESC),25 which recommend the use of a screening ECG during PPEs. Routine ECG screening is supported by Italian data showing a 90% decrease in SCD rate with the inclusion of ECG in PPE cardiovascular screening.14 The dispute in recommendations among societies is largely based on studies performed in Italy26–28 which demonstrated that an ECG had a 77% greater power to detect HCM than did a history and physical examination alone.28 There are important sex and race differences in SCD rates that may influence the decision to use the ECG as part of the PPE. It has been shown that there is an increased likelihood of obtaining abnormal ECGs with PPEs of older adolescent males and a decreased likelihood with females.29 Male athletes have been shown to be at 5 to 6 times greater risk than female athletes for SCD.30 In addition, the rate of SCD among black athletes has been shown to be 3 to 5 times higher in comparison with all other ethnic groups.30 A systematic approach to interpreting screening ECGs as part of the PPE are the Seattle Criteria.31 These criteria were initially created to balance the sensitivity and specificity of ECG use, while maintaining a practical and concise checklist for physicians to use for ECG interpretation with athletes. The goal of the Seattle Criteria is to aid physicians in distinguishing ECG abnormalities that may be considered normal in athletes from abnormal ECG findings that are concerning for pathology. However, use of the Seattle Criteria has not been shown to decrease morbidity or reduce incidence of SCD among athletes.31–33 The Refined Criteria published in 2014 for ECG interpretation have been shown to decrease the occurrence of false-positive and falsenegative results.33 Data suggest that the Refined Criteria outperform the ESC recommendations and Seattle Criteria by reducing false-positive rates of ECG interpretation in black athletes from 40.4% (ESC) and 18.4% (Seattle Criteria) to 11.5%, and in white athletes from 16.2% (ESC) and 7.1% (Seattle Criteria) to 5.3%.33,34 These studies suggest that established criteria and standardized guidelines for ECG interpretation are useful to avoid false-positive interpretations and potentially costly and unnecessary additional workup. Recently, the American Medical Society for Sports Medicine (AMSSM) formed a task force to address the need for preparticipation cardiovascular screening in young competitive athletes. Although the AMSSM supported the position that the ECG increases early detection of cardiac disorders associated with SCD, the absence of clear outcome-based research precluded the endorsement of using the ECG as a universal cardiovascular

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screening strategy.15 If physicians choose to incorporate routine ECG screening into their PPEs, proficiency in accurate ECG interpretation and access to cardiology resources are of paramount importance to maximize its utility without unnecessary cost escalation. However, the use of ECG as a global cardiovascular preparticipation screening modality in athletes is limited by the low prevalence of SCD in athletes. A newer area of debate is use of an echocardiogram as part of the routine PPE cardiac screening protocol. It has been demonstrated that ECGs have a higher rate of false-positives as a screening modality in comparison with echocardiogram for detection of causative risk factors for HCM.17 This is in large part due to the similarities between ECG changes that are physiologic resulting from physical conditioning and the structural and electrical changes found in HCM. The increasing availability of portable ultrasound has led to the development of the Early Screening for Cardiac Abnormalities with Preparticipation Echocardiography (ESCAPE) protocol, which produced accuracy and reliability in diagnosing results indicative of HCM and aortic root dilation.35 The protocol demonstrated that limited echocardiography measurements by noncardiologists were not statistically different from values obtained from cardiologists trained in echocardiography interpretation.34,35 However, as with ECG interpretation, the ability of the team physician, not frequently a cardiologist, to accurately and efficiently interpret echocardiograms is paramount to this modality being as useful as is reported in the literature. Reducing the incidence of SCD is a noble goal, but clinicians should be aware of the high false-positive rates associated with PPE ECGs, along with high costs, increased use of medical resources, potentially erroneous disqualification of athletes from participation, and the potential for lost “life-years” following needless sedentary lifestyle recommendations.36 Therefore although controversial, at present there are insufficient data available to promote universal use of screening ECGs or echocardiograms in asymptomatic individuals for detecting cardiovascular disease. A rational decision to include ECG or echocardiography as part of the PPE could conceivably be made in the appropriate setting and with sufficient provider training and resources.

Pulmonary System It is imperative that athletes be questioned regarding a personal or family history of asthma or exercise-induced bronchoconstriction (affecting 50% to 90% of athletes), asthma-like symptoms and their severity, use of bronchodilators, degree of asthma control, and the use of tobacco or exposure to secondhand smoke.37 A thorough auscultation of the lung fields should be performed during the PPE. Proper diagnosis may require provocative pulmonary function testing, and in patients with exercise-induced bronchospasm, this is imperative to evaluate for undiagnosed asthma.32 Because an athlete’s symptoms may be related to the environment, these tests may need to be performed in environmental conditions that stimulate symptoms.37 Athletes who are recovering from an asthma exacerbation and who are actively wheezing must be restricted from sports activity until stabilized.32 Vocal cord dysfunction should be considered as a potential diagnosis in athletes with asthma-like symptoms who fail to respond

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to usual bronchodilator therapy. Athletes with stable asthma or exercise-induced bronchoconstriction can usually be cleared to participate in sports, unless they are recovering from a recent asthma exacerbation. It may be indicated for athletes with severe underlying asthma or pulmonary disease to have a rescue inhaler available as a condition for athletic participation.32

Gastrointestinal/Genitourinary System The abdomen should be thoroughly examined for masses, tenderness, rigidity, or enlargement of the liver or spleen. The AMSSM, among other sports medicine professional organizations, recommends that a detailed genitourinary examination should be performed to assess for masses, testicular descent, tenderness, and hernias in male athletes.2 Liver or spleen enlargement is a contraindication to participation in sports. The athlete with a solitary kidney or testicle may be cleared to participate in contact sports; however, each athlete should be counseled on an individual basis about the harmful consequences of injury, and appropriate protective gear should be mandated during practice and competition. Acute diarrheal illness is a contraindication to participation in sports unless symptoms are mild and the athlete remains well hydrated.2 Musculoskeletal System The musculoskeletal history has a very high sensitivity (92%) for detecting abnormalities, and thus the physician should inquire about current injuries and a history of injuries requiring evaluation, casting, bracing, surgery, or missed participation.5,38 Given the high sensitivity of the history, a screening musculoskeletal examination is sufficient but should be supplemented with a more in-depth joint-specific examination when pathology is suspected.2 Box 11.3 reviews the 11-step general musculoskeletal screening examination. In general, literature suggests that generalized joint laxity, imbalance in strength ratios, excessive foot pronation or supination, level of physical maturity, multidirectional BOX 11.3  General Musculoskeletal

Screening Examination

The general musculoskeletal screening examination consists of the following: (1) inspection, athlete standing, facing toward examiner (symmetry of trunk, upper extremities); (2) forward flexion, extension, rotation, lateral flexion of neck (range of motion, cervical spine); (3) resisted shoulder shrug (strength, trapezius); (4) resisted shoulder abduction (strength, deltoid); (5) internal and external rotation of shoulder (range of motion, glenohumeral joint); (6) extension and flexion of elbow (range of motion, elbow); (7) pronation and supination of forearm or wrist (range of motion, elbow and wrist); (8) clench fist, then spread fingers (range of motion, hand and fingers); (9) inspection, athlete facing away from examiner (symmetry of trunk, upper extremities); (10) back extension, knees straight (spondylolysis/spondylolisthesis); (11) back flexion with knees straight, facing toward and away from examiner (range of motion, thoracic and lumbosacral spine; spine curvature; hamstring flexibility); (12) inspection of lower extremities, contraction of quadriceps muscles (alignment, symmetry); (13) “duck walk” 4 steps (motion of hip, knee, and ankle; strength; balance); (14) standing on toes, then on heels (symmetry, calf; strength; balance). From Bernhardt DT, Roberts WO, eds. Preparticipation Physical Evaluation. ed 4. Elk Grove Village, IL: American Academy of Pediatrics; 2010.

balance, and body mass all may be predictive for risk of injury in the adolescent athlete population.39,40 The PPE-4 recommends functional testing with the duck walk and single-leg hop as part of the musculoskeletal examination.2 These physical examination tests are time-efficient, require no additional equipment, and may help clinicians to effectively assess multiple physical attributes during the PPE. Clearance for sport participation is determined based on the degree and type of injury or condition, the ability of the injured athlete to compete safely, and the necessities of a given sport. In general, if the athlete has no tenderness to palpation, has normal range of motion (ROM) and normal strength in the affected area, and performs adequately on functional tests, clearance for sport participation can typically be given. Use of protective padding, taping, or bracing may also enable the athlete to participate in sports safely.2

Neurologic System Physicians should inquire about prior concussions or head injuries, seizure disorders, frequent or exertional headaches, problems with recurrent burners or stingers (transient brachial plexopathy), or a prior transient quadriparesis or cervical cord neuropraxia.2 A positive history demands a thorough neurologic examination, including assessment of cognition, cranial nerves, motor-sensory function, muscle tone, reflexes, coordination testing, and gait evaluation.5 Athletes who have a history of multiple concussions or who have prolonged postconcussive symptoms should be counseled about risks and encouraged to discuss with their families the potential for harm, although not presently well understood, that may result from repeated concussions.5 The Sport Concussion Assessment Tool (SCAT),41 exercise testing such as the Buffalo Concussion Treadmill Test,42 vestibuloocular system testing such as the Vestibular/Ocular Motor Screening Assessment,43 vestibulospinal testing such as the Balance Error Scoring System,32 and neuropsychological testing44 may increase the sensitivity of detecting residual concussion symptoms. Athletes with persistent symptoms should be disqualified and cleared for participation only after they have successfully completed a graded return-to-sport protocol without recurrence of concussion-related signs or symptoms.41 Likewise, after sustaining a single stinger, athletes must be asymptomatic with a normal neurologic examination prior to medical clearance, although further diagnostic testing may be necessary for persistent symptoms or recurrent injury.45 Athletes who have had transient quadriparesis should have an MRI to evaluate for spinal stenosis.46 For atypical, exerciserelated headaches, advanced intracranial imaging may be necessary to evaluate for occult causes of secondary headaches.47 Although a history of seizures does not preclude athletic participation, sports-specific modifications may be needed, particularly for persons involved in water sports.2 Hematologic and Infectious Disease The risks of transmission of human immunodeficiency virus, hepatitis B, and hepatitis C during routine sports participation are considered minimal, and the presence of these infections is not considered a contraindication to participation.48,49 However, guidelines from the National Hemophilia Foundation advise

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that athletes with bleeding disorders such as hemophilia be restricted from contact or collision sports. In addition, a diagnosis of infectious mononucleosis should preclude all sports participation for the first 3 weeks because of a significantly elevated risk of splenic rupture.50 Light, noncontact activity may be recommended 3 weeks after diagnosis if the athlete is asymptomatic and without complications. Participation in full-contact sports should be deferred for at least 28 days from the start of symptoms or from clinical diagnosis if the symptom onset date is imprecise.2 Febrile illness is also a contraindication to participation in sports because of increased susceptibility to heat illness and because it may occasionally accompany conditions such as myocarditis that may make sports participation unsafe.2 Sickle cell trait (SCT) is associated with 2% of deaths in National Collegiate Athletic Association (NCAA) football players.51 Athletes should be questioned about a personal or family history of SCT or sickle cell disease (SCD). Phenotypic expression is varied, and thus medical clearance or exercise modifications should be made on an individual basis. To prevent exertional sickling collapse, athletes with SCT should avoid strenuous activity in extreme heat and high-altitude environments, especially when they are poorly acclimated.52 Deaths from exertional sickling have reportedly been more common among football players as well.53 In recognition of these risks, the NCAA in 2010 mandated that all Division I and II athletes be screened for SCT and that the status be established at the time of the PPE32; however, athletes may decline screening.51 This requirement by the NCAA was extended to Division III competitors as of 2014.54 If SCT is confirmed with screening, affected athletes are offered counseling on its implications to their health, athletics, and family planning.55 Debate still exists on universally screening athletes for SCT. Some proponents have estimated that universal screening of NCAA Division I student athletes would save seven lives over 10 years.54 Based on the available evidence, we recommend that all active individuals be screened for SCT with a 1-time hemoglobin electrophoresis test.

Endocrine System Persons with types I and II diabetes mellitus can participate in sports without restriction but are encouraged to monitor blood glucose more frequently, maintain a balanced diet, adjust medications appropriately, and hydrate suitably.2 Education regarding activities with relatively higher risk of cutaneous foot injury such as hiking, rock climbing, or surfing is also recommended. Obese patients should not be discouraged from participating in sports but should receive counseling on lifestyle changes such as dietary and activity modifications, as well as prevention of heat-related illness.2 Athletes in weight-sensitive sports such as wrestling and boxing, and aesthetic sports such as diving and figure skating are at risk for eating disorders, particularly in females.32 The female athlete triad consists of disordered eating, amenorrhea, and decreased bone mineral density. A history of stress fractures with prolonged healing in a female athlete should increase clinical suspicion for this treatable yet potentially deadly medical condition. These patients should undergo a multidisciplinary treatment program with further risk stratification before they return to sports. It is recommended that sports medicine

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professionals include female athlete triad risk assessment in the standard PPE and consider expanding the history to include full menstrual history, reasons for hormonal therapy use, and questions concerning eating disorders and eating irregularities.56

Dermatology Athletes should be asked about a history of dermatologic pathology, with particular attention to highly communicable infections such as herpes or methicillin-resistant Staphylococcus aureus.2 The athlete should be inspected for evidence of common cutaneous infections such as herpes gladiatorum, tinea gladiatorum, impetigo, molluscum contagiosum, warts, and communityacquired methicillin-resistant S. aureus.2 Prevention of transmission is critical and may be achieved by covering the infected site, using prophylactic medications as indicated, refraining from sharing personal items, thoroughly cleaning athletic equipment, or ultimately restricting the athlete from participation for a specific period based on the characteristics of the sport, the type of microorganism involved, and governing body guidelines.2 Immunizations Lack of immunizations does not inherently affect sports participation, but many states require them for school enrollment, and thus the PPE provides a good opportunity to discuss vaccinations.2 Athletes traveling internationally for competition should be aware of local immunization guidelines recommended by the Centers for Disease Control and Prevention.2 Medications and Allergies It is imperative that medical personnel are familiar with regulations established by drug-enforcing agencies such as the World Anti-Doping Agency. Some medications are strictly prohibited, whereas others, such as albuterol, may be used with therapeutic use exemption.5 Over-the-counter drugs and supplements may contain banned substances and should also be thoroughly reviewed. The PPE provides a good opportunity to address the detrimental effects of illicit drug and alcohol use, particularly in the adolescent population. Medication, food, and environmental allergies should be documented in detail. Specifications should include the name of the allergen, the type of reaction, and whether athletes require an epinephrine autoinjector.2 Four recommendations for persons with a history of anaphylaxis include: 1. All medical personnel and athletes with allergies who may potentially require treatment with an epinephrine autoinjector should be trained in how to use it. 2. All medical kits should be stocked with an epinephrine autoinjector and over-the-counter diphenhydramine. 3. Athletes with allergies should carry an epinephrine autoinjector in their backpacks, have an additional one in their homes or dormitory rooms, and have over-the-counter diphenhydramine readily available at all times. 4. An emergency action plan (EAP) should be detailed for athletes with allergies during the PPE. Heat Illness Athletes with a history of exertional heat illness (EHI) are at enhanced risk for recurrent heat illness.57 Such athletes should be

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educated about preventive measures, including adequate hydration and gradual acclimatization over a period of 10 to 14 days. If possible, use of stimulant and antihistamine medications should be avoided during warm-weather activities.5 Athletes who use stimulant medications (e.g., for attention-deficit/hyperactivity disorder) and team health care professionals should be informed about the possible deleterious effects of using these medications in hot environments. The National Athletic Trainers’ Association (NATA) has guidelines for athletes to help mitigate risks involved with EHI.58 It is recommended that individuals are gradually acclimatized to heat over 7 to 14 days to prevent the risk of EHI. Athletes who are currently sick with any viral infection or fever or have a skin rash should be withheld from participation until the condition is resolved. It is recommended that players have access to fluids at all times. Athletes should consume sodiumcontaining food or fluids to help replace loss of sodium in sweat and/or urine. Monitoring proper fluid consumption and replacement can help to minimize body mass loss to 2% during activity participation, which should be measured before and after the activity. Athletes should also be encouraged to sleep a minimum of 7 hours per night in a cool environment, eat a balanced diet, and properly hydrate before, during, and after exercise. Of most importance, rest periods should consist of at least 3 hours for food, nutrients, and electrolytes to be properly digested and absorbed before the next practice or game. Cold-water or ice towels should be readily accessible for all patients because immediate whole-body cooling is essential to treat EHI.

Athletes With Special Needs The PPE-4 includes a chapter that discusses athletes with special needs and a separate form to aid the provider with unique issues affecting this patient population. The history and physical examination should be similar to that used with athletes who do not have special needs but may need to focus on diseases more common in this population such as seizures, hearing loss, vision loss, congenital heart disease, and renal disease.2 Athletes with Down syndrome should always be assessed for a history of atlantoaxial instability (AAI), and athletes with spinal cord injuries should be asked about difficulties with thermoregulation, autonomic dysreflexia, pressure ulcers, and use of urinary catheterization.2 The physical examination should focus on the visual, cardiovascular, musculoskeletal, neurologic, and dermatologic systems. Congenital heart disease is present in up to half of all athletes with Down syndrome and may require a cardiology referral for further testing prior to participation in sports.59 The neurologic examination in athletes with Down syndrome should include evaluation for symptomatic AAI, which may present with upper motor neuron signs such as spasticity, hyperreflexia, clonus, and clumsiness. Persons with symptomatic AAI should undergo lateral cervical spine flexion and extension plain x-ray views to assess stability.2 Wheelchair athletes should be evaluated for nerve entrapments, pressure ulcers, and overuse injuries of the shoulders, hands, and wrists.2

Conclusion The PPE has continued to evolve, with updated recommendations to perform a PPE for all children in an office-based setting. Despite these broad recommendations, evidence showing that the PPE reduces morbidity and mortality is scarce.4 The PPE-4 emphasizes that history, rather than physical examination, is most sensitive for gleaning information relevant to medical clearance for sports participation. Nonetheless, a thorough PPE using a systematic approach and current guidelines may help to identify those athletes who need additional investigation prior to safe athletic participation and may also aid in preparation by the sports medicine team and the athlete for any injuries or medical complications that may result from sports.

ON-FIELD EMERGENCIES The preceding section outlined the limitations in preventing potentially life-threatening events. Although rare, medical emergencies in sports will inevitably occur despite thorough preventive measures. This section outlines the core components of managing sports-related emergencies, including development of an effective EAP, the general approach to the collapsed athlete, and select examples of medical emergencies encountered on the playing field.

Emergency Action Plan Before hosting athletic events, every institution has a duty to formulate an EAP,60 which should be developed and reviewed annually as a coordinated effort by the medical team, school administrators, local emergency medical services (EMS), and first responders. The key components of the EAP are (1) effective communication, (2) training personnel, (3) acquiring equipment, (4) emergency transportation, (5) practice and review, and (6) postevent guidelines.61 Effective communication with local EMS is a critical link in the chain of survival. Communication systems such as telephones or two-way radios should be tested before each game. An EAP coordinator should be identified at each institution, and all other potential first responders should receive training in EAP guidelines, as well as in CPR and AED use. Resuscitation equipment should be centrally located and well marked for easy access. Personnel trained in basic life support (BLS) should have quick access to barrier masks for rescue breathing and an on-site AED. Providers trained in advanced cardiac life support (ACLS) may consider having advanced airways, oxygen delivery systems, and cardiac medications available.61 Other critical contents of a sideline physician’s emergency kit are listed in Box 11.4. A plan for efficiently directing EMS to the field of play should be in place, and on-site ambulance coverage is ideal at particularly high-risk events. In the event that medical personnel must leave the playing field to tend to an injured athlete, a plan for continued event coverage should be established.60 The EAP should be rehearsed on an annual basis, which will ensure a coordinated team effort, and the EAP should be evaluated frequently to ensure its durability. Lastly, a protocol for release of medical information should be established and an incident form should be available for documentation and evaluation purposes.61

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BOX 11.4  Recommended Contents of the Sideline Physician’s Emergency Bag Medications • Aspirin • Beta-agonist inhaler • Epinephrine • Oral glucose solution

• Skin stapler • Sterile drapes or towels • Nylon sutures: 3-0, 4-0, 5-0, 6-0 • Polyglactin sutures: 3-0, 4-0, 5-0 • Liquid cyanoacrylate adhesive • Compound benzoin tincture • Bacitracin or triple antibiotic ointment • Adhesive strips: Y4-, Y2-, and 1-in. wide • Nonadherent pads • Sterile gauze pads • Sterile adhesive dressings in various sizes • Hydrocolloid dressings • Protective skin covering • Aluminum chloride solution • Athletic tape • Latex and nonlatex (e.g., nitrile) gloves • Aftercare instructions for patients

Wound Care • Bandage scissors • Bandage tape • Sterile saline and sterile bowl (0.5–1 L) • 60-mL syringe for irrigation • Large-bore needles: 18 gauge or angiocatheter • Antibacterial cleansing agent • 1% lidocaine with and without epinephrine • Lidocaine jelly (2%) or LET gel for abrasions • Sterile scrub brush • Povidone-iodine • 5-mL syringes • 25-gauge needles (1 Y2-in. long) • Needle driver • Tweezers

Airway Devices • Pocket mouth-to-mouth mask • Cutting tool for facemask loops

Modified from Daniels JM, Kary J, Lane JA. Optimizing the sideline medical bag preparing for school and community sports events. Phys Sportsmed. 2005;33(12):9–16; Bouchard M. Sideline care of abrasions and lacerations: preparation is key. Phys Sportsmed. 2005;33(2):21–29.

TABLE 11.2  Initial Approach to the Collapsed Athlete Nontraumatic

Traumatic

BLS Assessment49 1. Check for responsiveness. 2. Activate the emergency response system; obtain and activate the AED. 3. Check for breathing and a carotid pulse for 5–10 s. If no pulse is present, initiate CPR with chest compressions first and then rescue breathing. If a pulse is present, begin rescue breathing. 4. Perform defibrillation with the AED when indicated.

ATLS Primary Survey41 Airway maintenance with cervical spine control Breathing and ventilation Circulation and hemorrhage control Disability/drugs: assessment of neurologic status Exposure: completely undress the patient but prevent hypothermia

ACLS Primary Assessment49 Airway: Maintain airway patency and use advanced airway management if needed. Breathing: Monitor ventilation and oxygenation and provide supplementary oxygen if needed. Circulation: Monitor CPR quality; monitor for arrhythmias; provide defibrillation, cardioversion, and administer cardiac drugs when needed; obtain intravenous or intraosseous access and provide fluids if needed; monitor glucose, temperature, and perfusion. Disability: Check neurologic function; check for responsiveness, levels of consciousness, and pupil dilation. Exposure: Remove clothing and observe for signs of trauma, bleeding, or medical alert bracelets.

ATLS Secondary Survey41 History: Allergies Medications Past illness/Pregnancy Last meal Events/Environment related to injury Physical examination: Thorough head-to-toe physical examination

ACLS, Advanced cardiac life support; AED, automated external defibrillator; ATLS, advanced trauma life support; BLS, basic life support; CPR, cardiopulmonary resuscitation.

General Approach to the Collapsed Athlete A pivotal duty of physicians is to be a keen observer of on-field emergencies, because the injury mechanism is often critical to the initial management of the athlete. For example, the clinical approach to a 65-year-old masters track athlete who clutches his chest before collapsing in the middle of a race will differ from the care of a 15-year-old football cornerback who collapses after “spear tackling” an opponent. In the first nontraumatic case, cardiac etiology would be suspected, and thus the BLS and

ACLS assessments would be used (Table 11.2). Conversely, the approach to the trauma patient should follow the advanced trauma life support (ATLS) guidelines (see Table 11.2).62 With ATLS, the rapid primary survey assesses vital functions with simultaneous stabilization of any life-threatening conditions. After stabilization, a thorough history and physical examination of the secondary survey should commence.62 Physicians covering a sporting event may not always be able to determine the injury mechanism or extent of the injury, particularly when the patient remains unconscious or the inciting event was not witnessed.

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In these situations, it should be assumed that the cervical spine is compromised, and physicians should follow appropriate precautions (outlined later in this chapter).

Head Injury Head injuries account for 69% of fatalities in American football athletes.63 The leading cause of death after a sports-related head injury is intracranial hemorrhage,64 which may present as either an epidural, subdural, intracerebral, or subarachnoid hematoma. Epidural hematomas, which typically result from a tear of the middle meningeal artery as a complication of fracture of the temporal bone, are the most rapidly progressive intracranial hemorrhage and may cause death within 30 to 60 minutes.64 In contrast, subdural hematomas evolve at a considerably slower rate, over a period of days to months, and yet they are the most common cause of fatal head injury in athletics.63 Fortunately, most head injuries are less severe, with concussions being more common. A concussion is defined as a traumatic brain injury induced by direct or indirect biomechanical forces.41 The sideline physician should be trained to recognize the symptoms of concussion, which vary greatly and include combinations of different symptoms including but not limited to headaches, nausea, dizziness, photophobia, and difficulties with concentration and memory.65 The approach to a collapsed athlete with a suspected head injury should always begin with the ATLS survey. An unconscious athlete should be assumed to have a cervical spine injury and should be appropriately stabilized. For conscious athletes, the primary survey should involve rapid assessment of circulation, airway, and breathing, followed by an assessment for spinal tenderness and neurologic assessment of the upper and lower limbs.65 The athlete who remains unconscious for greater than 1 minute, has focal neurologic deficits, or has deteriorating mental status should be transferred emergently for advanced imaging to assess for intracranial hemorrhage. Stable athletes should be removed from play, and a thorough neurologic examination should be performed either on the sideline or in the locker room. The SCAT41 provides a systematic approach to concussion evaluation both immediately on the field and for more extensive evaluation in the locker room, training room, or medical office. Following a potential head injury during athletic participation, serial examinations are essential because epidural hematomas frequently present with a lucid interval prior to rapid neurologic deterioration.64 The concussed athlete should never return to play (RTP) the same day and should follow a gradual stepwise return-to-sport protocol, returning to play only after symptoms have resolved and medical clearance has occurred.41 Current guidelines no longer allow for “rare exceptions” to be made with respect to same day RTP guidelines for elite adult athletes. We recommend that team physicians, in concert with athletic trainers and other medical personnel involved in the care of athletes, establish a written policy regarding concussion management. The policy should detail a stepwise algorithm to carefully assess clinical progress, cognitive function (using computerized testing when available), a graded return-to-sport protocol, and, as needed, a plan for specialist consultation.

Cervical Spine Injury Approximately 12,000 new spinal cord injuries occur each year in the United States, with 8% resulting from sports participation.66 The injury typically results from traumatic axial loading of the cervical spine, which creates transient, geometric changes in the spinal column with resultant injury to neural structures.67 The recommendations provided in this section are primarily based on the NATA position statement on prehospital management of the spine-injured athlete. At the time of press, the NATA was completing a position statement update process, and the recommendations herein are reflective of changes outlined in the corresponding executive summary; however, these updates had not been officially endorsed by the NATA and participating professional organizations. The authors encourage the reader to review the NATA website for updates (https://www.nata.org/ news-publications/pressroom/statements/consensus). The management of suspected cervical spine injury requires a coordinated team effort, and prior to each season, neck stabilization techniques, methods of transferring injured players, airway and equipment management, and immobilization techniques should be rehearsed carefully. EAPs should be developed and coordinated with local emergency responders prior to the season, and on-site sports medicine teams should perform a “time out” prior to competition to review EAPs. Considerations should include the personnel and equipment available for that event, stabilization and transportation plans, and the use of a hospital that can deliver immediate, definitive care for cervical spine injuries.68 In a collapsed athlete, symptoms and signs that raise the index of suspicion for severe traumatic cervical spine injury include (1) unconsciousness or an altered level of consciousness, (2) bilateral neurologic findings or complaints, (3) significant midline spine pain with or without palpation, and (4) obvious spinal column deformity.69 An ATLS survey should commence immediately with special attention to cervical spine precautions. Moving the patient to a supine position with use of the log-roll maneuver may be obligatory if the athlete is found prone and the primary survey cannot be performed. The head and neck should be manually maintained in a neutral position without traction.69 Airway patency and accessibility should be established, and rescue breathing should be initiated if necessary, which may entail the removal of a facemask or mouth guard. A cordless screwdriver is the initial equipment of choice for removal of a facemask because it induces less movement than other tools. However, an appropriate manual tool for cutting helmet loops should also be available at all times, and medical personnel should rehearse the use of these tools before the season begins. Helmet screws also should be routinely inspected and maintained throughout the season by equipment managers and/or athletic trainers. Removal of helmets and pads prior to transfer when appropriate should be done by three rescuers trained and experienced with equipment removal, or at the earliest possible time three such trained rescuers are available in order to have unhindered access to the athlete to facilitate delivery of care.68,69 Manual stabilization should be augmented, but not replaced, by mechanical stabilization with use of a cervical collar. A full-body stabilization should be

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facilitated by transfer to a spine board. Supine athletes should be transferred via the “lift-and-slide” technique, whereas prone athletes should be transferred with use of the “log-roll” method. Head and neck stabilization should continue during transportation and until a destabilizing injury has been excluded. For an in-depth review, we recommend perusal of the NATA position statement68 on acute management of the cervical spine–injured athlete.69

Cardiac Arrest The most common cause of SCD in athletes younger than 35 years is congenital cardiac disease, and in athletes older than 35 years, the most frequent etiology is atherosclerotic heart disease.70 The initial presenting feature of occult cardiac disease may be SCD, and thus the PPE is designed to screen for potential symptoms and signs that may be representative of underlying cardiac disease. In the event of a nontraumatic collapse of an athlete, a potential cardiac etiology should be strongly considered and a thorough evaluation and cardiology consultation are imperative before the athlete is allowed to resume participation. After cardiac arrest, the inclusive goal is to support and restore effective oxygenation, ventilation, and circulation with return of neurologic function.71 Keys to ensuring successful resuscitation are (1) immediate recognition of cardiac arrest and activation of the emergency response system, (2) early initiation of CPR with an emphasis on high-quality chest compressions, (3) rapid defibrillation, (4) effective use of advanced life support measures, and (5) integrated post–cardiac arrest care.71 Initial evaluation should follow the BLS assessment and ACLS primary assessment (see Table 11.2). For unconscious athletes with cardiac or respiratory arrest, initial management should move to the ACLS primary assessment once the BLS assessment is completed. For conscious athletes, the ACLS primary assessment should be conducted first.71 The 2015 AHA BLS guidelines recommend beginning CPR with chest compressions immediately, without a delay for administering rescue breaths first. Factors for effective CPR include a rate of 100 to 120 chest compressions per minute, adequate depth of compressions to 5 cm, allowing complete chest recoil after each compression, minimizing interruptions of chest compressions, avoiding excessive ventilation, and switching the CPR provider who is administering the chest compressions to avoid fatigue, ideally changing positions during cardiac rhythm interpretation by the AED, as applicable.71 At a minimum, we recommend that all medical providers involved in the care of athletes maintain BLS certification, and ACLS certification for team physicians should be strongly considered.

Tension Pneumothorax Pneumothorax (PTX) is the presence of air in the pleural space, which occurs spontaneously as a result of a traumatic tear of the pleura after a chest injury or may be iatrogenic as a result of a medical procedure.72 Tension PTX is a rare form of PTX that may develop as a result of a chest wall defect or a displaced fracture, or as a progression of a simple PTX. The underlying mechanism is a “one-way valve” air leak that forms through a defect in the

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lung or chest wall, which leads to a progressively enlarging PTX with each inspiration.62 Typical symptoms include dyspnea and ipsilateral pleuritic chest pain. Physical examination may reveal tachycardia, tachypnea, hypotension, hyperresonance to percussion, unilateral absence of breath sounds, tracheal deviation, and distended neck veins.72 Sideline diagnosis of this medical emergency is dependent on symptoms and signs noted with clinical evaluation, and clinicians should not await radiographic imaging to confirm this diagnosis.62 Initial management entails immediate decompression via insertion of a large-caliber (11to 16-gauge) needle into the affected hemithorax by way of the second intercostal space in the midclavicular line.62 Definitive treatment involves emergent hospital transportation, tube thoracostomy, and supplementary administration of oxygen. RTP guidelines should be individualized, yet it is possible for athletes to resume participation 3 to 4 weeks after a traumatic PTX has occurred.72 We recommend a thorough workup for occult connective tissue disorders (e.g., MFS) in athletes who experience a spontaneous PTX.

Anaphylaxis Anaphylaxis is an acute, alarming, and accelerated life-threatening systemic reaction with varied mechanisms, clinical presentations, and severity that results from the abrupt systemic release of mediators from mast cells and basophils.73 The overall incidence is estimated to be 1%–2% worldwide, and food and drugs are thought to be the most common causes.74 Exercise-induced anaphylaxis is a well-described phenomenon in which exercise triggers symptoms, including extreme fatigue, warmth, flushing, pruritus, and urticaria, occasionally progressing to angioedema, wheezing, upper airway obstruction, and collapse.73 The precise pathophysiology is ill defined, yet co-triggers such as nonsteroidal antiinflammatory drugs, pollen, or specific foods have been implicated and should be identified if possible.75 Anaphylaxis as a result of insect stings is also a concern; symptoms are similar to those previously described but may also include a large, localized skin reaction.73 The circulation, airway, breathing, and level of consciousness of athletes with a possible anaphylactic reaction should be evaluated. EMS should be activated followed by the rapid administration of an age-appropriate dose of epinephrine intramuscularly into the anterolateral thigh. Epinephrine injections can be repeated every 5 minutes for protracted symptoms. It is important to note that epinephrine injections alone do not definitively treat anaphylaxis in all cases and further emergent care may still be indicated. Athletes should be placed in a supine position with their lower limbs elevated. Vital signs should be monitored diligently, and oxygen and intravenous fluids should be administered if available. An advanced airway may be necessary for persons with respiratory compromise. Other adjunctive medications include nebulized bronchodilators, antihistamines, and glucocorticoids. After stabilization, athletes should undergo a workup to identify possible triggers of anaphylaxis, and future prevention should include appropriate prophylactic medications and avoidance of triggers. An epinephrine autoinjector should be prescribed, and a personalized EAP should be developed (as detailed in the PPE section).73

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Limb-Threatening Injuries Knee Dislocation Defined as complete disruption of the integrity of the tibiofemoral articulation, knee dislocation is typically accompanied by rupture of at least two of the four major knee ligaments.76 Sports activities account for one-third of all cases of knee dislocation.77 The most feared complication is potential limb amputation as a result of vascular compromise. Dislocations are classified according to tibial dislocation in relation to the femur. Anterior dislocation as a result of hyperextension is the most common type of dislocation.78 Clinical signs may be subtle if the dislocation reduced spontaneously, yet hemarthrosis and severe multidirectional instability are suggestive of a possible dislocation. If the knee remains dislocated, closed reduction should be attempted emergently. Common fibular nerve and popliteal artery function and integrity should be tested and documented. Distal pulses may remain intact despite significant popliteal artery compromise, which necessitates more definitive evaluation with angiography.79 The athlete should be emergently transported for orthopedic and vascular surgery consultation. Traumatic Amputation The primary clinical goals after a traumatic amputation occurs are hemorrhage control and digit/limb salvage. Even small digital amputations may result in significant bleeding. Pressure should be applied to the area, and the affected limb should be elevated. A tourniquet should be applied only if significant hemorrhaging continues. The residual limb should be rinsed with sterile saline solution and wrapped with sterile gauze. The amputated portion should be wrapped in moist sterile gauze, sealed in a plastic bag, placed in an ice bath, and sent with the athlete during emergency transport to the hospital.80 Acute Compartment Syndrome Acute compartment syndrome (ACS) is caused by altered tissue homeostasis within a closed muscle compartment. Tissue pressure greater than vascular perfusion pressure reduces capillary blood flow and induces local tissue hypoxia and necrosis.81 ACS can occur in any limb but is much more common in the lower limbs. Causes of ACS in sports include fractures and crush injuries. Symptoms typically present within a few hours of the initial injury and include progressive pain, paresis, and paresthesias.81 Passive and active ROM worsen pain, and severe cases present with diminished pulses, pallor, and paralysis.82 Clinical suspicion for ACS mandates rapid transportation to a hospital for an emergent fasciotomy.

Environmental Factors Heat Illness EHI includes heat cramps, heat exhaustion, and heat stroke. Exertional heat stroke (EHS), the most severe type of heat illness, is defined by a core temperature greater than 40.5°C (105°F) at collapse, accompanied by central nervous system changes.83 EHS manifests when body organ temperature rises above critical levels, leading to cell membrane damage and cell energy disruption. Early symptoms of EHS include clumsiness, stumbling, headache, nausea, dizziness, apathy, confusion, and impairment of

consciousness.83 Risk factors include obesity, prior heat stroke, dehydration, certain medications, poor fitness, hot and humid environments, and lack of acclimatization.83 Early recognition and treatment are fundamental to reducing morbidity and mortality. Circulation, airway, and breathing should be assessed, along with rectal temperature in athletes exhibiting signs of EHS. The goal is to lower core body temperature to less than 38.9°C (102.5°F) within 30 minutes of collapse. Confirmation of EHS should result in initiation of immediate cooling measures, ideally in the form of whole-body ice-water immersion, which should be performed prior to emergency transportation.83,84 The water should be approximately 1.7°C (35°F) to 15°C (59°F) and stirred continuously to maximize cooling. The patient should be removed from cold water immersion once core body temperature reaches 38.9°C (102°F) to prevent overcooling. Establishing intravenous access with volume resuscitation may help to prevent cardiovascular collapse and end-organ damage. A rectal temperature should be obtained every 3 to 5 minutes, and cooling should continue until body temperature is less than 39°C.85 All persons experiencing EHS should be transported to a medical facility for advanced care and monitoring.

Lightning Injuries from lightning kill approximately 24,000 people annually worldwide.85 Participants in outdoor recreational activities have the greatest risk of sustaining an injury from lightning.62 Lightning can cause injuries via direct contact, contact with an object that is struck, or “side splash,” which occurs when the electrical current jumps from an object to the victim.85 The most common cause of fatality resulting from a lightning injury is cardiopulmonary arrest.86 Other sequelae may include burns, fractures, and dislocations resulting from violent muscle contraction and neurologic conditions such as loss of consciousness, seizure, headache, paresthesia, confusion, memory loss, and transient paralysis.85,86 Initial management may require movement of the injured person if ongoing thunderstorms threaten the safety of first responders. It should be noted that after a lightning strike, the injured person does not retain an electrical charge, and thus treatment should not be delayed.87 After the scene of the lightning strike is deemed secure, management should follow the ATLS primary and secondary surveys. A tenet of triage after lightning trauma dictates that the “apparently dead” should be resuscitated first. This tenet pertains to the unique pathophysiology of cardiopulmonary arrest in lightning strikes that necessitates immediate ventilatory support to prevent secondary hypoxic arrhythmias.86

Conclusion Paramount to the management of on-field emergencies are the precepts of preparation and anticipation. Team physicians should coordinate EAPs and have them rehearsed annually by all staff involved in the care of athletes. In addition, the physician’s kit should be restocked adequately on a periodic basis to help ensure effective and timely treatment. Physicians should remain alert on the sideline, monitoring play vigilantly so they can view injuries as they occur, which will facilitate optimal care.

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Lastly, thorough assessment of injured and ill athletes can be enhanced by meticulous adherence to the BLS, ACLS, and ATLS guidelines.

ETHICAL AND LEGAL ISSUES IN SPORTS MEDICINE Ancient Greeks were credited with the birth of both rational medicine and professional sports.65 With Western medicine in its infancy, the physician’s role in the sporting microcosm was neither well defined nor respected. Greek athletes sought advice from their trainers regarding their inclusive training methods, including diet and physiotherapy.88 The awkward inception of medicine in the sporting arena was broadened by the sometimes contrasting goals of the athletes and physicians. Although the health of the athletes takes precedence for physicians, athletes often view victory as the ultimate goal.88 Some persons believe that it is these opposing philosophies that lie beneath most ethical and legal issues in modern-day sports medicine. In addition, the evolution of the traditional dyad of the patient-physician relationship into a triad of patient-teamphysician has been further recognized as a source of potential medicolegal conflict.89 This section is intended to serve as a general guide for ethical and legal issues and should not be perceived as binding legal advice. For detailed advice regarding specific medicolegal issues, we recommend that legal counsel be obtained.

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payments, or transmit claims to a health plan in an electronic form.90 Regardless of the clinical scenario, revealing whether an athlete is “cleared” or “not cleared” is considered an exception to HIPAA.90

High School Athletics At the high school level, with rare exception, sideline coverage is voluntary and does not involve any form of billing, and thus the information obtained during these encounters would not be considered under the jurisdiction of HIPAA. Theoretically, information could be shared with coaches and team administrators without fear of prosecution from the Department of Health and Human Services, which implements HIPAA. Although no legal precedent exists, some persons believe that HIPAA guidelines should be adhered to in high schools.90 Regardless, if medical services are billed, for example, as an in-office follow-up visit, HIPAA guidelines are enforceable.

Inherent to the integrity of any patient-physician relationship is the concept of trust. In modern medicine, a primary approach to maintain the trust of our patients is to preserve confidentiality. The following case example illustrates potential problems surrounding trust.

Collegiate Athletics HIPAA guidelines are usually the rule in collegiate athletics. One particular exception is clinical scenarios that involve health information governed by the Federal Education Records Protection Act (FERPA). At private or public colleges and universities that receive federal educational funding, information obtained during clinical encounters may be covered by this act. Information governed by FERPA guidelines are exempt from HIPAA and enable health information to be released to administrators and coaches who have an educational interest in the athlete without formal consent by the patient.90 School-based athletic training room records maintained by team physicians or certified athletic trainers are often considered to be governed by FERPA. Given the complex nature of FERPA and HIPAA regulations, it is advisable to review privacy policies with the institution’s legal counsel.2

Case 1 A 21-year-old star running back cuts to the sideline during a midseason game. He hears a “pop” in his right knee, which is accompanied by immediate pain and swelling. As the team physician, you evaluate him, and examination reveals positive right knee Lachman and anterior drawer tests. Immediately following your examination, you are approached by the athletic trainer, the head coach, and a member of the media who ask for returnto-play prognosis. During this encounter, you have not asked the player for his consent to release medical information. Question: Who can you talk to, and what can you tell them? Many clinicians reflexively cite confidentiality guidelines outlined in the Health Information Portability and Accountability Act (HIPAA). Remarkably, the primary goal of HIPAA was not to enforce confidentiality but rather to improve the portability and continuity of health insurance coverage.90 A section of HIPAA details the principles of patient confidentiality and subsequently had far-reaching effects on patient information when it was enacted in 2003. A key determinant to the enforcement of HIPAA guidelines depends on whether the information is “protected.” These regulations apply only to clinical encounters for which physicians bill for their services, receive

Professional Athletics In the arena of professional athletics, athletes sign an employment contract with the team, and health information can be considered to be a part of the employment record. Thus health information gathered by a team physician may be shared with employers who have a vested interest in the athlete’s health, such as coaches and administrators.90 As previously illustrated, the issue of whether information can be divulged to coaches varies with the clinical situation. To avoid controversy when dealing with sensitive medical information, most professional teams have their athletes sign a preparticipation waiver that details with whom health information can be shared as needed. Thus consent for release of information does not have to be obtained repeatedly throughout the season. In the absence of such a waiver, if an athlete begins to reveal information to the team physician that could potentially restrict him or her from play, it is recommended that the physician preempt any further revelations by notifying the athlete that if further information is shared, he or she may need to share this information with the team’s administration. At that juncture, the athlete can consent to the release of medical information or refuse to reveal additional information and request a referral to another provider.91

Confidentiality

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TABLE 11.3  Key Components of Informed

Consent

Component

Description

Disclosure

Relevant information must be provided regarding the proposed treatment including potential risks, benefits, and alternatives. Athletes must have the ability to understand information and its relevance. Athletes must voluntarily express their wishes in a noncoercive environment.

Capacity Voluntariness

Informed Consent Informed consent is one of the primary means of ensuring patient autonomy when making nonemergent medical decisions.92 Most physicians are familiar with the concept of informed consent in the context of preprocedure planning, but any medical decision affecting an athlete’s health and future should involve three key components of informed consent: disclosure, capacity, and voluntariness (Table 11.3).93 To illustrate the importance of informed consent, we provide the following case.

Case 2 A 20-year-old female middle distance runner reports recurrent right medial ankle pain and swelling consistent with a previous diagnosis of posterior tibial tendinopathy. She is scheduled to participate in a regional qualifying meet for the national championships in 1 week. She requests a steroid injection into the posterior tibial tendon sheath and states that a prior injection by her primary care physician allowed her to successfully obtain a national qualifying result last year. Question: Should you proceed with the injection or opt for more conservative measures? In this example, pressure from the coach and athlete to do whatever it takes to win may affect clinical judgment by the team physician. Further complicating the scenario is the fact that she had a prior injection in the past with good results, and as such, it is reasonable for the coach and athlete to expect similar treatment. Referring to the basic components of informed consent (see Table 11.3), it is imperative to reestablish the three criteria in the current scenario because it is unlikely that the athlete can still recite the potential risks, benefits, and alternatives. It is also incorrect to assume that informed consent was actually obtained prior to her last injection. The short-term, antiinflammatory, and analgesic effects of the injection would need to be weighed with the short-term risks of acute rupture and long-term risk of chronic weakening and progression of posterior tibialis tendon dysfunction.94 By educating the patient about the risks, benefits, and alternatives, the physician is fulfilling a protective role in medical decisionmaking. This scenario does not involve a life-threatening injury; accordingly, it is reasonable that if informed consent is obtained, an injection may be justified. Conversely, in rendering return-toplay decisions for potentially catastrophic injuries such as cervical spine instability, patient autonomy would be less important than

the principles of beneficence and nonmaleficence. In addition, when athletes join a sports team, they voluntarily sacrifice a certain degree of their autonomy by agreeing to abide with the decisions of team physicians.93 Another potential pitfall is the assumption that a signed consent form automatically fulfills the medicolegal criteria needed to substantiate informed consent. A legal precedent exists indicating that a signed consent form does not necessarily guarantee legal immunity. Medical jargon may be overly complicated, and the patient may not fully understand the potential risks of the procedure. It is recommended that if doubt exists about whether the patient fully understands the ramifications of a medical decision, the patient should write a letter in his or her own words detailing his or her understanding of the risks, benefits, and alternatives.95

Drug Use A trend in modern sports is the use of performance-enhancing drugs. In opposing the use of performance-enhancing drugs, most physicians cite the potential harms and the unfairness for the spirit of competition and good sportsmanship. The practice of physicians supplying banned substances to athletes is entirely unacceptable, and yet numerous well-publicized examples of such practices exist.96 Although condemnation of the distribution of performance-enhancing drugs by a physician is clear-cut, other potential scenarios may be unclear.

Case 3 You are the primary care physician for an 18-year-old male sprinter who is competing on the junior national track team. He presents to your clinic with a report of acne. Upon further questioning, he reveals that he has recently started taking anabolic steroids. Questions: Should this information be kept confidential? Should you continue to treat the patient? Would your decision change if you were the national team physician? The physician may believe that it is necessary to inform his patient’s coaches and potentially an antidoping agency that governs the sport. However, in this case, the athlete has addressed his use of steroids during a clinic visit with his primary care physician, who does not have a legal obligation to disclose this information. Some persons have suggested that athletes who use performance-enhancing drugs should not be viewed any differently from those who abuse alcohol or tobacco,96,97 because with the latter forms of abuse, physicians would provide counseling regarding potential adverse effects. Likewise, it is beneficial for physicians to advise athletes on the potential detrimental effects of performance-enhancing drugs, without overstating risks, to maintain their trust. In addition, psychosocial triggers that may have fueled drug use should be considered and addressed. On the other hand, in this scenario, if the physician was taking care of an athlete on the national team rather than serving as a primary care provider, an obligation to divulge information to administrators is logical. However, in most instances at the national level, the athlete will have signed an agreement acknowledging forfeiture from participation for use of performance-enhancing drugs.

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Disagreements With Coaches Sideline medical coverage can exemplify the potentially incompatible goals of physicians and coaches. Occasionally, coaches may disagree with medical assessments, as illustrated in the following case.

Case 4 A 16-year-old football cornerback tackles an opposing player in the second quarter of play. You witness him jog back to the huddle with his right arm held at his side. He reports having radiating pain down his arm. A preliminary examination reveals no neck tenderness and 4 5 shoulder abduction and elbow flexion strength. You instruct him not to RTP and tell him you plan to reexamine him in 10 minutes. The coach cannot understand why you have restricted play because the coach “used to play with stingers.” Questions: What should you tell the coach? Could this situation have been avoided? The RTP guidelines with regard to transient brachial plexopathies (also known as stingers) were different in the past, and athletes often returned to play relatively soon. However, current guidelines clearly state that RTP is contraindicated in the presence of residual neurologic deficits.45 Knowledge of current guidelines and education of athletes and coaches can be of great help to team physicians.98 A thorough explanation of the potential immediate and long-term sequelae of premature RTP should suffice for most coaches. Perhaps a solution to avoid a power struggle with a coach on the sideline is to preemptively delineate duties as team physician in writing. This approach typically would not be feasible in a situation in which a team physician is at odds with an opposing team’s coach, especially when only one physician is on site at a game. In this situation, the physician should arrive early, introduce himself or herself to the opposing team’s athletic trainer(s) and coaching staff, and delineate his or her role during the contest. To make unbiased medical decisions on either sideline, it is recommended that team physicians avoid excessive emotional involvement with their team and maintain a sense of objectivity throughout the contest.93

Conclusion The team physician encounters unique bioethical issues when interacting with coaches and athletes. Most of these issues stem from the nontraditional patient-doctor relationship and the dichotomous goals of “health first” versus “victory at all costs.” Team physicians should rely on their knowledge of current medical guidelines and the basic principles of medical ethics.

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In addition, it is recommended that physicians strictly adhere to the rule of “full disclosure” and notify all athletes of potential risks and conflicts of interest, which will facilitate autonomous and informed decision-making.92

ACKNOWLEDGMENT The authors and editors are grateful for the contributions of the previous authors of this chapter, C. Joel Hess and Dilaawar J. Mistry. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Bernhardt DT, Roberts WO, eds. Preparticipation Physical Evaluation. 4th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2010.

Level of Evidence: V, expert opinion

Summary: A product of six author societies, the fourth edition of the preparticipation physical evaluation guides the team physician through the intricacies of preseason screening for sport participation.

Citation: McCrory P, Meeuwisse W, Dvorak J, et al. Consensus statement on concussion in sport – the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;[Epub ahead of print].

Level of Evidence: V, expert opinion

Summary: The most recent and widely accepted concussion management guideline, including in-depth discussion on RTP decisions.

Citation: Swartz EE, Boden BP, Courson RW, et al. National athletic trainers’ association position statement: acute management of the cervical spine-injured athlete. J Athl Train. 2009;44(3):306–331.

Level of Evidence: V, expert opinion

Summary: A consensus statement of the on-field management of the athlete with a cervical spine injury.

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REFERENCES 1. Herring SA, Kibler WB, Putukian M. Team physician consensus statement: 2013 update. Med Sci Sports Exerc. 2013;45(8): 1618–1622. 2. Bernhardt DT, Roberts WO, eds. Preparticipation Physical Evaluation. 4th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2010. 3. Wingfield K, Matheson GO, Meeuwisse WH. Preparticipation evaluation: an evidence-based review. Clin J Sport Med. 2004;14(3):109–122. 4. Hulkower S, Fagan B, Watts J, et al. Clinical inquiries: do preparticipation clinical exams reduce morbidity and mortality for athletes? J Fam Pract. 2005;54(7):628–632. 5. Peterson AR, Bernhardt DT. The preparticipation sports evaluation. Pediatr Rev. 2011;32(5):e53–e65. 6. Seto CK. The preparticipation physical examination: an update. Clin Sports Med. 2011;30(3):491–501. 7. Carek PJ, Futrell M. Athletes’ view of the preparticipation physical examination. Attitudes toward certain health screening questions. Arch Fam Med. 1999;8(4):307–312. 8. Koester MC, Amundson CL. Preparticipation screening of high school athletes: are recommendations enough? Phys Sportsmed. 2003;31(8):35–38. 9. Krowchuk DP, Krowchuk HV, Hunter DM, et al. Parents’ knowledge of the purposes and content of preparticipation physical examinations. Arch Pediatr Adolesc Med. 1995;149(6): 653–657. 10. Preparticpation Physical Evaluation History Form. American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, American Medical Society for Sports Medicine, American Orthopaedic Society for Sports Medicine, and American Osteopathic Academy of Sports Medicine. https://www.amssm.org/Content/pdf%20files/ PPE2010RevisedForm.pdf. Accessed September 24, 2017. 11. Smith J, Laskowski ER. The preparticipation physical examination: Mayo Clinic experience with 2,739 examinations. Mayo Clin Proc. 1998;73(5):419–429. 12. Dunn TP, Pickham D, Aggarwal S, et al. Limitations of current aha guidelines and proposal of new guidelines for the preparticipation examination of athletes. Clin J Sport Med. 2015;25(6):472–477. 13. Maron BJ, Thompson PD, Ackerman MJ, et al. Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive athletes: 2007 update: a scientific statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: Endorsed by the American College of Cardiology Foundation. Circulation. 2007;115(12):1643–1645. 14. Harmon Kg, Zigman M, Drezner JA. The effectiveness of screening history, physical exam, and ECG to detect potentially lethal cardiac disorders in athletes: a systematic review/ meta-analysis. J Electrocardiol. 2015;48(3):329–338. 15. Drezner JA, O’Connon FG, Harmon KG, et al. AMSSM position statement on cardiovascular preparticipation screening in athletes: current evidence, knowledge gaps, recommendations and future direction. Curr Sports Med Rep. 2016;15(5): 359–375. 16. Maron BJ, Friedman RA, Kligfield P, et al. Assessment of the 12 lead electrocardiogram as a screening test for detection of cardiovascular disease in healthy general populations of young people (12-25 years of age). J Am Coll Cardiol. 2014.

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17. Mitchell ARJ, Hurry R, Maclachlan H. Pre-participation cardiovascular screening: is community screening using hand-held cardiac ultrasound feasible? Echo Res Pract. 2015;2(2):49–55. 18. Fudge J, Harmon KG, Owens DS, et al. Cardiovascular screening in adolescents and young adults: a prospective study comparing the Pre-participation Physical Evaluation Monograph 4th Edition and ECG. Br J Sports Med. 2014;48(15):1172–1178. 19. Corrado D, Biffi A, Migliore F, et al. Primary prevention of sudden death in young competitive athletes by preparticipation screening. Card Electrophysiol Clin. 2013;5(1):13–21. 20. Maron BJ, Zipes DP. 36th Bethesda conference: eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol. 2005;45(8):1318–1321. 21. Loeys BL, Dietz HC, Braverman AC, et al. The revised Ghent nosology for the Marfan syndrome. J Med Genet. 2010;47(7): 476–485. 22. Giese EA, O’Connor FG, Brennan FH, et al. The athletic preparticipation evaluation: cardiovascular assessment. Am Fam Physician. 2007;75(7):1008–1014. 23. Grazioli G, Merino B, Montserrat S, et al. Usefulness of echocardiography in preparticipation screening of competitive athletes. Rev Esp Cardio. 2014;67(09):701–705. 24. International Olympic Committee Medical Commission. Sudden cardiovascular death in sport: Lausanne recommendations on preparticipation cardiovascular screening. http://www.olympic.org/Documents/Reports/EN/en_report_886. pdf. Updated December 10, 2004. Accessed June 27, 2013. 25. Corrado D, Pelliccia A, Bjornstad HH, et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus statement of the study group of sport cardiology of the working group of cardiac rehabilitation and exercise physiology and the working group of myocardial and pericardial diseases of the European Society of Cardiology. Eur Heart J. 2005;26(5):516–524. 26. Corrado D, Basso C, Pavei A, et al. Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. JAMA. 2006;296(13):1593–1601. 27. Corrado D, Basso C, Rizzoli G, et al. Does sports activity enhance the risk of sudden death in adolescents and young adults? J Am Coll Cardiol. 2003;42(11):1959–1963. 28. Corrado D, Basso C, Schiavon M, et al. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med. 1998;339(6):364–369. 29. Burns KM, Encinosa WE, Peason GD, et al. Electrocardiogram in pre-participation athletic evaluations among insured youths. J Pediatr. 2015;167(4):804–809. 30. Kurtz JD, Kanter RJ, Olen M, et al. Screening the apparently healthy athlete for risk: a paradigm in transition. Cardiol Young. 2017;27(S1):S89–S93. 31. Drezner JA, Ackerman MJ, Anderson J, et al. Electrocardiographic interpretation in athletes: the ‘Seattle criteria’. Br J Sports Med. 2013;47(3):122–124. 32. Mirabelli MH, Devine MJ, Singh J, et al. The preparticipation sports evaluation. Am Fam Physician. 2015;92(5):371–376. http://www.aafp.org/afp/2015/0901/p371.html. Accessed June 14, 2017. 33. Sheikh N, Papadakis M, Ghani S, et al. Comparison of electrocardiographic criteria for the detection of cardiac abnormalities in elite black and white athletes. Circulation.

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35.

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2014;129:1637–1649. Doi: 10.1161/CIRCULATIONAHA .113.006179 #86. Gleason CN, Kerkhof DL, Lanyi MA, et al. Early screening for cardiovascular abnormalities with preparticipation echocardiography: feasibility study. Clin J Sport Med. 2016. Finnoff JT, Ray J, Corrado G, et al. Sports ultrasound: applications beyond the musculoskeletal system. Sports Health. 2016;8(5):412–417. Bar-Cohen Y, Silka MJ. The pre-sports cardiovascular evaluation: should it depend on the level of competition, the sport, or the state? Pediatr Cardiol. 2012;33(3):417–427. Weiler JM, Bonini S, Coifman R, et al. American Academy of Allergy, Asthma & Immunology work group report: exerciseinduced asthma. J Allergy Clin Immunol. 2007;119(6):1349–1358. Gomez JE, Landry GL, Bernhardt DT. Critical evaluation of the 2-minute orthopedic screening examination. Am J Dis Child. 1993;147(10):1109–1113. Dallinga JM, Benjaminse A, Lemmink KA. Which screening tools can predict injury to the lower extremities in team sports?: a systematic review. Sports Med. 2012;42(9):791–815. Onate JA, Everhart JS, Clifton DR, et al. Exam risk factors for lower extremity injury in high school athletes: a systematic review. Clin J Sport Med. 2016;26(6):435–444. McCrory P, Meeuwisse W, Dvorak J, et al. Consensus statement on concussion in sport – the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;[Epub ahead of print]. Leddy J, Baker JG, Haider MN, et al. A physiological approach to prolonged recovery from sport-related concussion. J Athl Train. 2017;52(3):299–308. Mucha A, Collins MW, Elbin RJ, et al. A Brief vestibular/ocular motor screening (VOMS) assessment to evaluate concussions: preliminary findings. Am J Sports Med. 2014;42(10):2479–2486. Van Kampen DA, Lovell MR, Pardini JE, et al. The “value added” of neurocognitive testing after sports-related concussion. Am J Sports Med. 2006;34(10):1630–1635. Standaert CJ, Herring SA. Expert opinion and controversies in musculoskeletal and sports medicine: stingers. Arch Phys Med Rehabil. 2009;90(3):402–406. Cantu RV, Cantu RC. Current thinking: return to play and transient quadriplegia. Curr Sports Med Rep. 2005;4(1):27–32. McCrory P. Headaches and exercise. Sports Med. 2000;30(3): 221–229. Human immunodeficiency virus and other blood-borne viral pathogens in the athletic setting. Committee on Sports Medicine and Fitness. Pediatrics. 1999;104(6):1400–1403. Human immunodeficiency virus and other blood-borne pathogens in sports. The American Medical Society for Sports Medicine (AMSSM) and the American Academy of Sports Medicine (AASM). Clin J Sport Med. 1995;5(3):199–204. Putukian M, O’Connor FG, Stricker P, et al. Mononucleosis and athletic participation: an evidence-based subject review. Clin J Sport Med. 2008;18(4):309–315. Klossner D. National Collegiate Athletic Association Division Manual August 2016–17. NCAA Sports Medicine Handbook. Ed. Baltimore, MD: The National Collegiate Athletic Association; 2016. Rice SG, American Academy of Pediatrics Council on Sports Medicine and Fitness. Medical conditions affecting sports participation. Pediatrics. 2008;121(4):841–848. Eichner ER. Sickle cell considerations in athletes. Clin Sports Med. 2011;30(3):537–549.

54. Shephard RJ. Sickle Cell Trait: what are the costs and benefits of screening? J Sports Med Phys Fitness. 2016;56(12):1562–1573. http://www.minervamedica.it/en/journals/sports-med-physicalfitness/article.php?cod=R40Y2016N12A1562. Accessed June 15 2017. 55. Roberts RO, Asplund CA, O’Connor FG, et al. Cardiac preparticipation screening for the young athlete: why the routine use of ECG is not necessary. J Electrocardiol. 2015;48(3):311–315. 56. Tenforde AS, Carlson JL, Chang A. Association of the female athlete triad risk assessment stratification to the development of bone stress injuries in collegiate athletes. Am J Sports Med. 2017;45(2):302–310. 57. Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior exertional heatstroke patients. Med Sci Sports Exerc. 1990;22(1):36–48. 58. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2015;50(9):986–1000. 59. Winell J, Burke SW. Sports participation of children with Down syndrome. Orthop Clin North Am. 2003;34(3):439–443. 60. Andersen J, Courson RW, Kleiner DM, et al. National Athletic Trainers’ Association position statement: emergency planning in athletics. J Athl Train. 2002;37(1):99–104. 61. Drezner JA, Courson RW, Roberts WO, et al. Inter-association task force recommendations on emergency preparedness and management of sudden cardiac arrest in high school and college athletic programs: a consensus statement. J Athl Train. 2007;42(1):143–158. 62. Advanced Trauma and Life Support for Doctors: ATLS Student Course Manual. 8th ed. Chicago, IL: American College of Surgeons; 2008. 63. Mueller FO. Catastrophic head injuries in high school and collegiate sports. J Athl Train. 2001;36(3):312–315. 64. Rich BSE, Betteridge BB, Richards SE. Management of on-site emergencies. In: McKeag DB, Moeller JL, eds. ACSM’s Primary Care Sports Medicine. 2nd ed. Philadelphia: Wolters Kluwer/ Lippincott Williams & Wilkins; 2007. 65. Fitch RW, Cox CL, Hannah GA, et al. Sideline emergencies: an evidence-based approach. J Surg Orthop Adv. 2011;20(2): 83–101. 66. National Spinal Cord Injury Statistical Center. Spinal cord injury facts and figures at a glance. https://www.nscisc.uab.edu/ PublicDocuments/fact_figures_docs/Facts%202013.pdf. Updated 2013. Accessed June 27, 2013. 67. Chang DG, Tencer AF, Ching RP, et al. Geometric changes in the cervical spinal canal during impact. Spine. 1994;19(8):973–980. 68. Appropriate Prehospital Management of the Spine-Injured Athlete Updated from 1998 document. National Athletic Trainers Association. https://www.nata.org/sites/default/files/ executive-summary-spine-injury-updated.pdf. Accessed September 24, 2017. 69. Swartz EE, Boden BP, Courson RW, et al. National Athletic Trainers’ Association position statement: acute management of the cervical spine-injured athlete. J Athl Train. 2009;44(3): 306–331. 70. Maron BJ. Sudden death in young athletes. N Engl J Med. 2003;349(11):1064–1075. 71. Advanced Cardiovascular Life Support: Provider Manual. USA: American Heart Association; 2015. 72. Putukian M. Pneumothorax and pneumomediastinum. Clin Sports Med. 2004;23(3):443–454.

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CHAPTER 11  Team Medical Coverage 73. Lieberman P, Nicklas RA, Oppenheimer J, et al. The diagnosis and management of anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol. 2010;126(3):477–480. 74. Lieberman P. Epidemiology of anaphylaxis. Curr Opin Allergy Clin Immunol. 2008;8(4):316–320. 75. Harada S, Horikawa T, Ashida M, et al. Aspirin enhances the induction of type I allergic symptoms when combined with food and exercise in patients with food-dependent exerciseinduced anaphylaxis. Br J Dermatol. 2001;145(2):336–339. 76. Howells NR, Brunton LR, Robinson J, et al. Acute knee dislocation: an evidence based approach to the management of the multiligament injured knee. Injury. 2011;42(11): 1198–1204. 77. Shelbourne KD, Porter DA, Clingman JA, et al. Low-velocity knee dislocation. Orthop Rev. 1991;20(11):995–1004. 78. Brautigan B, Johnson DL. The epidemiology of knee dislocations. Clin Sports Med. 2000;19(3):387–397. 79. Nicandri GT, Chamberlain AM, Wahl CJ. Practical management of knee dislocations: a selective angiography protocol to detect limb-threatening vascular injuries. Clin J Sport Med. 2009;19(2): 125–129. 80. Hunte GS. Sport and exercise-associated emergencies: On-site management. In: Brukner P, Khan K, eds. Clinical Sports Medicine. 3rd ed. Sydney; New York: McGraw-Hill; 2007:789–802. 81. Shadgan B, Menon M, Sanders D, et al. Current thinking about acute compartment syndrome of the lower extremity. Can J Surg. 2010;53(5):329–334. 82. Gaertner MC, Crown LA. Field-side emergencies. In: O’Connor FG, Sallis RE, Wilder RP, eds. Sports Medicine: Just the Facts. New York: McGraw-Hill, Medical Pub. Division; 2005:627. 83. Armstrong LE, Casa DJ, Millard-Stafford M, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556–572. 84. McDermott BP, Casa DJ, Ganio MS, et al. Acute whole-body cooling for exercise-induced hyperthermia: a systematic review. J Athl Train. 2009;44(1):84–93.

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85. DeFranco MJ, Baker CL 3rd, DaSilva JJ, et al. Environmental issues for team physicians. Am J Sports Med. 2008;36(11):2226–2237. 86. Davis C, Engeln A, Johnson EL, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of lightning injuries: 2014 update. Wilderness Environ Med. 2014;25(4S): S86–S95. 87. Walsh KM, Cooper MA, Holle R, et al. National Athletic Trainers’ Association position statement: lightning safety for athletics and recreation. J Athl Train. 2013;48(2):258–270. 88. Mathias MB. The competing demands of sport and health: an essay on the history of ethics in sports medicine. Clin Sports Med. 2004;23(2):195–214, vi. 89. Dunn WR, George MS, Churchill L, et al. Ethics in sports medicine. Am J Sports Med. 2007;35(5):840–844. 90. Magee JT, Almekinders LC, Taft TN. HIPAA and the team physician. Sports Medicine Update (March-April), 2003:4–8. 91. Waddington I, Roderick M. Management of medical confidentiality in English professional football clubs: some ethical problems and issues. Br J Sports Med. 2002;36(2):118– 123, discussion 123. 92. Bernstein J, Perlis C, Bartolozzi AR. Ethics in sports medicine. Clin Orthop Relat Res. 2000;(378):50–60. 93. Stovitz SD, Satin DJ. Professionalism and the ethics of the sideline physician. Curr Sports Med Rep. 2006;5(3):120–124. 94. Holmes GB Jr, Mann RA. Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot Ankle. 1992;13(2):70–79. 95. American Medical Association. Code of medical ethics. E-3.06 sports medicine. http://www.ama-assn.org/resources/doc/ code-medical-ethics/306a.pdf. Published June 1983. Updated 1994. Accessed June 27, 2013. 96. Hoberman J. Sports physicians and the doping crisis in elite sport. Clin J Sport Med. 2002;12(4):203–208. 97. Johnson R. The unique ethics of sports medicine. Clin Sports Med. 2004;23(2):175–182. 98. Sanders AK, Boggess BR, Koenig SJ, et al. Medicolegal issues in sports medicine. Clin Orthop Relat Res. 2005;433:38–49.

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12  Comprehensive Cardiovascular Care and Evaluation of the Elite Athlete Paul S. Corotto, Aaron L. Baggish, Dilaawar J. Mistry, Robert W. Battle

HISTORICAL PERSPECTIVE The elite athlete has enjoyed a celebrated status within our culture since ancient times. The Olympic Games solidified that status as early as 776 BC, and it was amplified by Pheidippedes, who was a legendary Greek Olympic champion in 500 BC. Ten years later when the Persians arrived at the plains of Marathon and threatened to conquer Athens, Pheidippedes was dispatched from Athens to recruit the assistance of the Spartans. While remembered most for his 26-mile run from Marathon to Athens to announce the Greek victory, this run was only part of a remarkable triathlon of events for this remarkable Greek athlete. He began the first leg of his journey with a 145-mile run over mountains and plains that included swimming across the aquatic obstacles on his way to reach Sparta in only 2 days and without sleep. The second leg included travel by boat from Sparta to Marathon, where he joined in the victorious battle against the Persians. Only then did he embark upon his now infamous run back to Athens, where he proclaimed victory before dying suddenly in front of his fellow Greek citizens.1 The remarkable athletic accomplishments of Pheidippedes emphatically etched the Marathon run into sports modernity and deeply engraved the tragic event of athletic sudden death (SD) into our cultural consciousness. The Oxford poet and scholar A. E. Housman captured the effect of sudden athletic death in the poem “To an Athlete Dying Young” (1896): The time you won your town the race We chaired you through the market place The metaphor of the winning athlete on the shoulders of the townspeople is an image we have all witnessed in some form many times. With the unexpected death of the athlete, Housman brings the same metaphor full circle from celebration to sadness with athlete’s coffin resting upon the shoulders of those same townspeople: Shoulder-high we bring you home, And set you at your threshold down, Townsman of a stiller town. Estimates of the incidence of athletic SD reassure us that this is a rare event.2-4 The consequences of athletic SD, however, resound far beyond the individuals directly affected. The advent of continuous media coverage through television, radio, and the internet that is now further augmented by social media has created instant access to any adverse event involving a previously healthy 158

and seemingly invincible athlete. Accordingly, a tragic athletic SD immediately affects family, friends, fellow athletes, students, coaches and administrators, and that effect can rapidly ripple into the minds of sports fans anywhere in the world. The sudden deaths on the soccer pitch of Marc Vivien Foe in 2003 (a Cameroon national player with hypertrophic cardiomyopathy) and Fabrice Muamba in 2012 (a player for Bolton in the English Premier league) illustrate the magnitude of the amplification of modern information. Disturbing videos of both events are widely available on the internet and have been viewed by millions of fans around the world. The SD of Hank Gathers in 1990 had a seminal impact upon the landscape of sports cardiology in the United States. Gathers played Division I college basketball for Loyola Marymount on a team that had realistic aspirations for a national championship. The previous season, he had become the second player in NCAA history to lead the nation in scoring and rebounding. Gathers fainted on the court, and both sustained and nonsustained ventricular arrhythmias were documented most likely as a result of underlying myocarditis.5 With the extraordinary success of this team from a small university, there was tremendous pressure for Gathers to continue to play. He ultimately returned to play later in the season and died tragically on the court during a tournament game. This case illustrates the entwined complexity inherent to any cardiovascular diagnosis in an elite athlete. Gathers was admittedly noncompliant with his propranolol. The reluctance to disqualify him under the circumstances was profound. The emotional cost to Gather’s family, friends, teammates, and the Loyola Marymount community at large is beyond measure. There was also a profound financial impact, with judgments and settlements against the physician and the university.6 Now that we are more than 25 years removed from this event, it is reasonable to assume that Loyola Marymount is still suffering beneath the dark cloud of this occurrence. Death during competition would intercede as “the most unwelcome spectator” (Jim Murray, The Los Angeles Times)1 for other notable athletes as well, including Tom Simpson, an English cyclist who died on Mont Ventoux in the 1967 Tour de France (likely from amphetamines); Flo Hyman, an Olympic volleyball player who died of aortic dissection from the Marfan syndrome four years before Gathers; basketball players Pete Maravich (anomalous coronary artery), Reggie Lewis, and Jason Collier; Sergei Grinkov (ice-skating), Jiri Fischer (hockey), Thomas Herrion (football), and Fran Crippen (swimming). In addition to elite athletes with national and international notoriety,

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CHAPTER 12  Comprehensive Cardiovascular Care and Evaluation of the Elite Athlete

Abstract

Keywords

A comprehensive review of the cardiovascular assessment of elite athletes. Specific topics include cardiovascular adaptations and remodeling, the role of epidemiologic factors, preparticipation cardiovascular screening, structural and congenital disease, and acquired cardiovascular pathologies. Content focuses of current guidelines and state-of-the-art practice with a focus on a multidisciplinary approach to the athlete’s “medical home.”

electrocardiogram transthoracic echocardiogram cardiac magnetic resonance imaging screening medical home

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SD has also had a profound impact in communities around the world coping with unexpected deaths of athletes of all ages and levels of ability. The amplification of athletic SD into our cultural consciousness has stimulated considerable research and medical practice interest into the causes of SD in athletes, potential preventive measures inclusive of screening, and the development of care and management guidelines for athletes with known cardiovascular abnormalities. In practice, the prevention of SD represents only a part of the comprehensive cardiovascular care of the elite athlete. In this chapter, we will discuss the current state of practice, controversy with regard to screening, and the detection and management of cardiovascular disorders, with particular emphasis on the normal physiologic cardiovascular remodeling that can occur with elite levels of training.

MEDICAL HOME OF THE ELITE ATHLETE It is imperative that the elite athlete begin with a medical home composed of a multidisciplinary team, ideally led by a primary care sports medicine provider. Athletic trainers are a vital part of this medical home as well, and bring a rapidly evolving expertise involving the overall health and wellness of the athlete. Trainers are keenly aware of the importance of cardiovascular health and are now familiar with a wide array of useful technology and equipment including blood pressure cuffs, stethoscopes, automatic external defibrillators (AEDs), and electrocardiogram (ECG) machines. In addition, smartphone technology has greatly enhanced the ability of the sports trainer to assess their athletes in real time. Trainers at some Division 1 programs now use a digital application that provides immediate rhythm analysis for symptomatic athletes. It is very helpful when trainers can accompany athletes to subspecialty encounters, because they can reliably relay important information onto the practice and playing field and report back on the development of any important signs, symptoms, or physical findings that may place the athlete at risk. There is increasing recognition that the medical home of an elite athlete should ideally include a dedicated cardiovascular specialist, with their scope of practice and depth of involvement depending on the specific needs of the individual. These cardiovascular specialists, often referred to as sports cardiologists, may be tasked with oversight of preparticipation screening as well as the evaluation and management of athletes with suspected or previously diagnosed cardiovascular disease. Given this evolving role of cardiovascular specialists in the care of elite athletes, both the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) have dedicated resources to define specific skills and core competencies to guide the practice of sports cardiologists.7

Preparticipation Screening The initial history and physical exam performed by the primary care sports medicine provider now includes the fourth edition of the Preparticipation Physical Evaluation (PPE-4)9 and has evolved to include a somewhat more reliable detection process for familial cardiovascular abnormalities that might increase the risk of SD and were adopted by the American Heart Association consensus panel for preparticipation cardiovascular screening.6

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However, the state of the current initial athlete evaluation suffers from significant limitations. There is a wide variation from state to state with regard to the type of provider performing the PPE-4 and the content of the PPE-4. In addition, the PPE-4 relies on self-reporting by the athletes themselves, which is inherently prone to error.10 Furthermore, the PPE-4 has been demonstrated to have poor sensitivity for the detection of cardiovascular disorders. Indeed, in a retrospective look at SD in athletes who had participated in preparticipation screening, only 3% were thought to have potential cardiovascular abnormalities, and none were restricted from participation.11 Following the PPE-4, referral of an athlete for more advanced cardiovascular care or evaluation occurs as a result of an abnormal physical finding, a family history of premature sudden death, or the development of new symptoms that elicit concern. Many of the most dangerous cardiovascular conditions that could threaten the athlete often are asymptomatic and have no physical finding that would trigger a referral. This includes conditions such as hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), congenital Long QT and Brugada syndromes, WolffParkinson-White (WPW), and the anomalous coronary artery. The absence of a positive family history for SD can be falsely reassuring in the autosomal dominant familial conditions (HCM, ARVC, Long QT, the Marfan syndrome), because up to 25% to 33% of affected individuals will have new spontaneous mutations with no previously affected family members.12,13 Accordingly, the current state of evaluation of the elite athlete in the United States is unlikely to detect most threatening cardiovascular conditions. Furthermore, the normal physiologic adaptations of hypertrophy of the left ventricle to rigorous isometric training (often referred to as the “athlete’s heart”) can very closely mimic HCM, which is the most prevalent and dangerous cardiovascular disease in young athletes.14 In addition, physiologic changes in left and right ventricular cavity size and systolic function can be difficult to distinguish from forms of dilated cardiomyopathy and ARVC. Perhaps nowhere in medicine does normalcy mimic disease as it does in this circumstance. As a result, further screening or evaluation of elite athletes requires a sophisticated and programmatic approach that is designed to avoid the pitfall of potentially lifechanging false-positive results that will be the inherent weakness in the evaluation of large populations of athletes with a low prevalence of disease. Because of these inherent complexities, expert consensus in the United States, including the American College of Cardiology and American Heart Association (ACC/ AHA), has not recommended routine evaluation of the athlete beyond the PPE-4. While this recommendation is well wrought and reasonable, evidence is lacking regarding the efficacy of the PPE-4 in prevention of morbidity and mortality in athletes.10 In addition, this differs from other expert guidelines, including the ESC and the International Olympic Committee (IOC), which recommend the addition of ECG screening in order to improve the sensitivity of preparticipation screening. Current practice in the United States varies in regard to the inclusion of diagnostic screening tools beyond the PPE-4. As an example, more than one third of National Collegiate Athletic Association (NCAA) Division-1 athletes undergo additional screening with either an ECG or echocardiogram.15

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Current recommendations have created an unanticipated consequence in the field of sports cardiology. There is a paucity of well trained and knowledgeable cardiovascular providers familiar with the nuances of the normal physiologic adaptations to elite training and how to differentiate normalcy from disease. Encounters with elite athletes are uncommon for most practicing cardiologists. Accordingly, athletes who undergo more extensive testing and evaluation by inexperienced providers are commonly sidelined unnecessarily, subjected to over testing, relegated to the emotional consequences of concern for survival, and temporary or permanent disqualification from sports altogether. The incorporation of cardiovascular care into the medical home of the athlete must be done very carefully with knowledgeable providers dedicated to understanding the complex world of the athlete.

CARDIOVASCULAR ADAPTATIONS AND REMODELING ASSOCIATED WITH RIGOROUS ATHLETIC TRAINING The earliest recognition of the physiologic changes commonly referred to as the “athlete’s heart” were astutely described in 1899 by a Swedish physician who detected cardiac enlargement in elite Nordic skiers utilizing remarkably accurate skills of auscultation and percussion. That same year, these findings were reinforced in a study of Harvard University rowers.16 It is not surprising that the earliest descriptions of cardiac enlargement were made in Nordic skiers and elite rowers, because these disciplines include extreme combinations of endurance training (isotonic, dynamic, aerobic) and strength training (isometric, static, anaerobic) that lead to more striking combinations of both left ventricular (LV) cavity dilation and hypertrophy. A few years later, Paul Dudley White would strengthen the legacy of sports cardiology in Boston by observing pulses in endurance-trained runners participating in the Boston Marathon17 and would later describe bradycardia associated with this level of endurance training.18 The evolution of more sophisticated technology would allow for the complex assessment of the electrophysiologic and structural cardiovascular adaptations to varying degrees and types of athletic training.19,20 Accordingly, any cardiovascular evaluation of an athlete inclusive of electrocardiography or any form of cardiovascular imaging must be undertaken with in-depth knowledge of the trainingspecific changes in cardiac structure and function. Pure endurance training involves prolonged activities with sustained increases in cardiac output without significant elevation in mean arterial pressure. This type of volume load can lead to dilation of all four chambers of the heart and to some degree the great vessels as well. Strength-training subjects the heart to more brief but dramatic increases in mean arterial pressure that in turn leads to an increase in myocardial muscle hypertrophy. Marathon running is a good example of pure endurance training, and weight lifting is an example of pure strength training. Most sports, however, will have varying degrees of both types of training that will also vary with the approach of the individual athlete. Therefore the heart of any athlete may manifest changes across a broad spectrum of physiologic adaptation.

Structural Adaptations to Rigorous Training Left Ventricle The effects of training on the LV are routinely detected on the ECG and increases in voltage have been documented for decades.21 Endurance training that also incorporates increasing degrees of isometric/strength training (cycling, rowing, cross country skiing, canoeing) are more likely to demonstrate these manifestations on the resting ECG.22 Transthoracic echocardiography (TTE) has been used extensively to document the spectrum of LV cavity dilation and increase in LV wall thickness/left ventricular hypertrophy (LVH) associated with rigorous training.14,23-25 LV cavity size across a large variety of sports is larger than sedentary controls and ranges from 43 to 70 mm (mean 55 mm) in men and 38 to 66 mm (mean 48 mm) in women.25 LV wall thickness is generally less than 13 mm in elite athletes,23 but larger increases in wall thickness (1.3 to 1.5 mm) that stray into the “gray zone” with hypertrophic cardiomyopathy are more commonly seen in older elite athletes (rowers) who train with large degrees of static and dynamic exercise.26 LV systolic function as measured by TTE is usually normal in elite athletes.27-29 It is important to recognize, however, that LV systolic function can be low normal to mildly depressed (mimicking mild forms of dilated cardiomyopathy), as shown in some of the fittest athletes in the world participating in the Tour de France.30 These adaptive changes in cavity dimension, wall thickness, and the associated increase in LV mass have also been demonstrated in magnetic resonance imaging (MRI) studies31,32 and have been recently reviewed in depth.33 LV diastolic function is usually normal in elite athletes and can be improved with endurance training, leading to more robust early diastolic filling.26,34 Less is known about the effects of strength training on diastolic function, but there is evidence that diastolic function may be impaired, which could be an untoward longterm effect of hypertrophy that warrants further study.20 Right Ventricle Sustained increases in cardiac output have a similar effect on the right ventricle (RV) as compared with the LV, particularly with regard to cavity dilation. Older M-mode and 2-D TTE studies in endurance-trained athletes showed symmetrical dilation in both the RV and the LV.35,36 Due to the unique geometry of the RV, echocardiography has struggled to assess RV size and function, and cardiac MRI has greatly enhanced our ability to evaluate the RV. More recent MRI studies in elite endurance athletes have reinforced the balanced dilation of the RV and LV demonstrating increases in LV and RV mass, LV and RV diastolic volumes, and LV and RV stroke volumes.31,32,37 Abnormalities in systolic function in endurance athletes can also be abnormal and generally seen in athletes with more extensive RV dilation.38 The impact of strength training on the RV is less clear but likely to be a topic of future clarification utilizing TTE and cardiac MRI. Atria As expected, increased right and left atrial volumes and sizes are also seen in endurance athletes with more numerous studies evaluating the left atrium.35,39-41 A large volume of data supports the physiologic effects of sustained endurance volume loading

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on all four cardiac chambers, including the atria. In the largest Italian series, 20% of athletes had left atrial dimensions of >40 mm measured by TTE, and supraventricular arrhythmias were not common in this group.42

Great Arteries and Veins The great arteries and veins are subject to the physiologic effects of endurance training. The aorta is of particular interest with regard to strength training, as extraordinary increases in both systolic and diastolic blood pressure (480/350 mm Hg!) have been documented in weight lifters.43 Studies have documented somewhat inconsistent aortic root dilation with regard to specific types of sports and training regimens. Strength-trained athletes have been shown to have larger dimensions of the aorta measured by TTE at the aortic annulus, the sinuses of Valsalva, sinotubular junction, and proximal aortic root when compared with controls, and this effect increased with the duration of training.43,44 Aortic root size was greater in taller athletes and typically measured between 3.0 and 4.0 cm, and only rarely measured greater than 4.0 cm. While aortic regurgitation was found in none of the controls, 9% of the strength-trained athletes had mild (n = 5) or moderate (n = 4) aortic regurgitation.44 Another large trial supported these findings comparing strength-trained with endurance-trained athletes.45 In a large trial of a wide range of sports in Italy, the largest measurements were found in endurancetrained athletes, particularly in the disciplines of cycling and swimming.46 This apparent inconsistency may be attributed the sustained combination of isometric and isotonic exercise associated with these sports. In totality, it is important to note that while athletic training in various disciplines may lead to increase in aortic root dimensions, these increases have not been shown to approach diameters typically concerning for pathologic dilatation. In this light, a meta-analysis investigating aortic root dimensions in athletes versus nonathlete controls found that elite athletes have a minor, and likely clinically insignificant, increase in aortic root dimensions.47 The authors rightfully noted that marked

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aortic root dilatation likely represents a pathologic process rather than an adaptation to exercise. The effects of training are also seen on a wide range of great vessels in endurance athletes and taller athletes, including larger caliber carotids, branch pulmonary arteries, superior and inferior vena cavae, and abdominal aorta as shown in cyclists, longdistance runners, and volleyball players.48 It has been our observation in endurance-trained athletes that the inferior vena cava is routinely larger than normal, and that published estimates of RA pressure based upon vena cava size and inspiratory collapse do not apply to the elite athlete.

The Athlete’s Electrocardiogram and Electrophysiologic Adaptations to Rigorous Training Training-induced alterations in cardiac structure and autonomic regulation are reflected on the ECG of the athlete in many ways, and the resting ECG will have a range of well-documented variations as compared with normal controls in most cases.18,49-51 Common training-related findings on the athlete’s ECG include sinus bradycardia, first degree atrioventricular (AV) block, incomplete right bundle branch block (RBBB), early repolarization, and voltage criteria for LVH (Fig. 12.1). Electrophysiologic aberrations, like their structural counterparts, are more common in endurance sports that include a significant amount of strength training as well (cycling, rowing, canoeing, and cross-country skiing).22

GENDER, GENETICS, AND RACE Gender, genetics, and race have a pronounced influence upon the structural and electrophysiologic adaptations to rigorous athletic training. Abnormal findings on the athlete’s ECG are more common in males and in athletes of African or Caribbean descent.22,52 Dramatic examples of LVH by voltage with markedly

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Fig. 12.1  The electrocardiogram (ECG) of a 17-year-old white freshman intercollegiate distance runner who had undergone several years of intense endurance training. The ECG shows a marked sinus bradycardia with a heart rate of 37 bpm at rest. Also note the diffuse, prominent, high-voltage T-waves (red arrows).

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B Fig. 12.2  (A) The resting electrocardiogram (ECG) of an intercollegiate 800-meter runner of Nigerian descent. Diffuse increased QRS voltage is present, particularly in leads V4 and V5, which is very common in endurance-trained athletes. This athlete has T-wave inversion in the inferior leads (red marker) and ST elevation with biphasic T-waves in the precordial leads (blue marker). These findings are uncommon in white athletes. (B) Transthoracic echocardiography showing the parasternal long-axis view in this same athlete. Left ventricular (LV) cavity size, wall thickness, and LV mass are all normal. This ECG is a normal variant for this athlete of African descent.

abnormal T-waves and repolarization abnormalities are commonly seen in elite African athletes (Fig. 12.2) and should not be mistaken for HCM. In 1962, these findings were described in the Bantu and Nilotic people of Africa, and in the case of an Olympic boxer, an ECG performed after prolonged detraining demonstrated complete regression of the ECG findings of LVH and T-wave abnormalities.53 Gender and ethnicity have a similar impact upon imaging studies (TTE). A study of 600 elite female athletes undergoing TTE screening demonstrated a low incidence of LV cavity dilation, and not one female athlete had an LV wall thickness greater than 12 mm.54 Black female athletes show a modest but more pronounced tendency toward hypertrophy with LV wall thickness measuring 6 mm greater when compared with Caucasian female athletes.55 In a study of elite rowers, a familial genetic influence was suggested when Baggish et al. found that athletes with a family history of hypertension developed a more pronounced increase in LV mass when compared with rowers without a family history of hypertension. The pattern of hypertrophy was different as well, with concentric hypertrophy more commonly seen in rowers with a family history of hypertension and eccentric hypertrophy seen in controls.56 In addition,

angiotensin converting enzyme gene polymorphisms have been shown to predispose athletes to more pronounced remodeling with increases in both LV mass and LV wall thickness.57,58 These studies underscore the complexity of the process of training induced cardiac remodeling. This process is influenced by the type and duration of training, the gender, and the genetic heterogeneity of the individual athlete.

CARDIOVASCULAR SCREENING OF THE ATHLETE Because of the devastating consequences of unexpected athletic SD, a wide array of approaches has been developed outside of recommended guidelines by individual universities, countries, and professional athletic teams to more reliably identify potential life-threatening and asymptomatic abnormalities that would not be detected on the PPE-4. The modern elite athlete stresses the cardiovascular system to remarkable levels of both strength and endurance. The examples of Pheidippedes and Fran Crippen, who died in a 10-kilometer open-water swim in extreme heat in 2010 in the United Arab Emirates, may both be examples of athletic SD occurring as a result of heroic athletic effort in the absence of any underlying cardiovascular abnormality. Accordingly, any undiagnosed cardiovascular abnormality could expose the athlete to distracting symptoms, impaired performance, and ultimately athletic SD. Landmark papers on the causes of SD in athletes under the age of 35 are well established.11,59 In the United States, athletic SD occurs at a rate of approximately 125 per year, and a spectrum of underlying pathologies are implicated. It was previously thought that HCM accounted for more than one third of these tragic occurrences,3 but recent data have challenged that assessment by demonstrating a lesser prevalence of autopsyproven HCM in SCD cases across various countries, in agematched noncompetitive athletes, and in US military personnel.60-64 In this light, it has been demonstrated that more than 30% of NCAA athletes and 40% of US military recruits had structural normal hearts at autopsy, with a sudden arrhythmia presumed to be the etiology of their death.65,66 In the most rigorous review of SCD in athletes to date, a British study of 357 consecutive cases of SCD demonstrated that HCM accounted for only 5% of cases.67 In this study, pathologic analysis was performed by a dedicated cardiac pathologist, a crucial detail, as it has been shown that up to a 40% disparity in documented cause of death exists when standard autopsy results are compared with those performed by a pathologist specializing in cardiac disease.68 When rigorous pathologic criteria for diagnosing HCM are applied, the percentage of SCD cases attributable to this disease state is significantly reduced as compared with earlier assessments.67 In British athletes, sudden arrhythmic death accounted for 42% of cases with a strong predilection for younger athletes, whereas myocardial disease accounted for just under 40% and in contrast had a predilection for older athletes. However, it should also be noted that there may be an inherent referral bias in that straightforward cases, such as easily identified HCM, may be not be referred for autopsy. Other congenital cardiac anomalies comprise the majority of the other causes of athletic SD, including the anomalous coronary artery, congenital aortic stenosis, ARVC,

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and ruptured aorta from the Marfan syndrome or related vascular disorders. A much smaller percentage of athletic SD in young athletes results from acquired heart diseases like myocarditis and coronary artery disease. In addition to serious cardiovascular disorders, there are many other less threatening congenital and acquired abnormalities that are often asymptomatic and may have subtle if any physical findings that could affect the future of the athlete’s health, cause symptoms in the athlete, or impair performance (Box 12.1). Accordingly, any programmatic attempt to screen athletes for potential cardiovascular abnormalities beyond the PPE-4 will need a very sharp edge, an edge that can reliably distinguish training related remodeling from real disease, and an edge that is familiar with the congenital anomalies that will be found and can distinguish the benign from the more serious disorders. Screening must remain non-invasive and pose no risk to the athlete; therefore ECG and TTE are the most widely utilized modalities. Unless exercise-induced arrhythmias or coronary artery disease (CAD) are suspected, routine stress testing is of little value, while computed tomography (CT) and MRI expose the athlete to radiation (CT) and intravenous contrast (CT and MRI). These tests along with Holter monitoring, and genetic testing should be performed only when significant cardiovascular BOX 12.1  Congenital and Acquired

Cardiovascular Disorders Often Undetected in Childhood 1. Bicuspid aortic valve—functionally normal or mild valve disorder: • Fifty percent will have an associated abnormality of the ascending aorta (congenital aortopathy) 2. ASD/left to right shunts: • Secundum ASD, which includes atrial septal aneurysm with small or multiple ASD/patent foramen ovale • Venosus ASD • Coronary sinus ASD • Partial anomalous pulmonary venous return 3. Hypertrophic cardiomyopathy 4. Anomalous coronary arteries, coronary artery fistulae 5. Marfan syndrome and related disorders: • Ehlers-Danlos syndrome • Loeys-Dietz syndrome • Mitral valve prolapse, aortic root diameter at upper limits of normal for body size, stretch marks of the skin, and skeletal conditions similar to Marfan syndrome (MASS) phenotype 6. Wolff-Parkinson-White syndrome 7. Long QT syndrome 8. Brugada syndrome 9. Ventricular tachycardia, pathologic premature ventricular contractions 10. Arrhythmogenic right ventricular cardiomyopathy 11. Coarctation of the aorta (particularly milder forms) 12. Pulmonary hypertension (particularly mild to moderate forms) 13. Myocarditis (acute or with chronically impaired ventricular function) 14. Congenital cardiomyopathy (including congenital noncompaction) 15. Mitral valve prolapse ASD, Atrial septal defect. From Battle RW, Mistry DJ, Malhotra R. Cardiovascular screening and the elite athlete: advances, concepts, controversies, and a view of the future. Clin Sports Med. 2011;30:503–524.

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disease is strongly suspected and interpreted by providers knowledgeable in sports cardiology.

Electrocardiogram Screening in Athletes The ECG is a widely available screening tool that can provide valuable information regarding cardiac structure and function. Accordingly, ECG is the most frequently used diagnostic test to screen athletes above and beyond the PPE-4. Mandatory ECG screening has been in place in the Veneto region of Italy since the 1971. Mandated by the Medical Protection of Athletes Act, ECGs were performed on Italian athletes from ages 12 to 35. Corrado et al.69 have published an extensive 25-year experience with athlete ECG screening in a variety of sports, and from the Italian perspective, this has been shown to be cost-effective.70 Investigators argue that the data from Italy support ECG screening, and that has led to the disqualification of athletes at risk (particularly with HCM), thereby shifting the demographics of athletic SD in Italy away from HCM as the most common cause of SD and toward ARVC.71 As a result of these findings, the IOC supported ECG screening of Olympic athletes in 2004,72 and the following year a similar recommendation emerged from the European Society of Cardiology.73 ECG screening has also been shown to more reliably identify college athletes with cardiovascular disorders in the in the United States, albeit with an increase in false-positive results,74 but because of the inherent interpretive complexity of this process, there has been considerable controversy regarding the routine addition of the ECG to athletic screening. In support of the European approach, the use of ECG has been advocated in the United States,75 while the complexity of cost and inherent limitation of widespread ECG screening have been elegantly argued,76 even discouraged,76,77 and thus it has not been endorsed by the US Olympic Committee, the American Heart Association, the American College of Cardiology, and has not been incorporated into the most recent Joint Conference on Eligibility Recommendations for Competitive Athletes with Cardiovascular Disorders.78 As stated by the ESC, the goal of ECG screening is to “differentiate between physiologic adaptive ECG changes and pathologic ECG abnormalities, with the aim to prevent adaptive changes in the athlete being erroneously attributed to heart disease, or signs of life-threatening cardiovascular conditions being dismissed as normal variants of athlete’s heart.”69 With this goal in mind, in recent years, both European and American researchers have made significant strides in improving ECG screening guidelines in an effort improve sensitivity as well as to decrease the rate of false-positive results. In 2010, the ESC published recommendations for ECG interpretation in athletes, commonly referred to as the “European guidelines.” These guidelines were the first to formally differentiate adaptive physiologic ECG patterns from those suggestive of underlying cardiovascular disease, a dichotomous approach that has subsequently become the standard of care. “Common and training-related” changes included sinus bradycardia, first-degree AV block, incomplete RBBB, early repolarization, and isolated QRS voltage criteria for LVH. “Uncommon or training-unrelated” changes included T-wave inversion, ST-segment depression, pathologic Q-waves, left atrial enlargement, left-axis deviation/left anterior hemiblock, right-axis deviation/left posterior hemiblock,

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right ventricular hypertrophy, ventricular pre-excitation, complete left bundle branch block (LBBB) or RBBB, long- or short-QT interval, or Brugada-like early repolarization (Figs. 12.3 and 12.4). When applied to a cohort of more than 1000 previously studied ECGs, it was demonstrated that greater than 70% of ECGs previously identified as being suggestive of cardiovascular disease could be reclassified as “physiologic” on the basis of either isolated voltage criteria for LVH or early repolarization.22 Such a significant decrease in the rate of false-positives demonstrated the significant advantage of a formal dichotomous approach in ECG screening of athletes; however, further investigation demonstrated that the false-positive rate still remained between 10% and 20%.79 In subsequent years, attempts were made to further improve the specificity of screening recommendations. The “Seattle Criteria” added sinus arrhythmia, ectopic atrial rhythm, junctional escape rhythm, and Mobitz Type I (Wenckebach) secondary AV block to the benign ECG changes included in the European guidelines, while refining the specific electrocardiographic changes required to define pathologic changes in regards to RVH or right-axis deviation, intraventricular conduction delay, and isolated anterior T-wave inversion, along with an increase in QTc required to define a long QT-interval.80 Subsequent analysis has shown that the Seattle criteria perform to a higher level of I

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Fig. 12.3  An electrocardiogram at rest shows long QT in a patient with torsades des pointes. The QT interval indicated by the bar in V6 is prolonged to approximately 600 ms. (From Battle RW, Mistry DJ, Malhotra R. Cardiovascular screening and the elite athlete: advances, concepts, controversies, and a view of the future. Clin Sports Med. 2011;30:503–524, with permission.)

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Fig. 12.4  An example of Brugada syndrome with “coved” type ST segment elevation >2 mm in V1 (arrow) followed by a negative/inverted T-wave. (From Battle RW, Mistry DJ, Malhotra R. Cardiovascular screening and the elite athlete: advances, concepts, controversies, and a view of the future. Clin Sports Med. 2011;30:503–524, with permission.)

specificity, and thus achieve a lower false-positive rate, primarily through this refinement in criteria to define an ECG change as pathologic.81 Further studies attempted to enhance specificity to an even greater degree by evaluating the pathologic relevance of “borderline variants,” including RVH, isolated axis deviation, and atrial enlargement specifically,82,83 as well as the applicability in subpopulations of athletes of African or Caribbean decent. In this light, the “Refined Criteria” were published in 2014 and defined a scheme that distinguished borderline variants identified in isolation, previously defined as abnormal by the European guidelines and some by the Seattle criteria as not requiring further workup.84 When applied to a cohort of both black and white athletes, the Refined Criteria improved specificity in white athletes from 73% to 84%, and even more substantially in black athletes from 40% to 80%. Further analysis has demonstrated that whereas the European guidelines, Seattle Criteria, and Refined Criteria were each 100% sensitive in identifying the case of HCM and WPW, the Refined Criteria greatly reduced the prevalence of ECGs identified as abnormal and significantly increased specificity across all ethnicities.85 In summary, we believe the ECG has considerable value particularly when applied with a comprehensive understanding of normal adaptations associated with training, the effects of race and gender, and when formally evaluated using newly defined criteria to distinguish normal adaptation from “uncommon and training unrelated ECG changes.”69 Use of the Refined Criteria specifically has been demonstrated to significantly reduce the rate of false-positive screenings while not compromising sensitivity in identifying pathology. In addition, these criteria can be used with confidence by providers who see larger volumes of athletes of African descent and thus will be exposed to a much wider range of repolarization abnormalities (ST elevation, biphasic T-waves) associated with dramatic increases in voltage as shown in Fig. 12.2 and Fig. 12.5A. When supplemented by available on-site high-quality TTE when necessary, these criteria can greatly reduce unnecessary withdrawal from participation.74,76 While current AHA guidelines do not support a universal ECG screening program for athletes, it does support the concept of formal and standardized ECG screening programs when adequate cardiology resources are available for further investigation of pathologic variants when discovered.86 While the controversy over the inclusion of ECG screening in preparticipation screening will undoubtedly continue, institutions and team physicians will be left to decide what is feasible, affordable, and what level of risk is acceptable within their particular circumstance. Accordingly, incorporation of ECG screening alone in conjunction with the PPE-4 will likely lead to unnecessary sidelining of athletes, particularly athletes of African and Caribbean descent, while further testing is performed at the expense of the athlete in question. Therefore any consideration of the cost effectiveness of ECG screening alone must incorporate the added and often unnecessary cost of downstream imaging (TTE) generated by a false-positive screening ECG.

Transthoracic Echocardiography Screening in Athletes TTE screening for athletic preparticipation has not been formerly included in any guidelines or recommendations in Europe or the

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Fig. 12.5  Examples of athlete’s hearts as shown by electrocardiogram (ECG) and transthoracic echocardiography (TTE). (A) The ECG of an African American Division I basketball player demonstrates diffusely increased QRS voltage without QRS widening (narrow arrows) and upwardly convex ST elevation followed by inverted T-waves (broad arrows). This ECG shows more pronounced abnormalities of the athletic heart seen in African American athletes. (B) This same athlete’s short-axis TTE image demonstrates a mild increase in septal wall thickness to 1.25 cm (thin arrows) with mild left ventricular (LV) cavity dilation of 6.0 cm (broad arrows) and a corresponding increase in LV mass. The image is a representative example of athlete’s heart in an elite African American athlete. (C) An 18-year-old white high school football player with hypertrophic cardiomyopathy (HCM). The ECG reveals increased QRS voltage but with mild prolongation in QRS duration (thin arrows) and prominent T-wave inversion (broad arrows). (D) A short-axis TTE image in an African American Division I basketball player with HCM and exertional angina. The septum is abnormally hypertrophied, measuring 1.6 cm (thin arrows), and the LV cavity size is 5.0 cm (broad arrows), which is considerably smaller than noted with the athletic heart. Stress echocardiography revealed complete systolic LV cavity obliteration. (From Battle RW, Mistry DJ, Malhotra R. Cardiovascular screening and the elite athlete: advances, concepts, controversies, and a view of the future. Clin Sports Med. 2011;30:503–524, with permission.)

United States, except when the abnormalities found during the PPE-4, screening ECG, or the development of new symptoms indicate the need for additional testing. TTE is far more expensive and logistically challenging than ECG, and it suffers from similar challenges with regard to the definition of acceptable limits of normal remodeling and the presence of true disease. Accordingly, inclusion of TTE also carries with it the important problem of false-positive results exceeding the detection of real disease states. Performance of TTE as a screening tool or as a consequence of concern for disease places the sports cardiologist in and around the “gray zone” defined by Maron as the overlap area between training related hypertrophy and HCM.14 This presents a strong challenge, but there are, however, tools to sharpen our discerning edge that allow for more precise separation of the two.14,23,87,88 The autosomal dominant mutation of the cardiac sarcomere known as HCM is a phenotypically very heterogeneous condition with LV wall thickness ranging from normal (2 mm in 2 or more adjacent leads (see Fig. 12.8) is uncommon in older athletes and may warrant further evaluation with MRI.69,111,115 T-wave inversion in precordial leads V1 to V3 occurs in 1% and thus five times more common than HCM. Examples of a familial BAV syndrome in two brothers that are Division I intercollegiate athletes are shown in Fig. 12.9. Both have right and left cusp fusion with mild to moderate aortic regurgitation,

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and one has mild aortic root dilation at the sinuses of Valsalva exceeding 40 mm. Both are followed every 6 to 12 months with TTE, and the athlete with aortic root dilation has been restricted from isometric weight training to avoid the impact of hypertension associated with rigorous isometric weight training. The Marfan syndrome is another autosomal dominant cardiovascular disorder that was first meticulously described by Edgar Allan Poe in a short story (“A Tale of the Ragged Mountains”), written about his earlier experience at the University of Virginia.121 The protagonist of this tale has all of the classic features of this syndrome, described by Poe more than 50 years before the first documented case in medical literature noted in Paris by Professor Antoine Marfan.122 The PPE-4 has been adapted to better detect the family history, medical history, and physical findings that might suggest the Marfan syndrome or related disorders such as Ehlers-Danlos or Loeys-Dietz syndrome.13,123 These syndromes all manifest genetic deficiencies of vital matrix proteins that can predispose the athlete to aortic dissection and, in the case of Ehlers-Danlos and Loeys-Dietz syndromes, to smaller arteries as well. In general, these athletes are restricted from all but lowintensity sports104 and usually do not develop into elite athletes. Exceptions do occur, however, and athletes with the Marfan syndrome may gravitate toward sports that require taller athletes, as illustrated by Flo Hyman who was an Olympic volleyball player before she died tragically of aortic dissection in a professional game. Furthermore, due to inconsistencies in administration of the PPE-4, athletes may inadvertently be allowed to participate, like the college swimmer in Fig. 12.10 with Marfan syndrome who was prescribed losartan and suffered a type B dissection of the aorta during practice. In the event of a positive family history of one of these autosomal dominant disorders, it may be prudent, as we suggested with family histories of HCM, to have the affected parent/relative genetically tested, followed by genetic testing of the athlete in question if appropriate.

ACQUIRED CARDIOVASCULAR CONDITIONS IN THE ATHLETE Myocarditis and myopericarditis should be considered in any athlete with new symptoms or evidence of arrhythmia, sustained chest pain, troponin elevation, or new findings of LV systolic dysfunction or ECG changes, particularly diffuse ST elevation and repolarization abnormalities. A Division I college basketball player with syncope and documented ventricular arrhythmia due to myocarditis is shown in Fig. 12.11. Previously difficult to diagnose in cases of preserved systolic function, this disorder is now readily detected utilizing gadolinium MRI with classic findings of sub-epicardial late gadolinium enhancement.124 Because the clinical course of myocarditis, and the arrhythmias and ventricular systolic dysfunction that may accompany it, varies widely, withdrawal and treatment recommendations must be individualized. It is prudent, however, to temporarily restrict any athlete with confirmation of this diagnosis at least temporarily and until any documented arrhythmias or LV systolic abnormalities resolve. CAD is a rare finding or cause of athletic SD in athletes 160/100 mm Hg) should be restricted from isometric training until the blood pressure is well controlled. All athletes with HTN should be closely followed so that ongoing counsel on diet and lifestyle is repeatedly provided, blood pressure is monitored, and the remodeling effects of training can be assessed when appropriate. Hyperlipidemia (including familial hyperlipidemia [FH] in particular) poses a difficult problem for sports medicine providers. Statin therapy for hyperlipidemia in the elite athlete is problematic, because many athletes will develop muscle pain in the absence of CK elevation,136 and in elite professional athletes, up to 80% will be intolerant to this class of drugs due to this side effect.137 Accordingly, treatment of this condition is close to incompatible with the activities associated with vigorous training and will prove a difficult challenge for most athletes, excepting those participating in less vigorous sports. Data to guide us in this area are few, yet it is reasonable to recommend at the minimum nonpharmacologic treatment according to guidelines138 and referral of any athlete with a family history of premature death from CAD with hyperlipidemia or FH to a lipid specialist, ensuring that, once retired from competition, this problem is readdressed.

Arrhythmias As discussed, conduction abnormalities and bradyarrhythmias are common in the trained athlete, including sinus bradycardia (which can be profound in endurance-trained athletes, see Fig.

12.1), junctional bradycardia, first-degree AV block, and Mobitz type I second-degree AV block. Mobitz type II and third-degree (complete) heart block are uncommon and should be judged abnormal, warranting referral to an electrophysiologist.139 Premature atrial and ventricular contractions and nonsustained ventricular tachycardia are also common in trained athletes and are typically overdriven and disappear at higher heart rates associated with exercise. In the absence of structural heart disease (normal resting ECG and TTE) and when suppressed by exercise, these findings are typically benign and do not have long-term implications.140-142 Atrial fibrillation (AF) is more common in elite endurance-trained athletes than sedentary controls.143-145 In athletes, AF may develop during training with high adrenergic tone (endurance athletes will suddenly feel a “power outage”) or during sleep and periods of more predominant vagal tone when AF may be focally initiated by premature atrial contractions arising from the pulmonary veins. Evaluation should include exclusion of structural heart disease, hyperthyroidism, and the intake of any type of inciting stimulant or supplement. Treatment is once again compromised by the performance-compromising effects of beta blockers and calcium blockers, neither of which suppress AF and which only slow the ventricular rate. We have found the Class IC agents flecainide and propafenone to be the most useful in athletes. For infrequent episodes, the “pill and pocket” approach as a single dose can effectively convert AF successfully to sinus rhythm.146 For athletes with a more significant clinical burden and/or impairment of performance during training or important competition, a daily dose of flecainide or propafenone may be required; and athletes with structurally normal hearts are also likely to respond favorably to radiofrequency ablation of the pulmonary veins. Following radiofrequency ablation, there is a required period of anticoagulation; therefore the timing of this procedure will have a temporary impact on participation depending upon the sport. WPW syndrome can be asymptomatic or cause symptomatic supraventricular re-entrant tachycardia (SVT); and in extreme cases, rapid atrial fibrillation with aberrant conduction that can degenerate into ventricular fibrillation. Accordingly, athletes with WPW should be referred to an electrophysiologist to discuss the risks and benefits of bypass tract ablation, which can be curative. Common forms of re-entrant SVT also occur frequently in athletes, and if event or Holter monitoring detects this in a symptomatic athlete, ablation can be curative in this circumstance as well. Brugada syndrome and the congenital long QT channelopathies can be life-threatening and warrant electrophysiology referral, whether found incidentally or due to symptoms. Once again, the future will see the current guidelines challenged with regard to participation with these diagnoses. In a recent publication of the Mayo experience with congenital long QT 130, patients continued to participate in a variety of sports and 20 of those had ICDs.147 Of that group, 25% participated in high school sports, with 6% participating at the college and professional levels. Only one case of ICD discharge was documented in a 9-year-old boy who received two shocks for ventricular fibrillation occurring during warm-ups in the setting of admitted beta-blocker noncompliance. Catecholamine polymorphic ventricular tachycardia (CPVT) is another genetic syndrome, with the triggering of VT/

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VF occurring with exercise-induced surges in adrenalin, and symptomatic patients have a poor prognosis unless treated with ICD.148 An example of an asymptomatic 17-year-old Division I pole-vaulter with CPVT detected on a screening ECG is shown in Fig. 12.12. Life-threatening arrhythmias will be one of the more difficult future challenges for the sports cardiologist. Athletes with ICDs and a strong inclination to participate are at the top of that list. These athletes will still be at risk for syncope with exercise and should be counseled with regard to risk of participation in sports and activities where syncope could be a threat to themselves, other athletes or spectators including but not restricted to: swimming, scuba diving, archery, shooting, race-car driving, sky diving, skiing, and snowboarding. Athletes and their families may focus on their own concerns and needs once limited or disqualified and not think about the emotional consequences an event such as aborted SD might have on teammates, coaches, friends, and spectators. Syncope is common in athletes and is unrelated to structural heart disease in the vast majority of cases, and typically occurs during nonexertional activities or immediately after exercise (likely due to sudden decrease in venous return).149 Accordingly, in this setting, neurocardiogenic syncope is the most likely cause; however, electrical and structural abnormalities should be excluded. Syncope with exercise should bring to mind more concerning diagnoses, including HCM, anomalous coronary artery, CPVT, and so on. Occasionally athletes with syncope at peak exercise will manifest recurrent vasodepressor (hypotension) and/or cardio-inhibitory (bradycardia) syncope, but this must be demonstrated during stress testing with reproduction of symptoms before the diagnosis can be reliably established. The presumed mechanism is the Bezhold-Jarish reflex mediated by hyperdynamic LV function stimulating receptors in the left ventricle, which in turn activate the dorsal medial nucleus of the vagal nerve.150,151 Athletes who we have found to have unique problems in this area are the elite rowers. It is common during training for upward of 60 intercollegiate rowers to line up side by side, often in confining spaces

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

II

Fig. 12.12  A 17-year-old female Division I collegiate pole-vaulter with premature ventricular contractions on a screening electrocardiogram (ECG). Exercise treadmill test revealed polymorphic ventricular foci (arrows). An epinephrine challenge corroborated the diagnosis of catecholaminergic polymorphic ventricular tachycardia. This athlete was disqualified and the arrhythmia was suppressed with a beta blocker. (From Battle RW, Mistry DJ, Malhotra R. Cardiovascular screening and the elite athlete: advances, concepts, controversies, and a view of the future. Clin Sports Med. 2011;30:503–524, with permission.)

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for erg training on rowing machines. These athletes are capable of extreme outputs under these circumstances, and coupled with the heat emanating from so many exercising athletes at this level in close proximity, syncope and presyncope with peak exertion can occur in the absence of structural or electrical abnormalities. Syncope while seated seems implausible, but this may in part be due to compromised return of inferior vena cava blood during the forward posture portion of the rowing stroke. Standard treadmill testing cannot reproduce this reliably, and erg testing on the portable rowing machine in the stress lab can simulate training and competition and thus be useful. Postural orthostatic tachycardia syndrome (POTS) and other disorders of autonomic regulation may also affect elite athletes causing symptoms and impairing performance.152 This condition has been a common cause for referral in our experience with university athletes, probably because of transmission of viral illnesses that can spread through large groups of athletes and may be responsible for many of these disorders. Affected athletes may have inappropriate increases in heart rate (sinus tachycardia), with upright posture and stress testing with varying degrees of postural hypotension. Most athletes will be reassured to know that compromised performance is physiologic and that patience and continued graduated training (usually to include isometric training) will be required. Many treatments have been proposed, but most, other than careful attention to proper hydration and perhaps salt tablets, have been disappointing. Commotio cordis is emerging as an important cause of athletic SD in the absence of structural or electrical cardiovascular abnormalities. SD during sports following blunt impact of a projected object (baseball, lacrosse ball, hockey puck) is uncommon but well described in the literature as commotion cordis, albeit with the mechanism unknown.153 In an elegant animal model, Link et al. demonstrated that a wooden object the size and weight of a regulation baseball projected into the chest of pigs at 30 miles per hour timed to 15 to 30 m/sec ahead of the T-wave induced VF in 9/10 impacts. This did not occur in any impacts at other times during the cardiac cycle.154 Furthermore, commercially available chest wall protectors fail to protect against this rare but often fatal event.155 A registry of commotio cordis has been established and has taught us that it more commonly affects children (mean age 12), presumably because of the underdeveloped thorax and that only 10% of individuals before 1999 survived the arrest.156 This research has resulted in a widespread appreciation of commotio cordis among sports medicine physicians and trainers, particularly in the vulnerable sports like baseball, softball, lacrosse, and hockey. VF induced by blunt impact is a time-sensitive rhythm, and knowledge by providers and availability of AEDs may have a beneficial impact on this rare but tragic occurrence in the future.

CONCLUSIONS AND AN OPTIMISTIC VIEW OF THE FUTURE Athletes who have suffered athletic SD have not done so in vain and are in large part responsible for many advances in this field. The feats of Pheidippides led to the reincarnation of the marathon race in Boston by the Boston Athletic Association in 1897. That race in turn would stimulate considerable interest in the

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cardiovascular adaptations to exercise and the diagnosis and evaluation of cardiovascular disease in those athletes. This sports cardiology tradition in Boston continues today and has gone well beyond its 100th year. Similar remarkable advances in basic science and the clinical spectrum of the athlete have come from around the world since the first description of the athlete’s heart by Henschen in 1899.157 We have optimism that this field will continue to grow beyond expert consensus and will bridge the gap between research and the clinical arena, and provide ample knowledgeable sports cardiologists to care for athletes of all ages in all locations. Incorporation of training in this discipline into standard cardiology fellowships should become routine rather than exceptional. Cardiologists entering this field will encounter complex relationships between athletes, their families, schools, teams, fans, and finally the media. It is also imperative that the role of the cardiologist within the medical home of the athlete continues to evolve within a shared decision-making framework alongside primary care sports medicine providers and athletic trainers. As stated by Dr. Andrew Krahn of the University of British Columbia in reference to the expanding role of specialized multidisciplinary clinics, “Shared decision-making supported by evidence-guided medical therapy and incremental interventions lays the foundation for a more permissive approach to not only allowing, but potentially encouraging participation in physical activity, including competitive sports.”158 Notably, the role of the physician in this complicated and often treacherous skein of relationships was thoughtfully and elegantly discussed by Harvard cardiologist Dr. Adolf Hutter Jr. in the keynote address prior to the 26th Bethesda Conference in 1994 and is mandatory reading for anyone entering this field.159 In closing, we emphasize the evolving improvements in the survival rate of athletic SD. The RACER investigators127 showed that during athletic SD from 2000 to 2010, the mortality of athletes dropped to 71%, which is a marked decrease in previously published mortality for out-of-hospital cardiac arrest. Bystander CPR was identified as a predictor of survival. Recently released unpublished data from the European Society of Cardiology Congress from the fall of 2012 reinforces this finding, comparing out-of-hospital cardiac arrest during athletic and nonathletic circumstances. SD with exercise was associated with a 45% survival as compared with nonexercise survival of 15%.160 None of the athletic survivors suffered significant cognitive brain damage. These advances in survival are likely due to heightened awareness, improved techniques of CPR, education and training of bystanders, accessibility of AEDs, and availability of sports medicine providers, all of which are more readily accessed at many sporting events. No example is more dramatic than the case of Fabrice Muamba, who arrested on the pitch during a soccer match and underwent CPR for 78 minutes, including multiple defibrillation attempts, directed by a bystanding cardiologist who was present as a fan. Sinus rhythm was restored only after admission to the hospital. Muamba survived, recovered, and received an ICD. Athletes, and the trainers, volunteers, and spectators who surround them, embody a culture of enthusiasm and accomplishment—a culture that will pursue success even under the most adverse circumstance. An inspirational example can be found in Grand Junction, Colorado, in response to the

survival of a female with ARVC. The not-for-profit foundation “ARVD Heart for Hope” founded by her mother has partnered with Western Orthopedics and Sports Medicine and Community Hospital of Grand Junction to provide 54 AEDs for all local schools. This remarkable initiative in Grand Junction (a community of athletes) is the result of caring people making their community safer for athletes and, indeed, for all of us. This chapter is dedicated to the memory of Fran Crippen (April 17, 1984, to October 23, 2010). Fran attended the University of Virginia, where he was an All-American swimmer and went on to earn six national titles. We honor and remember Fran as a student athlete whose character and commitment were commensurate to his remarkable athletic ability. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Williams RA. The Athlete and Heart Disease: Diagnosis, Evaluation, and Management. Philadelphia: Lippincott Williams and Wilkins; 1999.

Level of Evidence: I

Summary: An outstanding book on the entire subject that reviews the available data in depth.

Citation: Baggish AL, Wood MJ. The athlete’s heart and clinical cardiovascular care of the athletic patient: overview and scientific update. Circulation. 2011;123(23):2723–2735.

Level of Evidence: I

Summary: This article provides an excellent review of the athlete’s heart and the care of the athlete.

Citation: Battle RW, Mistry DJ, Malhotra R. Cardiovascular screening and the elite athlete: advances, concepts, controversies, and a view of the future. Clin Sports Med. 2011;30:503–524.

Level of Evidence: I

Summary: This article provides a recent and in-depth review of cardiovascular screening of the athlete

Citation: Hutter AM. Cardiovascular abnormalities in the athlete: role of the physician. Keynote address: 26th Bethesda Conference. J Am Coll Cardiol. 1994;24:851–853.

Level of Evidence: V

Summary: This article addresses the complex role of the physician in dealing with cardiovascular abnormalities in the athlete.

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58. Karjalainen J, Kujala UM, Stolt A, et al. Angiotensinogen gene m235t polymorphism predicts left ventricular hypertrophy in endurance athletes. J Am Coll Cardiol. 1999;34:494–499. 59. Maron BJ, Epstein SE, Roberts WC. Causes of sudden death in competitive athletes. J Am Coll Cardiol. 1986;7:204–214. 60. Eckart RE, Scoville SL, Campbell CL, et al. Sudden death in young adults: a 25-year review of autopsies in military recruits. Ann Intern Med. 2004;141:829–834. 61. Eckart RE, Scoville SL, Shry EA, et al. Causes of sudden death in young female military recruits. Am J Cardiol. 2006;97: 1756–1758. 62. Corrado D, Basso C, Thiene G. Sudden cardiac death in young people with apparently normal heart. Cardiovasc Res. 2001;50:399–408. 63. Solberg EE, Gjertsen F, Haugstad E, et al. Sudden death in sports among young adults in Norway. Eur J Cardiovasc Prev Rehabil. 2010;17:337–341. 64. Basso C, Calabrese F, Corrado D, et al. Postmortem diagnosis in sudden cardiac death victims: macroscopic, microscopic and molecular findings. Cardiovasc Res. 2001;50:290–300. 65. Harmon KG, Drezner JA, Maleszewski JJ, et al. Pathogeneses of sudden cardiac death in National Collegiate Athletic Association athletes. Circ Arrhythm Electrophysiol. 2014;7: 198–204. 66. Eckart RE, Shry EA, Burke AP, et al. Sudden death in young adults: an autopsy-based series of a population undergoing active surveillance. J Am Coll Cardiol. 2011;58:1254–1261. 67. Finocchiaro G, Papadakis M, Robertus JL, et al. Etiology of sudden death in sports: insights from a United Kingdom regional registry. J Am Coll Cardiol. 2016;67:2108–2115. 68. de Noronha SV, Behr ER, Papadakis M, et al. The importance of specialist cardiac histopathological examination in the investigation of young sudden cardiac deaths. Europace. 2014;16:899–907. 69. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J. 2010;31:243–259. 70. Corrado D, McKenna WJ. Appropriate interpretation of the athlete’s electrocardiogram saves lives as well as money. Eur Heart J. 2007;28:1920–1922. 71. Corrado D, Basso C, Pavei A, et al. Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. JAMA. 2006;296:1593–1601. 72. Bille K, Figueiras D, Schamasch P, et al. Sudden cardiac death in athletes: the Lausanne recommendations. Eur J Cardiovasc Prev Rehabil. 2006;13:859–875. 73. Corrado D, Pelliccia A, Bjornstad HH, et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus statement of the study group of sport cardiology of the working group of cardiac rehabilitation and exercise physiology and the working group of myocardial and pericardial diseases of the European Society of Cardiology. Eur Heart J. 2005;26:516–524. 74. Baggish AL, Hutter AM Jr, Wang F, et al. Cardiovascular screening in college athletes with and without electrocardiography: a cross-sectional study. Ann Intern Med. 2010;152:269–275. 75. Myerburg RJ, Vetter VL. Electrocardiograms should be included in preparticipation screening of athletes. Circulation. 2007;116:2616–2626, discussion 2626.

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CHAPTER 12  Comprehensive Cardiovascular Care and Evaluation of the Elite Athlete 76. Chaitman BR. An electrocardiogram should not be included in routine preparticipation screening of young athletes. Circulation. 2007;116:2610–2614, discussion 2615. 77. Maron BJ. National electrocardiography screening for competitive athletes: feasible in the United States? Ann Intern Med. 2010;152:324–326. 78. Pelliccia A, Zipes DP, Maron BJ. Bethesda conference #36 and the European Society of Cardiology consensus recommendations revisited: a comparison of U.S. and European criteria for eligibility and disqualification of competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol. 2008;52:1990–1996. 79. Sharma S, Ghani S, Papadakis M. ESC criteria for ECG interpretation in athletes: better but not perfect. Heart. 2011;97:1540–1541. 80. Drezner JA, Ackerman MJ, Cannon BC, et al. Abnormal electrocardiographic findings in athletes: recognising changes suggestive of primary electrical disease. Br J Sports Med. 2013;47:153–167. 81. Brosnan M, La Gerche A, Kalman J, et al. The Seattle criteria increase the specificity of preparticipation ECG screening among elite athletes. Br J Sports Med. 2014;48:1144–1150. 82. Gati S, Sheikh N, Ghani S, et al. Should axis deviation or atrial enlargement be categorised as abnormal in young athletes? The athlete’s electrocardiogram: time for re-appraisal of markers of pathology. Eur Heart J. 2013;34:3641–3648. 83. Zaidi A, Ghani S, Sheikh N, et al. Clinical significance of electrocardiographic right ventricular hypertrophy in athletes: comparison with arrhythmogenic right ventricular cardiomyopathy and pulmonary hypertension. Eur Heart J. 2013;34:3649–3656. 84. Sheikh N, Papadakis M, Ghani S, et al. Comparison of electrocardiographic criteria for the detection of cardiac abnormalities in elite black and white athletes. Circulation. 2014;129:1637–1649. 85. Riding NR, Sheikh N, Adamuz C, et al. Comparison of three current sets of electrocardiographic interpretation criteria for use in screening athletes. Heart. 2015;101:384–390. 86. Hainline B, Drezner JA, Baggish A, et al. Interassociation consensus statement on cardiovascular care of college studentathletes. J Am Coll Cardiol. 2016;67:2981–2995. 87. Sedehi D, Ashley EA. Defining the limits of athlete’s heart: implications for screening in diverse populations. Circulation. 2010;121:1066–1068. 88. Baggish A, Thompson PD. Thick hearts, high stakes, great uncertainties: screening athletes for hypertrophic cardiomyopathy. Heart. 2009;95:345–347. 89. Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA. 2002;287:1308–1320. 90. Rickers C, Wilke NM, Jerosch-Herold M, et al. Utility of cardiac magnetic resonance imaging in the diagnosis of hypertrophic cardiomyopathy. Circulation. 2005;112:855–861. 91. Maron MS, Maron BJ, Harrigan C, et al. Hypertrophic cardiomyopathy phenotype revisited after 50 years with cardiovascular magnetic resonance. J Am Coll Cardiol. 2009;54:220–228. 92. Maron MS, Appelbaum E, Harrigan CJ, et al. Clinical profile and significance of delayed enhancement in hypertrophic cardiomyopathy. Circ Heart Fail. 2008;1:184–191. 93. Ho CY, Lopez B, Coelho-Filho OR, et al. Myocardial fibrosis as an early manifestation of hypertrophic cardiomyopathy. N Engl J Med. 2010;363:552–563.

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94. Prakken NH, Velthuis BK, Cramer MJ, et al. Advances in cardiac imaging: the role of magnetic resonance imaging and computed tomography in identifying athletes at risk. Br J Sports Med. 2009;43:677–684. 95. Peritz DC, Vaughn A, Ciocca M, et al. Hypertrabeculation vs left ventricular noncompaction on echocardiogram: a reason to restrict athletic participation? JAMA Intern Med. 2014;174: 1379–1382. 96. Gati S, Chandra N, Bennett RL, et al. Increased left ventricular trabeculation in highly trained athletes: do we need more stringent criteria for the diagnosis of left ventricular noncompaction in athletes? Heart. 2013;99:401–408. 97. Gati S, Papadakis M, Papamichael ND, et al. Reversible de novo left ventricular trabeculations in pregnant women: implications for the diagnosis of left ventricular noncompaction in low-risk populations. Circulation. 2014;130:475–483. 98. Battle RW, Mistry DJ, Malhotra R, et al. Cardiovascular screening and the elite athlete: advances, concepts, controversies, and a view of the future. Clin Sports Med. 2011;30:503–524. 99. Paterick TE, Jan MF, Paterick ZR, et al. Cardiac evaluation of collegiate student athletes: a medical and legal perspective. Am J Med. 2012;125:742–752. 100. Teare D. Asymmetrical hypertrophy of the heart in young adults. Br Heart J. 1958;20:1–8. 101. Shapiro LM. Hypertrophic cardiomyopathy in the elderly. Br Heart J. 1990;63:265–266. 102. Maron BJ, Carney KP, Lever HM, et al. Relationship of race to sudden cardiac death in competitive athletes with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2003;41:974–980. 103. Maron BJ, Olivotto I, Spirito P, et al. Epidemiology of hypertrophic cardiomyopathy-related death: revisited in a large non-referral-based patient population. Circulation. 2000;102:858–864. 104. Maron BJ, Douglas PS, Graham TP, et al. Task force 1: preparticipation screening and diagnosis of cardiovascular disease in athletes. J Am Coll Cardiol. 2005;45:1322–1326. 105. Lampert R, Cannom D. Sports participation for athletes with implantable cardioverter-defibrillators should be an individualized risk-benefit decision. Heart Rhythm. 2008;5:861–863. 106. Maron BJ, Mitten MJ, Quandt EF, et al. Competitive athletes with cardiovascular disease–the case of Nicholas Knapp. N Engl J Med. 1998;339:1632–1635. 107. Basavarajaiah S, Wilson M, Junagde S, et al. Physiological left ventricular hypertrophy or hypertrophic cardiomyopathy in an elite adolescent athlete: role of detraining in resolving the clinical dilemma. Br J Sports Med. 2006;40:727–729, discussion 729. 108. Pelliccia A, Maron BJ, De Luca R, et al. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation. 2002;105:944–949. 109. Maron BJ, Maron MS, Semsarian C. Genetics of hypertrophic cardiomyopathy after 20 years: clinical perspectives. J Am Coll Cardiol. 2012;60:705–715. 110. Basso C, Maron BJ, Corrado D, et al. Clinical profile of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes. J Am Coll Cardiol. 2000;35: 1493–1501. 111. Pelliccia A, Spataro A, Maron BJ. Prospective echocardiographic screening for coronary artery anomalies in 1,360 elite competitive athletes. Am J Cardiol. 1993;72:978–979.

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112. Hoyt WJ, Dean PN, Schneider DS, et al. Coronary artery evaluation by screening echocardiogram in intercollegiate athletes. Med Sci Sports Exerc. 2017;49:863–869. 113. Kim SY, Seo JB, Do KH, et al. Coronary artery anomalies: classification and ECG-gated multi-detector row CT findings with angiographic correlation. Radiographics. 2006;26:317–333, discussion 333–334. 114. Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria. Eur Heart J. 2010;31:806–814. 115. Papadakis M, Basavarajaiah S, Rawlins J, et al. Prevalence and significance of T-wave inversions in predominantly Caucasian adolescent athletes. Eur Heart J. 2009;30:1728–1735. 116. Marcus FI. Prevalence of T-wave inversion beyond v1 in young normal individuals and usefulness for the diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia. Am J Cardiol. 2005;95:1070–1071. 117. Roberts WC. The congenitally bicuspid aortic valve. A study of 85 autopsy cases. Am J Cardiol. 1970;26:72–83. 118. Nistri S, Sorbo MD, Marin M, et al. Aortic root dilatation in young men with normally functioning bicuspid aortic valves. Heart. 1999;82:19–22. 119. Fernandes SM, Sanders SP, Khairy P, et al. Morphology of bicuspid aortic valve in children and adolescents. J Am Coll Cardiol. 2004;44:1648–1651. 120. Malhotra RSC, Eagle J, et al. Screening athletes with congenital echo: feasibility and findings in our first year. J Am Coll Cardiol. 2012;59-E1930. 121. Battle RW. Edgar Allan Poe: a case description of the Marfan syndrome in an obscure short story. Am J Cardiol. 2011;108: 148–149. 122. Marfan ABJ. Un Cas De Déformation Congénitale Des Quatre Membres, Plus Prononcée Aux Extrémités, Caractérisée Par L’allongement Des Os Avec Un Certain Degré D’amincissement. Paris: Impr. Maretheux; 1896. 123. Loeys BL, Schwarze U, Holm T, et al. Aneurysm syndromes caused by mutations in the TGF-beta receptor. N Engl J Med. 2006;355:788–798. 124. Gagliardi MG, Bevilacqua M, Di Renzi P, et al. Usefulness of magnetic resonance imaging for diagnosis of acute myocarditis in infants and children, and comparison with endomyocardial biopsy. Am J Cardiol. 1991;68:1089–1091. 125. Blumenthal RSMD. 2007 Johns Hopkins White Papers: Heart Attack Prevention: Medletter Assoc, 2007. 126. Maron BJ, Isner JM, McKenna WJ. 26Th Bethesda Conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 3: hypertrophic cardiomyopathy, myocarditis and other myopericardial diseases and mitral valve prolapse. J Am Coll Cardiol. 1994;24:880–885. 127. Kim JH, Malhotra R, Chiampas G, et al. Cardiac arrest during long-distance running races. N Engl J Med. 2012;366: 130–140. 128. Albert CM, Mittleman MA, Chae CU, et al. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med. 2000;343:1355–1361. 129. Lehmann M, Durr H, Merkelbach H, et al. Hypertension and sports activities: institutional experience. Clin Cardiol. 1990;13:197–208. 130. Gifford RW Jr, Kirkendall W, O’Connor DT, et al. Office evaluation of hypertension. A statement for health

131.

132. 133.

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147.

professionals by a writing group of the council for high blood pressure research, American Heart Association. Circulation. 1989;79:721–731. Tanji JL. Tracking of elevated blood pressure values in adolescent athletes at 1-year follow-up. Am J Dis Child. 1991;145:665–667. Niedfeldt MW. Managing hypertension in athletes and physically active patients. Am Fam Physician. 2002;66:445–452. Lenfant C, Chobanian AV, Jones DW, et al. Seventh report of the Joint National Committee on the prevention, detection, evaluation, and treatment of high blood pressure (JNC 7): resetting the hypertension sails. Hypertension. 2003;41:1178–1179. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. DASH-sodium collaborative research group. N Engl J Med. 2001;344:3–10. Ahmed S, Thompson PD. Management of hypertension in athletes. In: Lawless CE, ed. Sports Cardiology Essentials: Evaluation, Management and Case Studies. New York: Springer; 2011:235–246. Sinzinger H, Schmid P, O’Grady J. Two different types of exercise-induced muscle pain without myopathy and CK-elevation during HMG-co-enzyme-A-reductase inhibitor treatment. Atherosclerosis. 1999;143:459–460. Sinzinger H, O’Grady J. Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscular problems. Br J Clin Pharmacol. 2004;57:525–528. Jellinger PS, Smith DA, Mehta AE, et al. American Association of Clinical Endocrinologists’ guidelines for management of dyslipidemia and prevention of atherosclerosis: executive summary. Endocr Pract. 2012;18:269–293. Barold SS, Padeletti L. Mobitz type II second-degree atrioventricular block in athletes: true or false? Br J Sports Med. 2011;45:687–690. Biffi A, Pelliccia A, Verdile L, et al. Long-term clinical significance of frequent and complex ventricular tachyarrhythmias in trained athletes. J Am Coll Cardiol. 2002;40:446–452. Baldesberger S, Bauersfeld U, Candinas R, et al. Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists. Eur Heart J. 2008;29:71–78. Biffi A, Maron BJ, Di Giacinto B, et al. Relation between training-induced left ventricular hypertrophy and risk for ventricular tachyarrhythmias in elite athletes. Am J Cardiol. 2008;101:1792–1795. Molina L, Mont L, Marrugat J, et al. Long-term endurance sport practice increases the incidence of lone atrial fibrillation in men: a follow-up study. Europace. 2008;10:618–623. Mont L, Sambola A, Brugada J, et al. Long-lasting sport practice and lone atrial fibrillation. Eur Heart J. 2002;23:477–482. Karjalainen J, Kujala UM, Kaprio J, et al. Lone atrial fibrillation in vigorously exercising middle aged men: case-control study. BMJ. 1998;316:1784–1785. Alboni P, Botto GL, Baldi N, et al. Outpatient treatment of recent-onset atrial fibrillation with the “pill-in-the-pocket” approach. N Engl J Med. 2004;351:2384–2391. Johnson JN, Ackerman MJ. Competitive sports participation in athletes with congenital long QT syndrome. JAMA. 2012;308:764–765.

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155. Weinstock J, Maron BJ, Song C, et al. Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. Pediatrics. 2006;117:e656–e662. 156. Maron BJ, Link MS, Wang PJ, et al. Clinical profile of commotio cordis: an under appreciated cause of sudden death in the young during sports and other activities. J Cardiovasc Electrophysiol. 1999;10:114–120. 157. Skilanglauf und Skiwettlauf HS. Eine medizinische sportstudie. Mitt Med Klin Upsala (Jena). 1899;2:15–18. 158. Krahn AD, Sanatani S. Catecholaminergic polymorphic ventricular tachycardia. Activity as tolerated. JACC Clin Electrophysiol. 2016;2(3):263–265. 159. Lyon RM, Wiggins C. Do not move player requiring resuscitation on field until return of spontaneous circulation. BMJ. 2012;344. 160. Hutter AM Jr. Cardiovascular abnormalities in the athlete: the role of the physician. Med Sci Sports Exerc. 1994;26: S227–S229.

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13  Exercise-Induced Bronchoconstriction Virgil P. Secasanu, Jonathan P. Parsons

DEFINITION AND PREVALENCE Exercise-induced bronchoconstriction (EIB) describes acute, transient airway narrowing that occurs during and after exercise. EIB is characterized by symptoms of cough, wheezing, or chest tightness during or after exercise. Exercise is one of the most common triggers of bronchoconstriction in asthmatic patients. Approximately 80% of individuals with chronic asthma have exercise-induced respiratory symptoms.1 However, EIB can also occur in up to 10% of people who are not known to be atopic or asthmatic.2 These patients do not have the typical features of chronic asthma (i.e., frequent daytime symptoms, nocturnal symptoms, impaired lung function), and exercise may be the only stimulus that causes respiratory symptoms. The mechanism of EIB is characterized by the inspired volumes of relatively low-humidity air. Dry air leads to water loss from the airways, creating an osmotic change on the airway surface. The resultant hyperosmolar environment stimulates mast cell and eosinophil degranulation. The released mediators, predominantly leukotrienes, cause bronchoconstriction and airway inflammation. Inspiring cool air is thought to have a similar effect on the airways, albeit a less potent affect than hyperventilation with dry air. EIB occurs commonly in athletes. The prevalence rates of exercise-related bronchoconstriction in athletes range from 11% to 50% (Table 13.1).3 Holzer and colleagues4 found 50% of a cohort of 50 elite summer athletes had EIB. Wilber and associates5 found that 18% to 26% of Olympic winter sport athletes and 50% of cross-country skiers had EIB. The US Olympic Committee reported an 11.2% prevalence of EIB in all athletes who competed in the 1984 Summer Olympics.6 Despite numerous studies that investigate the prevalence of EIB in athletes, few studies have investigated the prevalence of EIB in cohorts of athletes without known history of asthma or EIB. Mannix and associates7 found that 41 of 212 subjects (19%) in an urban fitness center, none of whom had a previous diagnosis of asthma, had EIB. Rupp and colleagues8 evaluated 230 middle and high school student athletes and, after excluding those with known EIB, found that 29% had EIB. These studies suggest that EIB occurs commonly in subjects who are not known to be asthmatic and likely is underdiagnosed clinically. The prevalence of EIB may be further underestimated because patients with asthma and EIB have been shown to be poor perceivers of symptoms of bronchoconstriction.9,10 Specifically, athletes often suffer from lack of awareness of symptoms suggestive of

EIB.11,12 Health care providers and coaches also may not consider EIB as a possible explanation for respiratory symptoms occurring during exercise. Athletes are generally fit and healthy, and the presence of a significant medical problem often is not considered. The athlete is often considered to be “out of shape,” and vague symptoms of chest discomfort, breathlessness, and fatigue are not interpreted as a manifestation of EIB. Athletes themselves are often not aware that they may have a physical problem. Furthermore, if they do recognize they have a medical problem, they often do not want to admit to health personnel that a problem exists because of fear of social stigma or losing playing time.

SPECIFIC ATHLETIC POPULATIONS AT RISK Athletes who compete in high-ventilation or endurance sports may be more likely to experience symptoms of EIB than those who participate in low-ventilation sports13; however, EIB can occur in any setting. EIB is prevalent in endurance sports in which ventilation is increased for long periods of time during training and competition such as such as cross-country skiing, swimming, and long-distance running.13 EIB also occurs commonly in winter sports athletes.5 In addition, environmental triggers may predispose certain populations of athletes to an increased risk for development of EIB. Chlorine compounds in swimming pools14 and chemicals related to ice-resurfacing machinery in ice rinks,15 such as carbon monoxide and nitrogen dioxide, may put exposed athletic populations at additional risk. These environmental factors may act as triggers and exacerbate bronchoconstriction in athletes who are predisposed to EIB. Thus it is important for athletes, coaches, and athletic trainers supervising athletes in these sports to be aware of these important environmental issues.

CLINICAL PRESENTATION The clinical manifestations of EIB are extremely variable and can range from mild impairment of performance to severe bronchoconstriction and respiratory failure. Common symptoms include coughing, wheezing, chest tightness, and dyspnea. More subtle evidence of EIB includes fatigue, symptoms that occur in specific environments (e.g., ice rinks or swimming pools), poor performance for conditioning level, and avoidance of activity (Box 13.1).

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CHAPTER 13  Exercise-Induced Bronchoconstriction

Abstract

Keywords

Exercise-induced bronchoconstriction (EIB) is characterized by acute airway narrowing presenting with cough, wheezing, and chest tightness during and after exercise. This chapter discusses the clinical manifestations of EIB, diagnostic methods, and management approaches. EIB has been seen in many athletes with and without chronic asthma, and can occur at ages ranging from children to adults. Diagnosis can be challenging due to clinical similarities to other medical problems, such as vocal cord dysfunction, gastroesophageal reflux, and allergic rhinitis. Bronchoprovocation testing with eucapnic voluntary hyperventilation is considered the gold standard for diagnosis. First line treatments for EIB include bronchodilators such as short-acting beta agonist inhalers.

exercise induced bronchoconstriction exercise intolerance wheezing short-acting beta agonist sideline management

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TABLE 13.1  Prevalence of Exercise-

Induced Bronchoconstriction in Selected Studies Reference No.

Athletes

(5) (29)

Winter Olympians Elite figure skaters

(4)

Elite athletes

(11)

Collegiate athletes

EIB Prevalence (Bronchoprovocation Technique) 18%–26% (exercise) 41% (EVH) 31% (exercise) 50% (EVH) 18% (methacholine) 39% (EVH)

EIB, Exercise-induced bronchoconstriction; EVH, eucapnic voluntary hyperventilation.

BOX 13.1  Common Symptoms of

Exercise-Induced Bronchoconstriction • Dyspnea on exertion • Chest tightness • Wheezing • Fatigue • Poor performance for level of conditioning • Avoidance of activity • Symptoms in specific environments (e.g., ice rinks, swimming pools)

In general, exercise at a workload representing at least 80% of the maximal predicted oxygen consumption for 5 to 8 minutes is required to generate bronchoconstriction in most athletes.16 Typically, athletes experience transient bronchodilation initially during exercise, and symptoms of EIB begin later or shortly after exercise. Symptoms often peak 5 to 10 minutes after exercise ceases and can remain significant for 30 minutes or longer if no bronchodilator therapy is provided.17 However, some athletes spontaneously recover to baseline airflow within 60 minutes, even in the absence of intervention with bronchodilator therapy.17 Unfortunately, it is currently impossible to predict which athletes will recover without treatment. Athletes who experience symptoms for extended periods often perform at suboptimal levels for significant portions of their competitive or recreational activities.

DIAGNOSIS History and Differential Diagnosis The presence of EIB can be challenging to recognize clinically because symptoms are often nonspecific. A complete history and physical examination should be performed on each athlete with respiratory complaints associated with exercise. However, despite the value of a comprehensive history of the athlete with exertional dyspnea, the diagnosis of EIB based on self-reported symptoms alone has been shown to be inaccurate. Hallstrand and colleagues18 found that screening history identified subjects with symptoms or a previous diagnosis suggestive of EIB in 40% of the participants, but only 13% of these persons actually had EIB after objective testing. Similarly, Rundell and associates12

BOX 13.2  Mimics of Exercise-Induced

Bronchoconstriction

• Vocal cord dysfunction • Gastroesophageal reflux disease • Allergic rhinitis • Cardiac pathology (arrhythmias, cardiomyopathy, shunts)

demonstrated that only 61% EIB-positive athletes reported symptoms of EIB, whereas 45% of athletes with normal objective testing reported symptoms. The poor predictive value of the history and physical examination in the evaluation of EIB strongly suggests that clinicians should perform objective diagnostic testing when there is a suspicion of EIB. Other medical problems that can mimic EIB and should be considered in the initial evaluation of exertional dyspnea include vocal cord dysfunction, gastroesophageal reflux disease, and allergic rhinitis. Cardiac pathology such as arrhythmia, cardiomyopathy, and cardiac shunts are more rare, but these possibilities should also be considered (Box 13.2). A comprehensive history and examination is recommended to help rule out these confounding disorders, and specific testing such as echocardiography may be required. A history of specific symptoms in particular environments or during specific activities should be elicited. Timing of symptom onset in relation to exercise and recovery is also helpful. A thorough family and occupational history should be obtained because a family history of asthma increases the risk for other family members developing asthma.19

Objective Testing Objective testing should begin with spirometry before and after inhaled bronchodilator therapy, which will help to identify athletes who have asthma. However, many people who experience EIB have normal baseline lung function.20 In these patients, spirometry alone is not adequate to diagnose EIB. Significant numbers of false-negative results may occur if adequate exercise and environmental stress are not provided in the evaluation for EIB. In patients being evaluated for EIB who have a normal physical examination and normal spirometry, bronchoprovocation testing is recommended. A positive bronchoprovocation test indicates the need for treatment of EIB. Specific tests have varying positive values, but in general, a change (usually ≥10% decrease in forced expiratory volume in 1 second [FEV1]) between pretest and posttest values is suggestive of EIB.21 In a patient with persistent exercise-related symptoms and negative physical examination, spirometry, and bronchoprovocation testing, we recommend reconsidering alternative diagnoses. Not all bronchoprovocation techniques are equally valuable or accurate in assessing EIB in athletes. The International Olympic Committee recommends eucapnic voluntary hyperventilation (EVH) challenge to document EIB in Olympians.22 EVH involves hyperventilation of a gas mixture of 5% CO2 and 21% O2 at a target ventilation rate of 85% of the patient’s maximal voluntary ventilation in 1 minute (MVV). The MVV is usually calculated as 30 times the baseline FEV1. The patient continues to hyperventilate for 6 minutes, and assessment of FEV1 occurs at specified

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CHAPTER 13  Exercise-Induced Bronchoconstriction

intervals up to 20 minutes after the test. This challenge test has been shown to have a high specificity23 for EIB. EVH has also been shown to be more sensitive for detecting EIB than lab- or field-based exercise testing.23 In the United States, lab-based exercise testing is widely available, although often less sensitive than EVH. Lab-based exercise testing measures serial lung function tests before and after an exercise challenge. In general, FEV1 is measured because this value has shown good repeatability.24 Subjects are first asked to perform spirometry before an exercise challenge to measure the baseline FEV1 value. Subjects are then asked to exercise, and FEV1 is measured serially at 5, 10, 15, and 30 minutes after exercise. EIB is diagnosed as a 10% or greater drop in preexercise FEV1 measured during the 30-minute postexercise phase. Severity of EIB is characterized by the degree of reduction: mild (10% to 25% reduction), moderate (25% to 50% reduction), and severe (≥50% reduction).25–28 In contrast to lab-based testing, field-based exercise testing involves an athlete performing a sport and assessing FEV1 after exercise. Similar to lab-base testing, field-based testing has been shown to be less sensitive than EVH.29 Moreover, such field-based exercise testing allows for little protocol standardization. Pharmacologic challenge tests, such as the methacholine challenge test, have been shown to have a lower sensitivity than EVH for detection of EIB in athletes4 and are also not recommended for first-line evaluation of EIB.

TREATMENT OPTIONS Pharmacologic Therapy Pharmacologic therapy for EIB (Table 13.2) has been studied extensively. The most common therapeutic recommendation to minimize or prevent symptoms of EIB is the prophylactic use of short-acting bronchodilators (selective β-adrenergic receptor agonists) such as albuterol shortly before exercise.30 Treatment with two puffs of a short-acting β-agonist shortly before exercise (15 minutes) will provide peak bronchodilation in 15 to 60 minutes and protection from EIB for at least 3 hours in most patients. Long-acting bronchodilators work in a similar manner pharmacologically as short-acting bronchodilators; however, the bronchoprotection afforded by long-acting β-agonists has been shown to last up to 12 hours, whereas that of short-acting agents is no longer significant by 4 hours.31 Ferrari and associates32 demonstrated inhalation of formoterol, a long-acting β-agonist, is effective in protecting asthmatic athletes as early as 15 minutes TABLE 13.2  Treatment and Prevention of

Exercise-Induced Bronchoconstriction Pharmacologic Therapy

Nonpharmacologic Therapy

Short-acting β-agonists Inhaled corticosteroids Long-acting β-agonists Leukotriene modifiers Cromolyn compounds

Adequate preexercise warm-up Wearing a mask in cold environment Avoidance of triggers Nasal breathing

177

after dosing. However, tachyphylaxis also has been shown to occur after repeated use of long-acting β-agonists,33 and they are not recommended in patients with normal or near-normal baseline lung function tests or as monotherapy.28 Inhaled corticosteroids are first-line controller therapy for patients who have chronic asthma and experience EIB.30 Airway inflammation is also often present in athletes without asthma who have EIB14,34; therefore inhaled corticosteroids may be an effective medicine for treatment, but efficacy of corticosteroids in this cohort has not been studied. Inhaled corticosteroids are also valuable in athletes that train multiple times per day. Leukotriene modifiers have also been shown to be effective in treating EIB.35 Leff and colleagues36 evaluated the ability of montelukast, a leukotriene receptor antagonist, to protect asthmatic patients against EIB. Montelukast therapy offered significantly greater protection against EIB than did placebo therapy and was also associated with a significant improvement in the maximal decrease in FEV1 after exercise. In addition, tolerance to the medication and rebound worsening of lung function after discontinuation of treatment were not seen. In another study, daily zafirlukast treatment protected against EIB for at least 8 hours after regular dosing.37 Leukotriene modifiers are an effective second line agent for treatment of EIB. Mast cell stabilizers have been studied extensively for the prophylaxis of EIB. These medications prevent mast cell degranulation and subsequent histamine release. In a meta-analysis of the prevention of EIB in asthmatic patients, nedocromil sodium was found to improve FEV1 by an average of 16% and to shorten the duration of EIB symptoms to less than 10 minutes.38 Although these agents are effective and traditionally used to treat EIB, they are often used as a second line treatment because of their cost, lack of availability in the United States, and their decreased duration of action and efficacy compared with β2-agonists.27

Nonpharmacologic Therapy Many athletes find that a period of precompetition warm-up reduces the symptoms of EIB that occur during their competitive activity. Athletes often draw this conclusion without any guidance from health care specialists. It has been shown by investigators that this refractory period does occur in some athletes with asthma and that athletes can be refractory to an exercise task performed within 2 hours of an exercise warm-up.39,40 However, the refractory period has not been consistently proven across different athletic populations, and it is currently not possible to identify which athletes will experience this refractory period.41 Other nonpharmacologic strategies (see Table 13.2) can be used to help reduce the frequency and severity of symptoms of EIB. Breathing through the nose rather than the mouth will also help to ameliorate EIB42 by warming, filtering, and humidifying the air, which subsequently reduces airway cooling and dehydration. Wearing a facemask during activity warms and humidifies inspired air when outdoor conditions are cold and dry. Facemasks are especially valuable to elite and recreational athletes who exercise in the winter.43 In addition, people with knowledge of triggers (e.g., freshly cut grass) should attempt to avoid them if possible.28

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Authors’ Preferred Technique Our preferred method for diagnosis and treatment of exercise-induced bronchoconstriction (EIB) is shown in Fig. 13.1. The diagnosis of EIB based on symptoms alone is extremely inaccurate. Objective testing is necessary to make a confident diagnosis of EIB. We recommend using eucapnic voluntary hyperventilation (EVH) as the bronchoprovocation test of choice to document EIB; however, EVH may not be available to many health care providers. If EVH is not easily accessible, spirometry before and after an adequate exercise challenge is our second line recommendation. It is essential to ensure that the exercise challenge is strenuous enough to generate adequate ventilation rates in patients who have excellent physical fitness. In our experience, both pharmacologic and nonpharmacologic approaches are essential to minimizing the adverse effects of EIB. We recommend that athletes who have clinical evidence of EIB be treated with short-acting bronchodilators before exercise and be counseled on the importance of adequate warm-up and avoidance of known triggers. This regimen will prevent significant EIB in more than 80% of athletes.30 If symptoms persist, especially in athletes with asthma, we recommend adding corticosteroids as maintenance therapy. Although the efficacy of inhaled steroids in nonasthmatic athletes has not been evaluated, we recommend using them in nonasthmatic athletes whose symptoms are not completely controlled with short-acting bronchodilators. This recommendation is based on evidence of airway inflammation in subjects without known asthma as a result of hyperventilation and exercise.14,34,44 Alternatively, leukotriene modifiers or cromolyn compounds can be used in athletes inadequately controlled with β2-agonists.

Symptoms suggestive of EIB? History, physical examination, and spirometry Examination normal? No

Yes

Consider further work-up based on history/examination findings, e.g.: Obstruction on • Echocardiogram spirometry? • Videolaryngostraboscopy • Holter monitor • Pulmonary function tests No

Yes

EVH testing • If EVH unavailable: Alternative bronchoprovocation

Consider maintenance asthma therapy

Positive

Negative

• Albuterol before exercise • Proper warm-up • Avoidance of triggers Symptoms improved? Yes

Reconsider diagnosis • VCD • Cardiac arrhythmias • Shunts • Other pulmonary diseases No

No

Continue Add controller medication: Symptoms improved? • Inhaled corticosteroid • Leukotriene modifier • Cromolyn compound Yes Continue current therapy Fig. 13.1  Evaluation and management of exercise-induced bronchoconstriction (EIB). EVH, Eucapnic voluntary hyperventilation; VCD, vocal cord dysfunction. (Redrawn from Parsons JP, Mastronarde JG. Exerciseinduced bronchoconstriction in athletes. Chest. 2005;128:3966–3974.)

SIDELINE MANAGEMENT

BOX 13.3  Symptoms of Respiratory

Acute, sideline management of EIB requires athletic trainers and coaches to be prepared to intervene if an athlete experiences an acute episode of EIB. All athletic trainers should have pulmonary function–measuring devices such as peak flow meters at all athletic events, including practices.45 In addition, a rescue inhaler should be available during all games and practices. Spacers should be used with all rescue inhalers, and nebulizers should be readily available for emergencies in the event that inhalers are inadequate for control of acute symptoms. On-field management of asthma begins with awareness of the signs and symptoms of respiratory distress (Box 13.3). Any athlete presenting with respiratory distress should be removed from competition and immediately evaluated by a physician. It is recommended that any athlete with a peak expiratory flow lower than 80% of “personal best” be removed from activity until their peak flow returns to at least 80% of “personal best.”

Distress

• Increase in wheezing or chest tightness • Unable to speak in full sentences • A respiratory rate greater than 25 breaths/min • Persistent cough • Breathing with nostril flaring • Breathing with paradoxical abdominal movements

POTENTIAL COMPLICATIONS The goals of treating an athlete with EIB are to optimize pulmonary function before starting athletic competition and to attempt to prevent significant episodes of EIB from occurring during exercise. Unfortunately, EIB often goes unrecognized, and consequences of unrecognized or inadequately treated EIB

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KEY POINTS

Symptoms suggestive of EIB Remove athlete from activity Assess peak expiratory flow rate (PEFR) If PEFR is ≥10% below baseline, treat with two puffs of albuterol Reassess PEFR in 5-10 minutes

If PEFR back to baseline, may return to activity

If PEFR not back to baseline, repeat albuterol treatment Reassess PEFR in 5-10 minutes

If PEFR back to baseline, may return to activity

179

If PEFR not back to baseline, transfer from sideline to higher level health care facility

Fig. 13.2  Sideline management of exercise-induced bronchoconstriction (EIB) and criteria for return to play.

• Exercise-induced bronchoconstriction (EIB) occurs in athletes with and without chronic asthma. • EIB occurs more commonly in athletes than the general population. • The symptoms of EIB are often subtle and difficult to differentiate from normal manifestations of intense exercise. • Diagnosis of EIB based on subjective symptoms alone is extremely inaccurate. • Objective testing is strongly recommended to document a diagnosis of EIB. • The consequences of unrecognized or inadequately treated EIB can be significant. • Treatment of EIB with a short-acting bronchodilator before exercise is 80% effective. • Coaches and athletic trainers should be prepared to manage an athlete with an acute episode of EIB at all practices and competitive events. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation:

are significant. Becker and associates46 identified 61 deaths secondary to asthma over a 7-year period occurring in close association with a sporting event or physical activity. Of these deaths, 81% occurred in subjects younger than 21 years and 57% occurred in subjects considered elite or competitive. Strikingly, almost 10% of deaths in this review occurred in subjects with no known history of asthma. Similarly, Amital and colleagues47 found that asthma was the single greatest risk factor for unexplained death in a review of Israeli military recruits’ data over a 30-year period. Results from these reviews suggest that all individuals involved in organized sports or physical activity should be cognizant of the risk for EIB. Coaches, athletic trainers, parents, and team physicians who care for competitive athletes who have asthma or EIB should be specifically trained in the recognition and treatment of EIB.

Anderson SD, Argyros GJ, Magnussen H, et al. Provocation by eucapnic voluntary hyperpnoea to identify exercise induced bronchoconstriction. Br J Sports Med. 2001;35:344–347.

Level of Evidence: I

Summary: This article describes eucapnic voluntary hyperventilation protocol.

Citation: Parsons JP, Hallstrand TS, Mastronarde JG, et al; American Thoracic Society Subcommittee on Exercise-induced Bronchconstriction. An official American Thoracic Society Clinical Practice Guideline: exercise-induced bronchoconstriction. Am J Respir Crit Care Med. 2013;187:1013–1027.

Level of Evidence: I

Summary:

CRITERIA FOR RETURN TO PLAY

Expert position statement on exercise-induced bronchoconstriction

Criteria for safe return to play (RTP) after an acute episode of EIB are based on expert opinion only. Most experts agree that no athlete should RTP until lung function returns to baseline.45 However, no consensus RTP protocol exists, and each athlete must be evaluated for returning to play after an acute episode of EIB. An algorithm outlining acute, sideline management of EIB and suggested criteria for RTP are shown in Fig. 13.2.

Parsons JP, Mastronarde JG. Exercise-induced bronchoconstriction in athletes. Chest. 2005;128:3966–3974.

Citation:

Level of Evidence: I

Summary: Systematic review of EIB in athletes

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CHAPTER 13  Exercise-Induced Bronchoconstriction

REFERENCES 1. Parsons JP, Craig TJ, Stoloff SW, et al. Impact of exercise-related respiratory symptoms in adults with asthma: exercise-induced bronchospasm landmark national survey. Allergy Asthma Proc. 2011;32:431–437. 2. Gotshall RW. Exercise-induced bronchoconstriction. Drugs. 2002;62:1725–1739. 3. Rundell KW, Jenkinson DM. Exercise-induced bronchospasm in the elite athlete. Sports Med. 2002;32:583–600. 4. Holzer K, Anderson SD, Douglass J. Exercise in elite summer athletes: challenges for diagnosis. J Allergy Clin Immunol. 2002;110:374–380. 5. Wilber RL, Rundell KW, Szmedra L, et al. Incidence of exerciseinduced bronchospasm in Olympic winter sport athletes. Med Sci Sports Exerc. 2000;32:732–737. 6. Voy RO. The U.S. Olympic committee experience with exerciseinduced bronchospasm, 1984. Med Sci Sports Exerc. 1986;18: 328–330. 7. Mannix ET, Roberts M, Fagin DP, et al. The prevalence of airways hyperresponsiveness in members of an exercise training facility. J Asthma. 2003;40:349–355. 8. Rupp NT, Guill MF, Brudno DS. Unrecognized exercise-induced bronchospasm in adolescent athletes. Am J Dis Child. 1992;146:941–944. 9. Barnes PJ. Poorly perceived asthma. Thorax. 1992;47:408–409. 10. Barnes PJ. Blunted perception and death from asthma. N Engl J Med. 1994;330:1383–1384. 11. Parsons JP, Kaeding C, Phillips G, et al. Prevalence of exerciseinduced bronchospasm in a cohort of varsity college athletes. Med Sci Sports Exerc. 2007;39:1487–1492. 12. Rundell KW, Im J, Mayers LB, et al. Self-reported symptoms and exercise-induced asthma in the elite athlete. Med Sci Sports Exerc. 2001;33:208–213. 13. Holzer K, Brukner P. Screening of athletes for exercise-induced bronchoconstriction. Clin J Sport Med. United States; 2004;14(3):134–138. 14. Helenius IJ, Rytila P, Metso T, et al. Respiratory symptoms, bronchial responsiveness, and cellular characteristics of induced sputum in elite swimmers. Allergy. 1998;53:346–352. 15. Rundell KW. High levels of airborne ultrafine and fine particulate matter in indoor ice arenas. Inhal Toxicol. 2003;15: 237–250. 16. Parsons JP, Mastronarde JG. Exercise-induced bronchoconstriction in athletes. Chest. 2005;128:3966–3974. 17. Brudno DS, Wagner JM, Rupp NT. Length of postexercise assessment in the determination of exercise-induced bronchospasm. Ann Allergy. 1994;73:227–231. 18. Hallstrand TS, Curtis JR, Koepsell TD, et al. Effectiveness of screening examinations to detect unrecognized exercise-induced bronchoconstriction. J Pediatr. 2002;141:343–349. 19. London SJ, James Gauderman W, Avol E, et al. Family history and the risk of early-onset persistent, early-onset transient, and late-onset asthma. Epidemiology. 2001;12:577–583. 20. Rundell KW, Wilber RL, Szmedra L, et al. Exercise-induced asthma screening of elite athletes: field versus laboratory exercise challenge. Med Sci Sports Exerc. 2000;32:309–316. 21. Crapo RO, Casaburi R, Coates AL, et al. Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS board of directors, July 1999. Am J Respir Crit Care Med. 2000;161:309–329.

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22. IOC Medical Commission. Beta2 adrenoceptor agonists and the Olympic games in Beijing; 2008 June 16. Available from: http:// multimedia.olympic.org/pdf/en_report_1302.pdf. 23. Eliasson AH, Phillips YY, Rajagopal KR, et al. Sensitivity and specificity of bronchial provocation testing. An evaluation of four techniques in exercise-induced bronchospasm. Chest. 1992;102:347–355. 24. Enright PL, Beck KC, Sherrill DL. Repeatability of spirometry in 18,000 adult patients. Am J Respir Crit Care Med. 2004;169: 235–238. 25. Anderson SD, Brannan JD. Methods for “indirect” challenge tests including exercise, eucapnic voluntary hyperpnea, and hypertonic aerosols. Clin Rev Allergy Immunol. 2003;24: 27–54. 26. Clinical exercise testing with reference to lung diseases: indications, standardization and interpretation strategies. ERS task force on standardization of clinical exercise testing. European Respiratory Society. Eur Respir J. 1997;10: 2662–2689. 27. Parsons JP, Hallstrand TS, Mastronarde JG, et al. An official American Thoracic Society Clinical Practice Guideline: exercise-induced bronchoconstriction. Am J Respir Crit Care Med. 2013;187:1013–1027. 28. Weiler JM, Brannan JD, Randolph CC, et al. Exercise-induced bronchoconstriction update-2016. J Allergy Clin Immunol. 2016;138:1292–1295 e1236. 29. Mannix ET, Manfredi F, Farber MO. A comparison of two challenge tests for identifying exercise-induced bronchospasm in figure skaters. Chest. 1999;115:649–653. 30. National Asthma Education and Prevention Program. Expert panel report 3 (epr-3): guidelines for the diagnosis and management of asthma-summary report 2007. J Allergy Clin Immunol. 2007;120:S94–S138. 31. Bronsky EA, Yegen U, Yeh CM, et al. Formoterol provides long-lasting protection against exercise-induced bronchospasm. Ann Allergy Asthma Immunol. 2002;89:407–412. 32. Ferrari M, Balestreri F, Baratieri S, et al. Evidence of the rapid protective effect of formoterol dry-powder inhalation against exercise-induced bronchospasm in athletes with asthma. Respiration. 2000;67:510–513. 33. Ferrari M, Segattini C, Zanon R, et al. Comparison of the protective effect of formoterol and of salmeterol against exercise-induced bronchospasm when given immediately before a cycloergometric test. Respiration. 2002;69:509–512. 34. Parsons JP, Baran CP, Phillips G, et al. Airway inflammation in exercise-induced bronchospasm occurring in athletes without asthma. J Asthma. 2008;45:363–367. 35. Philip G, Villaran C, Pearlman DS, et al. Protection against exercise-induced bronchoconstriction two hours after a single oral dose of montelukast. J Asthma. 2007;44:213–217. 36. Leff JA, Busse WW, Pearlman D, et al. Montelukast, a leukotriene-receptor antagonist, for the treatment of mild asthma and exercise-induced bronchoconstriction. N Engl J Med. 1998;339:147–152. 37. Dessanges JF, Prefaut C, Taytard A, et al. The effect of zafirlukast on repetitive exercise-induced bronchoconstriction: the possible role of leukotrienes in exercise-induced refractoriness. J Allergy Clin Immunol. 1999;104:1155–1161. 38. Kelly KD, Spooner CH, Rowe BH. Nedocromil sodium versus cromoglycate for the pre-treatment of exercise induced bronchoconstriction in asthma. Cochrane Database Syst Rev. 2000;(2):CD002169.

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39. Anderson SD, Schoeffel RE. Respiratory heat and water loss during exercise in patients with asthma. Effect of repeated exercise challenge. Eur J Respir Dis. 1982;63:472–480. 40. McKenzie DC, McLuckie SL, Stirling DR. The protective effects of continuous and interval exercise in athletes with exerciseinduced asthma. Med Sci Sports Exerc. 1994;26:951–956. 41. Rundell KW, Spiering BA, Judelson DA, et al. Bronchoconstriction during cross-country skiing: Is there really a refractory period? Med Sci Sports Exerc. 2003;35:18–26. 42. Shturman-Ellstein R, Zeballos RJ, Buckley JM, et al. The beneficial effect of nasal breathing on exercise-induced bronchoconstriction. Am Rev Respir Dis. 1978;118:65–73. 43. Schachter EN, Lach E, Lee M. The protective effect of a cold weather mask on exercised-induced asthma. Ann Allergy. 1981;46:12–16.

44. Bonsignore MR, Morici G, Vignola AM, et al. Increased airway inflammatory cells in endurance athletes: What do they mean? Clin Exp Allergy. 2003;33:14–21. 45. Miller MG, Weiler JM, Baker R, et al. National Athletic Trainers’ Association position statement: management of asthma in athletes. J Athl Train. 2005;40:224–245. 46. Becker JM, Rogers J, Rossini G, et al. Asthma deaths during sports: report of a 7-year experience. J Allergy Clin Immunol. 2004;113:264–267. 47. Amital H, Glikson M, Burstein M, et al. Clinical characteristics of unexpected death among young enlisted military personnel: results of a three-decade retrospective surveillance. Chest. 2004;126:528–533.

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14  Deep Venous Thrombosis and Pulmonary Embolism Jason Thompson, Marc M. DeHart

Bleeding in the athlete can result from injury or after orthopedic surgery. Hemostasis—the body’s process to stop bleeding— prevents what can be a life-threatening hemorrhage. Immobilization and hypercoagulable states can also induce clotting at improper sites (thrombosis). If the resultant clot dislodges and migrates (thromboembolism), it can lead to devastating tissue damage and organ failure. The most feared complication of that cascade is a fatal pulmonary embolism (PE). Although rare, it can occur after minor orthopedic surgeries, including arthroscopic procedures. The majority of clots cause few symptoms and are not recognized clinically. A reduction in peak aerobic performance may be the only hint of a clot in the elite athlete.1 Chemical thromboembolic prophylaxis with anticoagulation therapy helps reduce the risk of thromboembolic events in the postoperative patient, but the use of these medications comes with significant risks of its own, as well as an added expense. Controversy surrounds the balance between the morbidity and mortality associated with thromboembolic events and the risks and costs of chemical prophylaxis.

NORMAL PHYSIOLOGY AND VIRCHOW TRIAD Hemostasis and thrombosis are physiologic mechanisms of the coagulation system, platelets, endothelial cells, and the vascular wall. Following an injury, hemostasis is our body’s ability to form a blood clot and is usually followed by the dissolution of that clot as injured tissues repairs. Thrombosis can be considered “hemostasis in the wrong place and the wrong time.”2 When a clot emerges in the arterial system, the subsequent loss of oxygenated blood can lead to stroke, myocardial infarction, and peripheral extremity necrosis. Clot formation within the venous system leads to local tissue congestion and decreased venous return, most often in the lower extremities. When the final destination of an embolus within the venous system is the lungs (PE), complications related to pulmonary infarction, abnormal gas exchange, and cardiovascular compromise may result. In honor of Rudolph Virchow, who is responsible for coining the term embolus, “Virchow triad” describes the three primary influences on thrombus formation. Endothelial damage exposes collagen and triggers the extrinsic clotting cascade by activating platelets to perform their three primary functions—adhesion (sticking to damage endothelium), secretion (releasing thrombotic chemicals), and aggregation (combining platelets into a group). (Fig. 14.1). Stasis permits the bonds of protein clotting factors 180

and platelets to assemble and results from immobility (from postoperative/postinjury pain, cast, limb paralysis, stroke), increased blood viscosity (from cancer, estrogens, polycythemia), decreased inflow (from intraoperative tourniquets, vascular disease),3 and increased venous pressure (from venous scarring, varicose veins, heart failure).4 Hypercoagulability is the result of activation of the catalytic system of plasma proteins known as the coagulation cascade, whose main product—thrombin—converts soluble fibrinogen to insoluble fibrin. The biologic goal of this network of interdependent enzyme-mediated reactions is to limit hemorrhage at sites where damage occurs by rapidly stabilizing the initial platelet plug with insoluble fibrin. Once formed, a thrombus has the ability to (a) undergo dissolution by the fibrinolytic system, (b) remain stationary with subsequent incorporation into the vein wall (organization and recanalization), (c) continue to grow (propagation), and/or completely or incompletely break free to travel downstream to imbed in the pulmonary vessels (embolization).4 Ninety percent of thrombi form in lower extremity veins, where those that form distal to the popliteal space occur in smaller veins of the calf and pose essentially no clinical threat because these typically dissolve spontaneously. However, a thrombus formed in the larger-diameter veins within the pelvis and proximal thigh are associated with increased risk of embolism.

PREOPERATIVE THROMBOEMBOLIC RISK FACTORS Thrombophilia is the predisposition to venous thromboembolism disease (VTE) and is caused by inherited (primary) and acquired (secondary) factors. Primary hypercoagulability is often a result of genetic mutations, which may lead to an abnormal quantity or quality of protein clotting factors. Screening for prothrombotic defects has not been shown to be effective in selecting a strategy for thromboembolic prophylaxis.5 The quality and quantity of the protein clotting factors can be a consequence of either malproduction or autoimmune alteration or destruction of these important factors. Clinical factors of secondary hypercoagulability are commonly found in orthopedic patients and play a significant role in the perioperative management of thrombosis. These classic, sometimes modifiable, preoperative risk factors for VTE include, but are not limited to, previous VTE, malignancy, pregnancy, age older than 40 years, obesity, smoking, peripheral vascular disease, and oral contraceptive (and/or estrogen) use.

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CHAPTER 14  Deep Venous Thrombosis and Pulmonary Embolism

Abstract

Keywords

Thromboembolic disease is a common complication of orthopedic surgery patients. This chapter includes a review of the basic science of hemostasis and discusses some of the sportsspecific areas of interest for clinical practice.

thromboembolism blood clot pulmonary embolism venous thrombosis hemostasis effort thrombosis

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1 2

A

3

4

D

B

E

C

Fig. 14.1  (A) Scanning electron micrograph (SEM) of free platelets. (B) SEM of platelet adhesion. (C) SEM of platelet activation. (D) Transmission electron micrograph (TEM) of aggregating platelets. 1, Platelet before secretion. 2 and 3, Platelets secreting contents of granules. 4, Collagen of endothelium. (E) SEM of fibrin mesh encasing colorized red blood cells. (Platelet EM courtesy James G. White, MD, Regents’ Professor, Department of Laboratory Medicine and Pathology, University of Minnesota School of Medicine.)

Studies have found an association of high-altitude locations with a two to nine times greater rate of VTE in both young health populations and in autopsy records.6–8 At high altitude, hypoxia, dehydration, hemoconcentration, low temperature, and use of constrictive clothing, as well as enforced stasis due to severe weather, would support the occurrence of thrombotic disorders.9 Ascending from a low elevation to an elevated altitude (4000 feet above sea level) initially causes an acute hypoxic ventilation period, followed by a respiratory system response where the lungs increase ventilation (minutes to hours). Higher altitudes stimulate renal and hepatic erythropoietin production that then stimulates erythropoiesis with an increase in size and concentration of red cells. This erythropoietin process is most active 2 days after introduction to the elevation but usually returns to sea level measurements after approximately 3 weeks at higher elevation. Physiologic changes occur to acclimatize over the course

of several years with sustained hyperventilation while at higher elevation. Changes occur to the oxygen-hemoglobin dissociation curve, pulmonary circulation, cardiac function, fluid hemostasis, and hematologic components.10 The relative risk of VTE after knee arthroscopy in residents of areas 4000 feet above sea level is as high as 3.8 times that of similar patients residing in and having their operations in areas at sea level (but the risk is still very low, clotting risk: IPC2 ≥10 days, consider 35 days1

Drugs and IPC1,2 D/C drugs when TKA mobile2 If VTE risks high and contraindication to prophylaxis2 Source http://www.aaos.org/research/guidelines http://journal.publications.chestnet.org/ http://effectivehealthcare.ahrq.gov/ http://guidance.nice.org.uk/CG92/

D/C, Discontinue; IPC intermittent pneumatic compression; IVC, intra-vena caval; US, ultrasound; VKA, vitamin K antagonist; VTE, venous thromboembolism. AAOS. Guideline on Preventing Venous Thromboembolic Disease in Patients Undergoing Elective Hip and Knee Arthroplasty. AAOS Clinical Practice Guidelines (CPG); 2011. http://www.aaos.org/research/guidelines/VTE/VTE_guideline.asp/. Accessed June, 20, 2012. AHRQ. Comparative Effectiveness Review, Number 49: Venous Thromboembolism Prophylaxis in Orthopedic Surgery; 2012. http:// effectivehealthcare.ahrq.gov/ehc/products/186/992/CER-49_VTE_20120313.pdf/. Accessed July 20, 2012. NICE. CG92 Venous thromboembolism—reducing the risk: NICE guideline; 2010. http://guidance.nice.org.uk/CG92/NICEGuidance/pdf/English/.

can lead to right heart failure and hypoxemia. Healthy individuals may remain asymptomatic if an occlusion obstructs less than 60% of the pulmonary circulation.28 The most common presenting symptoms in patients diagnosed with PE on pulmonary angiogram are chest pain (typically pleuritic) and sudden onset of shortness of breath (dyspnea). Objective physical exam findings seen in greater than 50% of patients are tachypnea (>20 breaths/min) and crackles with lung auscultation.28 Massive saddle emboli block all cardiopulmonary circulation and can cause immediate death. The nonspecific nature of the signs and symptoms of VTE can be confused for other diagnoses or even easily dismissed, and therefore these complaints demand a high clinical suspicion in patients particularly at high risk. There is no ideal objective test for VTE, but contrast venography, duplex compression ultrasound, spiral computed tomography (CT) venography, CT pulmonary angiography, ventilation-perfusion (V/Q) scintigraphy, and D-dimer levels, usually used in combination, can be useful. Duplex ultrasound is the most practical diagnostic tool for lower extremity DVTs because it is inexpensive, noninvasive, and easily administered at the patient’s bedside. Assessing blood flow and compressibility of the vein with real-time B-mode Doppler

ultrasound is more than 95% sensitive and specific for detecting proximal DVTs.26 When a DVT is suspected, an urgent outpatient screening is indicated where duplex ultrasound serves as the best first line test in a stable patient (see Fig. 14.2, lower panel).29 All guidelines agree that routine screening with duplex ultrasound at discharge from hospital is not cost effective and is not recommended.16,30 If nearby wounds, burns, or the presence of a cast or when DVT of the pelvis or inferior vena cava vessels are suspected, CT and magnetic resonance venography have shown good sensitivity and specificity.31 A postoperative patient who presents with chest pain, dyspnea, or cardiovascular collapse raises the clinical suspicion of PE; the diagnostic workup, provided that the patient is stable, should include a chest radiograph, electrocardiogram (ECG), and determination of an arterial blood gas (ABG) value. The plain film of the chest will often have subtle and nonspecific findings, whereas the ECG findings in patients with a PE potentially show sinus tachycardia, T-wave inversion, and ST abnormalities; however, these are not diagnostic alone. The tachypnea of a PE causes hyperventilation, which is represented by hypocapnia (low serum carbon dioxide level) in the ABG.32 D-dimer levels are often not helpful in the orthopedic setting because the trauma from

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TABLE 14.2  Common Drugs for Venous Thromboembolism Disease Prophylaxis/Treatment COMMON DRUGS FOR THROMBOEMBOLIC PROPHYLAXIS/TREATMENT Drug

Mechanism of Action

Complications

Notes

Reversal

Aspirina

Irreversibly blocks platelet COX-1 production of TXA2 Binds AT to inactivate Xa & II (thrombin) and IXa, XIa, XIIa Bind AT to inactivate Xa, & IIa (thrombin) Binds AT to selectively inactivate only Xa

Bleeding & GI issues Rare allergies Bleeding HIT and osteoporosis Bleeding Rare HIT Bleeding

Least effective chemical agent

None Protamine: 1 mg IV per 100 U UFH Protamine: 1 mg IV per 1 mg LMWH No antidote

VKAd Coumadin

Blocks γ-carboxylation of: factors II, VII, IX, X

Dabagitrand

Direct thrombin inhibitor

Bleeding Skin necrosis Fetal Warfarin syndrome Bleeding

Must monitor: aPTT or anti-Xa activity Monitor anti-Xa activity if: BMI >50 or CrCl 7 mm in diameter), or if the patient is considered high risk (unprovoked, history of prior VTE or cancer).38

SPORTS ISSUES, RETURN TO PLAY, AND TRAVEL Spontaneous DVTs and PEs in athletes with and without thrombophilia can occur.45–50 Comparison studies show a risk reduction

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Ventilation

A

L post R

RPO

R ant L

LAO

Perfusion

B

L post R

L RPO R

R ant L

R LAO L

Fig. 14.3  Left image, Helical computed tomography pulmonary angiography. (A) Patient with symptoms of syncope and hypoxia. Large clots (arrows) are present at the bifurcation of the main pulmonary artery and extend into the left and right pulmonary arteries. (B) Normal scan in a different patient at same level. Right image, High-probability pulmonary V/Q scan: Ventilation scan above demonstrates full lung fields. Perfusion scan below shows multiple areas lacking tracer. (Original image courtesy Austin Radiological Association and Seton Family of Hospitals.)

thromboembolic disease could potentially jeopardize performance.1,60 Multiple studies have made an association between taller individuals and increased risk of a first or recurrent venous thromboembolism.61–64 Injuries during competition and their treatment may put athletes at increased risk on their return journey. Prolonged air travel before surgery may also increase the risk of perioperative VTE.65–67 The risk of VTE is related to a person’s risk factors and the duration of the flight. The cause of the increased risk is likely related to a decrease in vascular flow of immobility; however, dehydration, decreased cabin pressure, and relative hypoxia may also play a role. The absolute risk of fatal PE is very low (2.57 per 1 million flights that last longer than 8 hours),68 but air travel lasting longer than 8 hours carries eight times the risk of fatal PE in nontravelers.69,70 Most patients who experience travel-related thrombosis have one or more other risk factors. Potential ways to help reduce the risk of VTE are by avoiding constrictive clothing, staying adequately hydrated, performing calf-stretching exercises, and taking frequent walks in the cabin. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: van Adrichem RA, Nemeth B, Algra A, et al. Thromboprophylaxis after knee arthroscopy and lower-leg casting. N Engl J Med. 2017;376(6):515–525.

Level of Evidence: II

in thromboembolic disease with activity51 and sports participation.52 Although DVTs usually affect athletes in the lower extremity, those who present with upper extremity pain, swelling, feeling of heaviness or dilated upper arm veins, the diagnosis of axillarysubclavian vein thrombosis or “effort thrombosis” (PagetSchroetter syndrome) should be entertained.53 Sports that involve shoulder abduction and extension (wrestling, gymnastics, weightlifting, throwing, and swimming) may have increased incidence in patients with anatomic abnormality of their thoracic outlet (cervical rib, congenital bands, hypertrophy of scalenus tendons, and/or abnormal insertion of the costoclavicular ligament). Upper extremity duplex ultrasound may help diagnosis, and thoracic outlet decompression may optimize their care.54,55 Athletes with DVT should be encouraged to start a gradual return to their usual daily activities when they begin anticoagulation therapy. A formal return-to-training program with progressively increasing intensity can be undertaken shortly thereafter, if the athlete is closely monitored for recurrence of VTE. Traditionally, athletes have been prohibited from contact or collision sports until anticoagulation therapy has been completed; however, the NOACs may allow protocols that allow earlier participation.56,57 Athletes involved in international competition may be at increased risk for “traveler’s thrombosis” (also known as “economy-class syndrome” or “rail coach syndrome”58) when facing travel durations longer than 4 hours.59 Young elite athletes who are at their peak physical condition are unlikely to experience significant health compromise; however, subclinical

Summary: A randomized controlled trial of patients important to sports medicine doctors looking at clinically relevant thromboembolic disease in both knee arthroscopy and cast immobilized patients. After studying more than 3000 patients, the conclusion is that chemical prophylaxis was not effective in preventing symptomatic VTE.

Citation: Kahn SR, et al. Compression stockings to prevent post-thrombotic syndrome: a randomised placebo-controlled trial. Lancet. 2014;383(9920):880–888.

Level of Evidence: II

Summary:. A multicenter randomized placebo-controlled trial of active versus placebo elastic compression stockings used for 2 years to prevent postthrombotic syndrome (PTS) after a first proximal DVT. Elastic compression hose did not prevent PTS after DVT, and their routine use was not supported.

Citation: Falck-Ytter Y, et al. Prevention of VTE in orthopedic surgery patients: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(suppl 2): e278S–e325S.

Level of Evidence: II

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TABLE 14.4  Treatment of Acute Venous Thromboembolism Disease

Drug Parenteral

IV heparin+ SC heparin+ LMWH– Fondaparinux–

Oral

Rivaroxaban–# Apixaban Edoxaban Dabigatran VKA

Dose 80 U/kg IV bolus 18 U/kg/h IV 333 U/kg SC then 250 U/kg SC BID 1 mg/kg BID SC 2 mg/kg QD SC 7.5 mg SC QD 5 mg if 100 kg 10 mg PO QD 5 mg PO BID 60 mg PO QD 150 mg PO QD

Duration ≥5 days

3 mos+

Monitoring aPTT:1.8–2.5 × control or Anti-Xa activity: 0.3–0.7 U/mL aPTT: 1.5–2.5 × control QAM 6 h after am dose None—unless RI or pregnancy Anti-Xa activity: 0.6–1.0 I U/mL None

3 mos+

None

3 mos+

None (aPTT/thrombin clotting time) INR: 2–3 QAM

5–10 mg PO QD Adjust dose

3 mos+

≥5 days ≥5 days

+ preferred for patients with severe renal impairment – avoid in patients with marked renal impairment (7% to 10%) present a solute load to the GI tract, which produces an osmotic drive for fluid to remain in the GI tract rather than being absorbed. This shift toward fluid deposition into the gut produces a “dumping syndrome” that overwhelms the colon’s absorptive abilities and results in diarrhea. For endurance athletes, it has been noted that when a beverage is consumed that contains multiple transportable

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carbohydrates such as glucose and fructose, gastrointestinal symptoms seem to be reduced compared with the consumption of the same amount of a single carbohydrate. Foods with high glycemic index and/or high fiber content may also contribute to osmotic “dumping,” whereas caffeine may produce diarrhea directly through its laxative properties.

Runner’s Diarrhea (“Runner’s Trots”) Although all athletes may be at increased risk for diarrhea, runners are at particular risk for a specific running-related diarrheal condition often referred to colloquially as “runner’s trots.” This condition is classically encountered in distance runners, but its exact pathophysiology is still largely unknown. Conjectured mechanisms include impairment in GI tract function as a result of the repetitive jarring associated with lengthy stints of running, fluid and electrolyte shifts associated with prolonged exercise, and relative ischemia of the GI tract. It is clear that unique intrinsic factors also may play a role in this condition because some endurance athletes rarely suffer with it whereas others are chronically affected. Clinically, athletes experience an urgent need to defecate mid-run with stools that may be loose or essentially normal. Management focuses on prevention, as noted next. Diarrhea Management Management centers on training and lifestyle modification to allow the gut to perform optimally in the face of high levels of exertion. Modifying physical stress through reduction of training intensity, duration, and/or distance for 1 to 2 weeks may lead to symptom resolution.5 The athlete should then transition to cross-training for several weeks, followed by resumption of running at progressively higher levels. Adequate hydration is always a crucial part of lifestyle management, and avoidance of NSAIDs, aspirin, antibiotics, and caffeine may also be helpful. Dietary modification to include a low-residue, low-fiber diet with avoidance of sports drinks and/or gels with carbohydrate concentrations greater than 8% should be recommended. Avoiding solid food at least 2 hours prior to exercise may help, as may adherence to an antidiarrheal diet such as the BRAT (bananas, rice, applesauce, toast) diet. Making an effort to have a bowel movement before exercise can greatly minimize the likelihood of midactivity GI distress. In general, anticholinergic medication use for exerciseassociated diarrhea is discouraged because the side effect profile and physiologic properties of these medications have a negative impact on sweat rate and thermoregulation. Opiate- and atropinebased preparations should also be avoided. Loperamide (Imodium) may be considered in athletes with nonbloody diarrhea who are at risk for dehydration and associated heat illness but are otherwise clinically well. Similarly, antispasmodic agents such as dicyclomine or hyoscamine may be considered for severe symptoms, but their use must be weighed against the risk of anticholinergic side effects. Stool studies should be obtained in athletes with “alarm” features, including gross hematochezia, profound diarrhea associated with dehydration, persistent diarrhea greater than 48 hours, fever, severe abdominal pain, recent travel, or possible exposure to infectious diarrheal pathogens. Consideration

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should also be given to studies in immunocompromised patients or older athletes,42 especially if they have comorbid medical conditions.

Lower Gastrointestinal Bleeding Microscopic heme-positive stools, rectal bleeding, or frank bloody diarrhea may be seen commonly with high-level training or competition particularly marathoning, ultramarathoning, or high-mileage cycling. Occult rectal bleeding has been demonstrated in approximately 25% of recreational triathletes, 20% of marathon runners, and almost 90% of 100-mile ultramarathoners.34 More dramatically, frankly bloody stools have been reported in up to 6% of postmarathon runners.43 As described earlier, long-duration events create prolonged ischemia in the GI tract, which compromises mucosal integrity, resulting in varying degrees of lower GI tract bleeding. This condition is generally benign and self-limited in the absence of underlying GI tract diseases. Pronounced or protracted rectal bleeding may predispose to anemia and may be a marker of a more worrisome underlying GI issue.

Ischemic Conditions There are four distinct ischemic syndromes seen in the GI tract.9 Although primarily seen in patients with vascular comorbidities such as hypertension, diabetes mellitus, or tobacco abuse, they must be considered by the sports medicine practitioner in light of the breadth and variable health characteristics of the exercising population. Colonic ischemia is the most common form of ischemic bowel disease. Crampy left lower quadrant abdominal pain and bowel movements of stool mixed with frank blood are the common presenting clinical features. Colonoscopy should be performed acutely in the setting of rectal bleeding to make a definitive diagnosis. Mucosal changes of ischemia, typically manifest by congestive and hemorrhagic vascular lesions, are the classic findings. This condition is self-limited and the associated colonic changes will typically resolve in 1 week, thus limiting the yield of diagnostic testing performed at that time or beyond. The less common ischemic syndromes include acute arterial mesenteric infarction (AAMI), chronic arterial mesenteric ischemia (CAMI), and mesenteric venous thrombosis. Although a discussion of these entities is beyond the scope of this text, it is important to consider them for older athletes presenting with severe abdominal pain and lower GI bleeding. Although some risk for GI ischemia is unavoidable in the most intense of activities, aggressive hydration and heat management remain the key means of attempting to prevent or minimize lower GI bleeding.

Irritable Bowel Syndrome A functional GI disorder without evidence of structural, biomechanical, radiologic, or laboratory abnormalities, IBS affects up to 15% of the general population.44 Two forms have been described—“diarrhea predominant” and “constipation predominant”—although the classic pattern typically involves alternating manifestations of both. IBS is twice as common in women and typically presents in the second or third decade of life.

Approximately 50% of patients who have IBS have comorbid psychiatric illnesses, most commonly depression and anxiety. Proposed mechanisms for IBS include increased GI sensitivity to various stimuli including stress, food, cholecystokinin secretion, impaired transit of bowel gas, visceral hypersensitivity, autonomic dysfunction, and altered immune activation.45 The clinical presentation of IBS is variable, with the most common symptoms including cramping abdominal pain relieved by defecation, altered stool frequency, altered stool form (watery, mucus, loose, hard), altered stool passage (urgency, strain), a sense of incomplete evacuation, and abdominal distention especially following meals. Athletes with IBS rarely have nocturnal symptoms and do not manifest features of systemic illness or gross GI bleeding. The diagnosis is generally made clinically based on presentation and lack of evidence of other GI disorders. Current evidence does not support the routine use of laboratory studies or imaging to exclude organic GI disorders in patients who have typical IBS symptoms and are lacking “alarm” features such as significant abdominal pain, fevers, GI bleeding, or weight loss.44 Primary management strategies focus on lifestyle measures including high-fiber diet, adequate hydration, and stress reduction techniques. For ongoing symptoms, drug treatment of IBS is based on the athletes’ predominant symptoms. For diarrheapredominant IBS, antidiarrheal (loperamide) or antispasmodic (dicyclomine, hyoscamine) medicines used as needed are typically efficacious. Constipation-predominant IBS is generally managed with an increase in the lifestyle measures noted previously coupled with nonstimulant laxatives such as polyethylene glycol (Miralax) or psyllium-containing products. Adequate hydration is particularly important in constipation-prone athletes.

Celiac Disease Celiac disease is a hereditary autoimmune disorder resulting in malabsorption in the GI tract. Hypersensitivity of the immune system to gluten- or gliadin-containing foods is the primary pathophysiologic mechanism. Gluten protein found in wheat, barley, and rye results in an immunologic reaction in the intestinal mucosa that causes villous atrophy and subsequent impairment in absorption of important nutrients. Increasingly, celiac disease is being recognized and diagnosed in the general population and, as such, is also being more commonly encountered in athletes and active individuals. Although its primary pathology is found in the GI tract, celiac disease may also have effects on blood, bone, brain, nervous system, and skin.46 Iron deficiency anemia has been reported in up to 70% of patients with newly diagnosed celiac disease,47 and calcium and vitamin D deficiencies are also common, which may increase the risk of stress fractures and osteopenia.48 The diagnosis of celiac disease is often delayed many months or even years because the presenting symptoms may be suggestive of other more common entities or may be sufficiently mild as to be largely ignored by the athlete. Signs and symptoms of classic celiac disease include chronic diarrhea, abdominal bloating/cramping/pain, malnutrition, fatigue, vomiting, anemia, myalgia/arthralgia, osteopenia/osteoporosis, menstrual irregularities, irritability, constipation, short stature, and dermatitis

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CHAPTER 15  Gastrointestinal Medicine in the Athlete

herpetiformis.49 Initial serologic testing is traditionally via serum tissue transglutaminase (tTG) antibody levels. More specialized studies are available but are beyond the scope of our discussion. The “gold standard” for definitive diagnosis of celiac disease is tissue biopsy of small intestinal mucosa demonstrating classic blunted villi. Eating a strict gluten-free diet is the only effective management of celiac disease, and this can be challenging on many levels for the competitive athlete. The elimination of all sources of wheat, rye, and barley requires that the athlete find ample alternative sources of carbohydrate to meet the recommended carbohydrate intake of 6 to 10 g/kg body weight. Beans, rice, corn meal, corn flour, nuts, potatoes, tapioca, and quinoa are excellent sources of gluten-free carbohydrates, along with fresh fruits and vegetables. Travel and team meals can be particular challenges for athletes with celiac disease who must ensure appropriate food choices to adequately meet their healthy fat, protein, and carbohydrate intake goals and to provide sufficient energy for maximum performance. In recent years, it has become increasingly popular for nonceliac athletes to consume a gluten-free diet because of perceived GI or general health benefits. However, research into the effects of gluten-free food intake in this group demonstrated no overall effect on performance, GI symptoms, well-being, indicators of intestinal injury, or inflammatory markers.50 For a complete list of references, go to ExpertConsult.com.

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SELECTED READINGS Casey E, Mistry DJ, MacKnight JM. Training room management of medical conditions: sports gastroenterology. Clin Sports Med. 2005;24:525–540. [Level of Evidence III, Systematic Review]. Cronin O, Molloy MG, Shanahan F. Exercise, fitness, and the gut. Curr Opin Gastroenterol. 2016;32(2):67–73. [Level of Evidence III, Systematic Review]. de Oliveira EP, Burini RC, Jeukendrup A. Gastrointestinal complaints during exercise: prevalence, etiology, and nutritional recommendations. Sports Medicine. 2014;44(suppl 1):79–85. [Level of Evidence III, Systematic Review]. Ho GWK. Lower gastrointestinal distress in endurance athletes. Curr Sports Med Rep. 2009;8(2):85–91. [Level of Evidence III, Systematic Review]. Leggit JC. Evaluation and treatment of GERD and upper GI complaints in athletes. Curr Sports Med Rep. 2011;10(2):109–114. [Level of Evidence I, Systematic Review]. Pfeiffer B, Stellingwerff T, Hodgson AB, et al. Nutritional intake and gastrointestinal problems during competitive endurance events. Med Sci Sports Exerc. 2012;44(2):344–351. [Level of Evidence III, Comparative Study]. Viola TA. Evaluation of the athlete with exertional abdominal pain. Curr Sports Med Rep. 2010;9:106–110. [Level of Evidence V, Expert Opinion]. Waterman JJ, Kapur R. Upper gastrointestinal issues in athletes. Curr Sports Med Rep. 2012;11(2):99–104. [Level of Evidence I, Systematic Review].

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CHAPTER 15  Gastrointestinal Medicine in the Athlete

REFERENCES 1. de Oliveira EP, Burini RC, Jeukendrup A. Gastrointestinal Complaints During Exercise: Prevalence, Etiology, and Nutritional Recommendations. Sports Med. 2014;44(suppl 1): 79–85. 2. Rehrer NJ, Janssen GM, Brouns F, et al. Fluid intake and gastrointestinal problems in runners competing in a 25-km race and a marathon. Int J Sports Med. 1989;10(suppl 1):S22–S25. 3. Peters HP, DeVries WR, Vanberge-Henegouwen GP, et al. Potential benefits and hazards of physical activity and exercise on the gastrointestinal tract. Gut. 2001;48(3):435–439. 4. Van Nieuwenhoven MA, Brouns F, Brummer RJ. Gastrointestinal profile of symptomatic athletes at rest and during physical exercise. Eur J Appl Physiol. 2004;91(4):429–434. 5. Brouns F, Beckers E. Is the gut an athletic organ? Digestion, absorption, and exercise. Sports Med. 1993;15(4):242–257. 6. Worobetz LJ, Gerrard DF. Effect of moderate exercise on esophageal function in asymptomatic athletes. Am J Gastroenterol. 1986;81(11):1048–1051. 7. Peters HP, Bos M, Seebregts L, et al. Gastrointestinal symptoms in long-distance runners, cyclists, and tri-athletes: prevalence, medication, and etiology. Am J Gastroenterol. 1999;94(6): 1570–1581. 8. Pals KL, Chang RT, Ryan AJ, et al. Effect of running intensity on intestinal permeability. J Appl Physiol. 1997;82(2):571–576. 9. Moses FM. Exercise-associated intestinal ischemia. Curr Sports Med Rep. 2005;4:91–95. 10. ter Steege RW, Van der Palen J, Kolkman JJ. Prevalence of gastrointestinal complaints in runners competing in a longdistance run: an Internet-based observational study in 1281 subjects. Scand J Gastroenterol. 2008;43:1477–1482. 11. Keeffe EB, Lowe DK, Goss JR, et al. Gastrointestinal symptoms of marathon runners. West J Med. 1984;141:481–484. 12. Lambert GP, Lang J, Bull A, et al. Fluid restriction during running increases GI permeability. Int J Sports Med. 2008;29: 194–198. 13. Pfeiffer B, Stellingwerff T, Hodgson AB, et al. Nutritional intake and gastrointestinal problems during competitive endurance events. Med Sci Sports Exerc. 2012;44(2):344–351. 14. Perko MJ, Nielsen HB, Skak C, et al. Mesenteric, celiac and splanchnic blood flow in humans during exercise. J Physiol. 1998;513(Pt 3):907–913. 15. Waterman JJ, Kapur R. Upper gastrointestinal issues in athletes. Curr Sports Med Rep. 2012;11(2):99–104. 16. Dimeo F, Knauf W, Geilhaupt D, et al. Endurance exercise and the production of growth hormone and hematopoietic factors in patients with anemia. Br J Sports Med. 2004;38:e37. 17. Leggit JC. Evaluation and treatment of GERD and upper GI complaints in athletes. Curr Sports Med Rep. 2011;10(2): 109–114. 18. Galmiche JP, Clouse RE, Balint A, et al. Functional esophageal disorders. Gastroenterology. 2006;130:1459–1465. 19. Simons SM, Kennedy RG. Gastrointestinal problems in runners. Curr Sports Med Rep. 2004;3:112–116. 20. Simren M. Physical activity and the gastrointestinal tract. Eur J Gastroenterol Hepatol. 2002;14:1053–1056. 21. de Oliviera EP, Burini RC. The impact of physical exercise on the gastrointestinal tract. Curr Opin Clin Nutr Metab Care. 2009;12:533–538. 22. Viola TA. Evaluation of the athlete with exertional abdominal pain. Curr Sports Med Rep. 2010;9:106–110.

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23. Peters HP, de Vries WR, Akkermans LM, et al. Duodenal motility during a run-bike-run protocol: the effect of a sports drink. Eur J Gastroenterol Hepatol. 2002;14:1125–1132. 24. Collings KL, Pierce Pratt F, Rodriguez-Stanley S, et al. Esophageal reflux in conditioned runners, cyclists, and weightlifters. Med Sci Sports Exerc. 2003;35:730–735. 25. Kiahrilas PJ, Shaheen NJ, Vaezi M. American Gastroenterological Association medical position statement on the management of gastroesophageal reflux disease. Gastroenterology. 2008;135: 1383–1391. 26. Parmalee-Peters K, Moeller JL. Gastroesophageal reflux in athletes. Curr Sports Med Rep. 2004;3:107–111. 27. Boyle JT. Pathogenic gastroesophageal reflux in infants and children. Pract Gastroenterol. 1990;14:25–38. 28. Sontag SJ, Harding SM. Gastroesphageal reflux and asthma. In: Goyal RK, Shaker R, eds. Goyal and Shaker’s GI Motility Online. New York: Nature Publishing Group; 2006. 29. Kiljander TO, Harding SM, Field SK, et al. Effects of esomeprazole 40 mg twice daily on asthma: a randomized placebo-controlled trial. Am J Respir Crit Care Med. 2006;173: 1091–1097. 30. Hirano I, Richter JE. The Practice Parameters Committee of the American College of Gastroenterology. ACG practice guidelines: esophageal reflux testing. Am J Gastroenterol. 2007;102:668–685. 31. Kraus BB, Sinclair JW, Castell DO. Gastroesophageal reflux in runners. Characteristics and treatment. Ann Intern Med. 1990;112(6):429–433. 32. Choi SJ, Kim YS, Chae JR, et al. Effects of ranitidine for exercise induced gastric mucosal changes and bleeding. World J Gastroenterol. 2006;12:2579–2583. 33. Thalmann M, Sodeck GH, Kavouras S, et al. Proton pump inhibition prevents gastrointestinal bleeding in ultramarathon runners: a randomized, double blinded, placebo controlled study. Br J Sports Med. 2006;40:359–362. 34. Baska RS, Moses FM, Deuster PA. Cimetidine reduces runningassociated gastrointestinal bleeding. A prospective observation. Dig Dis Sci. 1990;35:956–960. 35. Sullivan SN, Wong C, Heidenheim P. Does running cause gastrointestinal symptom? A survey of 93 randomly selected runners compared with controls. N Z Med J. 1994;107:328–331. 36. American Dietetic Association; Dietitians of Canada; American College of Sports Medicine, Rodriguez NR, Di Marco NM, et al. American College of Sports Medicine position stand. Nutrition and athletic performance. Med Sci Sports Exerc. 2009;41: 709–731. 37. Glace B, Murphy C, McHugh M. Food and fluid intake and disturbances in gastrointestinal and mental function during an ultramarathon. Int J Sport Nutr Exerc Metab. 2002;12:414–427. 38. Kahrilas PJ, Shaheen NJ, Vaezi MF. American Gastroenterological Association Institute, Clinical Practice and Quality Management Committee. American Gastroenterological Association Institute technical review on the management of gastroesophageal reflux disease. Gastroenterology. 2008;135:1392–1413. 39. Worobetz LJ, Gerrard DF. Gastrointestinal symptoms during exercise in Enduro athletes: prevalence and speculations on the etiology. N Z Med J. 1985;98(784):644–646. 40. Rao SSC, Beaty J, Chamberlain M, et al. Effects of acute graded exercise on human colonic motility. Am J Physiol Gastrointest Liver Physiol. 1999;276:G1221–G1226. 41. Sullivan SN, Champion MC, Christofides ND, et al. Gastrointestinal regulatory peptide responses in long-distance runners. Phys Sportsmed. 1984;12(7):77–82.

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42. Ho GWK. Lower gastrointestinal distress in endurance athletes. Curr Sports Med Rep. 2009;8(2):85–91. 43. Heiman DL, Lishnak DL, Trojian TH. Irritable bowel syndrome in athletes and exercise. Curr Sports Med Rep. 2008;7(2): 100–103. 44. Cash BD, Chey WD. Irritable bowel syndrome–an evidencebased approach to diagnosis. Aliment Pharmacol Ther. 2004;19(12):1235–1245. 45. Serra J, Azpiroz F, Malagelada JR. Impaired transit and tolerance of intestinal gas in the irritable bowel syndrome. Gut. 2001; 48(1):14–19. 46. Gasbarrini G, Malandrino N, Giorgio V, et al. Celiac disease: what’s new about it? Digest Dis. 2008;26:121–127.

47. Harper JW, Holleran SF, Ramakrishnan R, et al. Anemia in celiac disease is multifactorial in etiology. Am J Hematol. 2007;82: 996–1000. 48. Zanchi C, Di Leo G, Ronfani L, et al. Bone metabolism in celiac disease. J Pediatr. 2008;153(2):262–265. 49. Mancini LA, Trojian T, Mancini AC. Celiac Disease and the Athlete. Curr Sports Med Rep. 2011;10(2):105–108. 50. Lis D, Stellingwerff T, Kitic CM, et al. No Effects of a ShortTerm Gluten-free Diet on Performance in Nonceliac Athletes. Med Sci Sports Exerc. 2015;47(12):2563–2570.

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16  Hematologic Medicine in the Athlete John J. Densmore

Athletic performance depends on proper functioning of the blood. From problems with the oxygen-carrying function of red blood cells to the prevention of bleeding by the hemostatic system, many hematologic issues can affect athletes adversely. These hematologic issues include both acquired and inherited disorders that can affect athletes of all ages. This chapter reviews many of the hematologic issues that may arise in caring for athletes, focusing on those relating to red blood cells and the hemostatic system.

concentration.4 Intravascular hemolysis is also common in athletes. Initially referred to as march hemoglobinuria or foot-strike hemoglobinuria, the mechanism for hemolysis was thought to be induced by mechanical damage to red cells with each foot strike.5 However, others suggest that the effects of contracting muscles on red cells may contribute to hemolysis and the development of anemia in athletes.6

DISORDERS OF RED BLOOD CELLS

Anemia is a condition commonly experienced by persons in the United States. Rates are highest in children and adult women, largely because of iron deficiency. The most recent National Health and Nutrition Examination Surveys (2003–2012) estimate that 3.5% of men and 7.6% of women in the United States are anemic, with the highest rates among menstruating women.7 Iron deficiency is the most common cause of anemia in the United States and is the most common nutritional deficiency worldwide.8 A recent retrospective study evaluated the results of iron-related testing in 2749 individuals at a National Collegiate Athletic Association (NCAA) Division 1 institution.9 In women, 2.2% had iron deficiency anemia and another 30.9% had iron deficiency without anemia. The incidence for men was much lower, 1.2% with iron deficiency anemia and 2.9% with iron deficiency without anemia. Hemoglobin S is the most common inherited blood disorder in the United States. It is estimated that 1 in 12 African Americans carries one copy of the mutated gene, a condition referred to as sickle cell trait.10 The thalassemias are also common and are considered the most prevalent genetic mutation worldwide.2 Incidence varies geographically; alpha thalassemia is frequent in Southeast Asia and western Africa, whereas beta thalassemia is more common in the Mediterranean region of Europe.

Definition Anemia is defined as a reduction of red blood cells below the normal range, with the normal range differing for men and women. Hemoglobin and hematocrit are commonly used to identify the red blood cell concentration in the blood. Mild anemia can be asymptomatic, although compared with more sedentary persons, athletes generally notice it much earlier because of its effects on their performance. It is important to identify the underlying cause of the anemia, which can be due to decreased red cell production or increased red cell destruction. Hemoglobin is the oxygen-carrying protein in red blood cells. Normal hemoglobin (hemoglobin A) consists of two alpha chains and two beta chains.1 Inherited disorders of hemoglobin are referred to as hemoglobinopathies or thalassemia. A number of hemoglobinopathies have been identified that result from mutations in the alpha or beta chains and have varying degrees of anemia and symptoms. The most common hemoglobin mutation in the United States is hemoglobin S, which causes sickle cell disease in persons with two copies of the mutated gene. Thalassemia refers to decreased production of normal alpha or beta chains and can be clinically silent or markedly symptomatic.2 Thalassemias are referred to as alpha or beta, depending on which chain is affected. Thalassemias increase in clinical severity as the number of genes affected increases. In general, persons with one or two mutations are asymptomatic, a condition referred to as thalassemia minor. It also appears that some athletes have anemia that is caused by mechanisms not seen in nonathletes, including dilutional “pseudoanemia” and exercise-related intravascular hemolysis. Pseudoanemia refers to a temporary condition that occurs as a result of training-related expansion of the plasma volume.3 The degree of volume expansion relates to the duration and intensity of exercise and can result in a dilutional drop in the hemoglobin 196

Epidemiology

Pathophysiology As previously stated, anemia is caused by either decreased production or increased destruction of red blood cells. Red blood cell production problems (Table 16.1) can be due to a vitamin or mineral deficiency, inflammation, erythropoietin deficiency, or a primary bone marrow disorder. Iron deficiency is the most common cause and is most often the result of chronic blood loss. Menstruation or chronic gastrointestinal blood loss will lead to iron deficiency if oral absorption is not able to balance iron loss. Other avenues for iron loss in athletes are hemolysis leading to hemoglobinuria and increased sweat production.10

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CHAPTER 16  Hematologic Medicine in the Athlete

Abstract

Keywords

Athletic performance depends on proper functioning of the blood. From problems with the oxygen-carrying function of red blood cells to the prevention of bleeding by the hemostatic system, many hematologic issues can adversely affect athletes. These hematologic issues include both acquired and inherited disorders that can affect athletes of all ages. This chapter reviews many of the hematologic issues that may arise while caring for athletes, focusing on those relating to red blood cells and the hemostatic system.

anemia coagulation iron deficiency sickle cell trait thrombocytopenia

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TABLE 16.1  Types of Anemia in Athletes and Treatment Recommendations Condition

Frequency

Hemoglobin

Ferritin

Treatment Required

Dilutional pseudoanemia Iron deficiency without anemia Iron deficiency anemia Thalassemia minor

Common Common Less common Less common

Normal to mild decrease Normal Decreased Normal to mild decrease

Normal Decreased Decreased Normal to elevated

No Controversial Iron replacement indicated No

Another potential cause of iron deficiency in athletes is celiac disease, which results in iron malabsorption and can occur even in the absence of the gastrointestinal symptoms that are suggestive of celiac disease.11 Iron deficiency occurs in three stages.8 Stage I, also known as prelatent iron deficiency, is associated with an isolated decrease in serum ferritin. At this stage, stainable iron is not present in the bone marrow, but hemoglobin levels remain normal. Stage II is latent iron deficiency; at this stage, the ferritin drops further, serum iron and transferrin saturation decrease, and total ironbinding capacity rises. As in stage I, hemoglobin levels remain normal during stage II, although the mean corpuscular volume (MCV) of the red cells may start to decrease. However, in stage III, with progressive depletion of iron stores, an overt microcytic and hypochromic iron-deficiency anemia develops. Inflammatory conditions have long been known to lead to decreased red cell production, but only recently has the pathophysiology been understood fully. Hepcidin, a protein produced by the liver in response to infection or inflammation, inhibits iron absorption and its release from storage sites for use by developing red blood cell precursors.12 Although significant data are lacking in athletes, it appears that chronic inflammation from training can result in elevated hepcidin levels, contributing to disordered iron metabolism and resultant anemia. Erythropoietin is an important hormone that promotes red blood cell production.1 It is produced by the kidney but is also manufactured as a pharmaceutical agent for use in persons with kidney failure and some primary bone marrow disorders. Deficiency in an athlete would be unusual unless significant renal insufficiency was also present. Similarly, primary bone marrow disorders such as leukemia or multiple myeloma often cause significant anemia, but these disorders are rare in athletes. Hemoglobin S in red blood cells protects against malaria and has been shown to reduce mortality from the disease compared with hemoglobin A.13 Sickle cell trait has long been believed to be a benign condition, but evidence is increasing that carriers experience an increased number of adverse events.14 Exertional sickling, which was first reported in military recruits more than 25 years ago, has been associated with sudden death during exercise.15 Causes of sudden death include metabolic acidosis, rhabdomyolysis, renal failure, and cardiac arrhythmia. Risk for adverse events is increased by conditions that can promote sickling of red blood cells, including intense exercise, particularly at a high altitude or in extreme heat. In a recent review of NCAA athletes who died suddenly, it was determined that the relative risk for sudden death is 37 times higher for an athlete with sickle cell trait.16

Anemia Reticulocyte count

High (>100,000/µL) Bleeding Hemolysis

Low (200 units) daily doses of insulin, regular insulin can also be prescribed in 5× and 2× concentrations to reduce the volume of insulin injected. It is important for athletes, coaches, and trainers to be aware that insulin, as an anabolic agent, is included on the prohibited substances list of the World Anti-Doping Agency (WADA). For elite athletes requiring insulin for diabetes management, therapeutic use exemption (TUE) must be obtained. Information related to this process can be found at wada-ama.org.

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CHAPTER 18  The Athlete With Diabetes

Peak

Aspart (Novolog→) Glulisine (Apidra→) Lispro (Humalog→) Regulara Neutral protamine Hagedorn Detemir (Levemir→) Glargine (Lantus, Basaglar→)

5–15 min 5–15 min 5–15 min 30–60 min 1–3 h 1 h 1 h

45–90 min 45–90 min 45–90 min 2–4 h 4–6 h 6–8 h —

Plasma glucose concentration

Duration 3–4 h 3–4 h 3–4 h 5–6 h 8–12 h 12–24 h 24 h

Muscle

steady Insulin secretion

l ro ce ly

Onset

G

Insulin Preparations

Liver

inhibited

A

Preparations

FF

TABLE 18.1  Pharmacokinetics of Insulin

221

a

Regular insulin is also available in 5× (U-500) and 2× (U-200) concentrations. Fat

Incretin and Amylin Analog Therapy Incretins are peptides found in the gastrointestinal tract that act to lower glucose by pathways that are independent of the insulin receptor. The two currently recognized forms are glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide. GLP-1 agonists are injectable agents that lower blood glucose by delaying gastric emptying, inhibiting glucagon secretion, and increasing insulin secretion after a meal. DPP-4 is an endogenous enzyme that inactivates the incretins. Adverse effects of GLP-1 agonists include hypoglycemia, and therefore they should be used with caution before or during exercise. Amylin is a peptide that is normally cosecreted with insulin from the pancreas and which usually antagonizes its action. The amylin analog pramlintide is available as an injectable agent and is approved by the FDA for use in type 1 and type 2 diabetes. Its method of action is very similar to that of incretin therapy, and the risk of hypoglycemia with exercise is also a concern.

Fig. 18.1  The response to exercise in healthy persons and in insulindependent diabetic patients. When plasma insulin is normal or slightly diminished, hepatic glucose production increases markedly, as does skeletal muscle usage of glucose, whereas blood glucose remains unchanged. FFA, Free fatty acids. (From Ekoe JM. Overview of diabetes mellitus and exercise. Med Sci Sports Exerc. 1989;21:353–368. Copyright The American College of Sports Medicine.)

Liver Plasma glucose concentration

Muscle

Down Insulin concentration

ol

er

lyc

G

Glucose Regulation During Exercise in Athletes With Type 1 Diabetes Mellitus Soon after the discovery of insulin and its use in patients with type 1 diabetes, it was observed that physical activity could reduce insulin requirements. In addition, it was recognized that the decrease in blood glucose after an insulin injection was magnified by subsequent exercise.13 Exercise increases blood flow to muscles and skin, leading to an increased rate of insulin absorption in the athlete with type 1 diabetes (Figs. 18.1 and 18.2).14 This effect is most pronounced when insulin is administered less than 60 minutes before exercise. Because insulin is given exogenously in persons with type 1 diabetes, the body cannot

FF

A

PHYSIOLOGIC CHANGES OF EXERCISE IN HEALTHY ATHLETES AND IN ATHLETES WITH DIABETES A comprehensive review of the very complex changes that occur during exercise in healthy persons can be found elsewhere.12 However, because critical changes occur in glucose metabolism during exercise and recovery, it is important that persons who are managing athletes with diabetes have a basic understanding of what occurs during both aerobic and anaerobic metabolism.

Elevated

Fat Fig. 18.2  The response to exercise in hyperinsulinemic insulin-dependent diabetic patients. When plasma insulin is increased, skeletal muscle use of glucose during exercise increases markedly, but the increase in hepatic glucose production is smaller than normal: blood glucose levels decrease. FFA, Free fatty acids. (From Ekoe JM. Overview of diabetes mellitus and exercise. Med Sci Sports Exerc. 1989;21:353–368. Copyright The American College of Sports Medicine.)

decrease its release of insulin, and increased serum insulin levels inhibit hepatic glucose production and peripheral lipolysis. At the same time, continued insulin-independent glucose uptake by exercising muscles depletes energy stores. In type 1 diabetes, glucagon secretion in response to hypoglycemia is usually lost approximately 5 years after diagnosis; the epinephrine response to hypoglycemia is also attenuated in these persons.15 Deficiencies of these counterregulatory hormones further limit fuel availability during exertion (Table 18.2). The balance between energy supply and demand is often disrupted in the diabetic athlete by an excessive or inadequate insulin effect.

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TABLE 18.2  Actions of Major

Counterregulatory Hormones Hormone a

Glucagon Epinephrinea Growth hormone

Cortisol

Mechanism of Hyperglycemic Effect Activates hepatic glycogenolysis and gluconeogenesis Stimulates hepatic glucose production, limits peripheral glucose use, and suppresses insulin secretion After initial glucose-lowering effect, limits glucose transport into cells, mobilizes fat, and provides gluconeogenic substrate (glycerol) Initially inhibits glucose use; with time, mobilizes substrate (amino acids and glycerol) for gluconeogenesis

a

Hormones important in recovery from acute hypoglycemia.

Pathophysiologic Responses to Exercise in Persons With Diabetes Mellitus Data are inconclusive with regard to whether athletes with diabetes mellitus have inherently impaired exercise performance. It is possible that the associated epiphenomena of diabetes, such as acute hypoglycemia or chronic hyperglycemia, diminish the capacity of the athlete to perform at his or her highest capacity. In the setting of obesity or chronic illness, exercise performance is undeniably diminished, but in fit athletes with diabetes, particularly lean athletes with type 1 diabetes, this question remains unanswered. Therefore it is worth exploring the available literature so that both care and expectations can be managed accordingly. In a study that compared adolescent girls who had either type 1 or type 2 diabetes with either obese or normal-weight girls without diabetes, it was found that female adolescents with type 2 diabetes have reduced aerobic capacity and reduced heart rate response to maximal exercise.16 Moreover, investigators found that subjects with either type 1 or type 2 diabetes had a blunted stroke volume response compared with nondiabetic control subjects. However, subjects with either type 1 or type 2 diabetes had evidence of poor glucose control at baseline (hemoglobin A1c level = 8.8% and 8.2%, respectively). Moreover, no determinations of baseline activity levels were made. Therefore it is possible that the subjects with either type 1 or type 2 diabetes were more sedentary than their matched nondiabetic control subjects. This concept is supported by another study comparing aerobic capacity and pulmonary function in athletes with type 1 diabetes and both matched, nondiabetic control subjects and nonexercising, diabetic control subjects.17 In this instance, the glycemic control of the athletes with diabetes was much better than that of the nonathletes with type 1 diabetes (mean hemoglobin A1c = 7.5% vs. 9.0%), but the average glucose level was still much higher than that of the athletes without diabetes (mean hemoglobin A1c level = 4.4%). In addition, the type and duration of programmed exercise was not described. Nevertheless, aerobic capacity (as measured by VO2 max) was found to be similar in athletes both with and without diabetes and was higher in both groups than in nonathletes with diabetes. Of note, both forced expiratory volume in 1 second and anaerobic threshold (as measured by nonlinear increases of pulmonary ventilation and peak CO2 production compared with O2 consumption) were

lower in athletes with diabetes compared with nondiabetic athletes. Because aerobic capacity was normal, the authors speculated that other factors besides ventilation were adversely lowering the anaerobic threshold. They hypothesized that elastin and collagen abnormalities may negatively affect bronchial adaptation to air flow. With average glucose values significantly higher in the diabetic versus nondiabetic athlete subjects in this study (an average difference of greater than 80 mg/dL according to hemoglobin A1c levels), it is difficult to exclude the effect of chronic hyperglycemia alone on exercise performance in study subjects. In that regard, Wheatley et al.18 reported that the diffusing capacity for carbon monoxide and the membrane diffusing capacity were lower in athletes with uncontrolled type 1 diabetes compared with athletes with better glycemic control. However, an inverse relationship between glycemic control and pulmonary function was less clear after the investigators found that arterial oxygen saturation was lower in the subjects with well-controlled diabetes. Other investigators have used additional technologies to observe athletes with diabetes. Peltonen et al. used near-infrared spectroscopy to study local tissue deoxygenation rates during cycling in men with type 1 diabetes (mean hemoglobin A1c 7.7 ± 0.7%) and healthy control men, who were matched for age, body measurements, and baseline reported physical activity.19 Despite similar reported baseline physical activity, the men with type 1 diabetes were found to have lower aerobic capacity (VO2 peak). As a novel finding in this population, the men with diabetes had more rapid leg muscle deoxygenation at submaximal workloads. Because there was no difference in arterial oxygen saturation in the two groups of men, the authors noted that impaired alveolar gas transfer was an unlikely contributor to this observation. The investigators suggested that this finding instead could indicate inadequacy in circulatory capacity to amplify oxygen delivery to meet increasing tissue demand. Baldi et al. attempted to directly address the issue of glycemic status on exercise response in endurance athletes with type 1 diabetes.20 They reported no difference between aerobic capacity or cardiopulmonary exercise response between athletes with type 1 diabetes compared with subjects who did not have diabetes. However, significant differences were found between athletes with diabetes when the group was stratified into those with good glycemic control (hemoglobin A1c level 7%, mean = 7.8%), despite a similar time spent exercising per week. Multiple indicators of cardiopulmonary fitness were altered in the group with poorer glycemic control, including a lower resting cardiac output and higher systemic vascular resistance. In addition, the group with poor glycemic control had a 24% lower workload during peak exercise, a 10% lower VO2 max, and a 25% lower calculated cardiac output. All measured parameters of pulmonary function were lower in the group with poor glycemic control. When interpreting these findings, it is important to note that in most clinical settings, a hemoglobin A1c level of 7.0% to 7.8% would indicate glycemic control that was only minimally above target.5 Finally, Nguyen et al. studied children with and without type 1 diabetes to assess fitness levels in the setting of poor glycemic

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control (hemoglobin A1c ≥9.0% for the 9 months prior to the study period) versus good glycemic control (hemoglobin A1c ≤7.5% over the 9 months prior).21 The investigators assessed the children’s grip strength, short-term muscle power during cycling, aerobic capacity while cycling, and physical activity while wearing an accelerometer for 7 days. They found no significant differences between groups for grip strength or short-term muscle power but identified lower VO2 peak in the children with poorly controlled diabetes as compared with the controls or children with well-controlled diabetes. The groups of children had no significant differences in physical activity by minutes of activity per day or by activity intensity level. If poor glycemic control has a direct negative effect on exercise performance, several potential explanations exist. First, even acute elevations in blood glucose levels are known to diminish autoregulation of capillary blood flow, leading to diminished oxygen consumption.22 In addition, chronic hyperglycemia is associated with neuropathic changes, both autonomic and peripheral. Veves et al. noted reduced aerobic capacity and diminished heart rate in subjects with type 1 diabetes and neuropathy compared with subjects without neuropathy.23 As the distinction between exercise performance in athletes with good glycemic control compared with poor glycemic control becomes better defined, it is expected that additional mechanisms that might explain these differences will be determined.

MANAGEMENT OF ATHLETES WITH DIABETES DURING TRAINING AND COMPETITION Despite the fact that exercise is strongly recommended as a mainstay of therapy for persons with diabetes mellitus and that chronic athletic conditioning evokes positive metabolic changes, studies have shown a lack of improvement in hemoglobin A1c levels in patients with type 1 diabetes.24 Several possible explanations exist for this finding. First, exercise introduces variables of glucose utilization and insulin sensitivity that may cause difficulty in keeping glucose levels consistent, especially if exercise is not performed regularly. Perhaps more important is the justifiable concern of hypoglycemia both during but especially after competition. Anecdotally, concern for developing hypoglycemia leads many recreational, high school, and even collegiate athletes to induce hyperglycemia prior to training or competition either by consuming an excessive amount of simple carbohydrates or by underdosing insulin. The resultant hyperglycemia can offset any positive effects of athletic activity on long-term glycemic

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control. Therefore perhaps the most important advice for helping athletes manage their blood glucose levels is to encourage each athlete to meticulously record glucose levels and the conditions that are present during different types of training or competition. As an adjunct to capillary glucose values, the use of CGM may help to inform a more complete understanding of an athlete’s glucose trends before, during, and following exercise; importantly, CGM also can help to reduce athletes’ fear of developing exerciseinduced hypoglycemia. Altogether, glycemic data help the athlete and his or her care provider recognize patterns of glucose control and implement nutritional or pharmacologic strategies during athletic activities to prevent hypoglycemia or hyperglycemia. A prototype glucose log for this purpose is shown in Fig. 18.3. In addition, multiple apps and websites are available to help athletes with diabetes. A particularly useful site is Excarbs, developed by a University of Toronto team led by professor Michael Riddell. Recreational athletes can enter values for current glucose and the time and dose of last insulin bolus taken, and the app will recommend either additional carbohydrates or reduction in insulin to prevent hypoglycemia.25

Training Versus Competition It has long been known that different intensities of athletic activity lead to different compensatory hormonal responses,26 including those of the counterregulatory hormones epinephrine, cortisol, and growth hormone. Shetty et al. studied nine adolescents and young adults with type 1 diabetes at four different exercise intensities on 4 separate days.27 At low-to-moderate exercise intensities, they observed that exogenous glucose was necessary to maintain euglycemia, whereas at high exercise intensities (VO2 peak >80%) exogenous glucose requirements were absent. Furthermore, athletes at every level of competition have anecdotally reported that insulin requirements and postevent glucose excursions are generally higher on days of actual competition compared with days of training, despite the fact that the same activity is performed for the same interval of time. Little information exists in the scientific literature to explain this phenomenon. Indeed, it would be difficult to test in a clinical laboratory setting. Even if the intensity or duration of athletic activity was closely replicated, it would be challenging to control for the emotional response or other psychological elements that accompany actual competition. It is important for athletes to be aware of this phenomenon, and with regular sporting activity, to make adjustments for it as they learn their own responses.

Glycemic Log for Athletic Events Date/Time

Event and Duration Training Competition

Basal insulin adjustment

Last insulin bolus/amount

Timing/CHO (g) last meal

Timing/CHO (g) Glucose Conditions during event Before During After (Temp, Altitude)

Fig. 18.3  A proposed log that athletes with diabetes can use to record parameters affecting glycemic control and athletic performance. CHO, Carbohydrate.

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Management of Type 1 Diabetes Although the American Diabetes Association has a position statement regarding exercise and diabetes management,28 no single guideline or source of recommendations is available that athletes with type 1 diabetes can follow for management of their disease during training or athletic competition. As one elite athlete commented, it is an “independent disease,” and each athlete must know how his or her body will respond during different types of athletic conditions.29 However, some basic treatment principles and monitoring strategies can be used. • Glucose target: Although the target glucose value must be determined for each individual athlete, a general recommendation would be to attempt to keep glucose levels between 100 and 180 mg/dL during training and competition. Values less than 100 mg/dL may place the athlete at risk for hypoglycemia during activity, and values greater than 180 mg/dL are above the renal threshold for glucose. The resultant osmotic diuresis may lead to additional loss of fluids and electrolytes. Most athletes believe that they compete best when their glucose values are in the middle-to-upper portion of this target range, which allows a gradual decrease to occur without significant risk for hypoglycemia during activity. Note that athletes who use a low-glucose suspend insulin pump may be able to set their target glucoses considerably lower because their theoretic risk for hypoglycemic should be reduced or eliminated. However, data regarding this outcome are limited only to clinical trials at this time. • Glucose monitoring: For athletes not utilizing CGM, capillary glucose levels should be checked before, during, and after training or competition. Until patterns are recognized, it is advisable to check at 15-minute intervals prior to exercising to determine the rate of change of blood glucose. This is especially important if the athlete has injected an insulin bolus for a meal or snack within the previous 3 hours. If possible, athletes should also check their glucose levels during exercise or competition to determine its effect. This task will clearly be less practical during actual competition, although sports such as tennis or golf that have breaks between play or team sports with scheduled breaks or the ability to substitute players make this task more feasible. Athletes competing in individual sports, especially endurance sports such as running, cycling, or swimming, may have more difficulty with this recommendation and should use the help of others to assist with monitoring at various points in the competition. Although CGM devices should provide a superior option, these devices may not perform as well during exercise as they do at rest.30 However, a study comparing accuracy of one sensor (Dexcom G4 Platinum) during moderate versus intermittent high-intensity exercise found that, despite significant differences in mean glucose, lactate, and pH levels, the sensor was comparably accurate at both levels of activity.31 For persons who do not want or are unable to obtain a CGM device, one can be prescribed by their health care provider for a 72-hour to 7-day diagnostic period. The device captures glucose levels every 5 minutes during this period, and a graphic printout is provided at its completion. Ideally the

athlete would wear the device during both a training session and competition to maximize its utility in determining patterns of glucose levels. Finally, it is important for athletes to recognize when they are most at risk for hypoglycemia after exercise. Typically the period of highest risk occurs 6 to 15 hours following exercise, when glycogen stores are repleted.32 By regularly checking glucose levels during this period, the athlete can know whether insulin administration should be reduced or additional carbohydrates should be consumed in the postexercise period. • Insulin administration: Athletes must consider the level of insulin in their system and its duration of action when planning athletic activity. Unless a sufficient amount of carbohydrate is consumed before or during activity, it is generally ill advised to take a bolus of insulin directly prior to training or competition. The duration of action for the short-acting insulin analogs is approximately 3 hours, and the risk of hypoglycemia should be reduced if athletic activity is performed outside of this time frame. In addition, one must consider that once it is injected or infused, insulin will be bound to its receptor and biologically active for approximately 30 minutes. Therefore athletes should avoid reducing or suspending insulin pump basal rates immediately before an athletic event but rather should do so approximately 30 minutes beforehand. For new athletes or athletes beginning a new activity, basal insulin might be reduced by 50% before and during the activity until glucose patterns can be determined and a more tailored adjustment can be made. This should help prevent hypoglycemia during the event and help the athlete to avoid finishing the event with significant hyperglycemia. This objective is more easily accomplished with an insulin pump, and particularly so with sensor augmentation, meaning that when low-range glucoses are detected, the pump automatically suspends insulin infusion. Glycemic management is anticipated to be increasingly automated and safer with the emergence of closed-loop artificial pancreas systems. In research settings, artificial pancreas systems are being adapted to include mechanisms for detection of exercise. In a recent clinical trial, closed-loop systems integrated with heart rate detection appeared to improve adolescents’ glycemic management during exercise, specifically by reducing the amount of exercise time with glucose levels less than 70 mg/ dL.33 As the exercise detection mechanisms and functional algorithms for artificial pancreas systems are optimized, the artificial pancreas is anticipated ultimately to become the standard of care for athletes with insulin-dependent diabetes. Particularly, it should benefit those with a propensity to become hypoglycemic or hyperglycemic during and after activity. Comparatively, with injections of long-acting insulins such as insulin glargine or neutral protamine Hagedorn (NPH), additional carbohydrates may need to be consumed to counterbalance the effect of exogenous insulin (see the next section). As mentioned previously, glucose levels during and after intense competition are likely to be higher than those encountered during training, but use of additional basal insulin should be considered only after the athlete is confident of his or her individual glucose patterns during these times.

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• Carbohydrate consumption: In the authors’ experience in working with athletes who have diabetes, carbohydrate consumption is the area of most personal variability between individuals. Some athletes make adjustments to their insulin and will not require any additional carbohydrates before or during competition. Others will consume a small snack immediately prior to activity: in a survey of 91 adult endurance athletes with type 1 diabetes, 37% reported consuming preexercise carbohydrate snacks most or all of the time.34 Still others will use fast-acting glucose in the form of tablets, gels, or sports drinks at regular intervals while training or competing. In general, carbohydrates should be consumed shortly after exercise to prevent early postactivity hypoglycemia.35 Athletes should record both the type and amount of carbohydrate consumed to determine its effect on glucose levels during and after athletic activity. Of note, one study demonstrated that more carbohydrates should be consumed on the day after exercise to prevent hypoglycemia.36 Because this is beyond the expected period of glycogen repletion, it suggests that any increase in insulin sensitivity gained from exercise can be prolonged. Finally, the combination of CGM and an individualized algorithm for carbohydrate intake was shown to be effective in preventing hypoglycemia in children and adolescents involved in athletic activities at a summer camp.37 It is possible that strategies for athletic activity can be optimized by utilizing several treatment modalities at once (both for monitoring and adjusting glucose). • Monitoring ketones: In most situations, ketones do not need to be routinely monitored by athletes with diabetes. However, because athletic activity can worsen ketoacidosis in persons with very poor glycemic control, a general recommendation is to check urine ketones if capillary blood glucose is 250 mg/ dL or greater. If ketones are present, athletic activity should be postponed until glucose levels are lowered and ketonuria is resolved. For additional recommendations on managing athletes with type 1 diabetes from the viewpoint of the athletic trainer, see the comprehensive review by Jimenez et al.38

Management of Type 2 Diabetes Although patients with type 2 diabetes are generally sedentary and obese, they are occasionally both fit and athletic. It is the relative lack of insulin that leads to hyperglycemia, and this condition can occur with any body habitus. For patients with type 2 diabetes who are embarking on a new exercise program or athletic activity, several points should be kept in mind. • Risk of hypoglycemia: Although athletes with type 2 diabetes are more resistant to the effects of insulin than those with type 1 diabetes, any oral agent that increases endogenous insulin secretion or exogenous insulin injections can increase the risk for hypoglycemia if not properly managed. Therefore athletes with type 2 diabetes, especially those who are already at their ideal body weight, should use the same strategies previously listed for patients with type 1 diabetes. They should also log glucose levels and conditions and regularly analyze the recorded results to determine if and when nutritional or

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pharmacologic therapies need to be modified in the setting of athletic activity. • Screening for cardiovascular disease: Patients with type 2 diabetes and those with type 1 diabetes who have long-standing disease (>20 years) or microvascular complications are at increased risk for undiagnosed cardiovascular disease. Before the start of any new exercise or athletic activity, a complete medical evaluation should be performed and formal graded exercise testing should be considered for persons initiating more intense activities.39 Athletes with diabetes may take statins for primary cardiovascular risk reduction or in the setting of known cardiovascular disease. These athletes should not be discouraged from using an indicated statin or be restricted in appropriately planned exercise. For athletes engaging in training that gradually increases in intensity, muscular metabolic adaptation appears to reduce the risk of statin-induced muscle injury.40 Statin users who engage in vigorous exercise without appropriate training may be at heightened risk of rhabdomyolysis.41 • Weight loss: For athletes who weigh more than their ideal body weight, regular exercise should promote weight loss. Gradual modifications to the athlete’s pharmacologic and nutritional regimen may be needed to prevent hypoglycemia as the athlete becomes more insulin sensitive. In some cases, pharmacologic treatment may be discontinued altogether.

Additional Considerations for Elite Athletic Competition in Persons With Type 1 Diabetes In the authors’ experience, most athletes with type 1 diabetes who are engaged in recreational, high school, or collegiate sports are most concerned about becoming hypoglycemic during competition. The most common strategy is to allow or induce hyperglycemia, either by consuming extra carbohydrates with no insulin coverage or by reducing or withholding insulin. Experiencing a hypoglycemic event in the midst of competition would no doubt diminish performance. However, for the elite or professional athlete, significant or modest hyperglycemia could also be detrimental during athletic competition. Moreover, when an elite level of competition demands the most perfect of conditions, even mild hyperglycemia could negatively impact performance. There remains a notable lack of scientific investigation and clinical guidelines for glucose management during elite competition in athletes with diabetes. Individual elite athletes, often with teams of nutritionists, personal trainers, and exercise physiologists, are primarily responsible for determining the balance of insulin and nutrition that allows them to optimally train, compete, and recover from competition.

SUMMARY Athletes with diabetes mellitus face several challenges when training for and competing in athletic activity. To avoid hypoglycemia and hyperglycemia, many variables must be considered and adjusted to keep glucose levels in an optimal range, which is especially important because exercise itself significantly affects glucose levels. All persons involved with an athlete who has diabetes, including health care providers, coaches, athletic trainers,

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and most importantly, the athlete, must understand the basic principles of exercise physiology and the different types of medications used in the treatment of diabetes. This understanding is especially important as more children, adolescents, and young adults are diagnosed with diabetes. Despite significant challenges encountered during training and competition, performing well in athletic activity is very possible for athletes with diabetes. It is hoped that with continued technologic advancement, both in the arena of CGM and in the delivery of insulin, including the long-anticipated development of an artificial pancreas,42 the challenges faced by athletes with diabetes will continue to diminish.

ACKNOWLEDGMENT The authors thank their patients who have shared their many experiences with exercise and athletic competition over the years. For a complete list of references, go to ExpertConsult.com.

whether the degree of glycemic control is more responsible for aberrations in exercise physiology.

Citation: Jimenez CC, Corcoran MH, Crawley JT, et al. National Athletic Trainers’ Association position statement: management of the athlete with type 1 diabetes mellitus. J Athl Train. 2007;42:536–545.

Level of Evidence: V

Summary: This article includes useful recommendations for the athletic trainer who works with patients with type 1 diabetes. In addition to providing practical suggestions regarding supplies to carry and guidelines for travel, the recommendations focus on unique management issues for athletes with type 1 diabetes such as preparticipation physicals and healing of injuries.

Citation: Blauw H, Keith-Hynes P, Koops R, et al. A review of safety and design requirements of the artificial pancreas. Ann Biomed Eng. 2016;44:3158–3172.

SELECTED READINGS Citation: Baldi JC, Cassuto NA, Foxx-Lupo WT, et al. Glycemic status affects cardiopulmonary exercise response in athletes with type 1 diabetes. Med Sci Sports Exerc. 2010;42:1454–1459.

Level of Evidence:

Level of Evidence:

This article provides an updated and comprehensive review of the history, ongoing investigation, and expected future use of the technologies being applied to the development of a closed-loop system in the management of blood glucose.

V

Summary: This study is an important investigation into whether the underlying condition of diabetes negatively affects athletic performance or

V

Summary:

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REFERENCES 1. International Association of Diabetes in Pregnancy Study Groups Consensus Panel. International Association of Diabetes in Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care. 2010;33:676–682. 2. Geiss LS, Wang J, Cheng YJ, et al. Prevalence and incidence trends for diagnosed diabetes among adults aged 20 to 79 years, United States, 1980-2012. JAMA. 2014;312(12):1218–1226. 3. Centers for Disease Control and Prevention. National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014. Atlanta: US Department of Health and Human Services; 2014. 4. American Diabetes Association. Executive summary: standards of medical care in diabetes—2012. Diabetes Care. 2012; (suppl 1):54–60. 5. Diabetes Care. 2017;40(suppl 1):11–24. 6. Ziemer DC, Kolm P, Weintraub WS, et al. Glucose-independent, black-white differences in hemoglobin A1c levels: a crosssectional analysis of 2 studies. Ann Intern Med. 2010;152:770. 7. http://www.ajmc.com/newsroom/endocrine-society-endorsescgm-as-gold-standard-for-adults-with-type-1-diabetes. Accessed March 2017. 8. Laffel L. Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev. 1999;15:412–426. 9. Evert AB, Boucher JL, Cypress M, et al. Nutrition therapy recommendations for the management of adults with diabetes. Diabetes Care. 2013;36(11):3821–3842. 10. Heerspink JHJL, Perkins BA, Fitchett DH, et al. Sodium glucose co-transporter 2 inhibitors in the treatment of diabetes mellitus: cardiovascular and kidney effects, potential mechanisms, and clinical applications. Circulation. 2016;134:752–772. 11. U.S. Food and Drug Administration. The 670G System P160017. http://www.fda.gov/MedicalDevices/Productsand MedicalProcedures/DeviceApprovalsandClearances/Recently -ApprovedDevices/ucm522764.htm. Accessed February 15, 2017. 12. Vranic M, Berger M. Exercise and diabetes mellitus. Diabetes. 1979;28:147. 13. Lawrence RD. The effect of exercise on insulin action in diabetes. BMJ. 1926;1:648. 14. Farrannini E, Linde B, Faber O. Effect of bicycle exercise on insulin absorption and subcutaneous blood flow in the normal subjects. Clin Physiol. 1982;2:59–70. 15. Gerich JE, Langlois M, Naocco C, et al. Lack of glucagon response to hypoglycemia in diabetes: evidence for an intrinsic pancreatic alpha cell defect. Science. 1973;182:171–173. 16. Gusso S, Hofman P, Lalande S, et al. Impaired stroke volume and aerobic capacity in female adolescents with type 1 and type 2 diabetes mellitus. Diabetologia. 2008;51:1217–1320. 17. Komatsu WR, Chacra AR, Barros Neto TL, et al. Aerobic exercise capacity and pulmonary function in athletes with and without type 1 diabetes. Diabetes Care. 2010;33:2555–2557. 18. Wheatley CM, Baldi JC, Cassuto NA, et al. Glycemic control influences long membrane diffusion and oxygen saturation in exercise-trained subjects with type 1 diabetes. Eur J Appl Physiol. 2011;111:567–578. 19. Peltonen JE, Koponen AS, Pullinen K, et al. Alveolar gas exchange and tissue deoxygenation during exercise in type 1 diabetes patients and healthy controls. Respir Physiol Neurobiol. 2012;181(3):267–276.

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20. Baldi JC, Cassuto NA, Foxx-Lupo WT, et al. Glycemic status affects cardiopulmonary exercise response in athletes with type 1 diabetes. Med Sci Sports Exerc. 2010;42:1454–1459. 21. Nguyen T, Obeid J, Walker RG, et al. Fitness and physical activity in youth with type 1 diabetes mellitus in good or poor glycemic control. Pediatr Diabetes. 2015;16(1):48–57. 22. Tiedeman JS, Kirk SE, Srinivas S, et al. Retinal oxygen consumption during hyperglycemia in patients with diabetes without retinopathy. Ophthalmology. 1998;105: 31–36. 23. Veves A, Saouaf R, Donaghue VM, et al. Aerobic exercise capacity remains normal despite impaired endothelial function in the micro- and macrocirculation of physically active IDDM patients. Diabetes. 1997;46:1846–1852. 24. Zinman B, Zuniga-Guajardo S, Kelly D. Comparison of the acute and long-term effects of exercise on glucose control in type I diabetes. Diabetes Care. 1984;7:515–519. 25. http://www.excarbs.com, Accessed June 2017. 26. Kinderman W, Schnable A, Schmitt WM, et al. Catecholamines, growth hormone, cortisol, insulin, and sex hormones in anaerobic and aerobic exercise. Eur J Appl Physiol. 1982;49: 389–399. 27. Shetty VB, Fournier PA, Davey RJ, et al. Effect of exercise intensity on glucose requirements to maintain euglycemia during exercise in type 1 diabetes. J Clin Endocrinol Metab. 2016;101(3):972–980. 28. Colberg SR, Sigal RJ, Yardley JE, et al. Physical activity/exercise and diabetes: A position statement of the American Diabetes Association. Diabetes Care. 2016;39(11):2065–2079. 29. Personal communication, Sean Busby, 2012. 30. Taleb N, Emami A, Suppere C, et al. Comparison of two continuous glucose monitoring systems, Dexcom G4 Platinum and Medtronic Paradigm Veo Enlite system, at rest and during exercise. Diabetes Technol Ther. 2016;18(9):561–567. 31. Bally L, Zueger T, Pasi N, et al. Accuracy of continuous glucose monitoring during different exercise conditions. Diabetes Res Clin Pract. 2016;112:1–5. 32. MacDonald M. Postexercise late-onset hypoglycemia in insulin-dependent diabetic patients. Diabetes Care. 1987;10(5):584–588. 33. DeBoer M, Cherñavvsky D, Topchyan K, et al. Heart rate informed artificial pancreas system enhances glycemic control during exercise in adolescents with T1D. Pediatr Diabetes. 2016;doi:10.1111/pedi.12454. 34. Devadoss M, Kennedy L, Herbold N. Endurance athletes and type 1 diabetes. Diabetes Educ. 2011;37(2):193–207. 35. Nathan DM, Madnek SF, Delahanty L. Programming preexercise snacks to prevent post-exercise hypoglycemia in intensively treated insulin-dependent diabetics. Ann Intern Med. 1985;102:483–486. 36. Galassett P, Mann S, Tate D, et al. Effect of morning exercise on counterregulatory responses to subsequent afternoon exercise. J Appl Physiol. 2001;91:91–99. 37. Riddell MC, Milliken J. Preventing exercise-induced hypoglycaemia in type 1 diabetes using real-time continuous glucose monitoring and a new carbohydrate intake algorithm: an observational field study. Diabetes Technol Ther. 2011;13: 819–825. 38. Jimenez CC, Corcoran MH, Crawley JT, et al. National Athletic Trainers’ Association position statement: management of the athlete with type 1 diabetes mellitus. J Athl Train. 2007;42: 536–545.

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39. American Diabetes Association. Physical activity/exercise and diabetes. Diabetes Care. 2004;27:S58–S62. 40. Bouitbir J, Daussin F, Charles AL, et al. Mitochondria of trained skeletal muscle are protected from deleterious effects of statins. Muscle Nerve. 2012;46(3):367–373.

41. Antons KA, Williams CD, Baker SK, et al. Clinical perspectives of statin-induced rhabdomyolysis. Am J Med. 2016;119(5):400. 42. Blauw H, Keith-Hynes P, Koops R, et al. A review of safety and design requirements of the artificial pancreas. Ann Biomed Eng. 2016;44:3158–3172.

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19  Renal Medicine and Genitourinary Trauma in the Athlete Stefan Hemmings, Derek M. Fine

Trauma to the genitourinary (GU) tract is relatively uncommon because of the anatomic location of key internal GU organs, the kidneys and bladder. However, prompt recognition of the signs and symptoms associated with GU trauma will allow the clinician to order appropriate imaging tests and implement therapeutic plans that can save organs and even a person’s life.

DEFINITION (CLASSIFICATIONS) Table 19.1 summarizes the classification of kidney trauma injuries according to severity. This classification correlates with the need for surgical intervention.1

EPIDEMIOLOGY Of all the GU organs, the external genitalia (penis, scrotum, and vulva) are most likely to be injured. Of the internal GU organs, the kidneys are the most likely to be injured after a patient experiences abdominal trauma.2 Overall, the most common sport causing abdominal injury is cycling. Football, rugby, gymnastics, horseback riding, wrestling, martial arts, and hockey are a few of the sports that include activities capable of causing significant abdominal and consequent GU organ injury; the use of exercise equipment can do so as well.3,4 The overall incidence of renal injury as a result of trauma ranges from 1.4% to 3.25%.5 Sports-related trauma to the kidney is uncommon and is reported to constitute only 15% to 20% of all traumatic renal injuries.6 Most cases of renal trauma are the result of blunt trauma specifically relating to motor vehicle accidents and falls.5 Kidney injuries are particularly common when a person is subjected to rapid deceleration forces. One analysis shows that of the 23,666 sports-related injuries among high school–age varsity athletes, only 18 kidney injuries were reported, none of which was serious.4 In an analysis of more than 653,000 trauma cases from the National Trauma Data Bank, 16,585 were identified as trauma from bicycle injuries.7 Only 2% of the patients in these cases experienced a GU tract injury, with the kidneys being the organ most likely affected (in 75% of cases), followed by the bladder and urethra (in 15% of cases) and the penis and scrotum (in 10% of cases). Sixty percent of the patients with GU injuries had evidence of concomitant fractures of the spine or pelvis, suggesting that isolated GU trauma is uncommon.7 Compared with renal injuries, testicular injuries in sports occur

at a much lower rate. A review of a trauma registry of all cases of renal and testes injuries (1.4% of all injuries) showed that 92% involved the kidneys and 8% the testes.8 It is estimated that more than half of injuries to the testes occur during sporting events.9

PATHOBIOLOGY/PATHOPHYSIOLOGY The kidneys are located in the retroperitoneal space and are surrounded by visceral fat and the Gerota fascia. The kidneys lie on either side of the spinal column in front of the psoas muscle and medial to the quadratus lumborum muscle. The hepatic flexure of the colon on the right and the spleen and the splenic flexure on the left cover the kidneys anteriorly. Because the kidneys are protected by surrounding structures, traumatic kidney injuries during sporting activities occur mainly in association with major forces and are usually associated with injury to other organs. Injuries to the renal parenchyma constitute the vast majority of cases. Preexisting renal abnormalities such as hydronephrosis, renal cysts, or an abnormal renal anatomic position increase the likelihood of renal injury during trauma and are reported in 4% to 19% of adults and 12% to 35% of children.5,10-–12 These subjects have more severe symptoms and are more likely to require surgical intervention.10–12 Vascular injuries of the kidneys occur during deceleration forces and result from damage to the renal pedicle. These cases may present with thrombosis or rupture of the vasculature. Bladder injuries also occur as a consequence of blunt force trauma to the abdomen. The bladder’s anatomic location deep in the anterior bony pelvis makes it less frequently injured by trauma. However, the weakest part of the bladder is the dome, which is mobile and susceptible to injury when the bladder is full. The testes are particularly vulnerable to trauma because of their external location and lack of anatomic protection when blunt trauma forces the scrotum against the pelvic bone. Testicular rupture, scrotal wall hematoma, or intrascrotal hematocele are possible.13

DIAGNOSIS Obtaining a thorough history is imperative. The initial evaluation of patients should include attention to vital signs recorded on the field and upon arrival at the hospital. The lowest recorded

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CHAPTER 19  Renal Medicine and Genitourinary Trauma in the Athlete

Abstract

Keywords

Trauma to the genitourinary (GU) tract is relatively uncommon because of the anatomic location of key internal GU organs, the kidneys and bladder. However, prompt recognition of the signs and symptoms associated with GU trauma will allow the clinician to order appropriate imaging tests and implement therapeutic plans that can save organs and even a person’s life. Blunt trauma, often in the context of rapid deceleration, is the usual cause of kidney and bladder injury. Due the location of the kidneys, their injury is usually accompanied by simultaneous injury to other abdominal organs or bone fractures (spine and ribs). Hematuria is the most common presenting feature and should trigger evaluation of the GU tract. Although any hematuria should raise concern, gross hematuria is of particular concern. The presence of ascites in the context of abdominal trauma may be due to bladder perforation and associated urinary ascites. GU trauma may also be associated with renal metabolic complications including acute kidney injury, hyponatremia, and rhabdomyolysis. Although these are infrequent, they may be life threatening and should be considered given the appropriate presentation.

ascites bladder injury genitourinary tract trauma hematuria kidney injury kidney transplant solitary kidney

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TABLE 19.1  Organ Injury Severity Scale

for the Kidney (American Association for the Surgery of Trauma) Grade

Type

Description

I

Contusion

Microscopic or gross hematuria; urologic studies normal Subcapsular and nonexpanding without parenchymal laceration Nonexpanding perirenal hematoma confined to the renal retroperitoneum Less than 1 cm parenchymal depth of renal cortex without urinary extravasation Greater than 1 cm parenchymal depth of renal cortex without collecting system rupture or urinary extravasation Parenchymal laceration extending through the renal cortex, medulla, and collecting system Main renal artery or vein injury with contained hemorrhage Completely shattered kidney Avulsion of the renal hilum, devascularizing the kidney

Hematoma II

Hematoma Laceration

III

Laceration

IV

Laceration

Vascular V

Laceration Vascular

From Santucci RA, McAninch JW, Safir M, et al. Validation of the American Association for the Surgery of Trauma organ injury severity scale for the kidney. J Trauma. 2001;50:195–200.

Imaging Imaging studies specifically focused on the GU tract are required for all patients with rapid deceleration as the mechanism of blunt trauma (e.g., a motor vehicle accident or fall from a height), patients with hypotension, adults with gross hematuria, and children with microscopic hematuria.15 Hemodynamically stable patients with only microscopic hematuria may not require further imaging but should undergo a thorough follow-up evaluation for potentially harmful delayed effects of trauma.16 An abdominal computed tomography (CT) scan with use of intravenous contrast is the imaging modality of choice in patients with trauma to the GU tract. In one series, the most common findings on CT were perirenal hematoma (29.4%), intrarenal hematoma (24.7%), and parenchymal disruption (17.6%).17 Measurement of serum electrolytes and serum creatinine is useful in guiding diagnostic and treatment plans. Contrast should be avoided in those with severely reduced renal function, although emergent situations may necessitate its use. For suspected bladder injury, CT and plain retrograde cystography are equivalent imaging modalities that would demonstrate extravasation of contrast.18 Early diagnosis is essential for testicular salvage when there is trauma to the scrotum, the likelihood of which decreases with time. Scrotal ultrasonography is a safe, noninvasive, and valuable tool for rapid detection of testicular rupture, hematocele, hematoma, or traumatic torsion.13

Differential Diagnosis systolic blood pressure may indicate the need for radiologic assessment of subjects for a kidney injury. Careful examination of the abdomen, chest, and back is critical. Patients with evidence of abdominal or flank tenderness or hematoma, rib fractures, and penetrating injuries to the low thorax or flank may have sustained an injury to the kidney and require further assessment. Pelvic fractures in trauma may alert the physician to the potential of bladder injury. Increasing abdominal girth with “ascites” without hemodynamic instability and without a drop in hemoglobin levels should be cause for suspicion, as the diagnosis can be delayed.14 Persons with a testicular injury usually present with swelling, tenderness, and ecchymosis. Rupture of the testis is associated with immediate severe pain.13

Laboratory Findings Hematuria, either microscopic or gross, is the best indicator of injury to the urinary tract after trauma. Although hematuria is seen in 80% to 90% of cases of kidney trauma, lack of hematuria does not eliminate the possibility; therefore a high degree of clinical suspicion should be maintained if the mechanism of injury suggests renal trauma. In addition, the degree of hematuria may not correlate with the degree of injury. However, in general, gross hematuria associated with blunt trauma increases the likelihood of major injury. A rising serum creatinine in the absence of anuria/oliguria, especially in the context of ascites, could indicate bladder injury with intraperitoneal/intraabdominal urinary leak, as urinary ascites is resorbed across the peritoneum.

Exercise-induced hematuria is a relatively common, benign finding among athletes. The incidence ranges between 50% and 80%, with the highest incidence reported among swimmers, track athletes, and lacrosse players.19 A thorough medication history is critical, particularly for use of nonsteroidal inflammatory drugs (NSAIDs). In one study, more than half of the athletes with idiopathic hematuria regularly used NSAIDs.20 Preexisting glomerular or cystic kidney disease may be the source of microscopic hematuria and must be differentiated from trauma-induced hematuria. The presence of proteinuria may suggest a preexisting glomerular lesion.

TREATMENT A detailed discussion of specific surgical management is beyond the scope of this chapter. However, awareness of the following therapeutic considerations is important: 1. Surgical exploration of the kidney is required in cases with severe, persistent, or life-threatening renal hemorrhage, pedicle avulsion, or an expanding retroperitoneal hematoma.5 2. A nephrectomy may be required in persons who have sustained severe trauma and in unstable patients. However, patients who are more stable, especially those with a solitary kidney or with bilateral injuries, may be candidates for renovascular repair and reconstruction or the angioembolization of bleeding vessels.5 3. Hemodynamically stable patients who do not have hematuria and even patients with microscopic hematuria can be managed conservatively with careful monitoring.

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4. Vigorous hydration to dilute gross hematuria will facilitate the avoidance of clot formation and the potential for urinary obstruction. 5. Immediate surgical exploration is suggested for patients with testicular trauma when testicular rupture is suspected.13 6. Surgical intervention is recommended for complicated intra- or extraperitoneal bladder injury and conservative management with Foley catheter drainage for uncomplicated extraperitoneal injuries.18

RETURN-TO-PLAY GUIDELINES No specific guidelines are available to dictate the timing for a return to maximal activity after GU trauma; thus prudent decisions should take into account the severity of the injury and the required recovery period. Contact sport activities such as football should be avoided for a longer period during recovery, and specific protective padding to shield the flank regions may be indicated. Recommendations for safe athletic participation in special populations have been controversial. For example, athletes with either a single kidney or those who have undergone a kidney transplant are intuitively considered at higher risk for the effects of GU trauma. However, the American Academy of Pediatrics recommends a “qualified yes” for participation in contact/collision sports by athletes with a single kidney.21 Despite this recommendation, most physicians continue to discourage participation in contact/collision sports for patients with a single kidney.22 Patients who have had a renal transplant are also believed to be at higher risk for trauma to the allograft because of the unique location of the allograft in the preperitoneal space. Despite the potential for increased risk of trauma to the allograft, few actual reports of such trauma have surfaced, and the medical literature does not include any reports of allograft loss due to trauma.23,24 Given the risk of severe consequences with allograft trauma, the general consensus is that contact sports should be avoided altogether by patients who have undergone renal transplantation.24 Individual decisions should be made for other sports that have a theoretical reduced risk of injury, such as basketball, mountain biking, and other sports.

METABOLIC PROBLEMS IN RENAL SPORTS MEDICINE Acute Kidney Injury, Hyponatremia, and Rhabdomyolysis Acute kidney injury (AKI) is not an infrequent occurrence in endurance sports. In one study, 83.6% of 28 ultramarathon runners developed AKI with elevations in serum creatinine levels after the race concluded, but recovery of renal function was quick, within 24 hours. Dehydration and rhabdomyolysis are notable risk factors for AKI in endurance events.25 Acute hyponatremia (serum sodium pain No spasm (tetany) Alert, may become listless, rapid breathing Normal Often occurs early in training session

ExerciseAssociated Muscle Cramps Cramping pain ≥ weakness, spasm Listless, irritable, may become combative Normal or elevated Nearly always occurs late in training session

See references 57, 58.

Return to Play Our RTP criteria are listed in Box 21.3.38,54,55

Prevention ER can be prevented by gradually increasing training intensity and volume, and by ensuring adequate hydration and recovery between exercise bouts. ER has occurred in persons involved in activities, such as physical education, band, cheerleading, drill team, and Reserve Officers’ Training Corps, especially when excessive exercise is used as a reprimand. Persons involved in these activities should be provided free access to water and sufficient rest during exercise, and they should be educated about symptoms and signs of heat illness and muscle injury.

have a 37 to 67 times higher risk of exertion-related death compared with non-SCT athletes.5,56 Heat stress, dehydration, and intense exercise especially at high altitude can cause severe hypoxemia, acidosis, hyperthermia, and red cell dehydration, which may induce sickling of red blood cells, leading to ESC.57,58 Persons with SCT appear to be at greatest risk when they perform short bursts of repetitive, highintensity activity (e.g., sprints), especially during the preseason when they be deconditioned.

Diagnosis

Pathophysiology

Athletes who experience ESC have sudden onset of extreme weakness and may collapse on the field, appearing anxious, and tachypneic. Features that help distinguish an athlete with ESC from an athlete with exercise-associated muscle cramps are outlined in Table 21.1.58

Sickle cell trait (SCT) is defined as the presence of 30% to 40% hemoglobin-S. Persons with SCT are normally asymptomatic. SCT occurs in 7% to 10% of African Americans and is common in persons of Mediterranean ancestry. Football players with SCT

Laboratory Findings The presence and percentage of sickle hemoglobin (HgbS) is determined by hemoglobin electrophoresis. In the acutely ill

EXERTIONAL SICKLING COLLAPSE

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athlete, a complete blood cell count reveals anemia, and a blood smear reveals classic sickled red blood cells. Acutely, arterial blood gas findings reveal a partially compensated metabolic acidosis (low carbon dioxide, high pH, and increased anion gap). Muscle CPK is elevated and may continue to rise, akin to elevations observed in persons with ER.

Differential Diagnosis Conditions that may mimic ESC include collapse from cardiac abnormalities (conduction or structural), asthma, heat exhaustion, or EHS. Cardiac arrest or heat stroke are unconscious or obtunded, whereas an athlete who collapses with ESC is usually lucid.58

Treatment An athlete with suspected SCT-associated ER should not be allowed to perform any further exercise that day. EMS should be summoned and the athlete’s condition should be treated as a “medical emergency.” On-field measures should include oral rehydration, removal of the athlete to a cool environment, and the expeditious use of supplemental oxygen and IV fluids if available.

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treat EAMC.64,65 The syndrome of inappropriate antidiuretic hormone secretion (SIADH) will cause fluid retention when diuresis is needed. Tightly regulated osmotic control of body fluids can be overridden by nonosmotic stimuli, including nausea/vomiting, pain, exercise, elevated body temperature.66-70 Much less frequently, EAH can be related to excessive sweat sodium losses with relatively normal fluid replacement with hypotonic fluid.59

Diagnosis Increased body weight with decreased production of urine in an endurance athlete with the symptoms described above, especially with adequate water consumption, should raise suspicion of EAH.

Laboratory Findings Clinical suspicion of EAH should prompt evaluation of a basic metabolic panel. Mild or asymptomatic cases usually have a serum Na between 130 to 135 mmol/L while more severe cases are ≤129 mmol/L. Associated elevation urine osmolality indicates SIADH.

For general guidelines, medical staff may refer to the guidelines for RTP after ER (see Box 21.3).38,54,55

Differential Diagnosis Altered mental status associated with exercise may be caused alternatively by EHS, HS, or EAC, head trauma, seizure, drug ingestion, and diabetic ketoacidosis.

Prevention

Treatment

The sickle trait status should be known in all athletes born in states that mandate determination of hemoglobin status as part of the newborn metabolic screen. Universal screening for sports beyond the newborn period is controversial.58 Currently, the NCAA mandates screening of all athletes entering collegiate programs.56 In other settings, selective screening of high-risk groups, particularly African Americans, may be warranted. Athletes with SCT should be counseled to set their own pace, slowly build-up training with longer recovery between exercise bouts, maintain good hydration, avoid extreme performance tests, and to stop exercising immediately if they experience unusual muscle pain or weakness.58 The authors feel these guidelines should apply to all athletes regardless of whether their sickle trait status is known.

In mild cases, fluid restriction with free access to salty snacks and broth will prevent the progression to more severe hyponatremia. Reestablishment of the body’s homeostatic mechanisms is indicated with improving serum Na and the production of dilute urine. In severe cases with significantly altered mental status, an IV bolus of 100 mL 3% hypertonic saline should be given and can be repeated twice at 10-minute intervals for lack of clinical improvement.67 Rapid correction of serum Na in EAH poses minimal risk for central pontine myelinolysis, which is seen with rapid correction of chronic hyponatremia.59

Return to Play

EXERCISE-ASSOCIATED HYPONATREMIA Pathophysiology Exercise-associated hyponatremia (EAH) is defined as the serum sodium (Na) below normal reference values (usually 135 mmol/L) during or 24 hours following physical activity.59 EAH has been most frequently reported in endurance athletes, but has also been reported in the soldiers, hikers, and football players.60-63 EAH has a spectrum of severity from mild cases complaining of nausea, dizziness, and “not feeling right” to vomiting, headaches, and confusion, and ultimately to coma, seizures, pulmonary edema, and death. The most common etiology of EAH is exercising while over hydrating, which may be related to lack of education about proper hydration or attempts to

Return to Play The athlete with EAH may return to activity when asymptomatic, the serum Na is normal, and urine production is normal. Proper hydration practices must be instituted and exercise should be done at a moderate intensity and duration, at least during the initial 1 to 2 weeks, avoiding extreme environmental conditions.

Prevention Proper hydration is the best prevention and intervention. While some advocate drinking to thirst, replacing sweat loss using an individualized objective strategy will help novice athletes especially who may have difficulty in distinguishing thirst from fatigue. The sweat rate should be measured under different environmental conditions (Box 21.4). Secondary prevention can be achieved by measuring body weight before and after an event. Those who fail to lose weight during a marathon are seven times more likely to develop exercise-associated hyponatremia.65,70 Medical and

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BOX 21.4  Sweat Rate Measurement 1. Go to the bathroom and urinate/defecate if needed. 2. Towel off any sweat if needed. 3. Measure weight in minimal clothes/naked (PREWEIGHT). 4. Get dressed. 5. Perform planned exercise/practice for 1 hour with access to water in a container marked for volume. 6. Towel off any sweat. 7. Measure weight in minimal clothes/naked (POSTWEIGHT). 8. Measure the amount of fluid consumed (FLUID). SWEAT RATE FOR 1 HOUR = PREWEIGHT − POSTWEIGHT + FLUID

emergency response personnel should be educated about the possibility of EAH.

COLD INJURY Individuals participating in winter sports performed for a long periods at high levels of exertion are at an increased risk for cold injury, primarily hypothermia and frostbite.71-74

HYPOTHERMIA Pathophysiology Hypothermia, defined as a core body temperature of less than 35°C (95°F), is the most common cause of weather-related death, with individuals 65 years and older being at greatest risk.75-79 Mortality increases proportionately with the severity of the hypothermia.80 Dropping the core temperature results in nerve conduction delay, which leads to mental status changes, global depression of function, ataxia, and muscle stiffness. As hypothermia is neuroprotective, full neurologic recovery can occur even at remarkably low core temperatures.81-84 Hypothermia results in electrocardiogram (ECG) changes, including abnormal repolarization, atrial fibrillation, and the J wave (a positive deflection at the QRS and ST-segment junction).85,86 With dropping core temperature, there is sequential prolongation of the PR, QRS, and QT intervals.79 Vasoconstriction causes a relative hypervolemia, and leads to the “cold diuresis” that may in turn result in hypovolemia.

Heat Balance To avoid functional impairment in cold environments, core temperature must be maintained within a 4°C range by increasing heat production and decreasing heat loss. Body heat production, or thermogenesis, is achieved in four major ways.87 The resting (or basal) metabolic rate refers to energy expenditure at rest in a thermoneutral environment. During exercise 75% of muscle metabolic energy is released as heat, and 25% is converted to work. The absorption, breakdown, and storage of ingested food produce heat, called the “thermic effect,” and provides a minimal proportion of total body heat production.87 “Thermoregulatory thermogenesis” refers to shivering that can increase the metabolic rate up to five times the resting state.87-89 The amount of shivering is proportional to the amount of cold stress experienced, but can be maintained only

as long as glycogen stores are available.88 Shivering ceases at a core temperature of 30°C.82,84 About 90% of heat loss is through the skin, which is controlled by vasoconstriction. About 10% is lost through the lungs, which varies depending on the type and intensity of activity. Heat loss increases when an athlete is wet.85 Radiation accounts for about 60% of total heat loss.75 Radiation losses in children are higher due to their greater surface area-to-mass ratio.90

Other Factors Contributing to Thermal Balance Certain medical conditions such as hypothyroidism, hypoadrenalism, hypopituitarism, and diabetes can impair the body’s ability to produce heat.75,79,88 Altered heat balance occurs in the elderly, and in individuals with multiple sclerosis, Parkinson disease, certain skin conditions, and those taking certain drugs.75,91 Ethanol, the substance most commonly associated with hypothermia, leads to heat loss through peripheral vasodilation.75,91-93 Phenothiazine drugs impair shivering thermogenesis.94 Medications, such as benzodiazepines, barbiturates, and tricyclic antidepressants, decrease centrally mediated thermoregulation.95

Diagnosis The diagnosis of hypothermia requires an accurate and reliable measurement of the core temperature. An esophageal probe placed in the lower one-third of the esophagus is preferred if there is a secure airway. If an esophageal probe is not available or if the airway is not secured, an epitympanic probe is recommended, although these can give falsely low measurements in the field. Rectal or bladder thermometers should not be used until the patient is in a warm environment.82,84 Oral or axillary probes do not reliably reflect core temperature. In mild hypothermia (32°C to 35°C or 90°F to 95°F), the extremities are cool and pale, and performing fine movements of the hands is difficult. Shivering is evident. Neurologic exam reveals listlessness, confusion, disorientation, dysarthria, and ataxia. The person with moderate hypothermia (28°C to 32°C or 82°F to 90°F) exhibits markedly altered mental status, dysarthria, apathy, and amnesia. The mental status may deteriorate into stupor and coma. Deep tendon reflexes diminish and become absent. Vital signs become unstable; hypotension and bradycardia emerge. Shivering slows and ceases. Death will ensue without treatment.82,96 The person with severe hypothermia (90%

Rest, hydration, analgesics Descend as soon as possible to lowest possible altitude at which symptoms improve

Dexamethasone, load with 8 mg PO, IV, or IM, then 4 mg every 6 h If descent is delayed, add Acetazolamide 250 mg every 12 h

Nifedipine 10 mg by mouth initial dose, then 30 mg extended-release every 12 h Consider Salmeterol inhaled 125 µg every 12 h Consider dexamethasone if symptoms suggest HACE

2–6 L/min to maintain O2sat >90%

See references 116, 117, 120, 137, 139, 144, 145. a Arterial oxygen saturation. AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema; IM, intramuscular; IV, intravenous; LLS, Lake Louis Score; O2, oxygen; PO, per os (by mouth).

Laboratory Findings Arterial oxygen (O2) saturation less than 90% is characteristic of HAPE. Chest x-ray reveals engorgement of the pulmonary arteries and patchy infiltrates, although diffuse lung involvement may be seen in more severe cases. Arterial blood gas analysis reveals severe hypoxemia (30 to 40 mm Hg) and respiratory alkalosis.152 ECG may reveal right ventricular strain (e.g., rightaxis deviation and p-wave abnormalities) and a right bundle branch block.115 Differential Diagnosis Other causes of respiratory distress that may resemble HAPE include asthma, bronchitis, pneumonia, heart failure, myocardial infarction, and pulmonary embolus.

Treatment Treatment guidelines for HAPE are summarized in Table 21.2. Patients whose O2 saturation either fails to improve to 90% or greater who have evidence of HACE should descend immediately. Adding nifedipine, 30 mg by mouth twice a day, may be useful when either descent is not possible or oxygen is not available.152,155 The administration of high-dose salmeterol, five puffs (125 µg) twice a day may improve oxygenation.156

Return to Play Guidelines for RTP after AMS are applicable to persons with HAPE. Prophylaxis with dexamethasone, 8 mg twice a day, should commence 24 hours prior to ascent.157 Tadalafil, 10 mg by mouth twice a day, begun 24 hours prior to ascent, is almost as effective as dexamethasone in preventing HAPE.158 In a randomized controlled trial, nifidepine 30 mg twice a day afforded greater

reduction in HAPE recurrence than inhaled salmeterol 125 µg twice a day.156

Advice for the Team Physician Traveling to Altitude The physician accompanying a team to altitude for training or competition can implement measures to both minimize performance decrements and the risk of HAI. The team physicians and athletic training staff should review symptoms of HAI before traveling and regularly remind players to report symptoms, particularly headache, immediately.159 The strongest predictor of performance decrement at altitude is the HVR, a measure of how well the individual’s respiratory apparatus compensates for lower oxygen tension. Measuring the HVR could identify athletes who may require individualized acclimatization, but doing so requires special equipment, which is not always readily available. Athletes with positive risk factors for HAI, including a prior history of HAI, a history of migraine, a history of anemia or low iron stores, an increased BMI, and elevated blood pressure, should receive prophylaxis. Prophylaxis and treatment of HAI must be chosen with consideration of applicable antidoping regulations. Both dexamethasone and acetazolamide are on the World AntiDoping Agency (WADA) banned drug list.160 An acceptable prophylactic regimen is ibuprofen 600 mg by mouth 3 times/day begun 1 to 2 days before ascent for AMS.161 The authors recommend the coadministration of omeprazole 20 mg by mouth once daily to avoid gastritis. Prophylaxis of HAPE may consist of nifedipine or tadalafil. WADA allows a maximum daily dose of salmeterol of 200 µg, which also may be used for HAPE prophylaxis, equivalent to four puffs twice a day (which is 20% less than the

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recommended dose for prophylaxis).144,160 The team physician should always contemporaneously consult the latest applicable banned drug list. The ideal approach to guard against the effects of altitude would be to acclimatize. The use of techniques, such as intermittent hypoxemic exposure (IHE), intermittent hypoxemic training (IHT), and live high, train low (LHTL), have been shown to improve the HVR, but require hypobaric or hypoxemia chambers that are not readily available to most teams.162 Recommended graded ascent acclimatization to altitudes above 3000 m consists of increasing sleep altitude by no more than 500 m to 600 m per day, and a day of rest for each additional 1000 m if possible.163 Augmenting carbohydrates, such as pushing a carbohydratecontaining sport drink instead of water, may help to prevent performance decrements and dehydration.164-167 Individuals with a history of anemia or low iron stores should have their iron status rechecked several weeks prior to travel to altitude and should begin supplemental iron accordingly. Reducing the intensity of workouts and increasing recovery periods in the first 1 to 2 days at altitude may allow partial acclimatization. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS

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International Commission for Mountain Emergency Medicine (ICAR MEDCOM). Scan J Traum Rescuc Emerg Med. 2016;24(1):111.

Level of Evidence: III

Summary: This paper provides an up-to-date review of the management and outcome of accidental hypothermia patients with and without cardiac arrest.

Citation: McIntosh SE, Dow J, Hackett PH, et al. Wilderness Medical Society. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite: 2014 update. Wilderness Environ Med. 2014;25(suppl 4):S43–S54.

Level of Evidence: III

Summary: Evidence-based guidelines from an expert panel convened by The Wilderness Medical Society on the prevention and treatment of frostbite. The paper reviews pertinent pathophysiology, and discusses primary and secondary prevention measures and therapeutic management.

Citation:

Citation: Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainer’s Association position statement: exertional heat illness. J Athl Train. 2015;59(9):986–1000.

Level of Evidence:

Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of acute altitude illness: 2014 update. Wilderness Environ Med. 2014;25:S4–S14.

Level of Evidence:

III

III

Summary: Evidence-based, best-practice recommendations for the prevention, recognition, and treatment of exertional heat illnesses (EHIs) and description of the relevant physiology of thermoregulation.

Summary:

Bergeron MF, Devore C, Rice SG. Council on Sports Medicine & Fitness and Council on School Health. Policy statement—climatic heat stress and exercising children and adolescents. Pediatrics. 2011;128(3):e741–e747.

Best practices guidelines from an expert panel convened by the Wilderness Medical Society for the prevention and treatment of acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema. These guidelines present the main prophylactic and therapeutic modalities for each disorder and provide recommendations about their role in disease management. Recommendations are graded based on the quality of supporting evidence.

Level of Evidence:

Citation:

III

Bärtsch P, Swenson ER. Clinical practice: acute high-altitude illnesses. N Engl J Med. 2013;368:2294–2302.

Citation:

Summary: Evidence-based summary of differences in response to exercise heat stress between child and adult athletes, with specific recommendations for avoiding heat illness for child athletes.

Level of Evidence:

Citation:

An evidence-based clinical guideline on high-altitude illness, including a review of formal guidelines, as well as authors’ expert recommendations.

Paal P, Gordon L, Strapazzon G, et al. Accidental hypothermia—an update: the content of this review is endorsed by the

III

Summary:

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REFERENCES Exertional Heat Illness 1. Nelson NG, Collins CL, Comstock D, et al. Exertional heatrelated injuries treated in emergency departments in the U.S., 1997-2006. Am J Prev Med. 2011;40(1):54–60. 2. Centers for Disease Control and Prevention. Nonfatal sports and recreation heat illness treated in hospital emergency departments—United States, 2001-2009. MMWR. 2011;60(29): 977–980. 3. Centers for Disease Control and Prevention. Heat illness among high school athletes—United States, 2005-2009. MMWR. 2010;59(32):1009–1013. 4. Kerr ZY, Casa DJ, Marshall SW, et al. Epidemiology of exertional heat illness among U.S. high school athletes. Am J Prev Med. 2013;44(1):8–14. 5. Boden BP, Breit I, Beachler JA, et al. Fatalities in high school and college football players. Am J Sports Med. 2013;41(5):1108–1116. 6. Liljegren JC, Carhart RA, Lawday P, et al. Modeling the wet bulb globe temperature using standard meteorological measurements. J Occup Environ Hyg. 2008;5:645–655. 7. Cramer MN, Jay O. Biophysical aspects of human thermoregulation during heat stress. Auton Neurosci. 2016;196:3–13. 8. Epstein Y, Roberts WO. The pathophysiology of heat stroke: an integrative view of the final common pathway. Scand J Med Sci Sports. 2011;21:742–748. 9. Montain SJ, Latzka WA, Sawka MN. Control of thermoregulatory sweating is altered by hydration level and exercise intensity. J Appl Physiol. 1995;79:1434–1439. 10. Armstrong LE, Lopez RM. Return to exercise training after heat exhaustion. J Sport Rehabil. 2007;16(3):182–189. 11. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainer’s Association position statement: exertional heat illness. J Athl Train. 2015;59(9):986–1000. 12. Davis JM, Burgess WA, Slentz CA, et al. Fluid availability of sports drinks differing in carbohydrate type and concentration. Am J Clin Nutr. 1990;51:1054–1057. 13. Fallowfield JL, Williams C, Singh R. The influence of ingesting a carbohydrate-electrolyte beverage during 4 hours of recovery on subsequent endurance capacity. Int J Sport Nutr. 1995;5(4): 285–299. 14. Galloway SD, Maughan RJ. The effects of substrate and fluid provision on thermoregulatory and metabolic responses to prolonged exercise in a hot environment. J Sports Sci. 2000;18(5):339–351. 15. Osterberg KL, Pallardy SE, Johnson RJ, et al. Carbohydrate exerts a mild influence on fluid retention following exerciseinduced dehydration. J Appl Physiol. 2010;108:245–2010. 16. Anastasiou CA, Kavouras SA, Arnaoutis G, et al. Sodium replacement and plasma sodium drop during exercise in the heat when fluid intake matches fluid loss. J Athl Train. 2009;44(2):117–123. 17. Wemple RD, Morocco TS, Mack GW. Influence of sodium replacement on fluid ingestion following exercise-induced dehydration. Int J Sport Nutr. 1997;7(2):104–116. 18. Armstrong LE, Casa DJ, Millard-Stafford M, et al. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556–572. 19. Piet van Rosendal S, Osborne MA, Fassett RG, et al. Intravenous versus oral rehydration in athletes. Sports Med. 2010;40(4):327–346.

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20. World Anti-Doping Agency. TUE physician guidelines. Intravenous infusions and/or injections. https://www.wada -ama.org/sites/default/files/resources/files/intravenous _infusions_-_version_4.1_-_july_2016.pdf. 21. Bergeron MF, Devore C, Rice SG. Council on Sports Medicine & Fitness and Council on School Health: Policy Statement— Climatic heat stress and exercising children and adolescents. Pediatrics. 2011;128(3):e741–e747. 22. Casa DJ, Casillan D, Inter-Association Task Force for Preseason Secondary School Athletics. Preseason heat-acclimatization guidelines for secondary school athletics. J Athl Train. 2009;44:332–333. 23. National Federation of State High School Associations: Sports Medicine Advisory Committee. Position statement and recommendations for hydration to minimize the risk for dehydration and heat illness; October 2011 http://www.nfhs .org/search.aspx?searchtext=position%20statement%20 hydration. Accessed September 16, 2013. 24. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform; uncompensable heat stress and hyperthermic exhaustion. J Athl Train. 2010;45(2):117–127. 25. Bergeron MF, McKeag DB, Casa J. Youth football: heat stress and injury risk. Med Sci Sports Exerc. 2005;37(8):1421–1430. 26. Grundstein AJ, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int J Biometeorol. 2012;56(1):11–20. 27. Wendt D, van Loon LJC, van Marken Lichtenbelt WD. Thermoregulation during exercise in the heat. Sports Med. 2007;37(8):669–682. 28. Coris EE, Mehra S, Walz SM, et al. Gastrointestinal temperature trends in football linemen during physical exertion under heat stress. South Med J. 2009;102(6):569–574. 29. Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Br J Sports Med. 2015;49:1164–1173. 30. Yeargin SW, Casa DJ, Judelson DA, et al. Thermoregulatory responses and hydration practices in heat-acclimatized adolescents during preseason high school football. J Athl Train. 2010;45(2):136–146. 31. Binkley HM, Beckett J, Casa DJ, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2002;37(3):329–343. 32. Bouchama A, Knochel JM. Heat stroke. N Engl J Med. 2002; 346:1978–1988. 33. Zeller L, Novack V, Barksi L, et al. Exertional heatstroke: clinical characteristics, diagnostic and therapeutic considerations. Eur J Intern Med. 2011;22:296–299. 34. Miller KC, Long BC, Edwards J. Necessity of removing American football uniforms from humans with hyperthermia before cold-water immersion. Med Sci Sports Exerc. 2015;50(12):1240–1246. 35. Casa DJ, McDermott BP, Lee EC, et al. Cold water immersion; the gold standard for exertional heat stroke treatment. Sport Sci Rev. 2007;35:141–149. 36. Bouchama A, Dehbi M, Chaves Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 2007;11:R54. 37. Gagnon D, Lemire BB, Cas DJ, et al. Cold-water immersion and the treatment of hyperthermia: using 38.6°C as a safe rectal temperature cooling limit. J Athl Train. 2010;45(5):439–444. 38. Asplund CA, O’Connor FG. Challenging return to play decisions: heat stroke, exertional rhabdomyolysis, and

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39.

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41. 42.

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44. 45. 46.

47.

48.

49.

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51. 52.

53.

54.

55.

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57.

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exertional collapse associated with sickle trait. Sport Health. 2015;8(2):117–125. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine roundtable on exertional heat stroke— return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010;9(5):314–321. Moran DS, Heled Y, Still L, et al. Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit. 2004;10(6):CR252–CR257. Schwelllnus MP. Muscle cramping in the marathon. Aetiology and risk factors. Sports Med. 2007;37(4–5):364–367. Horswill CA, Stofan JR, Lacambra M. Sodium balance during U.S. football training in the heat: cramp-prone vs reference players. Int J Sports Med. 2009;30(1):789–794. Nelson NL, Churilla JR. A narrative review of exerciseassociated muscle cramps: factors that contribute to neuromuscular fatigue and management implications. Muscle Nerve. 2016;54:177–185. Maquirriain J, Merello M. The athlete with muscular cramps: clinical approach. J Am Acad Orthop Surg. 2007;15:425–431. Roberts WO. Exercise-associated collapse care matrix in the marathon. Sports Med. 2007;37(4–5):431–433. Krediet CT, van Dijk N, Linzer M, et al. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation. 2002;106(13):1684–1689. Giannoglou G, Chatzizisis YS, Misirili G. The syndrome of rhabdomyolysis: pathophysiology and diagnosis. Eur J Intern Med. 2007;18:90–100. Scalco RS, Snoeck M, Quinlivan R, et al. Exertional rhabdomyolysis: physiologic response or manifestation of an underlying myopathy? BMJ Open Sport Exerc Med. 2016;2(1): e000151. Kenney K, Landau ME, Gonzalez RS, et al. Serum creatine kinase after exercise: drawing the line between physiological response and exertional rhabdomyolysis. Muscle Nerve. 2012;45:356–362. Hoffman JD, Steiner RD, Paradise L, et al. Rhabdomyolysis in the military, recognizing late-onset very long-chain acyl co-A dehydrogenase deficiency. Mil Med. 2006;171(7):657–658. Clarkson PM. Exertional rhabdomyolysis and acute renal failure in marathon runners. Sports Med. 2007;37(4):361–363. Torres PA, Helmstetter JA, Kaye AM. Rhabdomyolysis: pathogenesis, diagnosis, and treatment. Oscher J. 2015;15: 58–69. Clarkson PM, Kearns AK, Rouzier P, et al. Serum creatine kinase levels and renal function measures in exertional muscle damage. Med Sci Sports Exerc. 2006;38(4):623–627. George M, Delgaudio A, Salhanick SD. Exertional rhabdomyolysis—when should we start worrying? Case repots and literature review. Pediatr Emerg Care. 2010;26:864–866. O’Connor FG, Brennan FH, Campbell W, et al. Return to physical activity after exertional rhabdomyolysis. Curr Sports Med Rep. 2008;7(6):328–331. Harmon KG, Drezner JA, Klossner D, et al. Sickle cell trait associated with a RR of death of 37 times in National Collegiate Athletic Association football athletes: a database with 2 million athlete-years as the denominator. Br J Sports Med. 2012;46:325–330. Bergeron MF, Cannon JG, Hall EL, et al. Erythrocyte sickling during exercise and thermal stress. Clin J Sport Med. 2004;14: 354–356.

58. Eichner ER. Sickle-cell trait in sports. Curr Sports Med Rep. 2010;9(6):347–351. 59. Hew-Butler T, Rosner MH, Fowkes-Godek S, et al. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, CA, 2015. Clin J Sports Med. 2015;25(4):303–320. 60. Backer HD, Shopes E, Collins SL, et al. Exertional heat illness and hyponatremia in hikers. Am J Emerg Med. 1999;7: 532–539. 61. Noe RS, Choudhary E, Cheng-Dobson J, et al. Exertional heat-related illnesses at the Grand Canyon National Park, 2004-2009. Wilderness Environ Med. 2013;24:422–428. 62. Zelingher J, Putterman C, Ilan Y, et al. Case series: hyponatremia associated with moderate exercise. Am J Med Sci. 1996;311:86–91. 63. O’Brien KK, Montain SJ, Corr WP, et al. Hyponatremia associated with overhydration in U.S. Army trainees. Mil Med. 2001;166:405–410. 64. Hew TD, Chorley JN, Cianca JC, et al. The incidence, risk factors, and clinical manifestations of hyponatremia in marathon runners. Clin J Sports Med. 2003;13:41–47. 65. Chorley J, Cianca J, Divine J. Risk factors for exerciseassociated hyponatremia in non-elite marathon runners. Clin J Sport Med. 2007;7:471–477. 66. Armed Forces Health Surveillance Center. Update: exertional hyponatremia, active component, U.S. Armed Forces, 19992013. MSMR. 2014;21:18–21. 67. Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014;170:G1–G47. 68. Hiller DB, O’Toole ML, Fortress EE, et al. Medical and physiological considerations in triathlons. Am J Sports Med. 1987;15:164–168. 69. Rowe JW, Shelton RL, Helderman JH, et al. Influence of the emetic reflex on vasopressin release in man. Kidney Int. 1979;16:729–735. 70. Takamata A, Mack GW, Stachenfeld NS, et al. Body temperature modification of osmotically induced vasopressin secretion and thirst in humans. Am J Physiol. 1995;269: R874–R880.

Cold Injury 71. Bangs C, Hamlet MD. Hypothermia and cold injury. In: Auerbach PS, Geehr EC, eds. Management of Wilderness and Environmental Emergencies. 2nd ed. St Louis: Mosby; 1989. 72. Whayne TF, DeBakey ME. Cold injury, ground type; 1958. Washington DC, Office of the Surgeon General, Department of the Army. 73. Danzl DF, Pozos RS, Hamlet MD. Accidental hypothermia. In: Auerbach PS, ed. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 3rd ed. St. Louis: Mosby; 1995. 74. Hamlet MD. An overview of medically related problems in the cold environment. Mil Med. 1987;152:393–396. 75. Ulrich AS, Rathlev NK. Hypothermia and localized cold injuries. Emerg Med Clin North Am. 2004;22:281–298. 76. Centers for Disease Control and Prevention. Hypothermiarelated deaths—United States, 1999-2002 and 2005. MMWR. 2006;55:282–284. 77. Berko J, Ingram DD, Saha S, et al. Deaths attributed to heat, cold, and other weather events in the United States, 2006-2010. Natl Health Stat Report. 2014;76:1–15.

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CHAPTER 21  Environmental Illness 78. Meiman J, Anderson H, Tomassalo C, et al. Hypothermiarelated deaths – Wisconsin, 2014, and United States, 2003-2013. MMWR. 2015;64(6):141–143. 79. Jurkovich CJ. Environmental cold-induced injury. Surg Clin North Am. 2007;87:247–267. 80. Danzl DF, Pozos RS, Auerbach PS, et al. Multicenter hypothermia survey. Ann Emerg Med. 1987;16:1042–1055. 81. da Silva IR, Frontera JA. Neurological complications of acute environmental injuries. Handbk Clin Neurol. 2017;141: 685–704. 82. Zafren K, Giesbrecth GG, Danzl DF, et al. Wilderness Medical Society practice guidelines for the out-of-hospital evaluation and treatment of accidental hypothermia. Wilderness Environ Med. 2014;25(4):425–445. 83. Paal P, Gordon L, Strapazzon G, et al. Accidental hypothermia – an update: the content of this review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM). Scan J Trauma Rescuc Emerg Med. 2016;24(1):111. 84. Zafren K. Out-of-hospital evaluation and treatment of accidental hypothermia. Emerg Med Clin North Am. 2017;35(2): 261–279. 85. Seto CK, Way D, O’Connor N. Environmental illness in athletes. Clin Sports Med. 2005;24:695–718. 86. Aslam AF, Aslam AK, Vasavada BC, et al. Hypothermia: evaluation, electrocardiographic manifestations, and management. Am J Med. 2006;119:297–301. 87. Vallerand AL. Exercise in the cold. In: Torg JS, Shephard RJ, eds. Current Therapy in Sports Medicine. 3rd ed. Philadelphia: Mosby; 1995. 88. Castellani JW, Young AJ, Ducharme MB, et al. Prevention of cold injuries during exercise. Med Sci Sports Exerc. 2006;38: 2012–2029. 89. Lampietro PF. Heat production from shivering. J Appl Physiol. 1960;15:632. 90. Keating WR. Accidental immersion hypothermia and drowning. Practitioner. 1977;219:183. 91. Young AJ, Sawka MN, Pandolf KB. Physiology of cold exposure. In: Marriott BM, Carlson SJ, eds. Nutritional Needs in Cold and High-Altitude Environments. Applications for Military Personnel in Field Operations. Washington, DC: National Academy Press; 1996. 92. White JD. Hypothermia: the Bellevue experience. Ann Emerg Med. 1982;11:417–423. 93. Shields CP, Sixsmith DM. Treatment of moderate-to-severe hypothermia in an urban setting. Ann Emerg Med. 1990;19: 1093–1097. 94. Reuler JB. Hypothermia: pathophysiology, clinical setting, and management. Ann Intern Med. 1978;89:519–527. 95. Danzl DF. Accidental hypothermia. In: Auerbach PS, ed. Wilderness Medicine. 6th ed. Philadelphia: Mosby; 2011. 96. Petrone P, Asensio JA, Marini CP. Management of accidental hypothermia and cold injury. Curr Probl Surg. 2014;51(10): 417–431. 97. Brown DJ, Brugger H, Boyd J, et al. Accidental hypothermia. N Eng J Med. 2012;367(20):1930–1938. 98. Froese G, Burton AC. Heat losses from the human head. J App Physiol. 1957;10:235–241. 99. Harirchi I. Frostbite: incidence and predisposing factors in mountaineers. Br J Sports Med. 2005;39:898–901. 100. Freer L, Imray CHE. Frostbite. In: Auerbach PS, ed. Wilderness Medicine. 6th ed. Philadelphia: Mosby; 2011.

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101. McIntosh SE, Dow J, Hackett PH, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite: 2014 update. Wilderness Environ Med. 2014;25(suppl 4):S43–S54. 102. Lewis T. Observations upon the reactions of the vessels of the human skin to the cold. Heart. 1930;15:177–208. 103. Dana H, Rex I, Samitz M. The hunting reaction. Arch Dermatol. 1969;99:441. 104. Cappaert TA, Stone JA, Castellani JW, et al. National Athletic Trainers’ Association position statement: environmental cold injuries. J Athl Train. 2008;43:640–658. 105. Handford C, Thomas O, Imray CHE. Frostbite. Emerg Med Clin North Am. 2017;35(2):281–299. 106. Shenaq DS, Gottlieb LJ. Cold injuries. Hand Clin. 2017;33(2): 257–267. 107. Cauchy E, Chetaille E, Marchand V, et al. Retrospective study of 70 cases of severe frostbite lesions: a proposed new classification scheme. Wilderness Environ Med. 2001;12: 248–255. 108. John AR, Jain A, Kishore B, et al. The role of 99mTc MDP bone scan in delineation of ischaemic zone in cases of severe frostbite. Indian J Nucl Med. 2017;32:203–207. 109. Cauchy E, Davis CB, Pasuier M, et al. A new proposal for management of severe frostbite in the austere environment. Wilderness Environ Med. 2016;27:92–99. 110. Ibrahim AE, Goverman J, Sarhane KA, et al. The emerging role of tissue plasminogen activator in the management of severe frostbite. J Burn Care Res. 2015;36:e62–e66.

High Altitude Illness 111. Muza SR, Beidleman BA, Fulco CS. Altitude preexposure recommendations for inducing acclimatization. High Alt Med Biol. 2010;11(2):87–92. 112. Khodaee M, Grothe HL, Seyfert JH, et al. Athletes at altitude. Sports Health. 2016;Mar-Apr:126–132. 113. Lundby C, Robach P. Does ‘altitude training’ increase exercise performance in elite athletes? Exp Physiol. 2016;101(7): 783–788. 114. Millet GP, Schmitt RL, Woorons X, et al. Combining hypoxic methods for peak performance. Sports Med. 2010;40(1):1–25. 115. Hackett PH, Roach RC. High-altitude illness. N Engl J Med. 2001;345:107–114. 116. West JB. The physiologic basis of high-altitude diseases. Ann Intern Med. 2004;141:789–800. 117. Derby R, de Weber K. The athlete and high altitude. Curr Sports Med Rep. 2010;9(2):79–85. 118. Peacock AJ. ABC of oxygen; oxygen at altitude. BMJ. 1998;317: 1063–1066. 119. Sagoo RS, Hutchinson CE, Wright A, et al. Magnetic resonance investigation into the mechanisms involved in the development of high altitude cerebral edema. J Cereb Blood Flow Metab. 2017;37(1):319–331. 120. Rodway GW, Hoffman LA, Sanders MH. High-altitude-related disorders—Part I: pathophysiology, differential diagnosis, and treatment. Heart Lung. 2003;32(6):353–359. 121. Alizadeh R, Ziaee V, Aghsaeifard Z, et al. Characteristics of headache at altitude among trekkers; a comparison between acute mountain sickness and non-acute mountain sickness headache. Asian J Sports Med. 2012;3(2):126–130. 122. Bartsch P, Mairbaurl H, Maggiorini M, et al. Physiological aspects of high-altitude pulmonary edema. J Appl Physiol. 2005;98(3):1101–1110.

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123. Maggiorini M. Prevention and treatment of high altitude pulmonary edema. Prog Cardiovasc Dis. 2010;52(6):500–506. 124. Sampson JB, Cymerman A, Burse RL, et al. Procedures for the measurement of acute mountain sickness. Aviat Space Environ Med. 1983;54:1063–1073. 125. Bloch J, Duplain H, Rimolid SF, et al. Prevalence and time course of acute mountain sickness in older children and adolescents after rapid ascent to 3450 meters. Pediatrics. 2009;123:1–5. 126. Hackett PH, Yarnell PR, Hill R, et al. High-altitude cerebral edema evaluated with magnetic resonance imaging. JAMA. 1998;280:1920–1925. 127. Roach RC, Bartsch P, Hackett PH, et al. The Lake Louise Acute Mountain Sickness Scoring Systems. In: Sutton JR, Coates G, Huston CS, eds. Hypoxia and molecular medicine: Proceedings of the 8th International Hypoxia Symposium. Burlington, VT, Queen City: 1993:272–274. 128. Pollard AJ, Niermeye S, Barry P, et al. Children at altitude: an international consensus statement by an ad hoc committee of the International Society for Mountain Medicine, March 12, 2001. High Alt Med Biol. 2001;2(3):389–403. 129. Weidman M, Tabin GC. High-altitude retinopathy and altitude illness. Ophthalmology. 1999;106:1924–1927. 130. Wilson MH, Newman S, Imary CH. The cerebral effects of ascent to high altitudes. Lancet Neurol. 2009;8:175–191. 131. Wu T, Ding S, Liu J, et al. Ataxia: an early indicator in high altitude cerebral edema. High Alt Med Biol. 2006;7(4):275–280. 132. Liu Y, Zhang JH, Gao XB, et al. Correlation between blood pressure changes and AMS, sleeping quality and exercise upon high-altitude exposure in young Chinese men. Mil Med Res. 2014;1:19–28. 133. Mairer K, Wille M, Burtscher M. The prevalence of and risk factors for acute mountain sickness in the Eastern and Western Alps. High Alt Med Biol. 2010;11(4):343–348. 134. Ren Y, Fu Z, Shen W, et al. Incidence of high altitude illness among unacclimatized persons who acutely ascended to Tibet. High Alt Med Biol. 2010;11:39–42. 135. Roach RC, Maes D, Sandoval D, et al. Exercise exacerbates acute mountain sickness at simulated high altitude. J Appl Physiol. 2000;88:581–585. 136. Schneider M, Bernasch D, Weyman J, et al. Acute mountain sickness: influence of susceptibility, preexposure, and ascent rate. Med Sci Sports Exerc. 2002;34(12):1886–1891. 137. Major SA, Hogan RJ, Yeates E, et al. Peripheral arterial desaturation is further exacerbated by exercise in adolescents with acute mountain sickness. Wilderness Environ Med. 2012;23(1):15–23. 138. Roach RC, Maes D, Sandoval D, et al. Exercise exacerbates acute mountain sickness at simulated high altitude. J Appl Physiol. 2000;88:581–585. 139. Karinen H, Peltonen JE, Kahonen M, et al. Prediction of acute mountain sickness by monitoring arterial saturation during ascent. High Alt Med Biol. 2010;11:325–332. 140. Richalet JP, Larmignat P, Poitrine E, et al. Physiological risk factors for severe high-altitude illness. A prospective study. Am J Respir Crit Care Med. 2012;185(2):192–198. 141. Tannheimer M, Albertini N, Ulmer HV, et al. Testing individual risk of acute mountain sickness at greater altitudes. Mil Med. 2009;174:363–369. 142. Kallenberg K, Dehnert C, Dörfler A, et al. Microhemorrhages in nonfatal high altitude cerebral edema. J Cereb Blood Flow Metab. 2008;28:1635–1642.

143. Morocz IA, Zientara GP, Gudbjartsson H, et al. Volumetric quantification of brain swelling after hypobaric hypoxia exposure. Exp Neurol. 2001;168:96–104. 144. Bärtsch P, Swenson ER. Clinical practice: acute high-altitude illnesses. N Engl J Med. 2013;368:2294–2302. 145. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of acute altitude illness: 2014 update. Wilderness Environ Med. 2014;25:S4–S14. 146. Basnyat B, Holck PS, Pun M, et al. Spironolactone does not prevent acute mountain sickness: a prospective, double-blind, randomized, placebo-controlled trial by SPACE Trial Group (spironolactone and acetazolamide trial in the prevention of acute mountain sickness group). Wilderness Environ Med. 2011;22(1):15–22. 147. Bates MGD, Thompson AAR, Baillie JK, et al. Sildenafil citrate for the prevention of high altitude hypoxic pulmonary hypertension: double blind, randomized, placebo-controlled trial. High Alt Med Biol. 2011;12(3):207–214. 148. Olfert IM, Loeckinger A, Treml B, et al. Sildenafil and bosentan improve arterial oxygenation during acute hypoxic exercise: a controlled laboratory trial. Wilderness Environ Med. 2011;22(3): 211–221. 149. Sepaul RA, Welch JA, Maika ST, et al. Pharmacologic prophylaxis for acute mountain sickness: a systematic shortcut review. Ann Emerg Med. 2012;59:307–317. 150. Luks AM. Which medications are safe and effective for improving sleep at high altitude? High Alt Med Biol. 2008;9(3): 195–198. 151. Luks AM. Clinician’s corner: what do we know about safe ascent rates at high altitude? High Alt Med Biol. 2012;13(3): 147–152. 152. Maggiorini M, Brunner-La Rocca HP, Peth S, et al. Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema. Ann Intern Med. 2006;145:497–506. 153. Pennardt A. High-altitude pulmonary edema: diagnosis, prevention, and treatment. Curr Sports Med Rep. 2013;12: 115–119. 154. Kobayashi T, Koyoma S, Kubo K, et al. Clinical features of patients with high altitude pulmonary edema in Japan. Chest. 1987;92:814–821. 155. Deshwal R, Iqbal M, Basnet S. Nifedipine for the treatment of high altitude pulmonary edema. Wilderness Environ Med. 2012;23:7–10. 156. Sartori C, Allemann Y, Duphain H, et al. Salmeterol for the prevention of high-altitude pulmonary edema. N Engl J Med. 2002;346:1631–1636. 157. Siebenmann C, Bloch KE, Lundby C, et al. Dexamethasone improves maximal exercise capacity of individuals susceptible to high altitude pulmonary edema at 4559 m. High Alt Med Biol. 2011;12(2):169–177. 158. Maggiorini M. High altitude-induced pulmonary edema. Cardiovasc Res. 2006;72:41–50. 159. DeFranco MJ, Baker CL, DaSilva JJ, et al. Environmental issues for team physicians. Am J Sports Med. 2008;36(11):2226–2237. 160. WADA Prohibited List. https://www.wada-ama.org/en/ what-we-do/prohibited-list. 161. Pandit A, Karmacharya P, Pathak R, et al. Efficacy of NSAIDs for the prevention of acute mountain sickness: a systematic review and meta-analysis. J Community Hosp Intern Med Perspect. 2014;4:24927.

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CHAPTER 21  Environmental Illness 162. Gore CJ, McSharry PE, Hewitt AJ, et al. Preparation for football competition at moderate to high altitude. Scand J Med Sci Sports. 2008;18(suppl 1):85–95. 163. McSharry PE. Altitude and athletic performance: statistical analysis using football results. Br Med J. 2007;335:1278–1281. 164. Bangsbo J, Mohr M, Kustrup P. Physical and metabolic demands of training and match-play in the elite football player. J Sports Sci. 2006;24:665–674. 165. Fulco CS, Kambis KW, Friedlander AL, et al. Carbohydrate supplementation improves time-trial cycle performance during

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energy deficit at 4,300-m altitude. J Appl Physiol. 2005;99: 867–876. 166. Fulco CS, Zupan M, Muza SR, et al. Carbohydrate supplementation and endurance performance of moderate altitude residents at 4300 m. Int J Sports Med. 2007;28:437–443. 167. Yanagisawa K, Ito O, Nagai S, et al. Electrolyte-carbohydrate beverage prevents water loss in the early stage of high altitude training. J Med Invest. 2012;59(1):102–110.

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22  Dermatologic Conditions Haoming Xu, Barbara B. Wilson, Michael A. Marchetti

The skin and its appendages constitute a complicated and highly regulated organ known as the integumentary system. Its functions are diverse and include protecting the body from an array of external insults by means of physical and immunologic mechanisms, regulating temperature homeostasis, providing sensory receptors for interactions with the environment, preventing water loss, and initiating vitamin D synthesis. As such, optimal athletic performance relies on the proper health and function of the integumentary system. It is therefore crucial that health care providers be able to recognize and effectively treat dermatologic disorders affecting the athlete. This chapter introduces disorders affecting athletes and focuses on providing a framework to evaluate the skin and effectively establish a diagnosis.

CUTANEOUS INFECTIONS Cutaneous infections are among the most common dermatologic disorders that affect athletes. Making an accurate diagnosis is critical because infections may result in morbidity and lead to missed practices or game ineligibility. Familiarity with returnto-play guidelines is essential. Readers are encouraged to consult published guidelines, such as the 2014–2015 NCAA Sports Medicine Handbook, which is emphasized in this chapter.1 Guidelines for skin infections are primarily for athletes in contact sports, particularly wrestlers, because they are at highest risk for acquisition and transmission of cutaneous infections.

Bacterial Infections Folliculocentric Infections: Bacterial Folliculitis, Furuncles, and Carbuncles Bacterial folliculitis, furuncles, and carbuncles are infections that begin within hair follicles and can be conceptualized as a disease continuum. All of these infections are common among athletes, and one study documented that 25% of a high school’s varsity athletes experienced an episode of furunculosis over 1 year.2 Bacterial folliculitis presents as tender, follicular-based pustules, whereas a furuncle is a deeper inflammatory nodule. Furuncles often, but not invariably, arise from folliculitis (Fig. 22.1). Carbuncles are more extensive, deeper, communicating masses that arise when multiple, closely set furuncles coalesce (Fig. 22.2). Patients with carbuncles often are ill and present with fever and malaise. All are most commonly caused by Staphylococcus aureus and can evolve into an abscess or a pus-filled cavity. These infections typically arise in hair-bearing sites, particularly in areas subject to friction, 246

occlusion, and perspiration, such as the neck, face, scalp, axillae, groin, extremities, and buttocks. Shaving of hair may promote infection, and any injury that disrupts skin integrity may lead to increased risk of infection. Diagnosis is made clinically, and if pus is obtainable, a bacterial culture should be submitted for organism identification and antibiotic sensitivity. The initial therapy for bacterial folliculitis includes washing the affected area daily with an antibacterial soap (e.g., a chlorhexidine gluconate 2% to 4% solution or a benzoyl peroxide 10% wash) and applying a topical antibiotic, such as mupirocin 2% ointment, two to three times daily. In resistant cases, short courses of oral antibiotics can be used as directed by culture results. Nonfluctuant furuncles can be treated with warm compresses to promote drainage. Fluctuant furuncles and carbuncles that have evolved into abscesses require incision, drainage, and culture. Oral antibiotic therapy has traditionally been considered on a case-by-case basis (e.g., suspicion for community-acquired methicillin resistant S. aureus [MRSA], severe or extensive disease, rapid progression, associated cellulitis, systemic illness, and/or the presence of comorbidities or immunosuppression). However, multicenter, prospective, double-blind, placebo-controlled, randomized trials in 2016 and 2017 have demonstrated that the use of clindamycin or trimethoprim-sulfamethoxazole in conjunction with incision and drainage improves short-term outcomes, including cure rate, in patients with uncomplicated, simple abscesses.3,4 Patients with recurrent disease should be evaluated for chronic nasal carriage of S. aureus, which may serve as a reservoir for infection. Eradication measures include intranasal application of mupirocin 2% ointment twice daily for 5 to 10 days, washing the skin and in particular the axillae and groin daily with chlorhexidine gluconate 2% to 4% solution, and use of dilute sodium hypochlorite (i.e., bleach) baths ( 1 4 cup bleach per 1 4 tub or 13 gallons of water). Oral antibiotic therapy is not routinely recommended for decolonization.5 National Collegiate Athletic Association (NCAA) wrestling guidelines require that wrestlers must be without any new skin lesions for 48 hours before competition, must have completed 72 hours of antibiotic therapy, must have no moist, exudative, or purulent lesions, and must not cover active purulent lesions, to allow for participation.1

Impetigo Impetigo is a superficial bacterial infection of the skin. Both S. aureus and Group A Streptococcus can produce impetigo, but S.

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Abstract

Keywords

The skin and its appendages constitute a complicated and highly regulated organ known as the integumentary system. Its functions are diverse and include protecting the body from an array of external insults by means of physical and immunologic mechanisms, regulating temperature homeostasis, providing sensory receptors for interactions with the environment, preventing water loss, and initiating vitamin D synthesis. As such, optimal athletic performance relies on the proper health and function of the integumentary system. It is therefore crucial that health care providers be able to recognize and effectively treat dermatologic disorders affecting the athlete. This chapter introduces disorders affecting athletes and focuses on providing a framework to evaluate the skin and effectively establish a diagnosis.

dermatologic conditions cutaneous infections mechanical dermatoses environmental dermatoses

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Fig. 22.1  A methicillin-resistant Staphylococcus aureus furuncle. (Courtesy Kenneth E. Greer.)

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Fig. 22.3  Nonbullous impetigo on the chin with golden crusting. (Courtesy Kenneth E. Greer.)

sensitivity results. Empiric MRSA coverage can be considered in areas with high prevalence of infection. Impetigo is contagious, particularly in its bullous form, and may spread among athletes practicing contact sports. Affected individuals should be advised against sharing towels or soap. Return-to-play (RTP) guidelines are identical to those for bacterial folliculitis (described in the previous section).

Fig. 22.2  Multiple furuncles coalescing to form a carbuncle. (Courtesy Kenneth E. Greer.)

aureus is the more common etiology in industrialized nations. Athletes who engage in contact sports are at higher risk for acquisition of disease via trauma and disruption of skin integrity. Two presentations are recognized: bullous and nonbullous impetigo. Nonbullous impetigo typically begins as a transient vesicle or pustule that evolves into a honey-colored crusted plaque with surrounding erythema (Fig. 22.3). Infection is most common on the central face. The differential diagnosis includes herpes simplex, contact dermatitis, and atopic dermatitis. Bullous impetigo is characterized by superficial vesicles and bullae that rupture after 1 to 2 days, leading to weeping erosions that eventually heal over. Contact dermatitis, herpes simplex, bullous arthropod bites, drug rash, burns, and erythema multiforme should be ruled out. Diagnosis is usually suspected based on the clinical appearance, but bacterial culture is recommended for diagnostic confirmation and antibiotic sensitivity, given the increasing prevalence of community-acquired MRSA infections. Initial treatment should include local wound care with soap and water and use of topical mupirocin 2% ointment three times daily. For widespread infections, penicillinase-resistant antistaphylococcal antibiotics (cephalexin or dicloxacillin) can be considered, pending antibiotic

Cellulitis/Erysipelas Cellulitis and erysipelas are common infections of the skin in athletes, usually caused by S. aureus and Group A Streptococcus. Cellulitis is defined as an infection of the dermis and subcutaneous fat, whereas erysipelas is a more superficial variant affecting the upper dermis and lymphatic vessels. Less common causative organisms include Haemophilus influenzae, groups B and G Streptococcus, enteric gram-negative rods, coagulase-negative Staphylococcus, and Streptococcus pneumoniae.6–10 Risk factors for the development of cellulitis include any injury or trauma to the skin that allows for bacterial entry, such as cuts and/or scrapes, which are more prevalent in athletes participating in direct contact sports. Cellulitis classically presents as a unilateral erythematous, warm, tender, indurated, and edematous plaque with indistinct margins. Erysipelas is similar in appearance but tends to be more sharply defined with a bright red color (Fig. 22.4). Occasionally cellulitis may undergo bullae formation with necrosis, resulting in localized skin sloughing and ulcer formation. Systemic symptoms are variable, with fever, chills, malaise, and regional lymphadenopathy being the most common. The absence of pain or pain out of proportion to the clinical appearance should prompt consideration of a deeper infection, such as necrotizing fasciitis or myonecrosis. Other clinical red flags for necrotizing fasciitis or myonecrosis include erythema evolving into a dusky gray color, malodorous watery discharge, and crepitus in the soft tissues. Diagnosis is primarily clinical, based on the history and clinical presentation. Culture studies of the leading edge of cellulitic plaques are not indicated in routine, uncomplicated cellulitis or erysipelas because of their low yield, but they should be obtained in the presence of open, fluctuant, or bullous lesions.

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Fig. 22.5  Pitted keratolysis. (Courtesy Kenneth E. Greer.)

Fig. 22.4  Erysipelas with bulla formation and subsequent erosion. Note the sharply defined border, which can help distinguish erysipelas from cellulitis. (Courtesy Kenneth E. Greer.)

The differential diagnosis is extensive and includes deep venous thrombosis, superficial thrombophlebitis, Sweet syndrome, contact dermatitis, stasis dermatitis, arthropod bites, panniculitides, necrotizing soft tissue infections, and erythema migrans. Treatment depends on the severity of infection, with more severe cases necessitating hospitalization and parenteral antibiotics. Routine, uncomplicated, and non-purulent cellulitis can be treated in the outpatient setting with β-lactam antibiotics (e.g., dicloxacillin and cephalexin) as empiric first-choice therapy. Studies have consistently shown that empiric β-lactam antibiotics continue to be the most cost-effective choice with fewer adverse events in the treatment of uncomplicated cellulitis.11,12 Furthermore, in a 2017 multicenter, double-blind, randomized, superiority trial among patients with uncomplicated, nonpurulent cellulitis, the use of cephalexin plus trimethoprim-sulfamethoxazole compared to cephalexin alone did not result in higher rates of clinical resolution of cellulitis.13 Simple measures including bed rest and elevation of the involved site should be routinely emphasized, but warm compresses should be avoided because they predispose the skin to vesicle formation. Empiric MRSA coverage (e.g., clindamycin, trimethoprim-sulfamethoxazole, and tetracyclines) should be reserved for patients with purulent cellulitis, systemic symptoms (i.e., fever, hypotension, tachycardia), a history of MRSA infection or colonization, a lack of clinical response to an antibiotic regimen that does not cover MRSA, risk factor(s) for MRSA infection (recent hospitalization or surgery, hemodialysis, and human immunodeficiency virus infection), or proximity of cellulitis to indwelling medical device (e.g., prosthetic joint or vascular graft).14 RTP guidelines are identical to those for bacterial folliculitis (described in the section “Folliculocentric Infections: Bacterial Folliculitis, Furuncles, and Carbuncles”).

Pitted Keratolysis Pitted keratolysis is a superficial bacterial infection of the feet caused by bacteria of the Corynebacterium genus, particularly Kytococcus sedentarius.15,16 Numerous small crateriform punchedout pits are seen predominantly on the thickest areas of the plantar surface and may coalesce to form large, irregular, scalloped lesions (Fig. 22.5). Less commonly, the toe web spaces are affected. Infection usually occurs in younger males with sweaty feet, but it can affect all ages and sexes. Patients note a distinctive malodor, and some may describe a slimy sensation. Moisture, occlusion, and tropical climates are predisposing factors. The clinical appearance is distinctive, but the differential diagnosis of interdigital involvement includes tinea pedis and erythrasma. Therapeutic options include thorough cleansing combined with use of a clindamycin 1% solution or a benzoyl peroxide 10% wash or 5% gel. Dilute sodium hypochlorite (bleach) soaks may speed resolution. Adjunctive and preventative measures aim at reducing moisture and include keeping feet dry by changing socks frequently, using absorptive foot powders (e.g., microporous cellulose and talc powder), and applying antiperspirants topically (e.g., aluminum chloride 20% solution nightly). Footwear should be replaced as indicated. Erythrasma Erythrasma is an underdiagnosed superficial bacterial skin infection caused by Corynebacterium minutissimum that is commonly confused with dermatophyte infections. The condition is most common in warm, temperate climates and leads to clinical disease, particularly in folds of the skin, such as the inguinal creases, axillae, or interdigital toe web spaces. Lesions are often pinkishtan, scaly patches, and unlike dermatophyte infections, they do not demonstrate an active, raised advancing border (Fig. 22.6). Erythrasma can be asymptomatic or mildly pruritic. The diagnosis can be confirmed by demonstrating coral-red fluorescence with Wood’s lamp (ultraviolet A [UVA]) examination. Of note, this finding may be absent in patients who have recently washed the involved area. Potassium hydroxide (KOH) preparations of skin scrapings will be negative. The differential diagnosis often includes other intertriginous eruptions, such as

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Fig. 22.7  A child with pseudomonas folliculitis after bathing in a hot tub. Fig. 22.6  Erythrasma affecting the axilla. (Courtesy Kenneth E. Greer.)

dermatophytoses (e.g., tinea cruris or tinea pedis), candidiasis, seborrheic dermatitis, contact dermatitis, and inverse psoriasis. First-line treatment is with topical erythromycin 2% solution, clindamycin 1% solution, or benzoyl peroxide 5% gel. Oral doses of clindamycin and erythromycin are also effective.

Pseudomonal Folliculitis (Hot Tub Folliculitis) Use of hot tubs, whirlpools, or swimming pools can lead to the development of a self-limited folliculitis caused by Pseudomonas aeruginosa. Lesions present as pruritic, follicular-based papules and pustules that develop 1 to 5 days after the use of bathing facilities (Fig. 22.7). Occasionally patients may experience fever, chills, and lymphadenopathy. Lesions may be generalized over the body, may appear underneath clothing, or may be localized if only a certain body site is immersed. The differential diagnosis includes staphylococcal folliculitis, Pityrosporum folliculitis, and arthropod bites. Bacterial culture of pustule contents can be performed to confirm the diagnosis. In immunocompetent persons without systemic involvement, the infection is self-limited and no treatment is necessary. For athletes who require treatment, ciprofloxacin, 250 mg by mouth twice daily for 7 days, is recommended. Suspected water sources should be inspected for adequate pH levels and chlorine content. RTP guidelines are identical to those for bacterial folliculitis (described in the section “Folliculocentric Infections: Bacterial Folliculitis, Furuncles, and Carbuncles”).

Fungal Infections Dermatophytoses The three fungal genera Trichophyton, Microsporum, and Epidermophyton comprise more than 40 species and are collectively referred to as “dermatophytes.” These fungi can be found living

in soil and on the skin of animals and humans. Common infections in humans are colloquially referred to as “jock itch” (tinea cruris), “athlete’s foot” (tinea pedis), and “ringworm” (tinea corporis). Dermatophytes can infect any superficial skin surface, including appendageal structures, such as hair follicles and nails, but they cannot penetrate into the dermis or infect mucous membranes. Athletes are at higher risk for infection, because perspiration and trauma facilitate growth and penetration of dermatophytes on the skin. Additionally, fungi are transmitted via skin-to-skin contact and the use of shared facilities and items (such as locker rooms and towels). Wrestlers in particular are at risk for tinea corporis. Dermatophyte infections of the skin—no matter the location— typically demonstrate a red, scaly, raised, advancing border, which is the most useful diagnostic clue on physical examination. Lesions on the body variably show an annular or ring-shaped appearance. Tinea cruris favors the inguinal folds and advances onto the thighs (Fig. 22.8). As opposed to candidiasis, tinea cruris almost never involves the scrotum. Tinea pedis classically presents with scaling, maceration, and erythema in the interdigital toe web spaces (particularly the fourth) but can involve the entire foot (Fig. 22.9). Tinea capitis is most common in children and presents as red, scaly patches of alopecia. The differential diagnosis is location dependent and extensive but most commonly includes seborrheic dermatitis, eczema, or alopecia areata in the scalp; contact dermatitis, atopic dermatitis, psoriasis, tinea versicolor, pityriasis rosea, or subacute cutaneous lupus erythematosus on the body; candidiasis, erythrasma, seborrheic dermatitis, psoriasis, or contact dermatitis in the groin; and dyshidrotic eczema, contact dermatitis, psoriasis, candidiasis, and scabies on the feet. Diagnosis can be suspected on clinical examination but should be confirmed with a diagnostic test. Scraping the advancing edge of a lesion for microscopic examination with 10% KOH is an in-office procedure that is easy to

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Fig. 22.8  Tinea cruris with characteristic sparing of the penis and scrotum. Note the active, advancing border typical of dermatophyte infections. (Courtesy Kenneth E. Greer.)

Fig. 22.10  Hypopigmented tinea versicolor. (Courtesy Kenneth E. Greer.)

for scalp lesions. Wrestlers with extensive and active lesions may be disqualified, with infection determined by KOH preparation or a review of the therapeutic regimen.1

Fig. 22.9  Interdigital tinea pedis. (Courtesy D. Stulberg.)

perform. The presence of septate, branching hyphae is diagnostic. Alternatively, hair shafts, skin scrapings, or swabs taken from the scalp can be submitted for fungal culture. Multiple systemic and topical antifungal agents are available to treat dermatophyte infections of skin, hair, and nails. Most cases of tinea corporis, cruris, and pedis can be successfully treated with topical therapy alone. Terbinafine 1% cream or ketoconazole 2% cream applied twice daily for several weeks are good firstline treatments. Consideration of an oral antifungal agent, such as fluconazole, 200 mg by mouth weekly for 2 to 4 weeks, or terbinafine, 250 mg by mouth daily for 1 to 2 weeks, can be considered in widespread, inflammatory, or refractory cases. Treatment of tinea capitis always requires systemic therapy, with griseofulvin ultramicrosized capsules, 15 mg/kg/day in divided doses for 8 weeks, remaining first-line treatment. Consultation with a dermatologist is recommended in severe cases, after treatment failure, and when the diagnosis is unclear. NCAA guidelines mandate that for wrestlers to return to competition, a minimum of 72 hours of topical therapy is required for skin lesions and two weeks of oral antifungal therapy is required

Malassezia The fungal genus Malassezia (formerly Pityrosporum) includes several species of lipophilic yeasts that form part of the normal skin flora and flourish in warm, moist, sebum-rich body areas. Under certain circumstances, proliferation of the yeast can produce the skin conditions tinea versicolor and Pityrosporum folliculitis. By the nature of their physical activity, young athletes are at higher risk for the development of these infections. Tinea versicolor presents as finely scaling macules that coalesce, forming irregularly shaped patches of pigment alteration. Lesions may be tan to brown or white to pink in color and are most commonly located on the back, chest, abdomen, proximal upper extremities, and neck (Fig. 22.10). A clue to the diagnosis includes the extensive dust-like scaling that can be produced by scratching the lesions. On microscopic examination with 10% KOH, the scale will show clusters of oval, budding yeast cells and short, septate hyphae. The differential diagnosis usually includes tinea corporis, pityriasis rosea, and progressive macular hypomelanosis. Tinea versicolor is neither transmissible nor caused by poor hygiene. Pityrosporum folliculitis presents as follicular, erythematous, 2- to 3-mm papules and pustules on the chest and back and is due to Malassezia yeast proliferating within the hair follicle (Fig. 22.11). The diagnosis is often confused with bacterial folliculitis and acne vulgaris. Both conditions are treated with topical antifungal agents, such as ketoconazole 2% shampoo and selenium sulfide 2.5% lotion, which are lathered onto the skin for 10 minutes and rinsed off. Patients should perform this treatment daily for at least 10 days, with tapering of frequency to weekly use thereafter for 1 to 2 months for prevention. Occasionally, oral antifungal drugs are used in persons with resistant disease.

Viral Infections Herpes Simplex Infection by human herpesvirus 1 (HSV-1) and human herpesvirus 2 (HSV-2) is common in both the general population and

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Fig. 22.11  Pityrosporum folliculitis. (Courtesy Kenneth E. Greer.)

among athletes, with herpes labialis and genital herpes being the most familiar clinical presentations. After primary acquisition of the virus from direct skin contact, the virus replicates at the site of inoculation, with variable production of a primary skin lesion. The virus spreads to infect sensory nerve terminals and travels by retrograde axonal transport to neuronal nuclei in regional sensory ganglia, where it establishes latent, lifelong infection. The virus will subsequently reactivate with anterograde axonal transport to the original site of primary infection. Contact sports place athletes at higher risk for both acquisition and transmission of the virus, whereas excessive UV radiation exposure (e.g., among skiers) may place certain athletes at risk for reactivation. HSV outbreaks are well described among wrestlers (“herpes gladiatorum”) and rugby players (“scrum pox”). HSV lesions are divided into primary and recurrent infection. Either may begin with a prodromal phase (marked by pain, burning, stinging, and itching), before development of erythema and edematous red papules, which subsequently become vesicles. Systemic symptoms (e.g., fever and malaise) are most common in primary infections. Classic skin lesions are small (2 to 5 mm) grouped vesicles on an erythematous base. Confluent vesicles may produce a scalloped border. Lesions soon ulcerate, develop an adherent crust, and eventually resolve within 5 to 14 days. Among wrestlers, the most common locations are the head and neck (Fig. 22.12), but they can occur anywhere, including the trunk and extremities.17 It is critical to note that the majority of patients with HSV are asymptomatic but can transmit the virus via asymptomatic shedding. The differential diagnosis of HSV is site-specific. Aphthous ulcers, syphilis, herpangina and erythema multiforme, or epidermal necrolysis may simulate orolabial HSV. On the trunk and extremities, contact dermatitis, herpes zoster, and impetigo should be considered. One study demonstrated that HSV in wrestlers is often misdiagnosed, with impetigo, tinea corporis, or eczema being the most common misdiagnoses.18 Clinical clues to the diagnosis include recurrences of disease at the same location, prodromal symptoms, and grouping of individual small vesicles. The definitive diagnosis of HSV can be made with an appropriate laboratory test. Viral culture of the vesicle fluid or ulcer base has been the gold standard for many years, but newer

Fig. 22.12  Herpes gladiatorum. (Courtesy Kenneth E. Greer.)

diagnostic modalities are available, including polymerase chain reaction and direct fluorescent antibody tests. Treatment, if indicated, is with oral antiviral medications such as acyclovir and valacyclovir, which may shorten lesion duration if they are begun soon enough. Numerous acceptable dosing regimens exist and are dependent on the site of infection and whether infection is primary or recurrent. Daily suppressive therapy can be considered in athletes who are prone to recurrences. The NCAA has developed stringent guidelines for wrestlers with HSV infections. In order to participate with a recent primary infection, the wrestler must be free of systemic symptoms, have developed no new vesicles in the last 72 hours, have all lesions covered by a firm, dried adherent crust, be taking appropriate oral antiviral therapy at least 120 hours before the time of participation, and not cover lesions to allow participation. Wrestlers with recurrent infection must meet the last three requirements before returning to event participation.1 The authors recommend caution for athletes in contact sports returning to competition with any lesions suspicious for HSV, because the infection is commonly misdiagnosed and can lead to widespread outbreaks.

Verruca vulgaris (Common Warts) Warts are one of the most common infections in humans and are particularly prevalent among children and young adults. They are caused by human papillomavirus, which infects epithelial cells. Disruption of the epithelial barrier by maceration and/or physical trauma and increased direct skin-to-skin contact places athletes at higher risk for infection. Warts typically present as rough, velvety, hyperkeratotic papules, plaques, and nodules with disruption of normal skin markings (Fig. 22.13). The hands, feet, fingers, toes, and periungual and subungual skin are particularly affected, but lesions can occur anywhere on the skin surface. The diagnosis is clinical, and the differential diagnosis

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Fig. 22.13  Plantar warts. Note the disruption of normal skin markings. (Courtesy Kenneth E. Greer.)

Fig. 22.15  Mycobacterium marinum. (Courtesy Kenneth E. Greer.)

on the body. The differential diagnosis includes common warts and, in immunocompromised patients, dimorphic fungal infections (Cryptococcus or Histoplasma). Treatment is not always necessary because the infection will eventually spontaneously resolve (in months to years), but if required, liquid nitrogen cryotherapy, topical cantharidin 0.7% liquid, and/or curettage are most effective. NCAA guidelines require that lesions on wrestlers must be curetted or removed before competition but that solitary or localized, clustered lesions can be covered with a gas-impermeable membrane, followed by application of tape that is appropriately anchored and cannot be dislodged.1

Mycobacterial Infections Fig. 22.14  Molluscum contagiosum. (Courtesy Kenneth E. Greer.)

on the palms and soles most commonly includes corns and calluses. Punctate black dots that represent thrombosed capillaries after paring are a useful diagnostic clue. Warts will often spontaneously regress after months to years. If treatment is desired, physical modalities, such as liquid nitrogen cryotherapy and daily use of over-the-counter salicylic acid 40% plasters, are most effective. Warts resistant to these therapies should be referred to a dermatologist for consideration of laser treatment, immunotherapy, or topical/intralesional chemotherapeutic agents. NCAA wrestling guidelines require that warts on the face be treated or covered by a mask and that other warts be adequately covered.1

Molluscum Contagiosum Infection with the poxvirus, molluscum contagiosum virus, results in a viral infection restricted to the skin. Transmission occurs mainly through direct skin contact; as a result, persons in closecontact sports are at higher risk. Furthermore, the use of school swimming pools and shared bathing fomites (i.e., sponges and towels) has been reported to increase the risk of infection.19,20 The virus most commonly affects children, but it can be a sexually transmitted infection in adults. Lesions present as small, dome-shaped, pink to flesh-colored papules with central dell or umbilication (Fig. 22.14). Patients typically have numerous lesions

Mycobacterium marinum (Swimming Pool or Fish Tank Granuloma) Mycobacterium marinum is an atypical mycobacterium that can infect persons exposed to freshwater and saltwater, including swimming pools, lakes, fish tanks, and ocean water. One epidemic involving a single swimming pool infected 290 individuals.21 Risk factors include immunosuppression and skin trauma. Skin lesions present as violaceous papules that evolve into granulomatous nodules and/or verrucous plaques (Fig. 22.15). Ulceration may be noted, and occasionally spread along lymphatic channels may produce a sporotrichoid pattern. In some cases, M. marinum infections can cause deeper infections including tenosynovitis, septic arthritis, and osteomyelitis. Skin biopsy with tissue culture establishes the diagnosis. Other mycobacterial infections, dimorphic fungal infections, and Nocardia can present with similar clinical findings. Consultation with a dermatologist and/or infectious disease expert is recommended for diagnosis, treatment, and return-toplay guidelines on an individual case basis.

Parasitic Infections Pediculosis Capitis Pediculosis capitis results from infestation by the head louse, Pediculus humanus capitis. Transmission occurs by direct head-to-head contact or via fomites such as hair care products, pillows, helmets, or other protective headgear. The most common presentation

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is the presence of eggs firmly attached to scalp hairs, which can be readily seen by the naked eye. Less commonly, adult lice and erythematous macules and papules corresponding to bites may be found. Often, secondary changes from scratching predominate, including excoriations, erythema, and scaling. Patients may report pruritus, regional lymphadenopathy, or low-grade fever. The differential diagnosis includes dandruff, pseudonits (from hair casts or hair spray), psoriasis, and eczema. Firstline therapy includes daily wet combing with a fine-toothed comb to physically remove eggs and the use of over-the-counter shampoos such as permethrin 1%, or synergized pyrethrins, or dimethicone 4% lotion. NCAA guidelines recommend that wrestlers be treated with an appropriate pediculicide and be reexamined for completeness of response before return to competition.1

Scabies Infestation by the mite Sarcoptes scabiei is common and produces a diffuse, pruritic eruption that is seen worldwide. Patients typically experience severe pruritus 4 to 6 weeks after initial infestation, although subsequent infections can present sooner. Scaly papules and plaques preferentially affect the interdigital web spaces, fingers, volar wrists, lateral palms, axillae, scrotum, penis, labia, and areolae (Fig. 22.16). Thin, thread-like burrows less than 1 cm in length are pathognomonic. Although the infection can be suspected clinically, diagnosis can be confirmed with microscopic confirmation of skin scrapings demonstrating scabies mites, eggs, or fecal pellets (scybala) or with use of a dermatoscope. The condition is commonly misdiagnosed, and the differential diagnosis includes atopic dermatitis, dyshidrotic eczema, contact dermatitis, insect bites, and other conditions characterized by pruritus. Treatment is with permethrin 5% cream applied

Fig. 22.16  Scabies affecting the penis, scrotum, and interdigital web space. (Courtesy Kenneth E. Greer.)

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topically to all areas of the body from the neck down and washed off after 8 to 14 hours, or with a single dose of ivermectin, 200 µg/kg orally. Both treatments should be repeated in 2 weeks.22 All cohabitants and close contacts must be simultaneously treated and living environments need to be thoroughly cleaned. Symptoms typically rapidly improve, but rash and pruritus may persist for up to 4 weeks or longer. NCAA recommendations for wrestlers include documenting negative scabies prep (i.e., microscopic examination of skin scrapings) at meet or tournament time.1

Cutaneous Larva Migrans Animal hookworms, particularly Ancylostoma braziliense and A. caninum, can infect athletes playing barefoot on sand or soil contaminated by animal feces.23 Lesions are characteristically erythematous raised serpiginous burrows that are 3 mm wide and several centimeters long and are intensely pruritic (Fig. 22.17). Occasionally, lesions may be vesicular. Burrows expand by several centimeters daily and are most commonly found on the feet and buttocks. Infection is most prevalent in tropical and subtropical climates.24 The clinical context of barefoot sand or soil exposure with serpiginous lesions on examination is diagnostic. Phytophotodermatitis or jellyfish stings may produce similarappearing serpiginous inflammatory lesions. Treatment is a single oral dose of ivermectin, 200 µg/kg or albendazole, 400 to 800 mg by mouth daily for 3 days.25 Footwear use can prevent infection. Cutaneous larva migrans is not transmissible.

MECHANICAL DERMATOSES Abrasions/Lacerations Abrasions and lacerations result from physical trauma to the skin but differ in their depth of involvement. Abrasions are superficial wounds that disrupt the epidermis and typically result from shearing forces, such as when an athlete falls on a turf field or road. Lacerations are deeper wounds that penetrate the epidermis and involve the dermis. Both forms of injury can result in bleeding and put athletes at risk for secondary infection or acquisition and/or transmission of blood-borne pathogens. Tetanus status

Fig. 22.17  Cutaneous larva migrans on the wrist. (Courtesy Kenneth E. Greer.)

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should be assessed with all forms of injury, and if necessary, a tetanus booster should be administered. Wounds should be generously irrigated with saline solution and all foreign material should be removed. Minor abrasions can be cleaned with antibacterial soap and covered with antibiotic ointment and an occlusive hydrocolloid dressing before returning to play. Lacerations may require local anesthesia for comfort of the athlete and closure of the defect with sutures, staples, or cyanoacrylate glues.

Friction Blisters Blisters are a common occurrence in athletes that result from repetitive shearing forces. Mechanical trauma leads to a split within the epidermis, with fluid collection resulting in tender vesicles and bullae. Blisters occur most commonly on thick skin of the palms and soles, and moisture increases the risk of development. Prevention includes the use of properly fitting footwear and keeping the skin dry. If excessive sweating is noted, therapies that reduce perspiration can be pursued, such as topical aluminum chloride 20% solution, and absorbent cellulose and talc powders. Treatment includes puncture of the blister edge to release fluid but leaving the blister roof intact to act as a biologic dressing. Additional protective bandages can be applied to encourage epithelization and provide cushioning.26 Excessive and dramatic blistering among multiple family members should raise suspicion for a genetically inherited trait, such as epidermolysis bullosa simplex. Athletes can resume competition if bleeding is stopped and wounds are firmly covered by occlusive dressings that are able to withstand the demands of activity.

An acute, painful subungual hematoma may need to be evacuated with electrocautery through the nail for pain relief. The differential diagnosis includes acral lentiginous melanoma. If uncertainty exists, referral to a dermatologist is prudent for a possible biopsy. Talon noir presents as pinpoint, blue-black dots on the posterior heel and represents an accumulation of red blood cells in the stratum corneum (Fig. 22.18). The differential diagnosis again includes melanocytic neoplasms, including melanoma. However, with paring of the skin, the lesion disappears. Trauma to the anterior ear sustained during contact sports such as wrestling, boxing, or rugby can lead to hemorrhage beneath the perichondrium. If recognized, the hematoma should be drained immediately with needle incision to prevent necrosis of the perichondrium with resulting fibrosis leading to deformity and a “cauliflower” appearance (Fig. 22.19).

Striae Striae (stretch marks) are common in the general population, especially during pregnancy and puberty. Their development among athletes is typically associated with intense training periods with rapid muscle growth and weight gain. Lesions are violaceous, linear atrophic streaks and favor the upper arms and thighs (Fig. 22.20). The sudden appearance of striae in athletes should prompt some consideration of the use of anabolic steroids, especially when coupled with other signs of anabolic steroid use (e.g., acne, male-pattern balding, deepened voice, personality change, and gynecomastia). Striae tend to improve in appearance with time. Treatment, which is usually not particularly effective, includes topical retinoids and the pulsed dye laser for vascular lesions.

Calluses and Corns

Acne Mechanica

Calluses and corns are common dermatologic conditions that result from prolonged mechanical shear, friction, and/or pressure placed on the skin. They are characterized by scaly papules and plaques and occur most commonly on the hands and feet. Athletes are at particular risk because of the forces applied during training and competition, and lesions can result in significant pain. If mechanical forces are applied over a broad skin surface, a callus forms. However, when forces are applied to a focused location, such as a bony prominence, a corn develops and is characterized by a central hard core. Warts should be considered in the differential diagnosis and can be differentiated by the loss of normal skin markings and the presence of punctate black dots that become evident after paring. Therapeutic options include paring and padding of lesions and topical use of keratolytics such as salicylic acid 40% plaster or urea 40% cream. Properly fitting footwear and the use of donut-shaped pads can help offset the pressure placed on corns, which often leads to improvement and/or their disappearance.

Acne mechanica is a variant of acne precipitated by any combination of pressure, friction, occlusion, rubbing, and heat.27 It is characterized by the appearance of inflammatory red papules and pustules in areas covered by clothing, uniforms or other protective equipment (Fig. 22.21). Lesions result from blockage of the pilosebaceous unit with comedo formation and eventual inflammation. The differential diagnosis includes acne vulgaris (i.e., typical teenage acne), acneiform drug reactions, Pityrosporum folliculitis, and anabolic steroid use. Acne mechanica is

Hemorrhage Mechanical trauma to the skin can result in damage to small capillaries in the dermis with local hemorrhage. Several characteristic presentations occur in athletes, including subungual hemorrhage, talon noir, and subperichondrial hematomas. Subungual hemorrhage is a frequent occurrence among athletes, presenting with brown-black discoloration underneath the toenail.

Fig. 22.18  Talon noir. (Courtesy Kenneth E. Greer.)

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Fig. 22.22  Athlete’s nodules on the dorsal feet in a runner. (Courtesy Kenneth E. Greer.)

Fig. 22.19  End-stage fibrosis from repeated subperichondrial hematomas in a wrestler, resulting in a “cauliflower ear.” (Courtesy Kenneth E. Greer.)

often challenging to treat. Simple therapy includes the use of cotton undershirts to minimize direct skin contact with occlusive equipment and immediate showers after practice with the use of benzoyl peroxide or sulfur-based washes (e.g., selenium sulfide 2.5% lotion).26 More severe presentations may require use of topical comedolytics at night (e.g., tretinoin 0.05% cream), topical antibiotic therapy (e.g., clindamycin 1% lotion or solution) and/or oral antibiotic therapy (e.g., a doxycycline hyclate capsule, 100 mg by mouth twice daily; cephalexin, 500 mg by mouth twice daily; or a trimethoprim-sulfamethoxazole doublestrength tablet by mouth twice daily). Athletes taking doxycycline should be counseled regarding potential sun sensitivity. Cessation of the precipitating etiology will lead to spontaneous resolution in the off-season.

Athlete’s Nodules (Collagenomas)

Fig. 22.20  Striae. (Courtesy Kenneth E. Greer.)

Athlete’s nodules are benign, nonpainful, reactive flesh-colored papules, plaques, or nodules that occur in areas exposed to longterm friction and trauma (Fig. 22.22). They have been found on the tibial tuberosities of surfers (“surfer’s nodules”), dorsal feet of runners (“Nike nodules”), knuckles of boxers (“knuckle pads”), and shins of hockey players (“skate bites”).26,28 These reactive growths have also been reported to develop in marbles players, skiers, soccer players, karate enthusiasts, and football players.28–30 Histopathology reveals reactive fibrosis with thickened and irregular collagen bundles.28 The differential diagnosis includes hypertrophic scar, callus, dermatofibroma, foreign-body reaction, verrucae, granuloma annulare, and other neoplastic growths. They can be distinguished from sports-related callosities by their failure to resolve after discontinuation of athletic activity. The clinical appearance and history are diagnostic. Treatment is unsatisfactory and is not required in the absence of symptoms; cessation of activity may lead to a decrease in size, but excision is usually required for definitive therapy.

Hidradenitis Suppurativa Fig. 22.21  Acne vulgaris aggravated by acne mechanica as a result of the use of athletic shoulder pads.

Hidradenitis suppurativa is a common, debilitating, chronic disorder of uncertain etiology that is under-recognized and often misdiagnosed.31 Sites rich in apocrine glands are preferentially

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against UVB radiation.35 Treatment of sunburn is symptomatic with use of cool compresses, oral antiinflammatory medications (e.g., acetaminophen or ibuprofen), and bland emollients.

Fig. 22.23  Hidradenitis suppurativa in the axillae with scarring and fibrosis. (Courtesy Kenneth E. Greer.)

affected, such as the axillae, perineum, and inframammary folds. Females are more likely to experience the disease, and smoking and obesity are known exacerbating factors.32 Lesions present after puberty in the second to third decade of life and begin as painful papules or nodules that evolve into sterile draining abscesses, scars, sinus tracts, and fistulae (Fig. 22.23). The restriction to intertriginous areas and disease chronicity are helpful diagnostic clues. Although bacteria are sometimes cultured from draining lesions, the role of bacterial infection in hidradenitis suppurativa is uncertain, and their presence most likely represents secondary colonization rather than primary infection.32 The differential diagnosis is extensive but most commonly includes bacterial infections and cutaneous Crohn disease. Patients are often treated for furunculosis for years before the disease is recognized. Consultation with a dermatologist is recommended. The NCAA states that a wrestler will be disqualified if extensive or purulent draining lesions are present and that lesions shall not be covered to allow participation.1

ENVIRONMENTAL DERMATOSES Photodermatoses Sunburn Acute exposure to UV radiation leads to sunburn, which is clinically visible as skin erythema but may progress to vesicles and bullae with associated warmth, pain, and swelling. The health risks of sunburn with respect to melanoma development cannot be overemphasized. One or more blistering sunburns in childhood or adolescence more than doubles a person’s chances of developing melanoma,33 and a person’s risk for melanoma doubles with more than five sunburns at any age.34 Protection from sunburns includes avoidance of peak hours of UV radiation (10 a.m. to 3 p.m.), wearing sun-protective clothing including hats and sunglasses, and the regular use of broad-spectrum, waterresistant sunscreen that protects against UVA and UVB wavelengths with at least a sun protection factor 15 rating. Fair-skinned athletes who spend significant time outdoors may benefit from use of oral polypodium leucotomos extract, which has been shown to have molecular and photobiologic protective effects

Skin Cancer Athletes who train and compete outdoors must be educated regarding an increased risk of skin cancer. UV radiation has been demonstrated to be one of the most important risk factors in the development of both malignant melanoma and nonmelanoma skin cancer. Particular efforts should be aimed at sun protection in young athletes, because tanning may be desired in this age group. Extreme UV radiation exposure has been documented among skiers, mountaineers, cyclists, and triathletes.36 In an ageand sex-matched study of 210 marathon runners, these athletes were found to have an increased risk for malignant melanoma and nonmelanoma skin cancer.37 Furthermore, sweating has been shown to potentially contribute to skin cancer development by lowering the sunburn threshold.38 Athletes should be counseled to avoid training and competition at peak hours of UV radiation, to wear adequate sun-protective clothing, and to consistently and repeatedly apply a broad-spectrum water-resistant sunscreen that protects against UVA and UVB wavelengths.

Aquatic Dermatoses Swimmer’s Itch and Seabather’s Eruption Swimmer’s itch results when miracidia of several species of Schistosoma cercariae penetrate the skin during fresh or saltwater activity. Lesions predominate in uncovered skin and are typically red papules and vesicles that are intensely itchy and painful. There is no risk of systemic infection because the organisms die in the superficial dermis. Treatment is symptomatic and includes the use of topical corticosteroids, antihistamines, and antipruritic lotions. Prevention is challenging but includes wearing protective clothing and coating the skin with emollients. Seabather’s eruption is caused by minute stings of coelenterate larvae of jellyfish and sea anemone, which become trapped underneath clothing during saltwater activity. Itchy papules or wheals are characteristically confined to areas covered by swimwear (Fig. 22.24). Treatment is symptomatic and includes the use of topical corticosteroids, antihistamines, and antipruritic lotions. Hair Discoloration Competitive swimmers may present with hair discoloration. A peculiar greenish discoloration occurs in persons with natural or tinted blond, gray, or white hair, and is caused by copper ions in the water.39 Treatment includes use of a hydrogen peroxide 2% to 3% solution or commercial chelating shampoos. In addition, discoloration of dark hair has been reported in Japan, with affected persons having golden hair. Electron microscopy has demonstrated cuticle damage, allowing hypochlorous acid to penetrate the hair cortex, leading to oxidation and the degeneration of melanosomes.40

Irritant Contact Dermatitis Irritant contact dermatitis is a nonimmunologic, inflammatory reaction of the skin that requires no previous sensitization and

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Fig. 22.25  Erythema ab igne from chronic heating pad use for knee pain. (Courtesy Kenneth E. Greer.) Fig. 22.24  Seabather’s eruption. Note that the lesions are confined to bathing suit distribution. (Courtesy Kenneth E. Greer.)

represents the majority of cases of contact dermatitis. Any chemical or physical insult that damages the integrity of the skin can lead to irritant contact dermatitis. Clinical presentations vary based on the acuity of disease and the specific etiologic agent, but can include vesicles and bullae, red and scaly plaques, cracks and fissures, hives, pustules, and acneiform papules. Etiologies specific to athletes include fiberglass used in hockey sticks, shin guards among soccer players, abrasive outdoor basketballs with a pebbled surface, alkaline lime used in field markings, chemicals in swimming pools, and seaweed, corals, sea cucumbers, sea mosses, and plants encountered by saltwater enthusiasts.41 Both surfers and runners can experience nipple dermatitis from chronic friction with surfboards or shirts, respectively, and swimmers can experience “swimmer’s shoulder” from an unshaven beard that repeatedly rubs the shoulder.41 Treatment centers on identification and avoidance of irritants and protection of the skin barrier with bland emollients.

Thermal Damage Athletes often use heat or ice packs to treat injuries, which can result in specific skin reactions. Inappropriate use of ice packs can result in frostbite with erythema and bullae. Rarely, panniculitis (i.e., inflammation of subcutaneous fat) can present as painful, firm, violaceous, indurated nodules 1 to 3 days after pronged cold exposure. Chronic use of heating pads on the skin surface may result in a rare condition called erythema ab igne (Fig. 22.25). A red–brown, nonblanchable, netlike discoloration of the skin occurs. It should be distinguished from livedo reticularis, which is violaceous and blanchable. The pigmentary changes are long lasting but eventually fade. Further use of heat should be avoided.

Chilblains (perniosis) are localized inflammatory lesions induced by prolonged exposure to cold and damp weather, and occur primarily on the fingers and toes. Lesions are nonblanching, erythematous-to-purple macules and papules that may be pruritic, burning, or painful (Fig. 22.26). Lesions are often misdiagnosed as vasculitis. Treatment is symptomatic with rewarming the area and using topical antipruritic agents.

URTICARIA, ANAPHYLAXIS, AND IMMUNOLOGIC DISORDERS Urticaria Urticaria is one of the most common skin disorders confronted by physicians across all specialties. Allergies, autoimmune conditions, medications, and infections are among the most common causes of urticaria in the general population. Specific subsets of urticaria, including cholinergic, solar, aquagenic, and cold urticaria may develop during athletic activity. Cholinergic urticaria presents as hives within a few minutes of sweat-inducing stimuli, such as physical exertion, hot baths, or sudden emotional stress. The lesions are typically small (2 to 3 mm) monomorphic wheals; they favor the upper half of the body and are surrounded by an obvious red flare (Fig. 22.27). Solar and aquagenic urticaria are defined by wheals and/or pruritus occurring within minutes of exposure to UV radiation, or visible light and water, respectively. Exposure to a cold stimulus results in cold urticaria. Management of these specific subsets of urticaria includes avoidance or protection from the inciting stimulus, and the use of oral antihistamines.

Exercise-Induced Anaphylaxis Anaphylaxis provoked by exercise is divided into exercise-induced anaphylaxis and food-dependent exercise-induced anaphylaxis.

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generalize and present as itchy, red, scaly plaques. Sources of contact allergens common to athletes include adhesives used in athletic tape, topical medications (e.g., anesthetics, antiseptics, and antibiotics), plus rubbers and rubber accelerators found in shoes, knee pads/guards, wet suits, and swimming goggles.41 The diagnosis is suspected based on the location and morphology of the rash and can be confirmed by the use of specialized patch testing. Treatment includes avoidance of the specific allergen and the use of topical corticosteroids. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Fig. 22.26  Chilblains (perniosis). (Courtesy Kenneth E. Greer.)

Citation: Daum RS, et al. A placebo-controlled trial of antibiotics for smaller skin abscesses. N Engl J Med. 2017;376(26):2545–2555.

Level of Evidence: I

Summary: In this multicenter, prospective, double-blind, placebo-controlled trial involving outpatient adults and children with simple abscesses, cure rates at day 10 were higher in patients receiving incision and drainage with clindamycin (83.1%), or incision and drainage with trimethoprim and sulfamethoxazole (81.7%) compared to incision and drainage with placebo [(68.9%), P < .001 for both comparisons].

Citation: Moran GJ, et al. Effect of cephalexin plus trimethoprim-sulfamethoxazole vs. cephalexin alone or clinical cure of uncomplicated cellulitis: a randomized clinical trial. JAMA. 2017;317(20):2088–2096.

Level of Evidence: I

Summary:

Fig. 22.27  Cholinergic urticaria. Note the distinctive erythematous flare surrounding each wheal.

The pathophysiology of either subset is not fully understood, but in food-dependent exercise-induced anaphylaxis, the ingestion of certain foods is required. Patients experience anaphylactic symptoms with hives and/or angioedema associated with exercise. The differential diagnosis includes anaphylaxis secondary to other etiologies (e.g., medications), cholinergic urticaria, exerciseinduced asthma, mastocytoses, and hereditary angioedema. The diagnosis is clinical and acute management is identical to other forms of anaphylaxis.

Allergic Contact Dermatitis Allergic contact dermatitis is an immunologically mediated delayed-type hypersensitivity response to a specific allergen. Lesions are usually localized to sites of skin contact but can

In this multicenter, prospective, double-blind, placebo-controlled trial of patients older than 12 years with uncomplicated cellulitis, there was no difference in clinical cure among participants receiving cephalexin plus trimethoprim-sulfamethoxazole (83.5%) compared to cephalexin plus placebo [(85.5%), P = .50].

Citation: National Collegiate Athletic Association (NCAA): 2014-2015 NCAA Sports Medicine Handbook. Retrieved February 5, 2017, from http://www.ncaapublications.com/ DownloadPublication.aspx?download=MD15.pdf: Accessed February 8, 2017.

Level of Evidence: V

Summary: This publication is a useful reference for NCAA sports medicine guidelines, including eligibility and return-to-play guidelines for skin infections.

Citation: Cordoro KM, Ganz JE. Training room management of medical conditions: sports dermatology. Clin Sports Med. 2005;24:565–598.

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Level of Evidence:

Citation:

V

Adams BB. Dermatologic disorders of the athlete. Sports Med. 2002;32(5):309–321.

Summary:

259

An excellent review article of the most relevant sports-related dermatoses with numerous representative clinical images.

Level of Evidence:

Citation:

Summary:

Kockentiet B, Adams BB. Contact dermatitis in athletes. J Am Acad Dermatol. 2007;56(6):1048–1055.

A well-organized general review of skin conditions seen in athletes.

V

Level of Evidence: V

Summary: This review article examines the published literature of contact dermatitis in athletes and provides a comprehensive resource of specific allergic and irritant contactants unique to athletes.

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REFERENCES 1. National Collegiate Athletic Association (NCAA). 2014-2015 NCAA Sports Medicine Handbook. Retrieved February 5, 2017, from http://www.ncaapublications.com/DownloadPublication. aspx?download=MD15.pdf. Accessed February 8, 2017. 2. Sosin DM, Gunn RA, Ford WL, et al. An outbreak of furunculosis among high school athletes. Am J Sports Med. 1989;17:828–832. 3. Talan DA, Mower WR, Krishnadasan A, et al. Trimethoprimsulfamethoxazole versus placebo for uncomplicated skin abscess. N Engl J Med. 2016;374(9):823–832. 4. Daum RS, Miller LG, Immergluck L, et al. A placebo-controlled trial of antibiotics for smaller skin abscesses. N Engl J Med. 2017;376(26):2545–2555. 5. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infection in adults and children. Clin Infect Dis. 2011;52(3):e18–e55. 6. Karppelin M, Siljander T, Vuopio-Varkila J, et al. Factors predisposing to acute and recurrent bacterial non-necrotizing cellulitis in hospitalized patients: a prospective case control study. Clin Microbiol Infect. 2010;16(6):729–734. 7. Sendi P, Johansson L, Norrby-Teglund A. Invasive group B streptococcal disease in non-pregnant adults: a review with emphasis on skin and soft tissue infections. Infection. 2008; 36(2):100–111. 8. Vayalumkal JV, Jadayji T. Children hospitalized with skin and soft tissue infections: a guide to antibacterial selection and treatment. Paediatr Drugs. 2006;8(2):99–111. 9. Böcher S, Tønning B, Skov RL, et al. Staphylococcus lugdunensis, a common cause of skin and soft tissue infections in the community. J Clin Microbiol. 2009;47(4):946–950. 10. Garcia-Lechuz JM, Cuevas O, Castellares C, et al. Streptococcus pneumonia skin and soft tissue infections: characterization of causative strains and clinical illness. Eur J Clin Microbiol Infect Dis. 2007;26(4):247–253. 11. Phillips S, MacDougall C, Holdford DA. Analysis of empiric antimicrobial strategies for cellulitis in the era of methicillinresistant Staphylococcus aureus. Ann Pharmacother. 2007;41(1): 13–20. 12. Madaras-Kelly KJ, Remington RE, Oliphant CM, et al. Efficacy of oral beta-lactam versus non-beta-lactam treatment of uncomplicated cellulitis. Am J Med. 2008;121(5):419–425. 13. Moran GJ, Krishnadasan A, Mower WR, et al. Effect of cephalexin plus trimethoprim-sulfamethoxazole vs. cephalexin alone or clinical cure of uncomplicated cellulitis: a randomized clinical trial. JAMA. 2017;317(20):2088–2096. 14. Raff AB, Kroshinsky D. Cellulitis: a review. JAMA. 2016;316(3): 325–337. 15. Blaise G, Nikkels AF, Hermanns-Le T, et al. Corynebacteriumassociated skin infections. Int J Dermatol. 2008;47(9):884–890. 16. Sims D, Brettin T, Detter JC. Complete genome sequence of Kytococcus sedentarius type strain (541). Strand Genomic Sci. 2009;1(1):12–20. 17. Belongia EA, Goodman JL, Holland EJ, et al. An outbreak of herpes gladiatorum at a high-school wrestling camp. N Engl J Med. 1991;325:906–910. 18. Dworkin MS, Shoemaker PC, Spitters C, et al. Endemic spread of herpes simplex virus type I among adolescent wrestlers and their coaches. Pediatr Infect Dis J. 1999;18:1108–1109.

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19. Nizeki K, Kano O, Yoshiro K. An epidemic study of Molluscum contagiosum: relationship to swimming. Dermatologica. 1984;169:197–198. 20. Choong KY, Roberts LJ. Molluscum contagiosum, swimming and bathing: a clinical analysis. Australas J Dermatol. 1999;40:89–92. 21. Philpott JA, Woodburne AR, Philpott OS, et al. Swimming pool granuloma: a study of 290 cases. Arch Dermatol. 1963;88: 158–161. 22. Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015; 64(RR-03):1–137. 23. Biolcati G, Alabiso A. Creeping eruptions of larva migrans—a case report in a beach volley athlete. Int J Sports Med. 1997; 18(8):612–613. 24. Davies HD, Sakuls P, Keystone JS. Creeping eruption. A review of clinical presentation and management of 60 cases presenting to a tropical disease unit. Arch Dermatol. 1993;129:588–591. 25. Hochedez P, Caumes E. Hookworm-related cutaneous larva migrans. J Travel Med. 2007;14(5):326–333. 26. Cordoro KM, Ganz JE. Training room management of medical conditions: sports dermatology. Clin Sports Med. 2005;24: 565–598. 27. Basler RS. Acne mechanica in athletes. Cutis. 1992;50(2): 125–128. 28. Dickens R, Adams BB, Mutasim DF. Sports-related pads. Int J Dermatol. 2002;41:291–293. 29. Cohen PR, Eliezri YD, Silvers DN. Athlete’s nodules: sportsrelated connective tissue nevi of the collagen type (collagenomas). Cutis. 1992;50(2):131–135. 30. Uchiyama M, Tsuboi R, Mitsuhashi Y. Athlete’s nodules. J Dermatol. 2009;36:608–611. 31. Kurzen H, Kurokawa I, Jemec GM, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17(5):455–456. 32. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol. 2009;60(4): 539–561. 33. Lew RA, Sober AJ, Cook N, et al. Sun exposure habits in patients with cutaneous melanoma: a case study. J Dermatol Surg Oncol. 1983;12:981–986. 34. Pfahlberg A, Kolmel KF, Gefeller O. Timing of excessive ultraviolet radiation and melanoma: epidemiology does not support the existence of a critical period of high susceptibility to solar ultraviolet radiation-induced melanoma. Brit J Dermatol. 2001;144(3):471–475. 35. Kohli I, Shafi R, Isedeh P, et al. The impact of oral polypodium leucotomos extract on ultraviolet B response: a human clinical study. J Am Acad Dermatol. 2017;77(1):33–41. 36. Moehrle M. Outdoor sports and skin cancer. Clin Dermatol. 2008;26(1):12–15. 37. Ambros-Rudolph CM, Hofmann-Wellenhof R, Richtig E, et al. Malignant melanoma in marathon runners. Arch Dermatol. 2006;142(11):1471–1474. 38. Moehrle M, Koehle W, Dietz K, et al. Reduction of minimal erythema dose by sweating. Photodermatol Photoimmunol Photomed. 2000;16:260–262. 39. Basler RS, Basler GC, Palmer AH, et al. Special skin symptoms seen in swimmers. JAAD. 2000;43(2):299–305. 40. Nanko H, Mutoh Y, Atsumi R, et al. Hair-discoloration of Japanese elite swimmers. J Dermatol. 2000;27(10):625–634. 41. Kockentiet B, Adams BB. Contact dermatitis in athletes. JAAD. 2007;56(6):1048–1055.

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23  Facial, Eye, Nasal, and Dental Injuries John Jared Christophel

Despite advances in protective gear for the face, facial trauma remains a common injury treated by sports medicine physicians. The face is a rather “high rent” district with sole proprietorship of four out of five senses (vision, hearing, taste, and smell) and 10 out of 12 cranial nerves (all but the vagus and spinal accessory cranial nerves). In addition, the face plays a large role in a person’s appearance, and his or her ability to communicate and eat. Injuries in this area carry a higher risk of detriment to an athlete’s quality of life.1 Given the central role of the face in a person’s functioning, even simple lacerations are often treated with greater care than a similar injury elsewhere on the body. This chapter addresses the most common sports injuries to the face, focusing on injuries that need to be referred to a specialist, and treatment of injuries that typically do not require referral.

SOFT TISSUE INJURIES TO THE FACE General Considerations Timing of Repair It is not necessary to repair facial wounds immediately. However, when possible, most wounds should be closed within 4 to 6 hours. The rate of infection in facial lacerations does rise significantly until after 24 hours, but the progressive tissue edema makes meticulous closure more difficult and therefore should be performed sooner rather than later.2 In the case of significantly contaminated wounds, it is appropriate to perform “delayed primary” closure after extensive débridement and a period of packing/cleansing over 24 to 72 hours to lessen the chance of infection. This procedure is usually only undertaken for extensive contaminated wounds that require closure in the operating room. Healing by secondary intention is less than ideal for soft tissue injuries on the face unless significant tissue loss has occurred; the scar from primary closure of a laceration is significantly better than that of a similar wound left to heal on its own. Anesthesia Simple lacerations that are not full thickness through the epidermis will, at a minimum, require cleaning prior to treatment; thus a topical anesthetic cream can be considered. Topical anesthetic creams include a eutectic mixture of local anesthetics (EMLA): tetracaine, liposome-encapsulated tetracaine, and liposome-encapsulated lidocaine.3 However, most patients will require injection of a local anesthetic prior to definitive treatment of their wounds, and prior application of a topical anesthetic 260

can deaden the pain of needle insertion to a small degree. This factor is probably most important in pediatric patients who have very little tolerance for pain before they become frightened, with a resultant need for sedation. In most adults, local anesthetic injections are well tolerated without prior application of topical anesthetic cream and allow the wound to be treated in the most expeditious manner. The pain from local anesthetic injection evolves from both the acidity in the commercially prepared anesthetic (to prolong shelf life) and the dermal distension from the volume of the anesthetic. The buffering of local anesthetic with sodium bicarbonate in a 10% volume to volume can significantly reduce the perception of pain.4 However, even if buffered anesthetic is used, poor injection technique will result in significant pain.5 Local anesthetic solution should be injected with a 27-gauge or smaller needle. Experienced practitioners often do not let patients see the needle to be used, and recent studies have shown that visualizing the needle increases the perception of pain.6 The plane of injection should be in the subcutaneous tissue immediately beneath the dermis. The most common mistake is to inject anesthetic intradermally, which will be exquisitely painful as the pain receptors in the dermis distend. Whenever possible, the subcutaneous plane should be entered through an existing laceration, because pain is experienced when the needle enters through intact skin. The use of an anesthetic combined with epinephrine is helpful both for increasing the duration of the anesthesia and for decreasing bleeding during wound repair. Epinephrine as dilute as 1:200,000 g/mL is as efficacious as more concentrated solutions in providing vasoconstriction.7 The onset of anesthesia after infiltration is rather rapid (60 min before activity

• Timing, amount and type of food and drink should match the practical needs of the event and the individual preferences • Foods higher in fat, protein, or fiber may cause gastrointestinal issues during activity • Carbohydrate goals: • Light: low intensity or skilled-based activity • 3–5 g/kg/day • Moderate: 1 h exercise program per day • Carbohydrate 5–7 g/kg/day • High: 1–3 h/day moderate/high intensity • 6–10 g/kg/day • Very high: extreme >4–5 h/day moderate/high intensity • 8–12 g/kg/day • Brief: 2.5 h • Up to 90 g of carbohydrate per hour • Focus on carbohydrate and protein food pairings • Carbohydrate: Replenishing glycogen stores and limiting cortisol-induced muscle damage during exercise • Recommendation: 1 g/kg • Protein: crucial to muscle protein synthesis and repair • Recommendation: 20 g of high-quality protein • Meal examples: • Example: 8 oz. chocolate milk with turkey sandwich (2 slices of whole grain bread & 3 oz. turkey) • Example: 1 cup ready-to-eat cereal (i.e., Cheerios) with 1 cup skim milk and 1 medium banana

During exercise

Post exercise Aim for 45–60 min after activity

Values adapted from reference 27, 29, 31, and 32.

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TABLE 25.4  Common Performance Enhancing Substances Substance

Purported Benefit

Usual Dose and Timing to Event

Comments

Creatine

3–5 g/day, not necessarily important when taken33 0.1 mmol/kg/day or 5–6 mmol/day over 5–6 days or more34

Muscle will hold more water and increase weight of athlete Complex pathway of conversion to nitric oxide in the body

Small doses multiple times per day, 4–6 g/ day in total for at least 4 weeks7

May cause tingling or paresthesia (thought to be harmless)

Pre-workouts

Increased muscle ATP allowing higher workload Precursor to nitric oxide (vasodilator) thus improving tissue oxygenation and metabolism Precursor to muscle carnosine thus improves muscle buffering allowing higher workload Decreases perception of fatigue centrally, or peripheral mechanism Help athlete increase arousal

Mass gainers

Help athlete gain lean mass

No set research numbers

Nitrates (e.g., beetroot juice) Beta alanine

Caffeine

3–6 mg/kg 1 h prior to event 1–2 mg/kg during later endurance tasks33 No set research numbers

SELECTED READINGS

Summary:

Citation: American College of Sports M, Sawka MN, Burke LM, et al. American College of Sports Medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc. 2007;39(2):377–390.

Level of Evidence: Various topics defined by position statement The American College of Sports Medicine on exercise and fluid replacement for athletes provides a review of current recommendations and strategies to optimize fluid-replacement practices of athletes.

Citation: Thomas DT, Erdman KA, Burke LM. Position of the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine: Nutrition and Athletic Performance. J Acad Nutr Diet. 2016;116(3):501–528.

Level of Evidence: Various topics defined by position statement

Summary: The Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine merged to create a Position Statement regarding Nutrition and Athletic Performance. These organizations provide guidelines for the appropriate type, amount, and timing of intake of food, fluids, and supplements to promote optimal health and performance across different scenarios of training and competitive sport.

Meeusen R, Duclos M, Foster C, et al. Prevention, diagnosis, and treatment of the overtraining syndrome: joint consensus statement of the European College of Sport Science and the American College of Sports Medicine. Med Sci Sports Exerc. 2013;45(1):186–205.

Level of Evidence: Various topics defined by position statement

Summary Within this consensus statement between the American College of Sports Medicine and European College of Sport Science the current state of knowledge on overtraining syndrome (OTS) including definition, diagnosis, treatment and prevention is discussed.

Citation: Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the Female Athlete Triad–Relative Energy Deficiency in Sport (RED-S). Br J Sports Med. 2014;48(7):491–497.

Level of Evidence: Various topics defined by position statement

Citation: Buell JL, Franks R, Ransone J, et al. National Athletic Trainers’ Association. National athletic trainers’ association position statement: evaluation of dietary supplements for performance nutrition. J Athl Train. 2013;48(1). Various topics defined by position statement

The National Athletic Trainer’s Position Statement on the evaluation of dietary supplements for performance nutrition promoting a “food-first” philosophy to support health and performance; to understand federal and sport governing body rules and regulations regarding dietary supplements and banned substances; and to become familiar with reliable resources for evaluating the safety, purity, and efficacy of dietary supplements.

Citation:

Summary:

Level of Evidence:

Ensure third-party verification to help avoid illegal ingredients such as stimulants Consider the extra calories in overall diet; ensure third-party verification to help avoid illegal ingredients such as anabolic agents

Summary: This Consensus Statement replaces the previous and provides guidelines to guide risk assessment, treatment, and return-to-play decisions. The IOC expert working group introduces a broader, more comprehensive term for the condition previously known as Female Athlete Triad. This Consensus Statement also recommends

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practical clinical models for the management of affected athletes. The “Sport Risk Assessment and Return to Play Model” categorizes the syndrome into three groups and translates these classifications into clinical recommendations.

Citation: IOC consensus statement on sports nutrition 2010. J Sports Sci. 2011;29(suppl 1):S3–S4.

Level of Evidence: Various topics defined by position statement

Summary: A practical guide to eating for health and performance prepared by the Nutrition Working Group of the International Olympic Committee.

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REFERENCES 1. Sports C, Wellness Nutrition. A Dietetic Practice Group of the Academy of Nutrition and Dietetics. Find a SCAN RD. 2017. Accessed June 15, 2017. 2. Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the Female Athlete Triad–Relative Energy Deficiency in Sport (RED-S). Br J Sports Med. 2014; 48(7):491–497. 3. Meeusen R, Duclos M, Foster C, et al. Prevention, diagnosis, and treatment of the overtraining syndrome: joint consensus statement of the European College of Sport Science and the American College of Sports Medicine. Med Sci Sports Exerc. 2013;45(1):186–205. 4. Burke L, Deakin V, Allanson B. Clinical sports nutrition. 2015. 5. Loucks AB. Energy availability, not body fatness, regulates reproductive function in women. Exerc Sport Sci Rev. 2003;31(3):144. 6. De Souza MJ, Nattiv A, Joy E, et al. 2014 Female Athlete Triad Coalition consensus statement on treatment and return to play of the female athlete triad: 1st International Conference held in San Francisco, CA, May 2012, and 2nd International Conference held in Indianapolis, IN, May 2013. Clin J Sport Med. 2014;24(2):96–119. 7. Trexler ET, Smith-Ryan A, Stout JR, et al. International Society of Sports Nutrition position stand: beta-alanine. J Int Soc Sports Nutr. 2015;12(Generic):30. 8. Aragon AA, Schoenfeld BJ, Wildman R, et al. International Society of Sports Nutrition position stand: diets and body composition. J Int Soc Sports Nutr. 2017;14(1):16. 9. IOC consensus statement on sports nutrition 2010. J Sports Sci. 2011;29(suppl 1):S3–S4. 10. Noakes T, Volek JS, Phinney SD. Low-carbohydrate diets for athletes: what evidence? Br J Sports Med. 2014;48(14):1077. 11. Romijn JA, Coyle EF, Sidossis LS, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol. 1993;265(3): E380–E391. 12. Burke LM, Collier GR, Broad EM, et al. Effect of alcohol intake on muscle glycogen storage after prolonged exercise. J Appl Physiol. 2003;95(3):983–990. 13. Casa DJ, Armstrong LE, Hillman SK, et al. National Athletic Trainers’ Association position statement: fluid replacement for athletes. J Athl Train. 2000;35(2):212–224. 14. American College of Sports M, Sawka MN, Burke LM, et al. American College of Sports Medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc. 2007;39(2): 377–390. 15. Hew-Butler T, Rosner MH, Fowkes-Godek S, et al. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, CA, 2015. Clin J Sport Med. 2015;25(4):303–320. 16. Schwellnus MP. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med. 2009;43(6):401–408.

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17. Minetto MA, Holobar A, Botter A, et al. Origin and development of muscle cramps. Exerc Sport Sci Rev. 2013;41(1):3–10. 18. Nelson NL, Churilla JR. A narrative review of exercise-associated muscle cramps: factors that contribute to neuromuscular fatigue and management implications. Muscle Nerve. 2016;54(2): 177–185. 19. Maughan RJ, Shirreffs SM. Development of individual hydration strategies for athletes. Int J Sport Nutr Exerc Metab. 2008;18(5): 457–472. 20. Hoffman MD, Hew-Butler T, Stuempfle KJ. Exercise-associated hyponatremia and hydration status in 161-km ultramarathoners. Med Sci Sports Exerc. 2013;45(4):784–791. 21. Bergeron MF. Exertional heat cramps: recovery and return to play. J Sport Rehabil. 2007;16(3):190–196. 22. Hinton PS. Iron and the endurance athlete. Appl Physiol Nutr Metab. 2014;39(9):1012–1018. 23. Lukaski HC. Vitamin and mineral status: effects on physical performance. Nutrition. 2004;20(7–8):632–644. 24. Benardot D. Advanced Sports Nutrition. Champaign, IL: Human Kinetics; 2012. 25. Willis KS, Peterson NJ, Larson-Meyer DE. Should we be concerned about the vitamin D status of athletes? Int J Sport Nutr Exerc Metab. 2008;18(2):204–224. 26. Visser M, Deeg DJ, Lips P. Longitudinal Aging Study A. Low vitamin D and high parathyroid hormone levels as determinants of loss of muscle strength and muscle mass (sarcopenia): the Longitudinal Aging Study Amsterdam. J Clin Endocrinol Metab. 2003;88(12):5766–5772. 27. Thomas DT, Erdman KA, Burke LM. Position of the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine: nutrition and athletic performance. J Acad Nutr Diet. 2016;116(3):501–528. 28. Buell JL. National Athletic Trainers’ Association position statement: evaluation of dietary supplements for performance nutrition. J Athl Train. 2013;48(1). 29. Kerksick C, Harvey T, Stout J, et al. International Society of Sports Nutrition position stand: nutrient timing. J Int Soc Sports Nutr. 2008;5:17. 30. Barnes MJ. Alcohol: impact on sports performance and recovery in male athletes. Sports Med. 2014;44:909–919. 31. Bolster DR, Pikosky MA, Gaine PC, et al. Dietary protein intake impacts human skeletal muscle protein fractional synthetic rates after endurance exercise. Am J Physiol Endocrinol Metab. 2005;289:E678–E683. 32. Ivy JL, Goforth HW Jr, Damon BM, et al. Early postexercise muscle glycogen recovery is enhanced with a carbohydrateprotein supplement. J Appl Physiol. 2002;93:1337–1344. 33. Tarnopolsky MA. Caffeine and creatine use in sport. Ann Nutr Metab. 2010;57(suppl 2):1–8. 34. Bailey SJ, Vanhatalo A, Winyard PG, et al. The nitrate-nitritenitric oxide pathway: Its role in human exercise physiology. Eur J Sport Sci. 2012;12:309–320.

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26  Doping and Ergogenic Aids Siobhan M. Statuta, Aaron J. Vaughan, Ashley V. Austin

SPORTS PHARMACOLOGY: ERGOGENIC DRUGS IN SPORT There is no room for second place. There is only one place in my game, and that’s first place. Vince Lombardi1 In this day and age, it is common for athletes to be scrutinized for using prohibited performance-enhancing drugs and methods. Our society places a high value on winning and rewards athletes who perform well. As a result, competitors are often motivated to do “whatever it takes” to perform at a higher level and thus improve in their sport. The word ergogenic is derived from the Greek éaargon, “to work,” and gennan, “to produce”; it literally means “increasing the ability to do work.” Athletes have sought ways to improve their performance for thousands of years. Athletes at the first Greek Olympics ate substances that they thought would give them a competitive advantage, including dried figs, mushrooms, large amounts of meat, and strychnine (a known poison). These ancient Greek athletes were willing to risk taking a potentially deadly substance in the hope of winning. History does repeat itself, because this trend continues today and has escalated to incomprehensible levels. The ensuing battle to weed out athletes who engage in unfair practices is a challenge to organizations that believe in the concepts of “an even playing field” and fairness in sport. The desire to win at all costs was confirmed by a poll of Olympic athletes conducted by Mirkin2 in the 1980s. The question was, “If you could take a pill that would guarantee you the Olympic gold medal but would kill you within a year, would you take it?” The shocking result was that more than 50% of the athletes would take the pill. Goldman3 subsequently conducted a modified poll in the 1990s and asked 198 aspiring Olympians, all elite athletes, two questions: 1. If you were offered a banned performance-enhancing substance that guaranteed that you would win an Olympic medal and you could not be caught, would you take it? 2. If you were guaranteed that you would not be caught, would you take a banned performance-enhancing drug that would allow you to win every competition for the next 5 years but would then cause you to die from the side effects of the substance?

Of 198 athletes, 195 answered yes to the first question; in response to the second question, more than 50% of the athletes said they would take the substance. The results of these two polls reveal that a high percentage of athletes are willing to use substances that are potentially fatal if they believe that those substances will help them win. Athletes want to win now and may not consider or even be concerned about the future consequences of taking a performance-enhancing substance.

Testosterone: Historical Perspectives In the 1950s it was discovered that Olympic weight lifters were gaining immense strength by injecting testosterone, a male hormone. An American physician, John Bosley Ziegler, saw the potential benefits, and in an effort to minimize the adverse androgenic effects that the weight lifters were experiencing, he developed the derivative methandrostenolone.4 Although it was initially considered a superior ergogenic drug compared with testosterone, it had its own adverse effects related to its potent androgenic properties. Since then many scientists have attempted and failed to develop a pure anabolic agent without androgenic features. To underscore the important point that derivatives of testosterone have anabolic and androgenic properties, we categorize all ergogenic derivatives of testosterone in this chapter as anabolic-androgenic steroids (AASs). Hundreds of ergogenic variants of testosterone are now being used by athletes. One of the first scientists to promote the ergogenic properties of testosterone was the prominent French physiologist Brown-Séquard.5 Although largely remembered in the medical world today for his description of a spinal cord syndrome, Brown-Séquard played an important role in the history of AASs. In June 1889, at the Société de Biologie meeting in Paris, the 72-year-old Brown-Séquard announced that he had found a “rejuvenating compound” that had reversed many of his physical and mental ailments related to aging. He reported that he had injected himself with a liquid extract made from the testicles of dogs and guinea pigs and that these injections had dramatically increased his strength, improved his mental acumen, relieved his constipation, and increased the arc of his urinary stream. Brown-Séquard’s findings were viewed with disdain, yet he had made an important discovery with enormous implications for the medical and athletic worlds. Brown-Séquard’s discovery of the positive properties of the testicular extract was based on the earlier work of Berthold, who had proposed that the implantation

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Abstract

Keywords

The plethora of available substances touting improved performance—be it powders, supplements, even vitamins—is widespread and growing. However, these aids are not without dangers and oftentimes can result in illness, worsened execution of the activities, disqualification from sport, and even death. Some of these are well known, such as testosterone and growth hormone, due to their role in publicly visible abuses across the long history of sports. Others, such as caffeine and alcohol, are commonly used and thus their effects on athletics is overlooked or not considered. Individuals interested in exploring and utilizing performance enhancing products should do so with a clear understanding of the benefits as well as the potential hazards.

performance enhancing drugs creatine doping ergogenic steroid recreational drugs

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of testicles in the abdomen of roosters reversed the effects of castration.6 Scientists continued the work of these two scientists, and several important discoveries were made that contributed to a better understanding of the properties of the testicular hormone. The Dutch scientist David and his colleagues first isolated testosterone in 1935.7 Soon thereafter, German scientists published an article describing the synthesis of testosterone from cholesterol.8 Subsequently, physicians and veterinarians started using testosterone and its intermediaries clinically,9 and testosterone was first used medically in humans to help chronically ill patients recover muscle mass.10 Testosterone was found to have positive effects on almost every organ of the body, and 60 years after Brown-Séquard announced his discovery, testosterone was promoted once again as a rejuvenation compound. In 1939 Boje10 suggested that male sex hormones might improve athletic performance. In 1941, after a racehorse dramatically improved its performance following injections of testosterone,11 human competitors who were looking for an advantage during competition started experimenting with testosterone use.12 The first systematic use of testosterone in sports was by Soviet Olympic athletes in the 1950s; by the 1960s, use of AASs was increasingly prevalent.13 During that time, no sanctions against the use of ergogenic drugs existed, and many athletes believed that it was necessary to use drugs to be able to remain competitive. By the 1968 Olympics, the use of AASs was pervasive across various disciplines of sport, including both strength and aerobic events. New drugs claiming to have superior anabolic qualities were being marketed openly, and male athletes in large numbers from other sports such as American football soon began taking AASs either knowingly or allegedly as “vitamins.”14 It was estimated that 40% to 90% of professional football players were using AASs by the 1980s,15 and soon thereafter, college football players followed suit.15 Female athletes began experimenting with the drugs to improve their own performance abilities. Before long, it was discovered that women who took AASs experienced increased muscular strength. In addition, the androgenic properties of AASs also induced masculinizing effects, including deepening of the voice, amplification of body hair, loss of breast tissue, and clitoral enlargement. The masculinization of female athletes from the Soviet Bloc nations was so dramatic that gender tests and chromosomal analyses were performed at the 1967 European Championships to ensure that male athletes were not masquerading as female athletes. Women in Western nations have been suspected of using ergogenic drugs. Florence Griffith Joyner became one of the most famous athletes in the world when she reappeared on the world stage after coming out of semiretirement and achieved tremendous success at the 1988 Olympic Games. Joyner had progressed from a good runner to a world champion whose record in the 100-m run was unsurpassed for 10 years. Her muscular physique, combined with her newfound athletic success, led to speculation that her athletic superiority was a result of the use of performance-enhancing drugs—a charge she vehemently denied.16 Joyner instead insisted that her athletic prowess was the result of a relentless training program supervised by her

husband, Olympian Al Joyner. When Florence Griffith Joyner died in her sleep at the young age of 38 years, speculation that her death may have been related to adverse effects from taking ergogenic drugs was rampant. To date, it has not been verified that Joyner used ergogenic aids or that her death was related to the use of drugs, and her death has been attributed to a seizure. Many young athletes believe that the use of ergogenic drugs is a worthwhile risk. An eye-opening study by Buckley and colleagues17 revealed that 6.6% of high school seniors had, at some point, used anabolic steroids. Of these, 30% of users were nonathletes using ergogenic drugs to improve their appearance rather than their athletic performance. Evidence indicates that ergogenic drug abuse commences in middle school. The 2013 survey by the Partnership for Drug-Free Kids revealed that 11% of high school teens had tried synthetic human growth hormone (GH) at least once without a prescription—an increase of 5% in just 1 year!18 Furthermore, Yesalis and Bahrke19 found that the percentage of 14- to 18-year-old girls using anabolic steroids had almost doubled in 7 years, as many considered the use an effective means of obtaining college athletic scholarships.20 When a Danish cyclist died at the 1960 Olympics after ingesting a combination of nicotinic acid and amphetamines, concerns were raised regarding both fairness and safety, and a plan of action to address these issues was formulated. One of the first steps was to define the problem, and in 1963, the Council of Europe established a definition of doping as “the administration or use of substances in any form alien to the body or of physiologic substances in abnormal amounts and with abnormal methods by healthy persons with the exclusive aim of attaining an artificial and unfair increase in performance in competition.”18

Anabolic-Androgenic Steroids Physiologic Considerations The three main steroids in the human body are androgens, estrogens, and corticosteroids. The androgens are responsible for the development of male characteristics, whereas the estrogens express female characteristics. Corticosteroids—both glucocorticoids and mineralocorticoids—are responsible for a wide variety of essential body functions involving the immune, cardiovascular, metabolic, and hemostatic systems. Females produce small amounts of androgens in the ovary and adrenal gland, and males produce small amounts of estrogen, but it is the production of androgens that makes males “masculine” and the production of estrogen that makes females “feminine.” The most abundant androgen in males is testosterone, which is produced primarily in the testes. In many target cells of the body, testosterone is reduced at the 5α position to dihydrotestosterone, which serves as the intracellular mediator of the actions of testosterone.21 Dihydrotestosterone exhibits a greater affinity for androgen receptors compared with testosterone and is thus the more stable and potent androgen. Precursors in the metabolic pathway to testosterone, dehydroepiandrosterone (DHEA) and androstenedione, bind less strongly to the androgen receptors and are known as weak androgens. Other weak androgens that are metabolites of testosterone include etiocholanolone and androsterone. Although they are weak, these androgens can induce significant anabolic effects.

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In males, testosterone production peaks at three distinct phases of life. The first peak occurs during the fetal period, in the second trimester, and directs male fetal development. Subsequently, a smaller surge occurs during the first year of life and the largest surge occurs during puberty, resulting in several visible changes. Androgens cause laryngeal enlargement, thus deepening the voice; genital maturity; spermatogenesis in the testicles; and bone and muscle growth, with a relative decrease in body fat. The skin becomes thicker and oilier, and body hair on the face and in the axillae and groin grows to adult levels. On the cellular level, testosterone, or its more active metabolite, dihydrotestosterone, works by binding to an intracellular androgen receptor in the cytoplasm. The steroid–androgen receptor complex is transported to the nucleus, where it attaches to a specific hormone regulatory complex on nuclear chromosomes. Here the complex stimulates the synthesis of specific ribonucleic acids and proteins. The ribonucleic acid compounds are transported through the bloodstream to act on target organs and stimulate spermatogenesis, effect sexual differentiation, and increase protein synthesis in muscle tissues. The androgenic message is received and processed in all organs that have androgenic receptors. The metabolism of testosterone and its products occurs rapidly in the liver. Oral testosterone is absorbed immediately and metabolized so rapidly that it becomes ineffective. Scientists have therefore developed methods of altering the basic structure of the molecule to delay its metabolism and increase its half-life in the plasma. Alkylation at the 17α position with a methyl or ethyl group allows oral agents to be degraded slowly. Similarly, esterification of the 17β position allows parenteral agents to resist degradation. Testosterone esters, such as cypionate and enanthate esters, are more potent than testosterone. These compounds must be injected intramuscularly, usually at 1- to 3-week intervals. Newer preparations of testosterone can be administered transdermally.22 These preparations were originally applied to the scrotum, but new transdermal patches and creams can be applied to other parts of the body. In addition to promoting muscle development, androgens cause the skin to become unusually oily, which can lead to acne, increase body hair, and induce male pattern baldness, with hairline recession and thinning and loss of central scalp hair. The skin effects are crucial clues for physicians who suspect anabolic steroid use. The extent of the acne can be profound, and the back is often significantly affected. Lastly, the distinctive odor caused by the effects of anabolic steroids on the sebaceous glands is inimitable.

Athletic Performance Considerations Despite the perceptions of athletes, scientific data regarding the effects of anabolic steroids on athletic performance are varied. When used at therapeutic doses, neither strength nor performance gains are expected, because in a homeostatic state, hormonal levels are maintained within a narrow window. After a therapeutic dose of a hormone is administered, the body halts its own endogenous hormone production to maintain constant levels. Athletes who are cognizant of this fact have taken doses 50 to 100 times the therapeutic dose, which shuts down endogenous production

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of AASs. But does taking such high doses improve athletic performance? In the world of athletics, several popular theories foster steroid abuse. The first theory is that “In combination with training, AASs increase lean body mass and decrease body fat.” Early studies that evaluated this theory showed equivocal results.23 More recent studies have shown an increase in body weight and lean body mass but no significant decrease in the percentage of body fat.24 Another theory suggests that “AASs increase muscle strength.” Early studies in which mostly low-dose AASs were evaluated were inconclusive.25 Later, in 1996, Bhasin and colleagues26 studied the effect of supraphysiologic doses of testosterone on healthy men; this was the first prospective randomized study that looked at the effect of “super dosing” of AASs. In this study of 43 healthy men, the group that received steroids had definite increases in strength and muscle size compared with the placebo group. Notably, no significant adverse effects were observed in the steroid group; however, the study had limitations, including a short term (6 weeks) and inadequate follow-up. However, this study was the first to provide scientific evidence for the theory that athletes believed for decades—that steroids do work, especially at the amplified doses that are popular in athletics. Other investigations have shown distinct advantages for muscle, with both expansion in cross-sectional diameter and proliferation of new fibers. The upper regions of the body are more susceptible to gains from AASs because of the relatively larger number of androgen receptors in these areas. AASs, however, do not appear to improve athletic endurance.24 AASs work on several different levels in the body. They stimulate not only protein synthesis but also the production of GH, a potent ergogenic agent. Furthermore, AASs display some anticatabolic features because they delay the effects of cortisol, a stress hormone. Cortisol is released in response to physical and psychological stress and causes protein degradation and muscle atrophy.27 Testosterone slows this catabolism by displacing the corticosteroids from receptor sites.28 Additionally, AASs may increase oxygen uptake, cardiac output, and stroke volume.29 They are thought to improve athletic performance by increasing aggressive behaviors; however, the data on the relationship between testosterone levels and aggressive behavior remain inconclusive.30,31

Adverse Effects The use of anabolic steroids may result in several less than desirable side effects. Oily skin, acne, small testicles, gynecomastia, and changes in hair patterns are the most common. Small doses of androgens increase sebaceous gland secretions, leading to the changes in the skin and the development of acne.32 Enlargement of the male breast (gynecomastia) is characterized by the presence of firm glandular tissue and is usually associated with an increased production of estrogens or decreased levels of androgens. The specific pathophysiology of gynecomastia in men taking AASs remains unclear. One theory suggests that the body homeostatically shuts down the production of endogenous androgens. Once the user stops using AASs, an increase occurs in the relative level of estrogens, leading to the development of breast tissue. Gynecomastia is irreversible once levels of androgens return to normal. A means of offsetting the estrogen-related adverse effects

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of AASs is to take an antiestrogenic drug such as clomiphene citrate (Clomid). Clomid blocks the effects of increased estrogen in persons using AASs by binding and thus blocking estrogen receptors. Small testicles often also develop in men who use AASs. The testicles atrophy and shrink, which is a response to the homeostatic effect triggered by high exogenous AASs. Often the testicles remain smaller after discontinuation of the AASs. Other adverse effects on the male reproductive system include oligospermia (a decreased number of sperm) and azoospermia (the absence of sperm).33 Moreover, taking exogenous AASs decreases not only levels of endogenous testosterone but also the circulation of follicle-stimulating hormone and luteinizing hormone, which can lead to male infertility. Testosterone-dependent prostate enlargement and accelerated growth of prostate cancer have been documented.34 Women who take AASs experience virilization effects, including deepening of the voice, an increased amount of body hair, loss of breast tissue, and enlargement of the clitoris. Irregularities in the menstrual cycle as well as infertility or early menopause may result, and many of these adverse effects in women are irreversible.35 Musculoskeletal.  The musculoskeletal system may be affected adversely, especially in prepubertal athletes who take AASs. Although bone growth is stimulated immediately after the use of AASs, the growth plates of long bones may close prematurely. The resultant short stature is permanent.36 Disproportionate changes in strength of the muscle-tendon unit (greater) than tendon strength (lesser) increases the susceptibility to tendon rupture.37 Cardiovascular.  Numerous adverse changes occur in the heart of a person who takes AASs. Androgens are modulators of serum lipoprotein, thus increasing plasma levels of low-density lipoproteins (“bad” lipids) and decreasing levels of high-density lipoproteins (“good” lipids). Oral and synthetic AASs have more pronounced negative effects on lipid metabolism than do injectable or natural AASs.38 An altered lipid pattern may lead to atherosclerotic heart disease. Male and female users of AASs show similar adverse changes in lipid metabolism.39 Animal studies have suggested that AASs may cause myocardial damage.40 A study that investigated the relationship among resistance training, anabolic steroid use, and left ventricular function in elite bodybuilders showed concentric left ventricular hypertrophy. However, no effect on cardiac function was observed, which suggests that the heart may enlarge as a physiologic adaptation to the intensive training potentiated by use of AASs.41 In a set of bodybuilding twins, one twin used AASs for more than 15 years whereas the other abstained. No significant difference in cardiac function was found between the twins.42 However, noteworthy changes in cardiac function after the use of AASs have been reported in other cases, such as myocardial infarction and death in young athletes.43 These case reports are no doubt worrisome yet do not provide scientific “proof ” that the use of AASs directly leads to myocardial infarction or death. Nevertheless, cardiac pathology was evident upon postmortem examination in more than one-third of 34 persons (aged 20 to 45 years) who had used AASs and died as a result of accidents, suicides, and homicides.44 Cardiac abnormalities may not resolve after

the use of AASs is stopped. A study of former users of AASs showed that many years after discontinuing their use, strength athletes showed persistent left ventricular hypertrophy compared with strength athletes who had not used AASs.45 Hepatic.  Most AAS metabolism occurs in the liver, which is thus prone to liver damage. Athletes with preexisting liver dysfunction are at greatest risk for androgen-induced damage. Temporary liver disturbances are common in athletes who use oral androgens, although function appears to return to normal after discontinuation of the drugs.46,47 Several investigators believe that AAS-induced hepatotoxicity is overstated, attributing resultant transaminitis to skeletal rather than liver damage.48 A study of the effect of AASs on rats showed definite cellular damage to hep atocytes,49 yet long-term studies on the effect of AASs on the liver in human subjects have not been conducted; until we have scientific data, hepatotoxicity should remain a potential concern. Hepatotoxicity may manifest as peliosis hepatis, that is, the formation of blood-filled cysts in the liver. Enlarged liver cells block venous and lymphatic flow, producing cholestasis, necrosis, and peliosis cysts, which can rupture and may be life threatening. In contrast to most adverse effects of AASs, peliosis hepatitis does not appear to be dose related and can occur at any time after the use of AASs is started.50 Pathogenesis is speculated to be from AAS-mediated hepatocyte hyperplasia.51 Last, although there is no definite evidence to support a causal relationship between hepatocellular carcinoma and steroid abuse, there have been multiple reports of the development of hepatocellular carcinoma after AAS use.52 Psychiatric.  The most commonly associated psychiatric effect of AASs is an increase in aggressive behaviors, although only a few well-conducted prospective randomized studies confirm this observation. In fact, most studies using therapeutic doses of exogenous testosterone showed no adverse effects, and a short-term study of supratherapeutic dosing of AASs in athletes revealed no significant psychiatric effects.53 However, some studies have reported positive effects on mood.54 In Brown-Séquard’s 19thcentury study of the self-administration of testicular substrates, one of the reported positive effects was improvement in mood, which was accompanied by an enhancement of his physical stature.5 Subsequently, benefits of AASs on mood and other psychiatric maladies were further evaluated by physicians following the advent of synthetic testosterone derivatives in the 1930s.55,56 AASs were being researched during their use to treat a variety of conditions ranging from depression to psychoses, and although results were varied, some small studies revealed an increase in aggression, thought to be linked to other personality disorders such as antisocial, borderline, and histrionic personalities.57 Additional research suggests an association with AAS use and psychiatric disturbances. A study of 41 athletes using supra­ therapeutic doses of AASs for an average of 45 weeks revealed that 34% experienced symptoms of major mood disorders such as severe depression or mania. AAS users are also more likely to abuse alcohol, tobacco, and illicit drugs,58 and data suggest that AAS users tend to meet criteria for substance dependence disorder more commonly than nonusers.59 Disorders of body image have also been reported after use of AASs. Many weight lifters who may appear muscular compared

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with the average athlete consider themselves small or weak. This dysmorphic disorder is similar to that of women with anorexia nervosa who, despite being much thinner than the average woman, erroneously perceive themselves as fat.

Steroid Supplements In 1994, the US Congress passed legislation affecting all persons involved in the care of athletes—the Dietary Supplement Health and Education Act. This law permits numerous substances to be sold without prior approval from the US Food and Drug Administration (FDA) as long as they are sold as dietary supplements and not as “drugs.” The Dietary Supplement Health and Education Act also established a formal definition of a dietary supplement using several criteria. A dietary supplement is a product (other than tobacco) that is intended to enhance the diet. It bears or contains one or a combination of dietary ingredients, such as a vitamin, mineral, herb, or other botanical product. Products have included approved new drugs, certified antibiotics, or licensed biologic agents that were marketed as dietary supplements or food before approval, verification, or licensure. These products are not recommended for use as a conventional meal or diet and are labeled as a dietary supplement. Subsequent to this bill’s passage, several synthetic AASs have become commercially available as dietary supplements; as such they do not have to pass the safety requirements of the FDA and are not held to strict quality control standards.60 Claims regarding their effectiveness need not be substantiated by scientific proof as long as a disclaimer is listed on the product.

Dehydroepiandrosterone DHEA is a naturally occurring hormone produced in the adrenal glands of the human body. Its synthetic form, isolated from soy and wild yams, is marketed as a supplement61 and has become popular for its antiaging properties, fat-burning properties, and enhancement of muscle mass, strength, and energy. DHEA is a weak androgen, but it is the most abundant steroid in the body serving as a precursor to testosterone, estrogen, progesterone, and corticosterone. Levels are high in the prenatal period as well as in puberty, gradually decreasing as an individual ages. Some studies performed on patients older than 50 years (when DHEA levels have dropped significantly) showed beneficial results after DHEA supplementation.62 Conversely, other studies have revealed inconsistent improvements in strength.63 Many athletes use DHEA for its androgenic and anticatabolic effects. With its use come some undesired effects of feminization, as DHEA is a precursor to estrogen. Athletes attempt to combat this outcome by using clomiphene citrate (Clomid), an antiestrogenic drug, while taking DHEA. Little evidence exists to support claims for DHEA, either as a potent anabolic agent or as an antiaging drug.64,65 Furthermore, no studies of the long-term effects of taking DHEA have been published, particularly regarding the large doses used by athletes.66 Androstenedione Androstenedione, originally touted as the “secret weapon of the East Germans,” was first used in the 1970s, and its reputation as an effective anabolic agent encouraged worldwide use. In

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March 2004, the US Department of Health and Human Services announced that the FDA had asked manufacturers to stop distribution of androstenedione. By October 2004, President Bush signed into law the Anabolic Steroid Control Act, which added androstenedione to the list of banned nonprescription steroidbased drugs. Currently Major League Baseball, the National Football League, the Olympics, and the National Collegiate Athletics Association (NCAA) prohibit its use. Androstenedione received tremendous exposure in the media during the 1998 baseball season when St. Louis Cardinals slugger Mark McGwire was discovered to be using the supplement, albeit legally at the time, after which sales of androstenedione rose dramatically.67 Androstenedione is a potent AAS produced endogenously in the adrenal glands and gonads. In the liver, androstenedione is metabolized to testosterone. Similar to DHEA, during transformation it can be converted to testosterone and estrogen. As a result, a male athlete taking androstenedione can have elevated estrogen levels. One study observed that male subjects taking androstenedione experienced elevated estradiol levels equal to the estradiol levels seen in women during the follicular phase of the menstrual cycle, when levels are at their highest.68 Additionally, as a testosterone precursor, it can lead to decreases in high-density lipoprotein cholesterol and enhance cardiac risk. Priapism has been described in an otherwise healthy young man using androstenedione who had no other precipitating factors; other concerns such as prostatic enlargement and cancer exist. Notably, significant ergogenic improvement after androstenedione supplementation has not been proved in the medical literature.

Doping Historical Perspectives The word doping originates from the Dutch word dop, an opium mixture used to enhance the racing capacity of horses. In 1967, the International Olympic Committee (IOC) published a medical code that included a list of banned drugs to “protect the health of athletes and to ensure respect for the ethical concepts implicit in Fair Play, the Olympic Spirit, and medical practice.”69 The World Anti-Doping Agency (WADA) was established from this committee in 1999. Through its affiliation with various international, national, and private governing bodies, WADA has helped to establish strategies to tackle organized doping schemes, trafficking, and detection. It also publishes an annual listing of banned substances—an invaluable resource for athletes and medical providers.70 Erythropoietin WADA defines blood doping as “the misuse of certain techniques and/or substances to increase one’s red blood cell mass.”70 Bons­ dorff and Jalavisto71 were the first to discover and name the blood-stimulating hormone now commonly referred to as erythropoietin (EPO). Scientists later discovered its molecular structure, which served as a base for the development of recombinant human EPO (rhEPO). The first experiments with enhanced red blood cell mass and exercise showed that blood transfusion decreases submaximal heart rate for several weeks, predicting performance enhancement.72 Subsequent studies replicated the performance-enhancing effects of transfusion, including those

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of Berglund and Ekblom who showed a 17% increase in the time to exhaustion among male athletes after 6 weeks of EPO administration.73,74 The IOC eventually banned blood transfusion for the 1988 Olympics.75 In 1990, EPO was added to the IOC list of prohibited substances, and it has been on WADA’s prohibited list since the organization’s inception.

Mechanism of Action Essential to athleticism and performance is how well trained or “conditioned” the athlete is. Basic physiology reminds us that muscle cells require oxygen to function optimally and that oxygen is transported throughout the body by erythrocytes. EPO is a hormone that stimulates the production of these erythrocytes in the range of 2.5 × 1011 erythrocytes per day, each of which has a life span of approximately 120 days. Nearly 90% of EPO is produced in the peritubular renal cells, with the remainder being produced in the liver and brain. EPO production is triggered in response to hypoxia and stimulates an increase in erythrocyte production, leading to enhanced tissue oxygenation. Both epoetins and their synthetic analogues (erythropoiesis stimulating agents, or ESAs) have the ability to induce erythropoiesis by binding to EPO receptors on target cells. Testing WADA publishes an annual summary of prohibited substances and doping methods, the most recent having been released on January 1, 2017.76 This list is commonly referred to as the Prohibited List, comprising a total of 10 different classes of banned substances (S0–S9), three different groups of prohibited methods (M1–M3), and two classes of drugs (P1 and P2) that are banned from selected sports only. The traceability of EPO abuse has been a complex issue, laborious and time-consuming, and frequently challenged by athletes. Drug testing in athletes is riddled with many hurdles, including cost. The inception of new ergogenic aids and novel masking agents has made the detection of illegal doping a challenge.77 Allocation of innumerable research resources has been invested in improving analytical approaches as well as eliminating technical issues in detection. Given the negative ramifications of a positive drug test, it is critically important that the chain of custody be maintained and that testing protocols be updated and followed precisely to ensure the accuracy of sampling. Detection of rhEPO includes both direct detection of recombinant isoforms and indirect approaches via the measurement of markers of enhanced erythropoiesis.78 In the 1990s, the International Cycling Union introduced random blood tests to detect abnormalities in biologic parameters as a screening test for subsequent urinary detection of rhEPO. Although this technique was successful in preventing heavy use of rhEPO, it proved unable to discriminate against athletes with naturally elevated blood parameters. Individual reference ranges were introduced in 2007 in the form of “biologic transport,” or the method of tracking each athlete’s own blood numbers, known as the Athlete Biologic Passport hematologic evaluation. Markers that are currently tracked include hematocrit, hemoglobin, red blood cell count, reticulocyte percentage, reticulocyte number, mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular

hemoglobin concentration, among others. Blood results are then processed by a model that identifies any abnormal blood parameters as compared with the athlete’s individual baseline. These operating guidelines, in accordance with the WADA code, were implemented in 2009. Newer generations of these models have since been employed to include advances in electrophoresis techniques—isoelectric separation, Western blot analysis, antibody detection, and mass spectrometry—to help distinguish between physiologic EPO versus rhEPO. Although there is still a lack of total understanding, research continues in an attempt to further develop new testing methods, decrease false positives, and improve the sensitivity of the current testing measures. What is clear is that the combination of an athlete’s biologic passport (based on individual profiling) and urine tests targeting rhEPO has undoubtedly made it more challenging for athletes to compete illegally.79

Side Effects To some athletes, the benefits of using performance-enhancing agents clearly outweigh any risk. EPO and its synthetic analogues are known to increase red blood cell mass. Physiologic benefits include normalization of cardiac output and enhanced immune function, leading to improved exercise tolerance, reduced fatigue, and subjective improved quality of life. EPO excess has been associated with hazardous adverse effects, including increased blood viscosity. This hyperviscosity, in turn, can lead to headache, hypertension, congestive heart failure, venous thromboses, pulmonary emboli, encephalopathy, and stroke. There have been some reports that rhEPO administration leading to excessive erythropoiesis may result in reduced thickness of cortical bone, trending toward osteoporosis and theoretically increased fracture risk.80

Creatine Historical Perspectives Creatine is one of the most popular supplements currently used by athletes. It is a compound synthesized within the body and also absorbed exogenously from fish and meats. In 1992, creatine was manufactured as a supplement to potentially improve muscular performance. Shortly thereafter, it was touted as a supplement that delayed fatigue and enhanced athletic performance.81 Physiology Creatine has a fundamental role in the structure and function of adenosine triphosphate, the body’s prime energy source. It is synthesized largely in the liver from amino acids and subsequently transported to skeletal muscles, the heart, and the brain, where it is absorbed. Intracellularly, creatine is phosphorylated into creatine phosphate, and in this state it serves as an energy substrate that contributes to the resynthesis of adenosine triphosphate for energy.82 Creatine is also proposed to serve as a buffer to lactic acid produced during exercise. Lactic acid is a byproduct of intense exercise caused by the accumulation of H+ molecules. In excess, it limits exercise. Creatine binds these molecules, delays fatigue, and lengthens exercise duration. Creatine may also help athletic performance by promoting protein synthesis, thereby increasing muscle mass.81 Additionally, when combined with a

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high-carbohydrate diet, creatine enhances glycogen stores, which is advantageous during long-duration, high-intensity exercise.83 Creatine may benefit athletes who engage in sports that emphasize short bursts of intense anaerobic activity, such as football, soccer, lacrosse, hockey, basketball, and powerlifting. Short-term creatine supplementation has been shown to enhance the ability to maintain muscular forces during jumping,84 intense cycling,85 and weight lifting.81 It is important to note, however, that not all athletes appear to benefit from creatine supplementation.83,86 Some individuals are “responders” while others are “nonresponders” to creatine.87 It is estimated that about 30% of athletes are “nonresponders” because they already naturally possess a maximal amount of creatine—as much as can be stored by their muscle cells. Muscle creatine content is measured only by muscle biopsy, making it necessary for an athlete to use the supplement on a “trial and error” basis to determine if it will be beneficial. Early studies emphasized the importance of a loading phase with creatine. Athletes would use large doses (20 g/day of creatine for 5 days) before reaching a maintenance dose (2 g/day).88 More recent evidence has shown that loading is unnecessary and that a low-dose regimen of 3 g/day is just as effective, although it may take longer to for benefits to be noted.89,90

Adverse Effects An increase in body mass of up to 2 kg occurs frequently and is believed to be the result of water retention.83,91 According to some recommendations, creatine should not be consumed either before or during intense exercise.92 Case reports of gastrointestinal distress (diarrhea) are common, but a direct cause-and-effect relationship has not been defined. Concerns regarding nephrotoxicity have been raised, but creatine supplementation does not appear to negatively affect renal function in healthy persons without a previous history of renal disorder if they adhere to recommended dosing.93 Thus the use of creatine in athletes is popular because it is considered a legal means of improving performance. Despite findings from a few controversial studies, supplementation with creatine can increase fat-free mass and strength. Creatine may also be of benefit to athletes who engage in high-intensity sprints or endurance training, but these benefits seem to diminish with prolonged exercise.83

Growth Hormone Historical Perspectives One of the most popular ergogenic drugs used by athletes, human GH, was discovered in the 1920s, when researchers noted that after an injection of ox pituitary glands, normal rats grew abnormally large. Animal breeders later used these injections to increase muscle mass and decrease body fat in their breeds.94 In the 1950s, GH extracted from the brains of cadavers from Africa and Asia was administered to children whose growth was stunted by absence of this hormone.95 Thousands of short-statured children were successfully treated with human GH. However, as a result of treatment with cadaver extracts, Creutzfeldt-Jakob disease developed in many of these children. This disease causes progressive dementia, loss of muscle control, and death.96 By the early 1990s,

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the FDA had stopped distribution of GH, yet there was a need to treat children who had short stature induced by low levels of GH. The Genentech Company used recombinant deoxyribonucleic acid technology to manufacture a biosynthetic GH, somatrem (Protropin), enabling GH to be safely provided to children in need. However, the use of human GH as a supplement is universally illegal. GH affects almost every cell in the body. Because human GH levels dip with advancing age, it has been endorsed as an antiaging product. Human GH secretion can be stimulated throughout life by either sleep or exercise; thus combining exercise with rest may be beneficial. Currently long-term studies on the effectiveness of human GH are lacking.

Mechanism of Action Human GH is a polypeptide produced and stored in the anterior pituitary gland. Its secretion is high during puberty and it continues to be secreted throughout life. Secretion occurs daily in a pulsatile fashion, with the highest levels observed shortly after sleep initiation.94 Human GH works in two ways: first, by binding on target cells, it exerts its effects on adipocytes, which, in turn, break down triglycerides and prevent lipid accumulation; second, after reaching the liver, human GH is rapidly converted into insulin-like growth factor-1 and thus exerts its growth-promoting effects throughout the body. Athletes have used human GH and insulin-like growth factor-1 as ergogenic supplements. Human GH is an appealing supplement for athletes because it stimulates protein metabolism. It is also a potent regulator of carbohydrate metabolism by decreasing insulin sensitivity and cellular uptake of glucose. In addition, human GH stimulates the catabolism of lipids, making free fatty acids available for quick energy use and sparing muscle glycogen.97 Human GH also stimulates bone growth, which is crucial for growth in prepubertal youths. Adverse Effects Most notably, excess GH may cause problems with bone growth in adults. In adults, growth plates have fused but continue to enlarge in the presence of high levels of GH, resulting in dysmorphic, acromegalic features, particularly of the face, hands, and feet. Other problems include a predisposition to diabetes (attributed to decreased insulin sensitivity), cardiomyopathy, and congestive heart failure.97 Correlations have been noted between human GH and the enlargement of intracranial lesions, amplification of intracranial hypertension, and leukemia in patients treated with recombinant human GH.98 No scientific studies have been conducted to show improved athletic performance with use of human GH. Nevertheless, human GH has been widely used by athletes. Limitations of human GH include poor quality (because much of it is supplied from international sources), exorbitant cost (about $1000 per month), and availability only in the parenteral form (increasing risk of infection). Nonetheless, human GH is used frequently, especially because few solid testing methods exist aside from two tests performed within a few days of dosing. The isoform test detects the presence of synthetic human GH and is effective for detection of use within 12 to 72 hours of administration. The second

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test, called the “biomarker test,” evaluates the presence of chemicals produced by the body after human GH use99; it may be used alone or in conjunction with the isoform test.

to appropriately balance and maximize benefit without eliciting the negative side effects of use.

Caffeine

For centuries, athletes have been willing to risk death in an attempt to improve their ability to compete in sports. What can persons entrusted with the health of athletes do to protect athletes from themselves? The first step is “meaningful education” as reflected by an important tenet in medicine—“you only recognize what you know.” Most medical personnel receive very little education about doping and ergogenic aids during their schooling. To stay abreast with the practices of athletes, lifelong learning is essential. Health care professionals should be able to communicate openly with athletes regarding the health risks and legality of ergogenic aids and the importance of healthy nutrition and honest training as a viable and preferred alternative for promoting athletic superiority. Second, the medical community should conduct scientific controlled studies on athletes who are using ergogenic drugs. Obviously such studies would be difficult to conduct because many of these drugs are illegal, many ergogenic agents have significant adverse effects, and research oversight committees are often reluctant to approve studies using drugs with known or suspected adverse effects. Third, effective drug testing and stringent penalties for athletes, coaches, teams, and nations who use banned substances are imperative.

Historical Perspectives Caffeine is the most widely used legal ergogenic drug, with billions of people using it. The United States Olympic Committee (USOC) had previously placed caffeine in a restricted status, allowing no more than 12 µg/mL in urine; however, because of highly variable excretion rates, this restriction has been eliminated. Doses between 5 and 10 mg/kg 1 hour before an athletic contest are commonly used. Caffeine is not included on the 2017 Prohibited List of substances, having been removed since 2004. The drug is part of WADA’s monitoring program, a program that includes substances not prohibited from sport but monitored to detect misuse in sport. Since 2010, caffeine use among athletes has increased, although there have been no global indications of misuse.75 Mechanism of Action Caffeine has historically been used to enhance physical and mental performance. It employs its ergogenic effects both centrally and peripherally. Once in the bloodstream, caffeine is rapidly absorbed, leading to the stimulation of excitatory neurotransmitters. At a central location, caffeine increases perception of physical effort and improves neural activation of muscle transport. Peripherally, caffeine leads to the release of free fatty acids from adipose tissue, sparing muscle glycogen and maintaining blood glucose levels. It also stimulates potassium transport into tissue, maintaining muscle cell membrane excitability and decreasing muscle cell reaction time after neural stimulus, while reducing muscle fatigue. Side Effects Evidence indicates that caffeine ingestion helps with endurance while providing performance enhancement.100 Beneficial effects occur at modest doses of about 1 to 3 mg/kg 1 hour prior to exercise without noticeable dose dependency, although higher doses (>6 to 9 mg/kg) tend to incur adverse side effects. The most common detrimental effects include anxiety, restlessness, panic attacks, gastritis, reflux, and heart palpitations.101 Chronic users may experience withdrawal, including headache and fatigue with abrupt cessation of use. Acute caffeine intake is known to increase urinary loss of fluid, although a recent review proposes that there is little evidence that the drug affects overall fluid status.102 Doses of caffeine within the ergogenic range do not alter sweat rates, urinary losses, or indices of hydration status.103 The majority of studies highlighting caffeine use and athletic performance concern endurance sports. In long-distance cycling competitions, time to exhaustion at VO2 max was significantly improved.104 In another cycling study, a 7% increase in distance covered in 2 hours was noted.105 There is also evidence that caffeine can enhance performance in sustained, high-intensity activities. In one particular study, 1500-meter swim time was significantly improved in trained athletes.106 There is a strong need to educate athletes regarding the responsible intake of caffeine

Summary

SPORTS PHARMACOLOGY: RECREATIONAL DRUG USE Substance use among students and young adults continues to be a leading cause of morbidity and mortality. The Monitoring the Future Survey is an ongoing study of the behaviors, attitudes, and values of American secondary school students, college students, and young adults.107 The 2016 updated survey shows that nearly 50% of young Americans have used some type of illicit substance between grades 8 and 12, with nearly 25% having used such a substance in the past 12 months. Cigarette smoking and alcohol use have continued to decline and are at all-time lows. Even so, vaping (the inhalation of vapors such as e-cigarettes), alcohol, and marijuana remain the most consistently abused substances. Consistent with prior studies, there appears to be little difference in the prevalence of recreational drug use in athletes and nonathletes. Clinicians need to be aware of the effects of these drugs in order to appropriately educate their athletes on the risk of these substances not only on performance measures but, more importantly, also on general health and wellness.

Alcohol Epidemiology Alcohol continues to be one of the most frequently abused substances in collegiate, professional, and Olympic sports.108 The use of alcohol has declined since 1980, yet despite this fact, the National Institute of Drug Abuse reports that in 2016, approximately 33% of high school seniors acknowledged having consumed alcohol in the previous month.109 According to the Harvard School of Public Health Alcohol Study, 80% of college

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students consume alcohol. Compared with nonathletes, collegiate athletes exhibit a higher rate of binge drinking; they also experience more alcohol-related complications including academic problems, driving under the influence, gambling, illicit drug use, and sexual promiscuity.110,111

Pathophysiology and Adverse Effects Ethanol is the primary psychoactive constituent in alcoholic beverages; it exerts its effect on the central nervous system (CNS) via its action on gamma-aminobutyric acid receptors. It also interacts with acetylcholine, serotonin, and N-methyl-D-aspartate receptors. It is oxidized by the liver at a constant rate rather than having an elimination half-life. Systemic ethanol levels are typically quantified by the blood alcohol content (BAC). Adverse effects of ingestion often correlate with BAC levels; however, persons lacking effective forms of metabolizing enzymes may experience more severe symptoms, whereas those who have acquired tolerance may metabolize alcohol more rapidly. In general, persons with a low BAC level (0.05%) experience euphoria, talkativeness, and relaxation. BAC levels of 0.1% or higher frequently induce CNS depression, compromise motor and sensory function, and impair cognition. Levels in excess of 0.3% may lead to unconsciousness, with levels surpassing 0.4% placing individuals at risk of death. In 1982, the American College of Sports Medicine issued a position statement regarding alcohol and its effect on sports performance.112 The main points of the position statement are as follows: 1. Alcohol adversely affects coordination, balance, and accuracy. 2. Alcohol does not improve athletic performance. 3. Alcohol will not improve muscle work performance and negatively affects the ability to perform. 4. Alcohol may impair temperature regulation during prolonged exercise in a cold environment. Other Considerations In recognition of the epidemic of alcohol abuse among young Americans, the Surgeon General’s Office released its Call to Action against Underage Drinking in 2007. This document identified the following six goals to help lower the incidence of alcohol abuse and associated morbidity and mortality.113 1. Foster changes in society that facilitate healthy adolescent development and that help prevent and reduce underage drinking. 2. Engage parents, schools, communities, all levels of government, all social systems that interface with youths, and youths themselves in a coordinated national effort to prevent and reduce underage drinking and its consequences. 3. Promote an understanding of underage alcohol consumption in the context of human development and maturation that takes into account individual adolescent characteristics, along with environmental, ethnic, cultural, and gender differences. 4. Conduct additional research on adolescent alcohol use and its relationship to development. 5. Work to improve public health surveillance on underage drinking and on population-based risk factors for this behavior.

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6. Work to ensure that policies at all levels are consistent with the national goal of preventing and reducing underage alcohol consumption. Despite campaigns to decrease binge drinking by athletes, excessive drinking is a reality. Team physicians should work closely with coaching staffs and athletic departments to develop prevention programs and an action plan for penalties for alcohol-related infractions of established rules.

Marijuana Epidemiology Marijuana is the second most commonly abused drug by athletes and the most commonly used illicit drug, with nearly 1 in 15 high school seniors reporting daily or nearly daily use.114,115 According to the most recent National Survey on Drug Use and Health released by the CDC in 2015, an estimated 22.2 million Americans aged 12 years or older are current users. Though this is not an increase, use in individuals age 18 or older is on the rise. Despite legalization across several states, the NCAA continues its stance in considering this a banned substance. Nevertheless, the use of marijuana is still pervasive and persisting among student athletes. Pathophysiology and Adverse Effects All forms of cannabis are mind-altering (psychoactive) drugs. The main active chemical derivative, Δ-9-tetrahydrocannabinol, affects cannabinoid receptors found in the brain and peripheral tissues and also indirectly enhances dopamine release, producing its psychotropic influences. Marijuana is absorbed readily and has effects throughout the body, most predominantly in the CNS, the respiratory system, and the cardiovascular system. Short-term effects of marijuana use include distorted perception, difficulty in thinking and problem solving, and loss of coordination. The psychotropic effects of cannabis include general euphoria and a mild release from inhibitions, drowsiness, stimulated appetite, and freedom from anxiety. Other persons experience an altered sense of consciousness.116 Long-term use may be linked to behavioral changes similar to those caused by traumatic injury. Recent studies document a spectrum of cardiorespiratory ailments associated with the smoking of marijuana. A large epidemiologic study suggests that marijuana smoke can cause the same types of respiratory damage as tobacco smoke.117 The acute physiologic effects of marijuana on the cardiovascular system include a substantial dose-dependent increase in heart rate, a mild increase in blood pressure, and occasionally orthostatic hypotension. Athletic performance is affected, as marijuana use has been shown to decrease exercise test duration in maximal exercise tests, with premature achievement of maximal oxygen uptake.118 Other Considerations Discussions with athletes should not only emphasize the negative effects of marijuana on athletic performance but also stress the often forgotten fact that marijuana continues to be a Schedule I drug despite legalization in many states. Moreover, more potent and dangerous synthetic derivatives have been developed and are

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increasingly popular in attempts to bypass screening tests. These products, such as “Spice” or “K-2,” are herbal mixtures infused with chemicals to give effects similar to those of marijuana by their ability to bind to cannabinoid receptors throughout the body. Their popularity stems from the “marijuana-like high” and easy availability at retail outlets and via the Internet. Numerous reports of serious adverse effects—including convulsions, anxiety attacks, tachycardia, vomiting, psychosis, and disorientation— have necessitated their emergency classification in March 2011 as a Schedule I substance.119

Tobacco Epidemiology Smoking remains the most preventable cause of death in developed countries. The World Health Organization reports that tobacco use is responsible for more than 7 million deaths annually worldwide.120 The use of tobacco by adolescents has declined since the peak levels of the mid-1990s; however, 15% of individuals in the United States continue to smoke. In addition to cigarette smoking, other forms of tobacco use include smokeless tobacco, pipes, cigars, chewing tobacco, snuff, and, most recently, the e-cigarette. In 2014, sales of e-cigarettes surpassed those of traditional cigarettes. In a recent press release regarding the e-cigarette epidemic, the Surgeon General reported that 1 out of every 6 high school students in the United States has used e-cigarettes in the previous month.121 Although cigarette smoking is less of a problem in athletes than in nonathletes, use of smokeless or “spit” tobacco remains prevalent, particularly in the realms of baseball, football, and golf. Pathophysiology and Adverse Effects Nicotine is both a stimulant and a depressant. As nicotine enters the body, it crosses the blood-brain barrier within 10 to 20 seconds and exerts its effects by binding to nicotinic acetylcholine receptors, increasing levels of dopamine. Via this mechanism, tobacco is believed to have an addictive potential comparable to that of alcohol, cocaine, and morphine.122 The detrimental health consequences of tobacco use are well known. Smokeless tobacco users have an increased risk for oral cancer, including cancer of the lip, tongue, cheeks, gums, and the floor and roof of the mouth. Through its release of various chemical messengers—including acetylcholine, epinephrine, norepinephrine, serotonin, and dopamine, among others— nicotine appears to enhance concentration, memory, and alertness while decreasing appetite and promoting relaxation. Nicotine is considered a mood- and behavior-altering drug, often helping athletes to deal with stressful situations. Other effects, due to nicotine’s vasoactive properties, include increases in pulse rate by 10 to 20 beats/min and blood pressure by 5 to 10 mm Hg. Nicotine also stimulates platelet aggregation, which may increase the risk for blood clots. Other Considerations In an effort to curtail tobacco use, both professional baseball (minor leagues) and junior hockey (Western Hockey League) have banned the use of spit tobacco by players, coaches, and officials. Similarly, the NCAA bans the use of spit tobacco by

players, coaches, and officials during NCAA-sanctioned events. Dental screening, which can often detect precancerous lesions that may be caused by nicotine, is highly recommended for all athletes. Last, nicotine addiction is difficult to overcome. Epidemiologic studies indicate that the likelihood of addiction increases when cigarette smoking commences during adolescence. Thus addressing the dangers of nicotine in youth sports and its potential for refractory addiction is critical for prevention.

Cocaine Epidemiology The Monitoring the Future Survey documented that in 2006, 8.5% of 12th graders had used cocaine.123 Since then, use has dropped to a historical low of 3.7% among this same cohort.123 Cocaine abuse can lead to physical dependence. It is a controlled substance (Schedule II) and is banned in sport, with the IOC testing athletes routinely. Pathophysiology and Adverse Effects Cocaine is a naturally occurring alkaloid that is present in the leaves of Erythroxylon coca. It is commercially available and can be applied to mucous membranes of the oral, laryngeal, and nasal cavities for use as a topical anesthetic; however, it is most known for its abuse potential via its various processed forms. Cocaine exerts its adverse effects as a result of excessive sympathetic activity. Unlike other local anesthetics, cocaine affects the nervous system by potentiating catecholamines and leads to increased energy levels. It also results in the inhibition of presynaptic reuptake of norepinephrine, dopamine, and serotonin. Cocaine causes an acute dopamine release and inhibits synaptic dopamine reuptake, which produces euphoria, reduced fatigue, elevated sexual desire, and increased mental ability as well as sociability. At higher doses, tremors and tonic-clonic convulsions may occur. Long-term use of cocaine can result in nasal congestion, rhinitis, chronic sinusitis, and increased risk for upper respiratory infection. CNS toxicity is extremely common with cocaine use, including agitation, anxiety, apprehension, confusion, headache, dizziness, emotional lability, euphoria, excitement, hallucinations, seizures, and psychosis. Effects on Athletic Performance The significant morbidity and mortality in athletes is a result of the effects of cocaine on the cardiovascular system. Through its sympathomimetic effects, cocaine augments ventricular contractility, blood pressure, heart rate, and myocardial oxygen demand. Myocardial ischemia is induced by coronary vasoconstriction, platelet aggregation, and accelerated atherosclerosis. The ensuing supply-demand deficit may manifest as angina, and cocaine-induced coronary spasm may lead to acute myocardial infarction and death. Cocaine is markedly pyrogenic because it induces muscular activity, augments heat production, and potentiates vasoconstriction—all of which can enhance the risk for heat stroke and death. Cocaine dependence is a significant problem in our society; it is associated not only with the outlined spectrum of medical complications but also with crime and violence. Educational programs regarding the hazards of cocaine use and addiction are highly recommended for all athletes.

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Inhalants Epidemiology and Classification Inhalant use is the deliberate inhalation of volatile substances to induce a mind-altering effect. Purchase and possession are legal, and inhalants are cheap and easily accessible. National surveys of adolescents in the United States have reported that second to marijuana, inhalants are the most widely used class of illicit drugs among 8th and 10th graders. Fortunately, their use has continued to decrease. The American Academy of Pediatrics has taken the initiative to educate clinicians, parents, and children of the dangers of inhalant abuse.124 Inhalants are divided into three groups on the basis of the inhalant pharmacology, as follows: 1. Type I agents include volatile solvents such as paint thinner, acetone, glue, rubber cement, butane, aerosols, hair spray, and gasoline. 2. Type II agents are nitrous oxide and whipping cream aerosols, which contain nitrous oxide. 3. Type III agents include volatile alkyl nitrites known as “poppers,” “snappers,” “boppers,” and “Amys.” Inhalant agents are abused through a variety of methods. Glue or solids are emptied into a bag, held close to the nose, and inhaled either through the nose (snorting or sniffing) or through the mouth (huffing). Other methods include placing one’s entire head into a bag (bagging) and inhalation of either air fresheners (e.g., Glade, referred to as glading), or computer cleaning aerosols (dusting). Pathophysiology and Adverse Effects Inhalants contain different solvents, each with its own unique toxicity, but all inhalants induce CNS depression, likely involving a γ-aminobutyric acid agonist or altered neuronal membrane function.125 Death can occur as a result of the use of inhalant agents because of cardiac complications that occur as a result of asphyxia, ventricular fibrillation, or cardiac arrhythmia. Cerebral death may occur as a result of asphyxia, edema, and hyperpyrexia.125 Inhalants do not augment or improve athletic performance; in fact, their use can lead to serious health consequences. Some glues are metabolized and may cause peripheral neuropathy, characterized by muscle weakness and wasting. Inhalants have also been known to sensitize and potentiate the myocardium to epinephrine, which, during exercise, may increase an athlete’s risk of an acute, fatal arrhythmia. No specific antidotes exist for inhalant toxicity, and treatment is rooted in prevention.

Conclusion The use of recreational drugs and their potential for deadly consequences are a realities for athletes and our society. Most treatment entails meaningful educational programs. Athletes who are well informed about the potential dangers of using recreational drugs may be best able to avoid the temptation to “try” these drugs, which are readily available. Additionally, coaches should be involved in the education process; they should stress

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the importance of sobriety and healthy habits as core requirements for optimal health and the development of a successful team. The ongoing Monitoring the Future surveys have clearly demonstrated that all the drugs discussed in this chapter are used by many youth at very young ages, often in middle or elementary school. It is therefore imperative that the education of athletes, coaches, and parents commence in the earliest recreational leagues. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Cooper R, Naclerio F, Allgrove J, et al. Creatine supplementation with specific view to exercise/sports performance: an update. J Int Soc Sports Nutr. 2012;9:33.

Level of Evidence: II

Summary: More and more information is being discovered about the use of creatine, particularly with regard to its relevance in improving sports performance. This article reviews recent advances in understanding the science relating to creatine use and the methods of supplementation to make cellular and subcellular changes.

Citation: Green GA, Uryasz FD, Petr TA, et al. NCAA study of substance use and abuse habits of college student-athletes: clinical investigations. Clin J Sport Med. 2001;11(1):51–56.

Level of Evidence: III

Summary: Monitoring the Future is an ongoing study that entails the administration of a series of annual surveys among representative samples of secondary school students throughout the United States, using a standard set of questions to determine usage levels of various substances. Cigarettes/e-cigarettes, alcohol, and marijuana continue to be the most frequently abused substances among adolescents, with synthetic marijuana recently falling under the Drug Enforcement Administration’s list of prohibited substances.

Citation: World Anti-Doping Agency. The 2012 Prohibited List. Available at: http://www.wada-ama.org/Documents/World_Anti-Doping_ Program/WADP-Prohibited-list/2012/WADA_Prohibited_ List_2017. Accessed June 12, 2017.

Level of Evidence: V

Summary: The World Anti-Doping Agency annually updates its list of prohibited substances among athletes. A review of and familiarity with the list is critical for providers so they can comply with up-to-date guidelines.

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CHAPTER 26  Doping and Ergogenic Aids

REFERENCES 1. http://www.cmgww.com/football/lombardi/print1.htm. 2. Mirkin G. Eating for competing. Semin Adolesc Med. 1987;3:177–183. 3. Goldman B. Death in the Locker Room II. Chicago: Elite Sports Medicine Publications; 1992: 23–24. 4. Cowart V. Steroids in sports: after four decades, time to return these genies to bottle. JAMA. 1987;257(421). 5. Hoberman JM, Yesalis CE. The history of synthetic testosterone. Sci Am. 1995;272:76–80. 6. Berthold AA. Transplantation der Hoden. Arch Anat Physiol Wiss. 1849;16:42–46. 7. David K, Dingemanse E, Freud J, et al. Uber krystallinischesmannliches Hormon aus Hoden (Testosteron), wirksamer als aus Harn oder aus Cholesterin bereitetes Androsteron. Hoppe Seylers Z Physiol Chem. 1935;233:281–282. 8. Butenandt A, Hanisch G. Uber die Umwandulung des Dehydroandrosterons in Androstenol-17-one-(3) (Testosterone): um Weg zur Darstellung des Testosterons auf Cholesterin. Ber Deutsch Chem Ges. 1935;68:1859–1862. 9. Millhorn HT Jr. Anabolic steroids: another form of drug abuse. J Miss State Med Assoc. 1993;32:293–297. 10. Boje O. Doping. Bull World Health Organ. 1939;8:439–469. 11. Knopp WD, Wang TW, Bach BR Jr. Ergogenic drugs in sport. Clin Sports Med. 1997;16:375–392. 12. De Kurd P. The Male Hormone, Garden City, NY, 1945, Garden City. 13. Yesalis CE. Medical, legal and societal implications of androstenedione use. JAMA. 1999;281:2043–2044. 14. Gilbert B. Drugs in sport: Part 2. Something extra on the ball. Sports Illus. 1969;30–42. 15. Yesalis CE, ed. Anabolic Steroids in Sport and Exercise. Champaign, Ill: Human Kinetics; 1993:35–47. 16. Hunter M. Shadows of doubt: did drug use kill sprinter Florence Griffith Joyner? Macleans. 1998;62. 17. Buckley W, Yesalis C, Friedl K, et al. Estimated prevalence of anabolic steroid use among high school seniors. JAMA. 1988;260:3441–3445. 18. Partnership for Drug-Free Kids. PATS KEY FINDINGS. Released July 23, 2014. https://drugfree.org/research-reports/. Retrieved June 23, 2017. 19. Yesalis C, Bahrke M. Doping among adolescent athletes. Bailliéagre’s Best Pract Res Clin Endocrinol Metab. 2000;14: 25–35. 20. Gorman C. Girls on steroids: among young athletes these dangerous drugs are the rage: is your daughter using them? Time. 1998;93. 21. Wilson JD. Androgens. In: Goodman LS, Limbird LE, eds. Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 9th ed. New York: McGraw-Hill; 1996:1441–1457. 22. Arver S, Dobs AS, Meikle AW, et al. Long-term efficacy and safety of a permeation-enhanced testosterone transdermal system in hypogonadal men. Clin Endocrinol (Oxf). 1997;47: 727–737. 23. Bhasin S, Storer T, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med. 1996;335:1–7. 24. Hartgens F, Kuipers H. The effects of androgenic-anabolic steroids in athletes. Sports Med. 2004;34(8):513–534. 25. Alen M, Hakkinen K, Komi PV. Changes in neuromuscular performance and muscle fiber characteristics of elite power

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athletes self-administering androgenic and anabolic steroids. Acta Physiol Scand. 1984;122:535–544. Bhasin S, Storer T, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med. 1996;335:1–7. Haupt H. Anabolic steroids and growth hormone. Am J Sports Med. 1993;21:468–473. Bahrke MS, Yesalis CE III, Wright JE. Psychological and behavioral effects of endogenous testosterone and anabolicandrogenic steroids: an update. Sports Med. 1996;22:367–390. VanHelder WP, Kofman E, Tremblay MS. Anabolic steroids in sport. Can J Sport Sci. 1991;16:248–257. Su TP, Pagliaro M, Schmidt PJ, et al. Neuropsychiatric effects of anabolic steroids in male normal volunteers. JAMA. 1993;269:2760–2764. Bamberger M. Under suspicion. Sports Illus. 1997;72–75. Strauss JS, Pochi PE. Hormones and cellular metabolism. The human sebaceous gland: its regulation by steroidal hormones and its use as end organ for assaying androgenicity in vivo. Recent Prog Horm Res. 1963;19:385–444. Reese T, Exum WR. Anabolic-androgenic steroids. In: Salis J, ed. Essentials of Sports Medicine. St. Louis: Mosby; 1997: 237–241. Tentori L, Graziani G. Doping with growth hormone, IGF-1, anabolic steroids or erythropoietin: is there a cancer risk? Pharmacol Res. 2007;10:1–11. Bamberger M, Yaeger D. Over the edge. Sports Illus. 1997; 61–70. Blue JG, Lombardo JA. Steroids and steroid-like compounds. Clin Sports Med. 1999;18:667–689. Michna H. Tendon injuries induced by exercise and anabolic steroids in experimental mice. Int Orthop. 1987;11:157–162. Blue JG, Lombardo JA. Steroids and steroid-like compounds. Clin Sports Med. 1999;18:667–689. Melchert RB, Welder AA. Cardiovascular effects of androgenicanabolic steroids. Med Sci Sports Exerc. 1995;27:1252–1262. Appell HJ, Heller-Umpfenback B, Feraudi M, et al. Ultrastructural and morphometric investigations on the effects of training and administration of anabolic steroids on the myocardium of guinea pigs. Int J Sports Med. 1983;4:268–274. Dickerman RD, Schaller F, Zachariah NY, et al. Left ventricular size and function in elite bodybuilders using anabolic steroids. Clin J Sport Med. 1997;7:90–93. Sullivan ML, Martinez CM, Gallagher EJ. Atrial fibrillation and anabolic steroids. J Emerg Med. 1999;17:851–857. Dickerman RD, Schaller F, Prather I, et al. Sudden cardiac death in a 20-year-old bodybuilder using anabolic steroids. Cardiology. 1995;86:172–173. Petersson A, Garle M, Holmgren P, et al. Toxicological findings and manner of death in autopsied users of anabolic androgenic steroids. Drug Alcohol Depend. 2006;81(3):241–249. Urhausen A, Albers T, Kindermann W, et al. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart. 2004;90:496–501. Overly WL, Dankoff JA, Wang BF, et al. Androgens and hepatocellular carcinoma in the athlete. Ann Intern Med. 1984;100:158–159. Wilson JD. Androgen abuse by athletes. Endocr Rev. 1988;9: 181–199. Dickerman RD, Pertusi RM, Zachariah NY, et al. Anabolic steroid-induced toxicity: is it overstated? Clin J Sport Med. 1999;9:34–39.

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SECTION 2  Medical

49. Boada LD, Zumbado M, Torres S, et al. Evaluation of acute and chronic hepatotoxic effects exerted by anabolic-androgenic steroid stanozolol in adult male rats. Arch Toxicol. 1999;73: 465–472. 50. Soe KL, Loe M, Gluud C. Liver pathology associated with the use of anabolic-androgenic steroids. Liver. 1992;12:73–79. 51. Paradinas FJ, Bull TB, Westaby D, et al. Hyperplasia and prolapse of hepatocytes into hepatic veins during long term methyltestosterone therapy: possible relationships of these changes in the development of peliosis hepatis and liver tumors. Histopathology. 1977;1:225–246. 52. Gleeson D, Newbould MJ, Taylor P, et al. Androgen associated hepatocellular carcinoma with an aggressive course. Gut. 1991;32:1084–1086. 53. Bhasin S, Storer T, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med. 1996;335:1–7. 54. Blue JG, Lombardo JA. Steroids and steroid-like compounds. Clin Sports Med. 1999;18:667–689. 55. Salmon UJ, Geist SH. Effects of androgens upon libido in women. J Am Endocrinol. 1943;3:235–238. 56. Vest SA, Howard JE. Clinical experiments with the use of male sex hormones. J Urol. 1938;40:154–183. 57. Perry PJ, Kutscher EC, Lund BC, et al. Measures of aggression and mood changes in male weightlifters with and without androgenic anabolic steroid use. J Forensic Sci. 2003;48:646–651. 58. Blue JG, Lombardo JA. Steroids and steroid-like compounds. Clin Sports Med. 1999;18:667–689. 59. Ip EJ, Barnett MJ, Tenerowicz MJ, et al. The Anabolic 500 survey: characteristics of male users versus nonusers of anabolic-androgenic steroids for strength training. Pharmacotherapy. 2011;8:757–766. 60. Parasrampuria J. Quality control of dehydroepiandrosterone dietary supplement products. JAMA. 1998;280:1565. 61. Clarkson PM, Rawson ES. Nutritional supplements to increase muscle mass. Crit Rev Food Sci Nutr. 1999;39:317–328. 62. Blue JG, Lombardo JA. Steroids and steroid-like compounds. Clin Sports Med. 1999;18:667–689. 63. Baker WL, Karan S, Kenny AM. Effect of dehydroepiandrosterone on muscle strength and physical function in older adults: a systematic review. J Am Geriatr Soc. 2011;59:997–1002. 64. Wallace MB, Lim J, Cutler A, et al. Effects of dehydroepiandrosterone vs androstenedione supplementation in men. Med Sci Sports Exerc. 1999;31:1788–1792. 65. Nair K, Rizza R, O’Brien K, et al. DHEA in elderly women and DHEA or testosterone in elderly men. N Engl J Med. 2006;355(16):1647–1659. 66. Corrigan AB. Dehydroepiandrosterone and sport. Med J Aust. 1999;171:206–208. 67. Yesalis CE. Medical, legal and societal implications of androstenedione use. JAMA. 1999;281:2043–2044. 68. King DS, Sharp RL, Vukovich MD, et al. Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men: a randomized controlled trial. JAMA. 1999;281:2020–2028. 69. Segura J. Summary of International Olympic Committee regulations on doping aspects. In: Karch SB, ed. Drug Abuse Handbook. Boca Raton, FL: CRC Press; 1997:16–17. 70. World Anti-Doping Agency. http://www.wada-ama.org/en. Accessed July 29, 2013. 71. Bonsdorff E, Jalavisto E. A humoral mechanism in anoxic erythrocytosis. Acta Physiol Scand. 1948;16(2–3):150–170.

72. Pace N, Consolazio WV, Lozner EL. The effect of transfusions of red blood cells on the hypoxia tolerance of normal men. Science. 1945;102(2658):589–591. 73. Ekblom B, Glodbarg AN, Gullbring B. Response to exercise after blood loss and reinfusion. J Appl Physiol. 1972;33: 175–180. 74. Berglund B, Ekblom B. Effect of recombinant human erythropoietin on blood pressure and some hematological parameters in healthy men. J Intern Med. 1991;229:125–130. 75. Giraud S, Sottas PE, Robinson N, et al. Blood transfusion in sports. Handb Exp Pharmacol. 2010;195:125–130. 76. World Anti-Doping Agency. The 2017 Prohibited List. Available at: http://www.wada-ama.org/Documents/World_AntiDoping_Program/WADP-Prohibited-list/2012/WADA_ Prohibited_List_2012_EN.pdf. Accessed June 23, 2017. 77. Reichel C, Gmeiner G. Erythropoietin and analogs. Handb Exp Pharmacol. 2010;195:251–294. 78. Ekblom BT. Blood boosting and sport. Baillieres Best Pract Res Clin Endocrinol Metab. 2000;14(1):89–98. 79. Jelkmann W, Lundby C. Blood doping and its detection. Blood. 2011;118(9):2395–2404. 80. Nelson AE, Howe CJ, Nguyen TV, et al. Erythropoietin administration does not influence the GH-IGF axis or makers of bone turnover in recreational athletes. Clin Endocrinol (Oxf). 2005;63:305–309. 81. Greenhaff PL, Casey A, Short AH, et al. Influence of oral creatine supplementation on muscle torque during repeated bouts of maximal voluntary exercise in man. Clin Sci. 1993;84:565–571. 82. Harris RC, Soderlund K, Hultman E. Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci (Colch). 1992;83:367–374. 83. Cooper R, Naclerio F, Allgrove J, et al. Creatine supplementation with specific view to exercise/sports performance: an update. J Int Soc Sports Nutr. 2012;9:33. 84. Bosco C, Tihanyi J, Pucspk J, et al. Effect of oral creatine supplementation on jumping and running performance. Int J Sports Med. 1997;18:369–372. 85. Birch R, Noble D, Greenhaff PL. The influence of dietary creatine supplementation on performance during repeated bouts of maximal isokinetic cycling in man. Eur J Appl Physiol. 1994;69:268–276. 86. Balsom PD, Harridge SD, Soderlund K, et al. Creatine supplementation per se does not enhance endurance exercise performance. Acta Physiol Scand. 1993;149:521–523. 87. Ingwall JS, Morales MF, Stockdale FE. Creatine and the control of myosin synthesis in differentiating skeletal muscle. Proc Natl Acad Sci USA. 1972;69:2250–2253. 88. Hultman E, Soderlund K, Timmons JA, et al. Muscle creatine loading in man. J Appl Physiol. 1996;81:232–237. 89. Harris RC, Soderlund K, Hultman E. Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci (Colch). 1992;83:367–374. 90. Buford TW, Kreider RB, Stout JR, et al. International Society of Sports Nutrition position stand: creatine supplementation and exercise. J Int Soc Sports Nutr. 2007;30:4–6. 91. Green AL, Simpson EJ, Littlewood JJ, et al. Carbohydrate ingestion augments creatine retention during creatine feedings in humans. Acta Physiol Scand. 1996;158:195–202. 92. Bosco C, Tihanyi J, Pucspk J, et al. Effect of oral creatine supplementation on jumping and running performance. Int J Sports Med. 1997;18:369–372.

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CHAPTER 26  Doping and Ergogenic Aids 93. Pline KA, Smith CL. The effect of creatine intake on renal function. Ann Pharmacother. 2005;39:1093–1096. 94. Ascol M, Segaloff DL. Adenohypophyseal hormones and their hypothalamic releasing factors. In: Goodman LS, Limbird LE, eds. Goodman and Gilman’s the Pharmacological Basis of Therapeutics. 9th ed. New York: McGraw-Hill; 1996:1363–1370. 95. Raben MS. Treatment of pituitary dwarf with human growth hormone. J Clin Endocrinol. 1958;18:901–903. 96. Tan L, Williams MA, Khan MK, et al. Risk of transmission of bovine spongiform encephalopathy to humans in the United States: report of the Council on Scientific Affairs. JAMA. 1999;281:2330–2339. American Medical Association. 97. Ghaphery NA. Performance-enhancing drugs. Orthop Clin North Am. 1995;26:433–442. 98. Genentech: Recombinant GH. http://www.gene.com. Accessed September 2, 2017. 99. Wilson S. Scientists back improved HGH test; 2011. Available at: http://www.washingtontimes.com/news/2011/oct/3/ scientists-back-improved-hgh-test. 100. Collomp K, Ahmaidi S, Audran M, et al. Effects of caffeine ingestion on performance and anaerobic metabolism during the Wingate test. Int J Sports Med. 1991;12:439–443. 101. Pasman WJ, VanBaak MA, Jeukendrup AE, et al. The effect of different dosages of caffeine on endurance performance time. Int J Sports Med. 1995;16:225–230. 102. Armstrong LE. Caffeine, body-fluid electrolyte balance, and exercise performance. Int J Sport Nutr Exerc Metab. 2002;12: 189–206. 103. Burke LM. Caffeine and sports performance. Appl Physiol Nutr Metab. 2008;33:1319–1334. 104. Wiles J, Bird S, Hopkins J, et al. Effect of caffeinated coffee on running speed, respiratory factors, blood lactate and perceived exertion during 1500-m treadmill running. Br J Sports Med. 1992;26:116–120. 105. Ivy J, Costill D, Fink W, et al. Influence of caffeine and carbohydrate feedings on endurance performance. Med Sci Sports. 1979;11:6–11. 106. MacIntosh B, Wright B. Caffeine ingestion and performance of a 1500-metre swim. Can J Appl Physiol. 1995;20:168–177. 107. Monitoring the Future. National Results on Adolescent Drug Use: Overview of Key Findings; 2016. Available at: http://www .monitoringthefuture.org. Accessed June 10, 2017. 108. American College of Sports Medicine. Alcohol and athletic performance. Available at: http://www.acsm.org/docs/currentcomments/alcoholandathleticperformance.pdf. Accessed August 7, 2017. 109. Monitoring the Future Study: Trends in Prevalence of Various Drugs. National Institute on Drug Abuse. https://www .drugabuse.gov. Accessed June 25,2017.

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110. Nelson T, Wechsler H. Alcohol and college athletes. Med Sci Sports Exerc. 2001;33(1):43–47. 111. Grossbard JR, Lee CM, Neighbors C, et al. J Stud Alcohol Drugs. 2007;68(4):566–574. 112. Position stand: American College of Sports Medicine. The use of alcohol in sports. MSSE. 1982;14(6):ix–xi. 113. Moritsugu KP. Underage drinking: a call to action. J Am Diet Assoc. 2007;107(9):1464. 114. National Estimates of Marijuana Use and Related Indicators – National Survey on Drug Use and Health 2002 – 2015. https://www.cdc.gov. Accessed June 24, 2017. 115. Sidney S. Cardiovascular consequences of marijuana use. J Clin Pharmacol. 2002;42:645–705. 116. Jacques JP, Zombek S, Guillain CH, et al. Cannabis: experts agree more than they admit. Rev Med Brux. 2004;25(2):87–92. 117. Moore BA, Augustson EM, Moser RP, et al. Respiratory effects of marijuana and tobacco use in a U.S. sample. J Gen Intern Med. 2005;20(1):33–37. 118. Renaud AM, Cormier Y. Acute effects of marijuana smoking on maximal exercise performance. Med Sci Sports Exerc. 1986; 18(6):685–689. 119. Chemicals Used in “Spice” and “K2” type products under Federal control and regulation for additional 6 months: DEA continues studies to determine whether to permanently control five substances. United States Drug Enforcement Administration, 2011. Available at: www.justice.gov/dea/pubs/ pressrel/pr022912.html. 120. World Health Organization. Tobacco Fact Sheet–Updated 2017. http://www.who.int/mediacentre/factsheets. Accessed June 12, 2017. 121. E-Cigarette Use Among Youth and Young Adults A Report of the Surgeon General. https://e-cigarettes.surgeongeneral.gov/ documents/2016. Accessed June 12, 2017. 122. Miyata H, Kono J, Ushijima S, et al. Clinical features of nicotine dependence compared with those of alcohol, methamphetamine, and inhalant dependence. Ann NY Acad Sci. 2004;1025:481–488. 123. Monitoring the Future Study: Trends in Prevalence of Various Drugs. Available at: https://www.drugabuse.gov/trends -statistics/monitoring-future/monitoring-future-study-trends -in-prevalence-various-drugs. Accessed June 23, 2017. 124. About inhalants. Paediatr Child Health. 1998;3(2):132–133. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC2851284/. Accessed September 2, 2017. 125. Bass M. Sudden sniffing death. JAMA. 1970;212:2075–2079.

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27  The Female Athlete Letha Y. Griffin, Mary Lloyd Ireland, Fred Reifsteck, Matthew H. Blake, Benjamin R. Wilson THE GROWING IMPORTANCE AND RECOGNITION OF THE FEMALE ATHLETE Over the past several decades there has been a rapid development of competitive sporting events for women, and parallel to this, an emergence of increasing numbers of excellent competitive women athletes. Before the 1970s, few women participated in organized sport. However, the passage of Title IX of the Educational Assistance Act of 19721 required institutions receiving federal money to offer equal opportunities to both males and females in all programs including athletics. This sparked a rapid growth not only in collegiate women’s sport opportunities, but also in those sport opportunities available to high school and recreational female athletes (Table 27.1). The female athlete market is now a major target for businesses as exemplified by women’s clothing. Women’s sporting gear before the 1980s was difficult to find. However, with increased opportunities in sports for women following the passage of Title IX, the demand for female-specific sport clothes and equipment has increased. Prior to this time, female athletes often wore men’s shoes (a practice that was associated with an increase in foot problems), men’s warm-ups, and sport protection equipment (shin guards in soccer, eye protection in racket sports, mouth guards, etc.). However, in the 1990s the business of women’s sport gear—including warm-ups, shorts, skirts, shirts, sports bras, protective pads, and shoes—grew rapidly. Women traditionally spend more money on all clothing needs compared to men, and sport wear has become a fashion statement for women. Sized to the women’s figure, braces and other protective sport gear now have a more comfortable fit. Lightweight clothing that wicks away perspiration is prevalent and comes in pinks, purples, and other bright colors for stylish looks. Shoes made for women are now a more comfortable “fit,” which has resulted in fewer calluses, corns, and other foot issues. Before 1970, rarely were the results of women’s sports contests found in newspapers or within the pages of Sports Illustrated or on nightly TV news or radio; however, this trend is changing. Women’s golf and tennis events are now aired on primetime television. The Women’s National Basketball Association (WNBA) aired 45 regular season games in 2017. Fox reports that 6 of the top 10 searches of 2016 Olympic Athletes were for females.5 Parallel and (perhaps one could argue) secondary to the increased emphasis on women’s sport participation, there has 294

been an improvement in women’s sport performance in swimming and running events, and the speed of basketball, soccer, tennis, and volleyball games has increased with the improvement in women’s skills and overall athleticism. Not only have the numbers and recognition of highly competitive female athletes increased over the last 50 years, but also the prevalence of women of all ages participating in recreational athletics has skyrocketed, making it essential that those caring for the female athlete appreciate her uniqueness as gender-based differences are important when developing novel approaches to prevention, diagnosis, and treatment of injury and illness.6 The term “sexual dimorphism” is defined as: “The condition in which the two sexes of the same species exhibit different characteristics beyond the differences of their sexual organs.”7 In humans, these differences are related to the expression of genes on the X and Y chromosomes. These differences form the basis of this chapter and include not only anatomic and physiologic differences (Table 27.2) but also certain aspects of illnesses and injuries unique to the female athlete.

GENERAL CONSIDERATIONS Conditioning Conditioning has been defined as “a process in which stimuli are created by an exercise program performed by the athlete to produce a higher level of function.”9 A properly constructed conditioning program should maximize performance and minimize the chance of injury. There have been ongoing debates as to whether conditioning techniques used for males are appropriate for females. Little boys start out wishing to do weights with their fathers or older brothers or friends. This is infrequently true in girls. Hence, in the mid to late teenage years, boys are typically familiar with weight workouts and have already incorporated strengthening programs into their sport conditioning programs. At this time, girls most likely are just beginning to learn that a weight strengthening program is a needed part of a wellconstructed conditioning program. Some theorize that girls and young women may be leery of participating in a weight training program for fear of developing bulky muscles. They should be reassured that strength training does not necessarily have to involve lifting heavier and heavier weights and is associated with not only better performance but also a decrease in injury.9,10 Static and dynamic balance are vital for maximizing sport performance as well as enhancing injury prevention.11 Articles

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CHAPTER 27  The Female Athlete

Abstract

Keywords

Over the past several decades there has been a rapid development of competitive sporting events for women, and parallel to this, an emergence of increasing numbers of excellent competitive women athletes. Not only have the numbers and recognition of highly competitive female athletes increased over the last 50 years, but also the prevalence of women of all ages participating in recreational athletics has skyrocketed, making it essential that those caring for the female athlete appreciate her uniqueness as gender-based differences are important when developing novel approaches to prevention, diagnosis, and treatment of injury and illness. The term sexual dimorphism is defined as: “The condition in which the two sexes of the same species exhibit different characteristics beyond the differences of their sexual organs” (Wikipedia 2017 https://en.wikipedia.org/wiki/sexual_ dimoprhism#External_links). In humans, these differences are related to the expression of genes on the X and Y chromosomes. These differences form the basis of this chapter and include not only anatomic and physiologic differences but also certain aspects of illnesses and injuries unique to the female athlete.

female athlete foot/ankle concussion triad knee shoulder

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CHAPTER 27  The Female Athlete

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TABLE 27.1  Growth in Women’s Sports2–4 NUMBER OF WOMEN PARTICIPATING Participation Level

1971–1972

2000–2001

2010–2011

2015–2016

High school Collegiate Olympic

294,015 29,972 1264 (17.5% of Olympians)

2,784,154 150,916 4935 (37.5% of Olympians)

3,173,549 190,000 5091 (42.4% of Olympians)

3,324,326 216,286 5800 (43.5% of Olympians)

www.nfhs.org; www.ncaa.org; www.olympic.org.

TABLE 27.2  Anatomic and Physiologic Gender Differences8,a Parameter

Postpubertal Girls

Postpubertal Boys

Impact

Oxygen pulse (efficiency of cardiorespiratory system V02 max (reflects level of aerobic fitness) Metabolism (basal metabolic rate [BMR]) Thermoregulation

Lower

Higher

Lower

Higher

Higher oxygen pulse provides boys an advantage in aerobic activity. Boys have greater aerobic capacity.

6%–10% lower (when related to body surface area) Equals boys

6%–10% higher (when related to body surface area) Equals girls

Girls need fewer calories to sustain the same activity level as boys. They have equal ability to adequately sweat in a hot environment to decrease core body temperature.

Endocrine System Testosterone

Lower

Higher

Estrogen

Higher

Lower

Height

64.5 inches

68.5 inches

Boys have increased muscle size, strength, and aggressiveness. Unknown if it is related to increase in ligamentous laxity or in rate of ACL injuries. The increased height and weight in boys give them structural advantages.

Weight Limb length Articular surface

56.8 kg Shorter Smaller

70.0 kg Longer Larger

Body shape

%Muscle/total

Narrower shoulders Wider hips Legs 51.2% of height More fat in lower body −36%

Wider shoulders Narrower hips Legs 52% of height More fat in upper body −44.8%

%Fat/total body weight

−22% to 26%

−13% to 16%

Age at skeletal maturation Cardiovascular system Heart size Heart volume Systolic blood pressure Hemoglobin

17–19 years

21–22 years

Smaller Smaller Lower

Larger Larger Higher 10%–15% > per 100 mL blood

Smaller Smaller Smaller Smaller

Larger Larger Larger Larger

Pulmonary System Chest size Lung size Vital capacity Residual volume

Boys can achieve a greater force for hitting and kicking. May provide boys with greater joint stability; boys have greater surface area to dissipate impact force. Girls have lower center of gravity and therefore greater balance ability; girls have increased valgus angle at the knee that increases knee injuries; boys and girls have different running gaits. Boys have greater strength and greater body weighta speed. Girls are more buoyant and better insulated; they may be able to convert fatty acid to metabolism more rapidly. Girls develop adult body shape/form sooner than boys. Stroke volume in girls is less, necessitating an increased heart rate for a given submaximal cardiac output; cardiac output in girls is 30% less than in boys; the risk of hypertension may be less in girls. The oxygen carrying capacity of blood is greater in boys. Total lung capacity in boys is greater than in girls.

a

There are no appreciable differences in these parameters prior to puberty; therefore prepubertal boys and girls can compete on a fairly equal basis. ACL, Anterior cruciate ligament. From Yurko-Griffin LY, Harris S. Female athlete. In: Sullivan JA, Anderson SJ, editors. Care of the Young Athlete. Rosemont, IL: American Academy of Orthopaedic Surgery; 2000:138–148 with permission.

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have been written and comments made in scientific meetings regarding the need, or the lack of need, to alter training and conditioning in several women’s sports such as soccer, softball, basketball, volleyball, and lacrosse.12 Suggestions have been made for players to incorporate more agility and balance exercises to try to decrease the frequency of noncontact anterior cruciate ligament (ACL) injuries in these sports.13-15 The adage “stronger is better,” is now being modified since strong muscles that fire at inappropriate times can cause harm rather than ensure protection from injury during an athletic event. Programs for women’s sports where ACL risks are high are adopting training and conditioning routines that emphasize not only the traditional strength, flexibility, and aerobic conditioning exercises, but also they have drills aimed to enhance balance and agility.14,16-20 Incorporating plyometric drills appears to be appropriate in both male and female sport programs. (See section on ACL injuries in women in this chapter.) Greater emphasis on core strengthening may also be appropriate for females who have been reported to have more anterior pelvic tilt than men, a trait that is linked with patellofemoral pain syndrome.13 Medial quadriceps exercises are recommended for females with laterally tracking patellae especially those with increased Q ankle, increased tibial tubercle to tibial groove distance, and those with increased knee valgus.21 These exercises should commence during the prepubescent age and continue through the pubertal years and into post pubertal maturation. By building strength in the vastus medialis, hopefully the patella will sit more centrally in the trochlear groove decreasing patellofemoral pain by balancing patellar trochlear forces. Since postpubertal females are reported to have increased flexibility compared to males, strengthening scapular stabilizers and the muscles of the rotator cuff to prevent shoulder instability issues is recommended in swimmers; in volleyball, lacrosse, and softball players; and in those playing racket sports.22 Prevention rather than “cure” should be the norm and has been proven to be beneficial. Following puberty, training and conditioning programs should also account for inherent gender-based, physical, and physiologic differences (see Table 27.2). Males are more fully developed in the upper body with a narrow pelvis and hence, a higher center of gravity; whereas females have narrower shoulders compared to males, but proportionally a wider pelvis resulting in a lower center of gravity, but they have a more difficult time achieving the upper body strength of their male counterparts. Males have more muscle mass per body weight; whereas female athletes, even those who are considered to be well conditioned, have greater body fat than males (18% to 20% females vs. 10% to 15% males). Moreover, males have a greater thoracic capacity and hence, a greater VO2 max than do females. Overall aerobic capacity in females is less than that of males following puberty. Hence, one notes that although female athletes have improved significantly over the last 10 years, their times in anaerobic and aerobic running events are still not equal to those of males (Table 27.3). A few “conditioning tips” for female athletes are listed in Table 27.4. In the last decade there has been an emphasis on screening athletes at all levels of play from those who exercise for health and fitness to recreational players to highly trained competitive

TABLE 27.3  Improvements in Women’s

Anaerobic and Aerobic Running Events23 Collegiate Track 800 m 3200 m 10,000 m

1972 2 : 04 : 7 10 : 51 : 0 33 : 36 : 51

1998 2 : 06 : 30 10 : 25 : 99 32 : 56 : 63

2012 2 : 03 : 34 10 : 08 : 11 32 : 41 : 63

2017 2 : 02.36 10 : 00.13 32 : 38.57

Boston Marathon

1972 3 : 10 : 26

1996 2 : 27 : 12

2011 2 : 22 : 36

2017 2 : 21 : 52

www.ncaa.org; www.baa.org.

TABLE 27.4  Conditioning Tips for

Recreational Athletes24,25

Emphasize core strength to minimize stress on lower extremities. Emphasize strengthening of scapular stabilizers and muscles involved in dynamic stabilization of the glenohumeral joint to minimize laxity issues of the shoulder joint.a Emphasize vastus medialis obliques (VMO) strength when doing lower extremity strengthening exercises to improve patellar tracking.b Minimize loading the patellofemoral joint in a fully flexed knee position, that is, consider short arc extension and leg press exercises in place of squats, lunges, and full arc extension exercises.b Perform upper extremity strengthening exercises at shoulder height and below to minimize stress on the rotator cuff (pull downs, overhead dumbbell press, etc.). a

Kibler WB, Sciascia AD, Uhl TL, Tambay N, Cunningham T. Electromyographic analysis of specific exercises for the scapular control in early phases of shoulder rehabilitation. Am J Sports Med. 2008;36:1789. b www.healthline.com/health/fitness-exercises/vastus-medialis-exercises.

athletes for functional movement skills and balance to detect deficits that could predispose the athlete to injury. Exercises to correct these deficits can then be incorporated into the athlete’s exercise program not only to improve physical performance parameters (e.g., increased aerobic power, strength, speed, agility, and balance), but also to prevent injury. Such programs have proven to be very highly effective in achieving both of these goals.11,26-30

Nutrition and Hydration Sports nutrition is currently recognized as one of the most important aspects of improving sports performance. Inadequate nutritional intake has been reported to be more common in female than male athletes. Both the content and timing of optimal nutrition may significantly impact the female athlete’s performance. In individuals, dietary needs depend on not only sex, but also size, weight, and energy demands of the sport. A 5-foot female dancer may not require as high a caloric intake as a 6-foot female basketball player. Please see the chapter on nutrition for a more complete discussion of the nutritional needs in athletes in general. This section will focus on vitamin D, calcium, iron, and hydration—areas of particular concern for the female athlete. Adequate consumption of carbohydrates, protein, fat, and other macronutrients, are critical to replace glycogen stores, and repair exercise-induced tissue damage. On average, an energy

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intake of less than 1800 kcal per day in a female athlete can result in a persistent state of negative energy balance and diminish sports performance. Vitamin D is an emerging micronutrient with deficiency being linked to low bone mineral density (BMD), cancer, heart disease, autoimmune problems, and infections.31 Vitamin D is needed for the absorption of calcium, which is critical to bone health. Vitamin D is also important in nervous system and skeletal muscle development and function.32 Female athletes living in northern latitudes who participate in indoor sport are at risk for vitamin D deficiency. Indoor sport athletes are nearly twice as likely as outdoor athletes to be vitamin D deficient.31 While sun exposure is important for vitamin D levels, low dietary intake may also lead to deficiency. Vitamin D can be obtained by one of two methods. Endogenous vitamin D is synthesized in the skin following direct sun exposure; exogenous vitamin D is ingested in foods or can be obtained as a supplement. A recent very interesting observation related to vitamin D is the risk of upper respiratory tract infections due to a lowered immune system response in patients with low vitamin D levels.31 Respiratory infections are a leading medical cause of lost time for the female athlete. At-risk athletes, especially athletes aged 19 to 49, may benefit from 200 IU of vitamin D supplementation per day.32 Female athletes with the female athlete triad or risk factors for osteoporosis may need 400 to 800 IU per day. (See sections on the Female Athlete Triad and Osteoporosis and Osteopenia in this chapter.) Adequate calcium intake is essential for proper bone mineralization. Females may be more at risk than males for low calcium intake as females more frequently restrict caloric intake and often shun dairy products feeling they are too high in calories. However, this is not the case since we now have options such as low-fat milk, low-fat cottage cheese, low-fat yogurt, and low-fat string cheese that are high in calcium but low in calories. Table 27.5 lists the required daily calcium needs for women of various age ranges. Three servings of daily calcium products typically provide the needed daily requirements. Female athletes should be encouraged to drink low-fat milk for breakfast and eat two servings of low-fat yogurt or string cheese daily to fulfill their

calcium needs. Table 27.6 lists the calcium present in some commonly consumed foods. Iron is a mineral that has long been known to affect athletic performance in the female athlete. Iron deficiency has been shown to limit endurance training and sports performance.35 TABLE 27.6  Sources of Calcium Milligrams (mg) Food Yogurt, plain, low fat, 8 oz Mozzarella, part skim, 1.5 oz Sardines, canned in oil, with bones, 3 oz Yogurt, fruit, low fat, 8 oz Cheddar cheese, 1.5 oz Milk, nonfat, 8 ozb Soy milk, calcium fortified 8 oz Milk, reduced fat (2% milk fat) 8 oz Milk, buttermilk, low fat, 8 oz Milk, whole (3.25% milk fat), 8 oz Orange juice, calcium fortified, 6 oz Tofu, firm, made with calcium sulfate, 12 cupc Salmon, pink, canned, solids with bone, 3 oz Cottage cheese, 1% milk fat, 1 cup Tofu, soft, made with calcium sulfate, 12 cupc Ready-to-eat cereal, calcium fortified, 1 cup Frozen yogurt, vanilla, soft serve, 1 2 cup Turnip greens, fresh, boiled, 12 cup Kale, fresh, cooked, 1 cup Ice cream, vanilla, 12 cup Chinese cabbage, bok choy, raw, shredded, 1 cup Bread, white, 1 slice Pudding, chocolate, ready-to-eat, refrigerated, 4 oz Tortilla, corn, ready-to-bake/fry, one 6″ diameter Tortilla, flour, ready-to-bake/fry, one 6″ diameter Sour cream, reduced fat, cultured, 2 tablespoons Bread, whole wheat, 1 slice Kale, raw, chopped, 1 cup Broccoli, raw, 12 cup Cheese, cream, regular, 1 tablespoon

TABLE 27.5  Required Daily Calcium Needs 33,34,a

for Women

Age Group (years) 1–3 4–8 9–18 19–50 51–70 >70 Amenorrhoeic athletesb (all ages) Pregnant/lactating women 14–18 19–50 a

Suggested Intake (mg/day) 700 1000 1300 1000 1000 1200 1500 1500 1300 1000

Recommendation of National Osteoporosis Foundation (www.NOF.org) b https://ods.od.nih.gov/factsheets/calcium-HealthProfessional.

a

Per Serving

Percent DVa

415 333 325

42 33 33

313–384 307 299 299 293 284 276 261 253

31–38 31 30 30 29 28 28 26 25

181

18

138 138

14 14

100–1000

10–100

103

10

99 94 84 74

10 9 8 7

73 55

7 6

46

5

32

3

31

3

30 24 21 14

3 2 2 1

DVs were developed by the US Food and Drug Administration to help compare the nutrient content within the context of a total daily diet. b Calcium content varies slightly by fat content; the more fat, the less calcium the food contains. c Calcium content is for tofu processed with a calcium salt. Tofu processed with other salts does not provide significant amounts of calcium. DV, Daily value. https://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/#h2.

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Iron is required in hemoglobin and myoglobin production. Since hemoglobin is responsible for carrying oxygen to muscles, adequate levels are vital during exercise, especially for endurance sports. Female athletes are especially at risk for iron deficiency due to menstrual blood loss monthly and poor dietary intake. Vegetarian athletes especially are at risk since red meats are an excellent source of iron. Training at high altitudes, losses of iron in sweat, feces, urine, foot strike hemolysis, and intravascular hemolysis can contribute to iron loss and subsequent deficiency. The female athlete’s iron is best screened by measuring serum ferritin. The complete blood count is used to screen for anemia by measurement of the hemoglobin. The female athlete can have iron deficiency anemia where both the ferritin and hemoglobin are decreased. Replenishing iron in those who are significantly iron deficient can take 3 to 6 months of dietary changes and supplementation. Therefore diagnosing the deficiency early or identifying at-risk athletes is important in decreasing the potential of loss of performance. Increasing iron by supplementation in the deficient athlete results in increased work capacity by enabling increased oxygen uptake, decreasing lactate concentration, and reducing heart rate during exercise.32 Current recommendations for dietary iron intake are 15 mg/day for girls 14 to 18 years of age and 18 mg/day for women 19 to 50 years of age. The bioavailability of dietary iron can be enhanced by ascorbic acid and fermented foods, and the inclusion of lean meat, chicken, and fish into the diet. Heme iron (type of iron found in animal protein) is better absorbed than nonheme iron, which is particularly important in counseling vegetarian athletes. Examples of iron-rich foods are listed in Table 27.7. Athletes who are minimally dehydrated can experience increased core temperatures.36,37 Females have a higher thermoregulatory threshold than males and begin sweating at a higher core temperature than males. This may make it harder for females to cool during times of intense training.38 Nonreplaced sweat loss of 1% to 2% of body mass can impair performance. One can measure the degree of an individual’s hydration by urinespecific gravity or by computing differences between pre- and postexercise weight.39 Water is adequate replacement for fluid TABLE 27.7  Examples of Iron-Rich Foods • Liver • Lean red meats, including beef, pork, lamb • Seafood, such as oysters, clams, tuna, salmon, and shrimp, etc. • Beans, including kidney, lima, navy, black, pinto, soy beans, and lentils • Iron-fortified whole grains, including cereals, breads, rice, and pasta • Greens, including collard greens, kale, mustard greens, spinach, and turnip greens • Vegetables, including broccoli, swiss chard, asparagus, parsley, watercress and Brussels sprout • Chicken and turkey • Blackstrap molasses • Nuts • Egg yolks • Dried fruits, such as raisins, prunes, dates, and apricots • Curry powder, paprika, thyme

losses unless excessive sweat losses occur as in endurance events. In these instances, adding electrolytes to water or supplying a sport drink with electrolytes is recommended for females just as it is for males. A sport medicine provider along with a sports’ nutritionist can serve as a valuable resource for the female athlete in helping her plan her nutritional needs.

Female Athlete Triad The female athlete triad is a complex medical syndrome of three interrelated entities: low energy availability (with or without disordered eating), menstrual dysfunction, and low BMD. The latter two entities can be linked to dysfunction secondary to low energy availability (Fig. 27.1).40-42 The female athlete triad appears to be most common in sports where the “lean look” is valued (e.g., running, gymnastics, figure skating, and ballet) but can occur in any physically active female. A female athlete may present with one or more of the three components of the triad and may be mildly to severely affected in any of the three. However, up to 15.9% of athletes with the triad are reported to present severely affected in all three components.43 Energy availability is the term that refers to the total energy needed by a female athlete to perform all of her daily physiologic functions, including athletic activities. Energy availability is defined as energy intake (kcal) minus exercise energy expenditure (kcal) divided by kilograms of fat-free mass or lean body mass.43 Functional hypothalamic amenorrhea can be divided into primary amenorrhea, secondary amenorrhea, or oligomenorrhea. Primary amenorrhea is defined as the absence of menarche by 15 years of age. Secondary amenorrhea is defined as a previously menstruating female having no menstruation for three consecutive menstrual cycles. Oligomenorrhea is a menstrual cycle length greater than 35 days, or less than nine cycles per year. The Z-score measures BMD in premenopausal women. Low BMD (osteopenia) is a Z-score between −1.0 and −2.5, and osteoporosis is a Z-score of less than −2.5 with one or more secondary conditions resulting from low BMD (e.g., stress fractures). It may be difficult to recognize an athlete with the triad. Presenting symptoms can include disordered eating, hair loss, dry skin, fatigue, weight loss, increased healing time for injuries, increased incidence of stress fractures, and absent menses. The most important screening factors for the triad suggested by the 2014 Athlete Triad Coalition Consensus Statement on Treatment Low energy availability (with or without disordered eating)

Functional hypothalamic amenorrhea

Low bone mineral density

Fig. 27.1  Components of the female athlete triad.

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CHAPTER 27  The Female Athlete

TABLE 27.8  Suggested Screen Questions

for Diagnosing the Triada

Have you ever had a menstrual period? How old were you when you had your first menstrual period? When was your most recent menstrual period? How many periods have you had in the past 12 months? Are you presently taking any female hormones (estrogen, progesterone, birth control pills)? Do you worry about your weight? a

Committee on Obstetric Practice. Physical Activity and Exercise During Pregnancy and the Postpartum Period. No. 650. Washington, DC: The American College of Obsetricians and Gynecologists; 2015:135–142. DeSouza MJ, Nattiv A, Joy E, et al. 2014 female athlete coalition consensus statement on treatment and return to play of the female athlete triad: 1st international conference held in San Francisco, California, May 2012 and 2nd international conference held in Indianapolis, Indiana, May 2013. Br J Sports Med. 2014;48:289–309.

and Return to Play of the Female Athlete Triad expert panel are listed in Table 27.8.41 Psychologic characteristics that may be present in those with the triad include low self-esteem, depression, and anxiety disorders.42,44 Physical findings on exam include anemia, orthostatic hypotension, electrical irregularities, vaginal atrophy, and bradycardia.41,45 The diagnosis of low energy availability can be difficult to make because there is no single test to make this diagnosis. It is recommended that a body mass index (BMI) rather than merely a weight of athlete should be obtained. If the BMI is less than 17.5 kg/m2, the state of low energy availability is likely present. Low energy availability has been said to be less than 45 kcal/kg of lean body mass per day. Treatment for low energy availability focuses on a well-designed nutritional plan to attempt to reverse weight loss, achieve a BMI of ≥18.5 kg/m2 or 90% of predicted weight, and have a minimum energy intake of 2000 kcal/day.41 The diet needs to contain a balance of carbohydrates, fats, and proteins. Some athletes have low energy availability not because of inadequate energy intake but because of excessive exercise. In making the diagnosis of amenorrhea (now known as functional hypothalamic amenorrhea), one must first rule out pregnancy and/or other metabolic or hormonal conditions that can lead to amenorrhea. Some of these conditions include thyroid disorders, hyperprolactinemia, primary ovarian dysfunction, polycystic ovary syndrome, and hypothalamic or pituitary disorders. In the female athlete with primary amenorrhea, physical examination of the female genitalia is mandatory to rule out anatomic abnormalities. Additional testing with blood work and/or hormonal challenges may reveal a correctable metabolic or hormonal irregularity. The treatment for amenorrhea or the menstrual irregularity of the triad is oral contraceptives; however, this is not just to regulate a girl’s period but rather to resolve the major issue, which is energy imbalance. Low BMD can be diagnosed through dual energy x-ray absorptiometry (DEXA) scans. The indications for DEXA scanning include a history of eating disorders, low BMI (≤17.5 kg/m2), low body weight, menarche ≥16 years of age, decreased number of menses over the previous year, history of stress fractures, and

299

TABLE 27.9  Triad Coalition Panel

Recommendations for Dual Energy X-Ray Absorptiometry Scanning Who Should Get DEXA Scans for BMD Testing “High risk” triad risk factors: (need 1)   History of a DSM-V diagnosed ED  BMI ≤17./5 kg/m2, 55% for females, and >62.5% for males49,50 • 90% or greater LSI of gluteals at time of RTS • 90% or greater LSI at time of RTS56,58,59 • 4 cm related to increase risk of lower extremity injury64,66 • Y-Balance Test anterior reach LSI of 97% with 65% of LL for anterior, 99% of LL for posteromedial, and 94% of LL for posterolateral22 • LESS score >6 = poor; LESS score ≤4 = excellent24 • 46/54 passing score for RTS25 • Assessment of increased knee valgus angles and moments,63,72 and decreased knee flexion angles72–75 during dynamic activities that may lead to increased risk of injury or re-injury

This table provides objective measurements for the clinician to consider prior to making a decision about the participant’s ability to return to sport. These factors should be considered within the context of other variables such as patient-reported outcomes (IKDC, ACL-RSI) and acute to chronic workload ratio. ACL, Anterior cruciate ligament; IR, internal rotation; LL, leg length; LESS, landing error scoring system; LSI, limb symmetry indices; ROM, range of motion; RSI, Return to Sport After Injury.

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SECTION 3  Rehabilitation and Injury Prevention

Name

Athlete A

Training Week

Acute Load (Current week)

Chronic Load (4 week average)

Acute:Chronic Training Load Ratio (Previous 4 week average / current week)

1

2300

2

2420

3

2357

4

6000

3269.3

5

6856

4408.3

2.10

6

7236

5612.3

1.64

7

6000

6523.0

1.07

8

5199

6322.8

0.80

9

4919

6838.5

0.78

10

4816

5244.8

0.83

11

6432

5352.8

1.23

12

7450

5915.5

1.39

13

6942

6421.3

1.17

14

3856

6170.0

0.60

15

3237

5371.3

0.52

16

3324

4339.8

0.62

2.5

Acute and Chronic Training Load

8000 7000

2

6000 5000

1.5

4000 1

3000 2000

Acute chronic training load Acute load Chronic:load Threshold 1 Threshold 2

0.5

1000 0

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

0

Training Week

Fig. 35.8  Acute versus chronic training load. This table represents an example of a 16-week training load schedule for both the Acute (current week) and Chronic (4 weeks average) phases. The training load is calculated by multiplying the number of minutes in which participation in the activity occurred (internal load) and/or the external load (i.e., distance covered, balls thrown or hit, jumps, etc.) by the rating of perceived exertion (RPE) of the participant during the activity. This calculation provides the weekly value for total training load. The acute to chronic workload ratio can be calculated by dividing the current week’s training load by the previous 4 weeks’ training load average (acute load/chronic load).

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Likelihood of subsequent injury (%)

CHAPTER 35  Return to Activity and Sport After Injury

‘Sweet Spot’ injury risk

25

review and meta-analysis of the state of play. Br J Sports Med. 2011;45(7):596–606.

‘Danger Zone’ injury risk

Level of Evidence:

20

I

Summary:

15 10 5 0

391

.50

1.00 1.50 Acute:chronic workload ratio

2.00

This meta-analysis and systematic review describes key factors that determine readiness for return to sport following anterior cruciate ligament reconstruction. These findings are based on objective data from more than 5500 participants who were attempting a return to sport. In addition, the results suggest that return-to-sport levels are not as successful as one might believe, and one of the factors that is lacking might involve a psychological component.

Fig. 35.9  Acute to chronic workload ratio. In general, this ratio should be close to 1.0. An acute to chronic training load that falls between 0.8 and 1.3 (i.e., loads are approximately equal) carries a relatively low risk of injury, while a training load that exceeds 1.5 may represent a greater risk of suffering injury.

Citation:

Level of Evidence:

Level of Evidence:

V

III

Summary:

Summary:

This article provides functional clinical insight into evidence-based criteria that can be used to identify when an individual is ready to return to sport following anterior cruciate ligament reconstruction. An overview of functional tests is framed within an algorithm that helps clinicians qualitatively and quantitatively make clinical decisions.

An overview of objective and subjective changes that occur in individuals from 6 to 9 months following anterior cruciate ligament reconstruction suggests that time may play an important factor in successful return to sport. This article highlights the lack of readiness of return to sport in patients who have undergone anterior cruciate ligament reconstruction secondary to deficits in quadriceps strength and patient-reported perception of function.

Citation:

Welling W, Benjaminse A, Seil R, et al. Low rates of patients meeting return to sport criteria 9 months after anterior cruciate ligament reconstruction: a prospective longitudinal study. Knee Surg Sports Traumatol Arthrosc. 2018. doi:10.1007/s00167-018-4916-4.

Ardern CL, Webster KE, Taylor NF, et al. Return to sport following anterior cruciate ligament reconstruction surgery: a systematic

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CHAPTER 35  Return to Activity and Sport After Injury

REFERENCES 1. Comstock RD, Pierpoint LA, Erkenbeck AN, et al National High School Sports-Related Injury Surveillance Study: 2016-2017 School Year. 2017. 2. Patel DR, Yamasaki A, Brown K. Epidemiology of sports-related musculoskeletal injuries in young athletes in United States. Transl Pediatr. 2017;6(3):160–166. 3. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Preventing musculoskeletal sports injuries in youth: a guide for parents. 2016. 4. Kay MC, Register-Mihalik JK, Gray AD, et al. The epidemiology of severe injuries sustained by National Collegiate Athletic Association student-athletes, 2009–2010 through 2014–2015. J Athl Train. 2017;52(2):117–128. 5. Eime RM, Young JA, Harvey JT, et al. A systematic review of the psychological and social benefits of participation in sport for children and adolescents: informing development of a conceptual model of health through sport. Int J Behav Nutr Phys Act. 2013;10(1). https://doi.org/10.1186/1479-5868-1110-1198. 6. Wankel LM, Berger BG. The psychological and social benefits of sport and physical activity. J Leisure Res. 1990;22(2):167–182. 7. Toohey LA, Drew MK, Cook JL, et al. Is subsequent lower limb injury associated with previous injury? A systematic review and meta-analysis. Br J Sports Med. 2017:bjsports-2017-097500. 8. Ardern CL, Taylor NF, Feller JA, et al. Return-to-sport outcomes at 2 to 7 years after anterior cruciate ligament reconstruction surgery. Am J Sports Med. 2012;40(1):41–48. 9. Ardern CL, Webster KE, Taylor NF, et al. Return to the preinjury level of competitive sport after anterior cruciate ligament reconstruction surgery: two-thirds of patients have not returned by 12 months after surgery. Am J Sports Med. 2011;39(3):538–543. 10. Colombet P, Allard M, Bousquet V, et al. Anterior cruciate ligament reconstruction using four-strand semitendinosus and gracilis tendon grafts and metal interference screw fixation. Arthroscopy. 2002;18(3):232–237. 11. Langford JL, Webster KE, Feller JA. A prospective longitudinal study to assess psychological changes following anterior cruciate ligament reconstruction surgery. Br J Sports Med. 2009;43(5): 377–378. 12. Nakayama Y, Shirai Y, Narita T, et al. Knee functions and a return to sports activity in competitive athletes following anterior cruciate ligament reconstruction. J Nippon Med Sch. 2000;67(3):172–176. 13. Ardern CL, Webster KE, Taylor NF, et al. Return to sport following anterior cruciate ligament reconstruction surgery: a systematic review and meta-analysis of the state of play. Br J Sports Med. 2011;45(7):596–606. 14. Wiggins AJ, Grandhi RK, Schneider DK, et al. Risk of secondary injury in younger athletes after anterior cruciate ligament reconstruction: a systematic review and meta-analysis. Am J Sports Med. 2016;44(7):1861–1876. 15. Webster KE, Feller JA, Leigh WB, et al. Younger patients are at increased risk for graft rupture and contralateral injury after anterior cruciate ligament reconstruction. Am J Sports Med. 2014;42(3):641–647. 16. Whyte EF, Richter C, O’Connor S, et al. Effects of a dynamic core stability program on the biomechanics of cutting maneuvers: a randomized controlled trial. Scand J Med Sci Sports. 2017. doi:10.1111/sms.12931. [Epub ahead of print]. 17. Davies GJ, McCarty E, Provencher M, et al. ACL return to sport guidelines and criteria. Curr Rev Musculoskelet Med. 2017.

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18. Gokeler A, Welling W, Zaffagnini S, et al. Development of a test battery to enhance safe return to sports after anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2017;25(1):192–199. 19. Zwolski C, Schmitt LC, Quatman-Yates C, et al. The influence of quadriceps strength asymmetry on patient-reported function at time of return to sport after anterior cruciate ligament reconstruction. Am J Sports Med. 2015;43(9):2242–2249. 20. Neeter C, Gustavsson A, Thomeé P, et al. Development of a strength test battery for evaluating leg muscle power after anterior cruciate ligament injury and reconstruction. Knee Surg Sports Traumatol Arthrosc. 2006;14(6):571–580. 21. Thomeé R, Kaplan Y, Kvist J, et al. Muscle strength and hop performance criteria prior to return to sports after ACL reconstruction. Knee Surg Sports Traumatol Arthrosc. 2011;19(11):1798–1805. 22. Clagg S, Paterno MV, Hewett TE, et al. Performance on the modified star excursion balance test at the time of return to sport following anterior cruciate ligament reconstruction. J Orthop Sports Phys Ther. 2015;45(6):444–452. 23. Garrison JC, Bothwell JM, Wolf G, et al. Y Balance Test anterior reach symmetry at three months is related to single leg functional performance at time of return to sports following anterior cruciate ligament reconstruction. Int J Sports Phys Ther. 2015;10(5):602–611. 24. Padua DA, DiStefano LJ, Beutler AI, et al. The Landing Error Scoring System as a screening tool for an anterior cruciate ligament injury–prevention program in elite-youth soccer athletes. J Athl Train. 2015;50(6):589–595. 25. Garrison JC, Shanley E, Thigpen C, et al. The reliability of the Vail Sport Test as a measure of physical performance following anterior cruciate ligament reconstruction. Int J Sports Phys Ther. 2012;7(1):20–30. 26. Ardern CL, Taylor NF, Feller JA, et al. Psychological responses matter in returning to preinjury level of sport after anterior cruciate ligament reconstruction surgery. Am J Sports Med. 2013;41(7):1549–1558. 27. Lentz TA, Zeppieri G Jr, George SZ, et al. Comparison of physical impairment, functional, and psychosocial measures based on fear of reinjury/lack of confidence and return-to-sport status after ACL reconstruction. Am J Sports Med. 2015;43(2):345–353. 28. Webster KE, Feller JA, Lambros C. Development and preliminary validation of a scale to measure the psychological impact of returning to sport following anterior cruciate ligament reconstruction surgery. Phys Ther Sport. 2008;9(1):9–15. 29. Logerstedt D, Di Stasi S, Grindem H, et al. Self-reported knee function can identify athletes who fail return-to-activity criteria up to 1 year after anterior cruciate ligament reconstruction: a Delaware-Oslo ACL cohort study. J Orthop Sports Phys Ther. 2014;44(12):914–923. 30. Zwolski C, Schmitt LC, Thomas S, et al. The utility of limb symmetry indices in return-to-sport assessment in patients with bilateral anterior cruciate ligament reconstruction. Am J Sports Med. 2016;44(8):2030–2038. 31. Fong C-M, Blackburn JT, Norcross MF, et al. Ankle-dorsiflexion range of motion and landing biomechanics. J Athl Train. 2011;46(1):5–10. 32. Macrum E, Bell DR, Boling M, et al. Effect of limiting ankledorsiflexion range of motion on lower extremity kinematics and muscle-activation patterns during a squat. J Sport Rehabil. 2012;21(2):144–150.

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33. Rabin A, Portnoy S, Kozol Z. The association of ankle dorsiflexion range of motion with hip and knee kinematics during the Lateral Step-Down Test. J Orthop Sports Phys Ther. 2016;46(11):1002–1009. 34. Wahlstedt C, Rasmussen-Barr E. Anterior cruciate ligament injury and ankle dorsiflexion. Knee Surg Sports Traumatol Arthrosc. 2015;23(11):3202–3207. 35. Noll S, Garrison JC, Bothwell J, et al. Knee extension range of motion at 4 weeks is related to knee extension loss at 12 weeks after anterior cruciate ligament reconstruction. Orthop J Sports Med. 2015;3(5):2325967115583632. 36. Shelbourne KD, Gray T. Minimum 10-year results after anterior cruciate ligament reconstruction. Am J Sports Med. 2009;37(3): 471–480. 37. Shelbourne KD, Benner RW, Gray T. Results of anterior cruciate ligament reconstruction with patellar tendon autografts: objective factors associated with the development of osteoarthritis at 20 to 33 years after surgery. Am J Sports Med. 2017:0363546517718827. 38. Philippon MJ, Maxwell RB, Johnston TL, et al. Clinical presentation of femoroacetabular impingement. Knee Surg Sports Traumatol Arthrosc. 2007;15(8):1041–1047. 39. Roach SM, San Juan JG, Suprak DN, et al. Passive hip range of motion is reduced in active subjects with chronic low back pain compared to controls. Int J Sports Phys Ther. 2015;10(1):13–20. 40. VandenBerg C, Crawford EA, Enselman ES, et al. Restricted hip rotation is correlated with an increased risk for anterior cruciate ligament injury. Arthroscopy. 2017;33(2):317–325. 41. Gomes JLE, de Castro JV, Becker R. Decreased hip range of motion and noncontact injuries of the anterior cruciate ligament. Arthroscopy. 2008;24(9):1034–1037. 42. Tainaka K, Takizawa T, Kobayashi H, et al. Limited hip rotation and non-contact anterior cruciate ligament injury: a casecontrol study. Knee. 2014;21(1):86–90. 43. VandenBerg C, Crawford EA, Sibilsky Enselman E, et al. Restricted hip rotation is correlated with an increased risk for anterior cruciate ligament injury. Arthroscopy. 2017;33(2): 317–325. 44. Khayambashi K, Ghoddosi N, Straub RK, et al. Hip muscle strength predicts noncontact anterior cruciate ligament injury in male and female athletes: a prospective study. Am J Sports Med. 2016;44(2):355–361. 45. Lawrence RK, Kernozek TW, Miller EJ, et al. Influences of hip external rotation strength on knee mechanics during single-leg drop landings in females. Clin Biomech (Bristol, Avon). 2008;23(6):806–813. 46. Petersen W, Taheri P, Forkel P, et al. Return to play following ACL reconstruction: a systematic review about strength deficits. Arch Orthop Trauma Surg. 2014;134(10):1417–1428. 47. Pollard CD, Sigward SM, Powers CM. Gender differences in hip joint kinematics and kinetics during side-step cutting maneuver. Clin J Sport Med. 2007;17(1):38–42. 48. Schmitt LC, Paterno MV, Hewett TE. The impact of quadriceps femoris strength asymmetry on functional performance at return to sport following anterior cruciate ligament reconstruction. J Orthop Sports Phys Ther. 2012;42(9):750–759. 49. Hewett TE, Myer GD, Zazulak BT. Hamstrings to quadriceps peak torque ratios diverge between sexes with increasing isokinetic angular velocity. J Sci Med Sport. 2008;11(5): 452–459. 50. Myer GD, Ford KR, Foss KDB, et al. The relationship of hamstrings and quadriceps strength to anterior cruciate

51.

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62.

63.

64.

65.

ligament injury in female athletes. Clin J Sport Med. 2009;19(1):3–8. Wilk KE, Meister K, Andrews JR. Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med. 2002;30(1):136–151. Logerstedt D, Grindem H, Lynch A, et al. Single-legged hop tests as predictors of self-reported knee function after anterior cruciate ligament reconstruction: the Delaware-Oslo ACL cohort study. Am J Sports Med. 2012;40(10):2348–2356. Narducci E, Waltz A, Gorski K, et al. The clinical utility of functional performance tests within one-year post-ACL reconstruction: a systematic review. Int J Sports Phys Ther. 2011;6(4):333–342. Reid A, Birmingham TB, Stratford PW, et al. Hop testing provides a reliable and valid outcome measure during rehabilitation after anterior cruciate ligament reconstruction. Phys Ther. 2007;87(3):337–349. Noyes FR, Barber SD, Mangine RE. Abnormal lower limb symmetry determined by function hop tests after anterior cruciate ligament rupture. Am J Sports Med. 1991;19(5):513–518. Gokeler A, Welling W, Benjaminse A, et al. A critical analysis of limb symmetry indices of hop tests in athletes after anterior cruciate ligament reconstruction: a case control study. Orthop Traumatol Surg Res. 2017. https://doi.org/10.1016/j.otsr.2017 .1002.1015. Hartigan EH, Axe MJ, Snyder-Mackler L. Time line for noncopers to pass return-to-sports criteria after anterior cruciate ligament reconstruction. J Orthop Sports Phys Ther. 2010;40(3):141–154. Augustsson J, Thomeé R, Karlsson J. Ability of a new hop test to determine functional deficits after anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2004;12(5):350–356. Pinczewski LA, Lyman J, Salmon LJ, et al. A 10-year comparison of anterior cruciate ligament reconstructions with hamstring tendon and patellar tendon autograft. Am J Sports Med. 2007;35(4):564–574. Welling W, Benjaminse A, Seil R, et al. Low rates of patients meeting return to sport criteria 9 months after anterior cruciate ligament reconstruction: a prospective longitudinal study. Knee Surg Sports Traumatol Arthrosc. 2018. doi:10.1007/s00167-018 -4916-4. Beutler AI, Sarah J, Marshall SW, et al. Muscle strength and qualitative jump-landing differences in male and female military cadets: the jump-ACL study. J Sports Sci Med. 2009;8(4): 663–671. Myer GD, Ford KR, Hewett TE. Tuck jump assessment for reducing anterior cruciate ligament injury risk. Athl Ther Today. 2008;13(5):39–44. Paterno MV, Ford KR, Myer GD, et al. Limb asymmetries in landing and jumping 2 years following anterior cruciate ligament reconstruction. Clin J Sport Med. 2007;17(4): 258–262. Paterno MV, Schmitt LC, Ford KR, et al. Biomechanical measures during landing and postural stability predict second anterior cruciate ligament injury after anterior cruciate ligament reconstruction and return to sport. Am J Sports Med. 2010;38(10):1968–1978. Plisky PJ, Rauh MJ, Kaminski TW, et al. Star excursion balance test as a predictor of lower extremity injury in high school basketball players. J Orthop Sports Phys Ther. 2006;36(12): 911–919.

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CHAPTER 35  Return to Activity and Sport After Injury 66. Kokmeyer D, Wahoff M, Mymern M. Suggestions from the field for return-to-sport rehabilitation following anterior cruciate ligament reconstruction: alpine skiing. J Orthop Sports Phys Ther. 2012;42(4):313–325. 67. Smith CA, Chimera NJ, Warren M. Association of Y Balance Test reach asymmetry and injury in Division I athletes. Med Sci Sports Exerc. 2015;47(1):136–141. 68. Bell DR, Smith MD, Pennuto AP, et al. Jump-landing mechanics after anterior cruciate ligament reconstruction: a landing error scoring system study. J Athl Train. 2014;49(4):435–441. 69. Padua DA, Marshall SW, Boling MC, et al. The Landing Error Scoring System (LESS) is a valid and reliable clinical assessment tool of JUMP-landing biomechanics: the JUMP-ACL study. Am J Sports Med. 2009;37(10):1996–2002. 70. Gao B, Cordova ML, Zheng NN. Three-dimensional joint kinematics of ACL-deficient and ACL-reconstructed knees during stair ascent and descent. Hum Mov Sci. 2012;31(1): 222–235. 71. Markström JL, Tengman E, Häger CK. ACL-reconstructed and ACL-deficient individuals show differentiated trunk, hip, and knee kinematics during vertical hops more than 20 years post-injury. Knee Surg Sports Traumatol Arthrosc. 2017;1–10. doi:10.1007/s00167-00017-04528-00164. 72. Zazulak BT, Hewett TE, Reeves NP, et al. Deficits in neuromuscular control of the trunk predict knee injury risk. Am J Sports Med. 2007;35(7):1123–1130. 73. Hewett TE, Myer GD, Ford KR, et al. Biomechanical measures of neuromuscular control and valgus loading of the knee predict anterior cruciate ligament injury risk in female athletes. Am J Sports Med. 2005;33(4):492–501. 74. Di Stasi S, Hartigan EH, Snyder-Mackler L. Sex-specific gait adaptations prior to and up to 6 months after anterior cruciate ligament reconstruction. J Orthop Sports Phys Ther. 2015;45(3):207–214. 75. Herrington L, Alarifi S, Jones R. Patellofemoral joint loads during running at the time of return to sport in elite athletes with ACL reconstruction. Am J Sports Med. 2017: 0363546517716632. 76. Schmitt LC, Paterno MV, Ford KR, et al. Strength asymmetry and landing mechanics at return to sport after anterior cruciate ligament reconstruction. Med Sci Sports Exerc. 2015;47(7): 1426–1434. 77. Ardern CL, Österberg A, Tagesson S, et al. The impact of psychological readiness to return to sport and recreational activities after anterior cruciate ligament reconstruction. Br J Sports Med. 2014:bjsports-2014-093842. 78. Müller U, Krüger-Franke M, Schmidt M, et al. Predictive parameters for return to pre-injury level of sport 6 months following anterior cruciate ligament reconstruction surgery. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3623–3631.

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79. Goetschius J, Hart JM. Knee-extension torque variability and subjective knee function in patients with a history of anterior cruciate ligament reconstruction. J Athl Train. 2016;51(1): 22–27. 80. Ithurburn MP, Altenburger AR, Thomas S, et al. Young athletes after ACL reconstruction with quadriceps strength asymmetry at the time of return-to-sport demonstrate decreased knee function 1 year later. Knee Surg Sports Traumatol Arthrosc. 2017;1–8. 81. Bodkin S, Goetschius J, Hertel J, et al. Relationships of muscle function and subjective knee function in patients after ACL reconstruction. Orthop J Sports Med. 2017;5(7): 2325967117719041. 82. Reinke EK, Spindler KP, Lorring D, et al. Hop tests correlate with IKDC and KOOS at minimum of 2 years after primary ACL reconstruction. Knee Surg Sports Traumatol Arthrosc. 2011;19(11):1806. https://doi.org/1810.1007/s00167-00011 -01473-00165. 83. Briggs KK, Lysholm J, Tegner Y, et al. The reliability, validity, and responsiveness of the Lysholm Score and Tegner Activity Scale for anterior cruciate ligament injuries of the knee. Am J Sports Med. 2009;37(5):890–897. 84. Kanakamedala AC, Anderson AF, Irrgang JJ. IKDC subjective knee form and Marx Activity Rating Scale are suitable to evaluate all orthopaedic sports medicine knee conditions: a systematic review. J ISAKOS. 2016:jisakos-2015-000014. 85. Irrgang JJ, Anderson AF, Boland AL, et al. Development and validation of the International Knee Documentation Committee Subjective Knee Form. Am J Sports Med. 2001;29(5):600–613. 86. Lentz TA, Zeppieri G Jr, Tillman SM, et al. Return to preinjury sports participation following anterior cruciate ligament reconstruction: contributions of demographic, knee impairment, and self-report measures. J Orthop Sports Phys Ther. 2012; 42(11):893–901. 87. American Academy of Family Physicians, American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, et al. The team physician and conditioning of athletes for sports: a consensus statement. Med Sci Sports Exerc. 2001;33(10):1789–1793. 88. Blanch P, Gabbett TJ. Has the athlete trained enough to return to play safely? The acute: chronic workload ratio permits clinicians to quantify a player’s risk of subsequent injury. Br J Sports Med. 2015:bjsports-2015-095445. 89. Gabbett TJ, Whiteley R. Two training-load paradoxes: can we work harder and smarter, can physical preparation and medical be teammates? Int J Sports Physiol Perform. 2017;12(suppl 2): S250–S254. 90. Bourdon PC, Cardinale M, Murray A, et al. Monitoring athlete training loads: consensus statement. Int J Sports Physiol Perform. 2017;12(suppl 2):S2161–S2170.

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36  Shoulder Anatomy and Biomechanics Timothy S. Mologne

The shoulder can really be considered a complex (Fig. 36.1), consisting of four joints or articulations (all with important stabilizing ligaments), two spaces, and more than 30 muscles and their respective tendons. The shoulder complex is an intricate structure that requires synchronized/orchestral-type motions/ movements to function properly. A thorough understanding of the anatomy and complex biomechanics of the shoulder is helpful to clinicians in diagnosing disorders, applying appropriate surgical procedures, and implementing proper rehabilitation protocols.

PERTINENT BONY ANATOMY The proximal humerus consists of the humeral head and articular surface, the greater and lesser tuberosities, which are the attachment sites for the rotator cuff muscles, and the humeral shaft. Between the tuberosities is the bicipital groove, the location of the tendon of the long head of the biceps brachii muscle, as it exits the glenohumeral joint. The articular cartilage on the humeral head has been shown to vary from 0.2 to 2.0 mm and is thickest in the central portion of the humeral head.1 Multiple anatomic and radiologic studies have been performed in an attempt to better define the relationships and geometry of the various parts of the proximal humerus, glenoid, and glenohumeral joint.2–8 Different measuring techniques and reference points make comparisons between the studies difficult. The inclination of the humeral head articular surface, as referenced to the humeral canal, varies from 30 to 55 degrees.3,6–8 The mean radius of curvature of the humeral head is 24 ± 1.2 mm but can be as much as 30 mm.4 The superior-most portion of the humeral head is a mean of 8 mm higher than the greater tuberosity. This relationship varies between men and woman but is proportional to the radius of curvature of the articular surface.4 Retroversion of the humeral head, in reference to the center of the humeral canal, has been shown to be quite variable, ranging from 0 to 55 degrees (Fig. 36.2).6,7,9 Medial and posterior offset of the humeral head is variable with reference to the humeral shaft.3,6–8,10 The scapula is a relatively flat, triangular-shaped bone that is positioned on the posterolateral aspect of the thorax at the level of the second and seventh ribs. The scapula has three angles—superior, inferior, and lateral. The lateral angle, formed by the superior and lateral borders of the scapula, gives rise to the glenoid. Anatomic variants at the superior angle are sometimes the cause of snapping scapula syndrome.11 The scapular spine divides the dorsal aspect into the supraspinatus and

infraspinatus fossa. The subscapularis fossa is located on the ventral or anterior portion of the scapular body. Several muscles originate on the scapula, namely the supraspinatus, infraspinatus, subscapularis, teres major and minor, triceps, and deltoid muscles. Several other important muscles insert on the scapula: the serratus anterior, levator scapulae, rhomboid major and minor, trapezius, pectoralis minor, short head of the biceps brachii, and coracobrachialis muscles. The scapula has two processes or projections: the coracoid and the acromion. The coracoid projects from the superior and lateral aspect and projects anteriorly and laterally. The mean distance from the coracoid tip to the anterior border of the coracoclavicular ligament can vary from 22 to 28 mm.12,13 The mean width of the coracoid is 15.9 mm, and the mean thickness is 10.4 mm.13 The use of the coracoid as an extension of the glenoid for shoulder stabilization procedures is well described14,15 and has, once again, become a treatment option for patients with glenohumeral instability and bone deficiencies. The acromion process is the lateral and anterior extension of the scapular spine. The anteroinferior aspect of the acromion serves as the attachment site for the coracoacromial ligament (Fig. 36.3). The morphology of the acromion has been studied, and some correlations have been made between aggressive anterior acromial hooks/spurs and rotator cuff tears.16–20 Some evidence indicates that the coracoacromial ligament helps provide superior stability to the glenohumeral joint.21,22 The lateral portion of the coracoacromial ligament has been found to have decreased mechanical properties, is shorter in length, and has a larger cross-sectional area in patients with rotator cuff tears.19 Resection of the coracoacromial ligament can lead to anterosuperior humeral head escape in patients with massive rotator cuff tears. Biomechanical studies have shown that the rotator cuff becomes closest to the undersurface of the acromion between 60 and 120 degrees.23 The subacromial bursa is located in the anterior portion of the subacromial space and is under the coracoacromial arch and deltoid. The bursa helps reduce friction between the coracoacromial arch and the rotator cuff when the arm is elevated but can be impinged under the acromion in certain conditions. The bursa has significant nerve endings, including Ruffini endings, Pacinian corpuscles, and free nerve endings,24,25 and is a source of pain in the subacromial space. Just medial to the coracoid and anterior to the supraspinatus fossa is the suprascapular notch of the scapula. As the suprascapular nerve travels from the upper trunk of the brachial plexus,

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CHAPTER 36  Shoulder Anatomy and Biomechanics

Abstract

Keywords

The shoulder is a complex arrangement of four bones, four articulations, and several muscles, tendons, and ligaments. The shoulder complex requires healthy and ligamentously stable joints and numerous muscles working in synergy to allow the upper extremity to be placed in various positions and to perform activities that subject it to extremes of force and torque. The various articulations and muscles are kinetically linked, and abnormalities in any of the joints or muscles can result in pain, dysfunction, and possibly injury to other structures. An appreciation of the anatomy and biomechanics of the shoulder complex will be beneficial to clinicians in making diagnoses, applying safe and appropriate surgical procedures, and implementing appropriate rehabilitation protocols.

humerus scapula glenoid rotator cuff glenohumeral joint

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SECTION 4  Shoulder Shoulder

Acromioclavicular joint

Acromioclavicular joint Coracoclavicular ligament Sternoclavicular joint

Coracoacromial ligament Acromioclavicular ligament

Trapezoid ligament Conoid ligament

Transverse humeral ligament

Glenohumeral joint

Synovial sheath of biceps

Fig. 36.1  The shoulder complex consists of the glenohumeral, acromioclavicular, and sternoclavicular joints, along with the scapulothoracic articulation.

Distal end of humerus, 0°

Fig. 36.3  An anterior view of the shoulder demonstrating the coracoclavicular ligaments, acromioclavicular joint, coracoacromial ligament, and transverse humeral ligament.

Proximal end of humerus 30° retrograde

Fig. 36.2  With respect to the epicondylar axis of the distal humerus, the humeral head articular surface is retroverted from 0 to 55 degrees, averaging 30 degrees.

it enters this notch prior to innervating the supraspinatus. The nerve branches to innervate the supraspinatus within 1 cm of the notch.26 The superior transverse scapular ligament is the roof of the suprascapular notch. Anatomic studies have shown that the notch is U-shaped in three-fourths of specimens. The superior transverse scapular ligament can be partially or completely ossified in some people.27 The lateral angle of the scapula is the location of the glenoid. The glenoid has an average of 5 degrees of superior tilt, referencing the scapula (Fig. 36.4).28 The superior slope to the glenoid plays a role in preventing inferior subluxation of the humerus. The glenoid is also retroverted with respect to the transverse axis of the scapula. Measurements vary depending on the imaging study used to perform the measurements. However, most studies have shown that the glenoid has 1 to 3 degrees of retroversion29,30; however, retroversion can vary from 14 degrees of anteversion to 12 degrees of retroversion in normal shoulders.31 Retroversion may be overestimated on plain axillary radiographs and

5°

Glenoid

Fig. 36.4  Relative to the plane of the scapula, the fossa is angled slightly inferior and posterior, offering little bony support to inferior instability with the arm at the side.

is probably more accurately measured by computed tomography.30 The scapula is anteroverted approximately 30 degrees to the coronal plane. The glenoid is shaped like a pear; it is wider inferiorly. The average superior-inferior length of the glenoid is 39 mm, and the anteroposterior width in the lower half averages 29 mm.4,32 The glenoid has a bare spot, which has been shown to be in the center of the lower portion on the glenoid. The bare spot can be used as a reference in measuring anteroinferior glenoid bone loss.33 The radius of curvature of the glenoid is, on average, 2.3 mm more than the humeral head.4 Unlike the humeral head, where the articular cartilage is thickest in the center, the articular cartilage is thickest on the periphery of the glenoid and thinnest in the center.

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CHAPTER 36  Shoulder Anatomy and Biomechanics

The spinoglenoid notch is an indentation at the confluence of the lateral edge of the base of the scapular spine and glenoid neck. This notch connects the supraspinatus and infraspinatus fossae. The suprascapular nerve and vessels travel through this notch prior to the nerve innervating the infraspinatus. On average, the suprascapular nerve is 1.5 cm medial to the posterior glenoid rim.26 Knowledge of the location of this nerve is important when one is directly dissecting in the posterior aspect of the shoulder and when placing screws from anterior to posterior across the glenoid.34 Compression of the suprascapular nerve in this location can result in isolated weakness of the infraspinatus muscle. The spinoglenoid notch can have a ligament across it. This ligament is present in 14% to 61% of people.27,35 The clavicle is an S-shaped or double-curved bone that connects the shoulder complex to the axial skeleton via the sternoclavicular joint. It is formed by membranous bone but does have a physis at the medial aspect. As a strut from the sternum to the shoulder, it is important in maintaining proper scapular positioning and kinematics during shoulder movement. Shortening of the clavicle, as is seen in some clavicular fracture malunions, leads to significant changes in shoulder posture and scapular positioning during shoulder motions.36,37 In addition to its role in shoulder kinematics, the clavicle protects vascular structures to the upper extremities and the brachial plexus. The clavicle is the site of origin of a portion of the deltoid and pectoralis major muscles, as well as the insertion site of a portion of the trapezius muscle; all these muscles influence shoulder motion.

JOINTS AND ARTICULATIONS OF THE SHOULDER COMPLEX Glenohumeral Joint The glenohumeral joint is the most mobile joint in the body. The joint has 6 degrees of freedom, allowing for glenohumeral joint translations and rotations. Shoulder joint rotations occur in the coronal plane and are commonly referred to as abduction and adduction. Rotations in the sagittal plane are called flexion and extension. Rotations relative to the long axis of the humerus are called internal and external rotation (Fig. 36.5). The normal shoulder has substantial translational motion, with as much as 8 to 14 mm of translation anterior, posterior, and inferior with manual clinical testing.38,39 Examinations with use of an anesthetic have documented even greater laxity, with subluxation over the glenoid anteriorly in 81.6% of subjects and posteriorly in 57.5% of subjects.40 Given the mobility and wide range of motion, it is really not surprising that the shoulder is also the most unstable joint in the body. Shoulder stability is achieved through a combination of inherent joint characteristics, static stabilizers, and muscular or dynamic stabilizers. The shoulder is afforded some stability from the inherent negative intraarticular pressure. This negative articular pressure is due to the glenoid concavity’s “plunger” effect on the humeral head. The loss of the intra-articular vacuum as a result of an opening in the joint capsule results in less shoulder stability.41,42 Some inherent stability is also achieved as a result of an adhesioncohesion effect that occurs when two wet surfaces come in contact. Concavity-compression is another mechanism that has been

Y

395

X

3 2

Z

1 1. Abduction 2. External rotation 3. Horizontal abduction Fig. 36.5  Shoulder motions are rotations along an axis. Rotations along the X axis or coronal plane are referred to as abduction and adduction. Rotations along the long axis of the humerus, when the arm is at the side, occur through the Y axis and are referred to as internal and external rotation. Rotations in the sagittal plane or Z axis (when the arm is at the side) are referred to as flexion and extension.

found to play a role in glenohumeral stability.43 A compressive load provided by the rotator cuff forces the convex humeral head into the concave glenoid. Static stability of the glenohumeral joint is provided by the glenoid labrum, glenohumeral ligaments, and joint capsule. The glenoid labrum is a fibrocartilaginous structure that is attached along the periphery of the glenoid. The labrum is wedge shaped, which increases the effective depth of the glenoid by approximately 50%.44 Increasing the concavity of the glenoid contributes to overall shoulder stability because of the concavity-compression and the suction effect as a result of the intraarticular vacuum that occurs. The labrum contributes to glenohumeral stability by providing a bumper effect to prevent abnormal translations of the humeral head. The morphology and attachment of the labrum varies in the different quadrants of the shoulder. Inferiorly, the labrum is well attached to the glenoid, becoming an extension of the articular cartilage.45 The firm attachment in the anteroinferior quadrant increases the diameter of the glenoid and increases the contact surface area. Removal of the anteroinferior labrum results in up to a 15% loss in glenohumeral contact area.46 In the superior and anterosuperior quadrant, the labrum is less well adhered to the glenoid. In some incidences, the labrum has the appearance of a knee meniscus. The glenoid labrum in the anterosuperior quadrant can be quite variable, with sublabral foramen common. Absence of the anterosuperior labrum, in conjunction with a cordlike middle glenohumeral ligament, has been described as a Buford complex.47,48 The labrum is the insertion of the glenohumeral ligaments and capsule. It is also the origin of the tendon of the long head of the biceps brachii muscle along the superior aspect. The glenohumeral joint capsule has several areas of thickening that are called glenohumeral ligaments (Fig. 36.6). The inferior glenohumeral ligament is a hammocklike structure, with bands extending both anteriorly and posteriorly along the inferior aspect of the glenohumeral joint. The ligament originates along the inferior aspect of the humeral metaphysis and inserts onto the

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SECTION 4  Shoulder

Opening into subscapularis bursa Infraspinatus Biceps Sup. glenohumeral ligament

Teres minor

Middle glenohumeral ligament Anterior inferior glenohumeral ligament Labrum

Fig. 36.6  A sagittal view of the glenohumeral joint showing the glenohumeral ligament, glenoid labrum, and biceps tendon. Sup., Superior.

inserts onto the lesser and greater tuberosities and over the bicipital groove. It also contains the SGHL, which arises from the superior labrum and supraglenoid tubercle, travels over the medial portion of the rotator interval, and blends with the coracohumeral ligament prior to inserting into the lesser tuberosity. The rotator interval also contains the joint capsule, which can be quite thin and variable. The rotator interval capsule can be as thin as 0.06 mm, and congenital defects are found in up to 75% of specimens.59 Sectioning of the coracohumeral ligament has been shown to result in increased inferior and posterior translation of the humerus, and imbrication and tightening of the coracohumeral ligament has been shown to decrease inferior and posterior translation.60 During the past 15 years, as arthroscopic shoulder stabilizations have become more common, rotator interval closures have been advocated as an adjunctive procedure to help with postoperative stability, particularly when the instability is inferior and posterior. However, arthroscopic rotator interval closures have not been shown to be of benefit in adding posterior or inferior stability in a cadaveric model.61

Glenohumeral Joint Capsule anteroinferior and posteroinferior glenoid labrum. The inferior glenohumeral ligament is considered one of the most important stabilizing structures in the abducted, externally rotated shoulder.49–51 The glenoid insertion site of the anterior band of the inferior glenohumeral ligament consists of two attachments, one to the glenoid labrum and the other directly to the anterior neck of the glenoid.52 The middle glenohumeral ligament is the most variable of the glenohumeral ligaments and has been shown to be absent in up to 36% of persons.53 It can vary from a thin fold of capsule to a thick cordlike structure. The middle glenohumeral ligament originates from the anterosuperior labrum or glenoid rim and crosses over the deep portion of the subscapularis prior to inserting onto the anatomic neck of the humerus. Although its presence and morphology vary, it has been shown to be important for anterior stability with the shoulder in 45 degrees of abduction.54 The superior glenohumeral ligament (SGHL) arises from the anterosuperior labrum, runs parallel to the biceps tendon in the rotator interval, and inserts onto the lesser tuberosity.55 Fibers of the SGHL help create the biceps pulley, which stabilizes the biceps in the bicipital groove. The function of the SGHL has generated considerable debate, with one study reporting that the SGHL was the most important stabilizer for inferior translation.56 Other investigators have concluded that the coracohumeral ligament is a more important stabilizer for inferior translation.57 Yet other investigators have concluded that the inferior glenohumeral ligament is the most important stabilizer for inferior translation of the adducted shoulder.58 The rotator interval is a triangular space that is bordered inferiorly by the subscapularis tendon, anteriorly by the supraspinatus tendon, and medially by the glenoid. The rotator interval has been associated with shoulder instability, adhesive capsulitis, and isolated defects and tears. The rotator interval contains the coracohumeral ligament, which is a trapezoidal structure that originates on the lateral coracoid, traveling in two bands as it

The glenohumeral joint capsule is important in maintaining the intra-articular vacuum that helps to stabilize the joint. The joint capsule varies from 1.3 to 4.5 mm. It is thickest in the anteroinferior quadrant, which accounts for the anterior band of the glenohumeral ligament, and it is thinnest in the rotator interval and posterior quadrant.62,63 A complex arrangement of the collagen fibers is present in the capsule, with a pattern of crosslinking in the superior capsule and a crossing pattern of spirals in the anterior and inferior capsule. The fibers in the ligamentous reinforcements radiate obliquely from the glenoid but vary greatly in orientation.64 The inferior humeral attachment of the capsule may extend well below the articular surface. The inferior capsule has distinct internal and external folds.65 Contracture of the glenohumeral joint capsule affects glenohumeral motion, which ultimately affect shoulder mechanics. This mechanism is commonly seen in patients with adhesive capsulitis. Another example is posterior capsular contractures, a diagnosis commonly seen in overhead throwers. Posterior capsular contracture results in a loss of internal rotation of the shoulder. The contracture and loss of internal rotation force the humeral head into a posterosuperior position as opposed to the normal posteroinferior position found in a normal shoulder when externally rotating in the cocking phase.66 Ruffini end organs and Pacinian corpuscles are found in the inferior, middle, and SGHLs.25 It is possible that these mechanoreceptors signal the dynamic muscle stabilizers when the capsule is stretched in the abducted-external rotated position. The tendon of the long head of the biceps brachii originates from the superior labrum and supraglenoid tubercle (see Fig. 36.6). Anatomic variations of the biceps origin have been described, including a bifid origin,67 an extraarticular origin,68 and origin from the rotator cable.69 The biceps tendon has been shown to be an additional dynamic stabilizer of the shoulder. Loading the biceps tendon has been shown to decrease both anterior-posterior and superior-inferior translation70–72 and also

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has been shown to increase torsional rigidity against rotation force, limiting both external and internal rotation.72,73 The biceps tendon travels out of the glenohumeral joint in the rotator interval prior to traveling distally in the bicipital groove of the proximal humerus. The tendon is stabilized in the proximal portion of the groove by the biceps pulley. The biceps pulley is a capsuloligamentous complex that is composed of fibers from the SGHL, the coracohumeral ligament, and the distal portions of the subscapularis tendon. More distally in the bicipital groove, the tendon is stabilized by the transverse humeral ligament. Recent evidence has suggested that the transverse humeral ligament is an extension of the subscapularis tendon (see Fig. 36.3).74

Acromioclavicular Joint The articulation between the distal end of the clavicle and acromion is called the acromioclavicular joint (see Fig. 36.3). The acromioclavicular joint is a synovial joint that consists of the articular facet of the acromion, the distal end of the clavicle, an intra-articular disk, and a joint capsule with thickening called the acromioclavicular ligaments. When viewed from the anterior position, the acromioclavicular joint is usually slightly medially or vertically oriented. With respect to the shaft of the clavicle, the inclination averages 12 degrees.75 The joint is stabilized by the bony articulation but also by the acromioclavicular and coracoclavicular ligaments.76 Several anatomic studies have assessed the location of the acromioclavicular ligaments and capsule.75,77,78 Measurements in these studies are different, but one must be aware that the superior acromioclavicular ligament begins to insert as close as 2.3 mm from the lateral end of the clavicle.78 The ligament does blend with the periosteum along the superior clavicle, and fibers of the ligament can be seen as far as 12 mm from the distal clavicle.77 It is generally accepted that superior-inferior stability of the acromioclavicular joint is due to the trapezoid and conoid ligaments, commonly referred to as the coracoclavicular ligaments (see Fig. 36.3). The lateral of the two, the trapezoid ligament, originates from the base of the coracoid, anterior and lateral to the conoid ligament. It has a broad insertion on the undersurface of the clavicle. The trapezoid ligament helps to reduce axial compression forces at the acromioclavicular joint.79 The coneshaped conoid ligament originates from the posteromedial aspect of the base of the coracoid and inserts on the conoid tubercle of the clavicle.80 The conoid ligament is the most important ligament for superior-inferior stability of the acromioclavicular joint.79 Anterior-posterior stability is also due to the coracoclavicular ligaments and the acromioclavicular ligaments. The trapezoidal ligament has been shown to provide the majority of restraint to the posterior translation of the clavicle.76,81 Some motion occurs at the acromioclavicular joint, but the motion is relatively small. Joint compression and translation occur as a result of protraction, retraction, and tilting of the acromion with overhead motion. Some clavicular rotation also occurs during abduction and adduction of the shoulder. Innervation of the acromioclavicular joint is from sensory branches from the suprascapular nerve.82 Distal clavicle resections are commonly performed, and this procedure can result in acromioclavicular joint instability.

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Arthroscopic distal clavicle resection has been shown to increase acromioclavicular joint motion with a posterior applied force.83 The acromioclavicular joint capsule is thickest superiorly and posteriorly. Preserving the superior and posterior acromioclavicular ligaments has been shown to be important in preserving joint stability when a distal clavicle resection is performed.84 This preservation can usually be accomplished if less than 8 mm of bone is resected from the distal clavicle in men78; however, it is necessary to confirm that ligamentous tissue is present superiorly at the end of the procedure.

Sternoclavicular Joint The sternoclavicular joint is truly the only connection of the shoulder complex to the axial skeleton. The proximal end of the clavicle has an irregular surface, being concave in the anteroposterior plane and convex superiorly. The articular surface along the sternum is small and not congruent to the end of the clavicle. Like the acromioclavicular joint, the sternoclavicular joint also has an intra-articular disk. As a result of the joint incongruity, the articular surfaces offer no significant stability to this joint. The stability of the sternoclavicular joint is therefore due to its surrounding capsular and ligamentous support (Fig. 36.7). The capsular ligament covers the anterosuperior and posterior aspects of the joint and helps to stabilize the clavicle against abnormal translations. The posterior capsule is the main stabilizer of the sternoclavicular joint against anterior and posterior translations. The costoclavicular and interclavicular ligaments do not seem to have a significant anteroposterior stabilizing effect on the joint,85 although the interclavicular ligament does help to stabilize the joint to superior translations. Most of the motion of the clavicle occurs at the sternoclavicular joint. Motion analysis has shown that the ligamentous support allows for up to 15 degrees of elevation, 30 degrees of retraction, and 30 degrees of rotation along the long axis of the clavicle with active arm elevation.86,87 The medial end of the clavicle does have a physis, which is the last physis in the body to fuse. In one radiographic study, the earliest observation of complete fusion was at 26 years of age.88 Sternoclavicular joint Anterior sternoclavicular ligament

Articular disk Interclavicular ligament

Costoclavicular ligament Fig. 36.7  A view of the sternoclavicular joint showing the anterior and posterior capsular ligaments, interclavicular ligament, articular disk, and costoclavicular ligament. The posterior capsular ligament provides the most stability against anterior and posterior translation of the sternoclavicular joint.

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Scapulothoracic Articulation The scapular motion along the thoracic rib cage is referred to as the scapulothoracic articulation. Motion of the scapula is a result of the various stabilizing muscles that insert on it. The serratus anterior is an important stabilizing muscle because it holds the medial scapula to the thorax. It also helps to rotate and elevate the scapula in normal shoulder motions. The serratus anterior, along with the trapezius muscle, have the most muscle activity during arm abduction.89 Smooth scapulothoracic motion is critical for normal shoulder kinematics. Alterations in scapular mechanics can lead to problems with glenohumeral instability and rotator cuff dysfunction. The biomechanics of normal shoulder motion, including scapular mechanics, will be discussed in more detail later in this chapter.

SHOULDER MUSCLES Rotator Cuff The rotator cuff consists of four muscles—the supraspinatus, infraspinatus, teres minor, and subscapularis (Fig. 36.8). The supraspinatus muscle originates in the supraspinatus fossa of the superior aspect of the scapula, passes in an anterolateral direction under the coracoacromial arch, and inserts on the greater tuberosity of the proximal humerus. The mean insertion footprint width of the supraspinatus is 14.7 mm, with the tendon insertion less than 1 mm lateral to the articular surface of the humeral head.90 The supraspinatus muscle is innervated by the suprascapular nerve. The supraspinatus muscle is one of the main abductors of the humerus, accounting for 50% of the power to abduct in the scapular plane.91 Other investigators have shown that paralysis of the supraspinatus and infraspinatus muscles results in a loss of 75% of abduction strength.92 The anterior portion of the supraspinatus muscle contributes to

Rotator cuff

internal rotation in adduction and works as an external rotator as the shoulder is abducted.93 Macroscopically the tendons of the rotator cuff interdigitate to form a common insertion on the humerus. The supraspinatus muscle, along with the infraspinatus and teres minor muscles, have an area of insertion on the greater tuberosity of 6.24 cm2.90 The attachment site consists of a complex arrangement of collagen fibers capable of distributing tensile loads in various shoulder positions.94 The cuff tendons have several layers, including a layer of tendon fibers that are both parallel and densely packed and another layer with obliquely oriented and loosely packed tendon fibers. The tendons also have layers composed of capsular and ligamentous tissue.95 The supraspinatus tendon has been shown to have a hypovascular area near the insertion,96–98 which may play a factor in the pathogenesis of tears of the rotator cuff. Histologic sections from surgical specimens of patients with bursal-sided tears have been shown to be avascular, with no evidence of reparative tissue.99 The articular side of the rotator cuff is subjected to and is more vulnerable to tensile forces, which might help to explain why partial rotator cuff tears occur more on the articular side compared with the bursal side.100 The main external rotators of the glenohumeral joint, the infraspinatus and teres minor muscles, originate on the posterior aspect of the scapula, with the infraspinatus muscle arising from the infraspinatus fossa (see Fig. 36.8). These muscles are inferior to the scapular spine and travel laterally to insert on the posterior aspect of the greater tuberosity. The infraspinatus muscle is innervated by the suprascapular nerve as it travels through the spinoglenoid notch. The teres minor muscle is innervated by the axillary nerve. The greater tuberosity has a small tubercle posteroinferiorly that is the site of the teres minor insertion. The infraspinatus muscle accounts for approximately 70% of the external rotation strength but also contributes approximately 45% of the abduction strength.92 Clinically, the infraspinatus

Supraspinatus Infraspinatus

Teres minor

Subscapularis

A

B Fig. 36.8  Anterior (A) and posterior (B) views of the shoulder showing the subscapularis muscle and tendon anteriorly and the infraspinatus and teres minor muscles and tendons posteriorly. The supraspinatus is seen in the supraspinatus fossa. It travels anterolaterally to insert onto the greater tuberosity.

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muscle is more functional at lower levels of abduction and elevation, whereas the teres minor muscle contributes more to external rotation power at higher levels of abduction and elevation. The subscapularis is the anterior-most muscle of the rotator cuff; it originates from the ventral surface of the scapula and inserts on the lesser tuberosity. The lesser tuberosity insertion is trapezoidal in shape, with a broad insertion in the proximal portion. The upper 60% of the insertion site has a mean width of 2.5 cm.101 As the subscapularis muscle travels laterally to insert, it passes under the coracoid process and the conjoined tendon of the short head of the biceps brachii and coracobrachialis. Narrowing of the distance from the lesser tuberosity to the coracoid may lead to subcoracoid impingement, which can lead to tearing of the subscapularis muscle.102 The subscapularis muscle internally rotates and helps to adduct the humerus and is innervated by the upper and lower subscapular nerves. The subscapularis muscle has been shown to help provide stability to the shoulder from 0 to 45 degrees of abduction.54 The function of the rotator cuff, as its name implies, is to rotate the humerus. The rotator cuff also functions to maintain the center of rotation of the humeral head in the glenoid. The cuff muscles are important dynamic stabilizers of the glenohumeral joint. A 50% reduction in rotator cuff force has been shown to significantly increase anterior and posterior translation of shoulder specimens subjected to applied loads.103 Because of its orientation and vector of force, the rotator cuff also functions as a humeral head depressor. The head depressor effect is mainly due to the effect of the subscapularis and the external rotators. The supraspinatus muscle does not appear to have an effect on humeral head depression when it is studied biomechanically.104 Although tears of the supraspinatus muscle can and do result in abnormal shoulder function, relatively normal kinematics can occur with active overhead motion with a balanced force couple of the subscapularis and infraspinatus/teres minor muscles.105

Scapular Muscles The scapular muscles are important to shoulder function because they ensure proper positioning of the scapula in conjunction with glenohumeral joint motion. The scapula, through its connections to the axial skeleton, is an important structure that is needed to help transfer energy from the lower extremities and lower torso to the upper extremities. The transfer of lower body energy to the shoulder is referred to as the “kinetic chain.”106 The scapular muscles stabilize the scapula, providing a stable base for shoulder movement. The scapular muscles include the serratus anterior, trapezius, levator scapulae, rhomboids, and pectoralis minor. Although all of these muscles have an important role, the serratus anterior and trapezius muscles appear to be most responsible for proper scapulothoracic motion. The serratus anterior muscle originates from the upper thorax, along the ribs. It has a broad insertion along the anterior portion of the medial border of the scapula and is innervated by the long thoracic nerve (C5-C6-C7). The main function of the serratus anterior muscle is to protract the scapula laterally along the thorax with overhead motion of the shoulder. The serratus anterior muscle also works together with the upper and lower portions of

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the trapezius muscle to rotate the scapula upward with overhead activities. The serratus anterior and upper and lower trapezius muscles have the most electromyographic-documented activity of the scapular muscles with arm elevation.89 The trapezius is a posterior muscle along the posterosuperior aspect of the scapula. It has three functional sections—the upper, middle, and lower trapezius. The superior trapezius originates from the occiput and inserts on the posterior portion of the lateral clavicle. The upper trapezius functions to help support the weight on the upper extremity. The middle portion originates from the spinous process of C7 to T3. The fibers of the middle portion insert onto the medial acromion and posteriorly along the medial portion of the scapular spine. The inferior trapezius originates from the spinous processes of T4 to T12 and travels superior and laterally to insert on the medial aspect of the scapular spine. The main function of the upper and lower trapezius is to upwardly rotate the scapula during overhead activity. The upper and lower trapezius also work with the middle trapezius to help retract the scapula. The trapezius muscle is innervated by the spinal accessory nerve, as well as the third and fourth cervical nerves. The levator scapulae muscle originates from the transverse processes of the cervical vertebra (C1-C4). It inserts on the superior angle of the scapula and helps to rotate the interior angle of the scapula medially. The levator scapulae muscle works with the rhomboids and pectoralis minor to rotate the medial scapula downward. It is innervated by the third and fourth cervical nerves. The rhomboid major and minor muscles originate from the spinous processes of the thoracic vertebra from T2 to T5 and insert on the medial border of the scapula. The rhomboid muscles are innervated by the dorsal scapula nerve, which arises from C5. The main function of the rhomboid muscles is to help stabilize the scapula along the thorax. The rhomboid muscles help to retract the scapula and, as such, are antagonists to the serratus anterior. The rhomboid muscles work with the levator scapulae muscle to elevate the medial scapula and rotate the scapula downward. The pectoralis minor muscle originates from the anterosuperior aspects of the anterior portions of ribs three through five. The muscle travels laterally to insert on the medial aspect of the coracoid. The main function of the pectoralis minor muscle is to pull the scapula inferiorly and medially. It is innervated by the medial pectoral nerve.

Other Muscles of the Shoulder Complex The deltoid is the most superficial muscle covering the glenohumeral joint. It originates from the clavicle, acromion, and scapular spine and inserts on the deltoid tubercle on the lateral aspect of the midhumerus. The deltoid muscle provides a significant contribution to abduction of the humerus91; this function is provided by the anterior and middle portions of the muscle. The anterior portion of the deltoid muscle helps to flex the humerus, whereas the posterior portion of the deltoid muscle helps to adduct and extend the humerus. The deltoid muscle is innervated by the axillary nerve as it travels out of the quadrilateral space (the space bordered by the teres minor muscle superiorly, the teres major muscle inferiorly, the long head of the triceps brachii

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medially, and the humeral shaft laterally). The posterior humeral circumflex artery also travels in this space. The axillary nerve travels around the lateral aspect of the shoulder as it innervates the deltoid muscle. The distance from the lateral acromion to the axillary nerve averages 5 cm but can be as little as 3 cm. The distance decreases with shoulder abduction.107 Surgical dissections through the deltoid muscle can injure the nerve if the deltoid muscle is split too far distally. The teres major muscle, along with the latissimus dorsi muscle, helps to extend, internally rotate, and adduct the humerus. The teres major muscle takes its origin from the inferior angle of the scapula and inserts on the medial aspect of bicipital groove. The latissimus dorsi muscle inserts on the medial aspect of the bicipital groove, just anterior to the teres minor muscle. The latissimus dorsi muscle originates from the spinous processes of T7 to L5, the thoracolumbar fascia, the posterior iliac crest, and the inferior angle of the scapula. The muscle fibers travel superiorly, laterally, and anteriorly to insert on the medial aspect of the floor of the bicipital groove. Is some persons, a conjoined tendon insertion with the teres major muscle occurs. The latissimus dorsi muscle helps to extend, adduct, and internally rotate the shoulder. It is innervated by the thoracodorsal nerve. The pectoralis major muscle originates from the medial portion of the clavicle (clavicular head), the anterior surface of the sternum, the upper ribs, and the aponeurosis of the abdominal external oblique muscle (sternal head). The fibers from the clavicular head travel inferiorly and laterally. The sternal head fibers travel laterally. The two heads converge to form a common tendon that inserts onto the lateral aspect of the bicipital groove. The pectoralis major muscle is innervated by the lateral and medial pectoral nerves. The pectoralis major muscle helps to internally rotate, adduct, and flex the humerus. The short head of the biceps brachii muscle and the coracobrachialis muscle originate from a common tendon at the tip of the coracoid. They are innervated by the musculocutaneous nerve, which pierces the muscles, on average, 5 cm distal to the coracoid. However, small branches of the nerve have been shown to innervate the muscle as close as 17 mm from the coracoid.108 An appreciation of the neural anatomy and the variations is important to potentially avoid nerve injury during surgeries that retract the conjoined tendon or osteotomize the coracoid.

BIOMECHANICS AND KINETICS OF NORMAL SHOULDER MOTION Normal glenohumeral and scapulothoracic biomechanics are prerequisites for achieving optimal shoulder function. Normal shoulder motion consists of a coordinated pattern of scapulothoracic and glenohumeral motion. The acromioclavicular and sternoclavicular joints also play a role in normal shoulder motion by guiding and limited scapular motion. The scapula has to move in conjunction with the humerus to maintain the humeral center of rotation in the various glenohumeral positions. In the normal shoulder, the center of rotation of the humeral head varies little with elevation or flexion/extension in the horizontal plane.

Coordinated scapular motion requires the scapula to protract and retract with elevation and lowering of the arm. Historically, glenohumeral to scapulothoracic motion has been described as being a 2 : 1 ratio after the initial 30 degrees of elevation.109 More accurate three-dimensional motion analyses have been performed to better define the normal scapulohumeral motion.86,87,110–116 Recent evidence would suggest that the ratio of glenohumeral elevation to scapular upward rotation is 2.3 : 1 during elevation and 2.7 : 1 when lowering the arm from overhead. Scapula upward rotation and posterior tilting increase until maximum elevation.111 Posterior tilting is needed to clear the acromion from the rotator cuff to avoid impingement with overhead activity. Motion during humeral elevation includes clavicle elevation, retraction, and posterior rotation; scapular upward rotation, internal rotation, and posterior tilting; and glenohumeral elevation with humeral external rotation.87 The largest amount of scapular rotation occurs between 80 and 140 degrees of arm abduction.117 Obligatory humeral external rotation occurs as the arm is elevated at or anterior to the scapular plane, partly because of the geometry of the humeral head and glenoid.87,110,118 Internal rotation is required from maximum elevation posterior to the scapular plane.110 Therefore one can easily see how capsular contractions that prevent rotation can adversely affect elevation and overall motion. Scapular dyskinesia is common in patients with shoulder instability and rotator cuff impingement syndrome.119–120 In fact, alternations in shoulder biomechanics can result from abnormalities in the scapular muscles, alterations in cervical and thoracic posture, abnormalities in joint mobility (such as seen in arthrosis or instability), and fractures of the scapula or clavicle that affect the position of the scapula or the length of the clavicle.

SUMMARY The shoulder is a complex arrangement of four bones, four articulations, and several muscles, tendons, and ligaments. The shoulder complex requires healthy and ligamentously stable joints and numerous muscles working in synergy to allow the upper extremity to be placed in various positions and to perform activities that subject it to extremes of force and torque. The various articulations and muscles are kinetically linked, and abnormalities in any of the joints or muscles can result in pain, dysfunction, and possibly injury to other structures. An appreciation of the anatomy and biomechanics of the shoulder complex will be beneficial to clinicians in making diagnoses, applying safe and appropriate surgical procedures, and implementing appropriate rehabilitation protocols. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Boileau P, Walch G. The three-dimensional geometry of the proximal humerus. Implications for surgical treatment and prosthetic design. J Bone Joint Surg Br. 1997;79B(5):857–865.

Level of Evidence: V, basic science study

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401

Summary:

Level of Evidence:

In this cadaveric study, the authors showed that the articular surface of the proximal humerus varies with respect to the inclination, retroversion, size, and medial and posterior offset. Findings from this study have influenced design features of newer shoulder prostheses, which now allow surgeons to reproducibly replicate the native anatomy.

V, basic science study

Citation:

Citation:

Gerber C, Blumenthal S, Curt A. Effect of selective experimental suprascapular nerve block on abduction and external rotation strength of the shoulder. J Shoulder Elbow Surg. 2007;16(6): 815–820.

Turkel S, Panio M, Marshall J. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am. 1981;63A(8):1208–1217.

Level of Evidence:

Level of Evidence:

V, basic science study

I, prognostic study

Summary:

Summary:

In this cadaveric study, the authors showed that the subscapularis muscle provides anterior stability to the adducted shoulder, the middle glenohumeral ligament provides stability at 45 degrees of abduction, and the inferior glenohumeral ligament provides anterior stability as the shoulder approaches 90 degrees of abduction.

In this well-designed and well-performed study, the authors showed that the infraspinatus muscle is responsible for 70% of the external rotation strength of the shoulder and that it also contributes to abduction strength. The authors also showed that the supraspinatus and infraspinatus muscles were responsible for 75% of the abduction strength in healthy volunteers.

Citation: Matsumura N, Ikegami H, Nakamichi N. Effect of shortening deformity of the clavicle on scapular kinematics: a cadaveric study. Am J Sports Med. 2010;38(5):1000–1006.

Level of Evidence:

Summary: In this cadaveric study, the authors demonstrated that the primary restraint to anterior and posterior translation of the abducted shoulder is the inferior glenohumeral ligament complex.

Citation: Kibler WB. The role of the scapula in athletic shoulder function. Am J Sports Med. 1998;26(2):325–337.

Level of Evidence: V, review article/expert opinion

Summary:

V, basic science study

Summary: In this cadaveric study, the authors showed that shortening of the clavicle by 10% of the original length had adverse effects on shoulder kinematics.

In this review article, the author thoroughly reviews the role of the scapula in normal shoulder biomechanics and in athletics involving overhead actions. The author introduces the concept of the kinetic chain (i.e., the transfer of lower extremity energy to the upper extremity) and reinforces the importance of the scapula in the kinetic chain.

Citation: O’Brien S, Schwartz R, Warren R. Capsular restraints to anterior-posterior motion of the abducted shoulder: a biomechanical study. J Shoulder Elbow Surg. 1995;4(4):298–308.

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CHAPTER 36  Shoulder Anatomy and Biomechanics

REFERENCES 1. Fox J, Cole B, Romeo A, et al. Articular cartilage thickness of the humeral head: an anatomic study. Orthopedics. 2008;31(3):216. 2. Boileau P, et al. The combined offset (medial and posterior) of the humeral sphere. J Shoulder Elbow Surg. 1994;3(1):S65. 3. Boileau P, Walch G. The three-dimensional geometry of the proximal humerus. Implications for surgical technique and prosthetic design. J Bone Joint Surg Br. 1997;79(5):857–865. 4. Iannotti J, Gabriel J, Schneck S, et al. The normal glenohumeral relationships. J Bone Joint Surg Am. 1992;74(4):491–500. 5. Pearl M, Volk A. Retroversion of the proximal humerus in relationship to prosthetic replacement arthroplasty. J Shoulder Elbow Surg. 1995;4:286–289. 6. Pearl M. Proximal humeral anatomy in shoulder arthroplasty: implications for prosthetic design and surgical technique. J Shoulder Elbow Surg. 2005;14(1):S99–S104. 7. Robertson D, Yuan J, Bigliani L, et al. Three-dimensional analysis of the proximal part of the humerus: relevance to arthroplasty. J Bone Joint Surg Am. 2000;82(11):1594–1602. 8. Tillet E, Smith M, Fulcher M, et al. Anatomic determination of humeral head retroversion: the relationship of the central axis of the humeral head to the bicipital groove. J Shoulder Elbow Surg. 1993;2:255–256. 9. Hernigou P, Duparc F, Hernigou A. Determining humeral retroversion with computed tomography. J Bone Joint Surg Am. 2002;84(10):1753–1762. 10. Holt E, Allibone R. Anatomic variants of the coracoacromial ligament. J Shoulder Elbow Surg. 1995;4:370–375. 11. Kuhne M, Boniquit N, Ghodadra N, et al. Current concepts. The snapping scapula: diagnosis and treatment. Arthroscopy. 2009;25(11):1298–1311. 12. Dolan C, Hariri S, Hart N, et al. An anatomic study of the coracoid process as it relates to bone transfer procedures. J Shoulder Elbow Surg. 2011;20(3):497–501. 13. Lo I, Burkhart S, Parten P. Surgery about the coracoid: neurovascular structures at risk. Arthroscopy. 2004;20(6): 591–595. 14. Helfet A. Coracoid transplantation for recurring dislocation of the shoulder. J Bone Joint Surg Br. 1958;40:198–202. 15. Latarjet M. A propos du traitement des luxations recidivantes de l’epaule. Lyon Chir. 1954;49:994–997. 16. MacGillivray J, Fealy S, Potter H, et al. Multiplanar analysis of acromion morphology. Am J Sports Med. 1998;26(6):836–840. 17. Nicholson G, Goodman D, Flatow E, et al. The acromion: morphologic condition and age-related changes. A study of 420 scapulas. J Shoulder Elbow Surg. 1996;5:1–11. 18. Ogata S, Uhthoff H. Acromial enthesopathy and rotator cuff tear: a radiologic and histologic postmortem investigation of the coracoacromial arch. Clin Orthop. 1990;254:39–48. 19. Soslowsky L, An C, Johnston S, et al. Geometric and mechanical properties of the coracoacromial ligament and their relationship to rotator cuff disease. Clin Orthop. 1994;304:10–17. 20. Shah N, Bayliss N, Malcolm A. Shape of the acromion: congenital or acquired—a macroscopic, radiographic, and microscopic study of acromion. J Shoulder Elbow Surg. 2001;10:309–316. 21. Lee T, Black A, Tibone J, et al. Release of the coracoacromial ligament can lead to glenohumeral laxity: a biomechanical study. J Shoulder Elbow Surg. 2001;10(1):68–72.

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22. Fagelman M, Sartori M, Freedman K, et al. Biomechanics of coracoacromial arch modification. J Shoulder Elbow Surg. 2007;16:101–106. 23. Flatow E, et al. Excursion of the rotator cuff under the acromion: patterns of subacromial contact. Am J Sports Med. 1994;22:779–788. 24. Ide K, Yasumasa S, Hiromoto I, et al. Sensory nerve supply in the human subacromial bursa. J Shoulder Elbow Surg. 1996;5:371–382. 25. Vangsness C, et al. Neural anatomy of the glenohumeral ligaments, labrum, and subacromial bursa. Arthroscopy. 1995;11:180–184. 26. Bigliani L, Dalsey R, McCann P, et al. An anatomical study of the suprascapular nerve. Arthroscopy. 1990;6:301–305. 27. Ticker J, Djurasovic M, Strauch R, et al. The incidence of ganglion cysts and other variations in anatomy along the course of the suprascapular nerve. J Shoulder Elbow Surg. 1998;7(5):472–478. 28. Basmajian J, Bazant F. Factors preventing downward dislocation of the adducted shoulder joint. J Bone Joint Surg Am. 1959;41(7):1182–1186. 29. Churchill R, Brems J, Kotschi H. Glenoid size, inclination, and version: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):327–332. 30. Nyffeler R, Jost B, Pfirrmann C, et al. Measurement of glenoid version: conventional radiographs versus computed tomography scans. J Shoulder Elbow Surg. 2003;12(5):493–496. 31. Friedman R, Hawthorne K, Genez B. The use of computed tomography in the measurement of glenoid version. J Bone Joint Surg Am. 1992;74(7):1032–1037. 32. Lo I, Parten P, Burkhart S. The inverted pear glenoid: an indicator of significant glenoid bone loss. Arthroscopy. 2004;20(2):169–174. 33. Burkhart S, Debeer J, Tehrany A, et al. Quantifying bone loss arthroscopically in shoulder instability. Arthroscopy. 2002;18:488–491. 34. Ladermann A, Denard P, Burkhart SS. Injury of the suprascapular nerve during latarjet procedure: an anatomic study. Arthroscopy. 2012;28(3):316–321. 35. Demirhan M, Imhoff A, Debski R, et al. The spinoglenoid ligament and its relationship to the suprascapular nerve. J Shoulder Elbow Surg. 1998;7(3):238–243. 36. Matsumura N, Ikegami H, Nakamichi N, et al. Effect of shortening deformity of the clavicle on scapular kinematics: a cadaveric study. Am J Sports Med. 2010;38(5):1000–1006. 37. Hillen R, Burger B, Pöll R. The effect of experimental shortening of the clavicle on shoulder kinematics. Clin Biomech (Bristol, Avon). 2012;27(8):777–781. 38. Harryman D, Sidles J, Harris S, et al. Laxity of the normal glenohumeral joint. J Shoulder Elbow Surg. 1992;1:66–75. 39. Harryman D, Sidles J, Clark J, et al. Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am. 1990;72:1334–1343. 40. Jia X, Ji J, Petersen S, et al. An analysis of shoulder laxity in patients undergoing shoulder surgery. J Bone Joint Surg Am. 2009;91(9):2144–2150. 41. Kumar V, Balasubramaniam P. The role of atmospheric pressure in stabilising the shoulder. J Bone Joint Surg Br. 1985;67(5):719–721. 42. Gibb T, Sidles J, Harryman D, et al. The effect of capsular venting on glenohumeral laxity. Clin Orthop. 1991;268: 120–127.

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43. Lippitt S, Vanderhooft J, Harris S. Glenohumeral stability from concavity-compression: a quantitative analysis. J Shoulder Elbow Surg. 1993;2:27–35. 44. Howell S, Galinat B. The glenoid-labral socket: a constrained articular surface. Clin Orthop. 1989;243:122–125. 45. Cooper D, Arnoczky S, O’Brien S, et al. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am. 1992;74(1):46–52. 46. Greis P, Scuderi M, Mohr A, et al. Glenohumeral articular contact areas and pressures following labral and osseous injury to the anteroinferior quadrant of the glenoid. J Shoulder Elbow Surg. 2002;11(5):442–451. 47. Kanatli U, Ozturk B, Bolukbasi S. Anatomic variation of the anterosuperior labrum: prevalence and association with type II superior labrum anterior-posterior (SLAP) lesions. J Shoulder Elbow Surg. 2010;19:1199–1203. 48. Williams M, Snyder S, Buford D. The Buford complex—the “cord-like” middle glenohumeral ligament and absent anterosuperior labrum complex: a normal anatomic capsulolabral variant. Arthroscopy. 1994;10(5):241–247. 49. O’Brien S, Schwartz R, Warren R, et al. Capsular restraints to anterior-posterior motion of the abducted shoulder: a biomechanical study. J Shoulder Elbow Surg. 1995;4(4): 298–308. 50. O’Brien S, Neves M, Arnoczky S. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med. 1990;18(5):449–456. 51. Urayama M, Itoi E, Hatakeyama Y, et al. Function of the 3 portions of the inferior glenohumeral ligament: a cadaveric study. J Shoulder Elbow Surg. 2001;10:589–594. 52. Eberly V, McMahon P, Lee T. Variation in the glenoid origin of the IGHL anterior band: implications for repair of the Bankart lesion. Clin Orthop. 2002;400:26–31. 53. Ide J, Maeda S, Takagi K. Normal variations of the glenohumeral ligament complex: an anatomic study for arthroscopic Bankart repair. Arthroscopy. 2004;20(2):164–168. 54. Turkel S, Panio M, Marshall J, et al. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am. 1981;63(8):1208–1217. 55. Kask K, Põldoja E, Lont T, et al. Anatomy of the superior glenohumeral ligament. J Shoulder Elbow Surg. 2010;19(6): 908–916. 56. Warner J, Deng X, Warren R, et al. Static capsuloligamentous restraints to superior-inferior translation of the glenohumeral joint. Am J Sports Med. 1992;20(6):675–685. 57. Boardman N, Debski R, Warner J, et al. Tensile properties of the superior glenohumeral and coracohumeral ligaments. J Shoulder Elbow Surg. 1996;5(4):249–254. 58. Soslowsky L, Malicky D, Blasier R. Active and passive factors in inferior glenohumeral stabilization: a biomechanical model. J Shoulder Elbow Surg. 1997;6:371–379. 59. Cole B, Rodeo S, O’Brien S, et al. The anatomy and histology of the rotator interval capsule of the shoulder. Clin Orthop Relat Res. 2001;90:129–137. 60. Harryman D, Sidles J, Harris S, et al. The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg. 1992;74A(1):53–66. 61. Mologne T, Zhao K, Hongo M, et al. The addition of rotator interval closure after arthroscopic repair of either anterior or posterior shoulder instability: effect on glenohumeral translation and range of motion. Am J Sports Med. 2008;36(6): 1123–1131.

62. Bey M, Hunter S, Kilambi N, et al. Structural and mechanical properties of the glenohumeral joint posterior capsule. J Shoulder Elbow Surg. 2005;14:201–206. 63. Ciccone W, Hunt T, Lieber R, et al. Multiquadrant digital analysis of shoulder capsular thickness. Arthroscopy. 2000;16(5):457–461. 64. Gohlke F, Essigkrug B, Schmitz F. The pattern of the collagen fiber bundles of the capsule of the glenohumeral joint. J Shoulder Elbow Surg. 1994;3:111–128. 65. Sugalski M, Wiater J, Levine W, et al. An anatomic study of the humeral insertion of the inferior glenohumeral capsule. J Shoulder Elbow Surg. 2005;14:91–95. 66. Grossman M, Tibone J, McGarry M, et al. A cadaveric model of the throwing shoulder: a possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am. 2005;87(4): 824–831. 67. Enad J. Bifurcate origin of the long head of the biceps tendon. Arthroscopy. 2004;20(10):1081–1083. 68. Hyman J, Warren R. Extra-articular origin of biceps brachii. Arthroscopy. 2001;17(7):E29. 69. Lang J, Vinson E, Basamania C. Anomalous biceps tendon insertion into the rotator cable: a case report. J Surg Orthop Adv. 2008;7(2):93–95. 70. Itoi E, Motzkin N, Morrey B, et al. Stabilizing function of the long head of the biceps in the hanging arm position. J Shoulder Elbow Surg. 1994;3:135–142. 71. Pagnani M, Deng X, Warren R, et al. Role of the long head of the biceps brachii in glenohumeral stability: a biomechanical study in cadavers. J Shoulder Elbow Surg. 1996;4:255–262. 72. Youm T, ElAttrache N, Tibone J, et al. The effect of the long head of the biceps on glenohumeral kinematics. J Shoulder Elbow Surg. 2009;18(1):122–129. 73. Rodosky M, Harner C, Fu F. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med. 1994;22:121–130. 74. Gleason P, Beall D, Sanders T, et al. The transverse humeral ligament: a separate anatomic structure or a continuation of the osseous attachment of the rotator cuff? Am J Sports Med. 2006;34(1):72–77. 75. Stine I, Vangsness C. Analysis of the capsule and ligament insertions about the acromioclavicular joint: a cadaveric study. Arthroscopy. 2009;25(9):968–974. 76. Lee K, Debski R, Chen C, et al. Functional evaluation of the ligaments at the acromioclavicular joint during anteroposterior and superoinferior translation. Am J Sports Med. 1997;25(6): 858–862. 77. Boehm T, Kirschner S, Fischer A, et al. The relation of the coracoclavicular ligament insertion to the acromioclavicular joint: a cadaver study of the relevance to lateral clavicle resection. Acta Orthop Scand. 2003;4(6):718–721. 78. Renfree K, Riley M, Wheeler D, et al. Ligamentous anatomy of the distal clavicle. J Shoulder Elbow Surg. 2003;12(4): 355–359. 79. Fukuda K, Craig E, An K, et al. Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am. 1986;68(3):434–440. 80. Takase K. The coracoclavicular ligament: an anatomic study. Surg Radiol Anat. 2010;32(7):683–688. 81. Dawson P, Adamson G, Pink M, et al. Relative contribution of the acromioclavicular joint capsule and coracoclavicular ligaments to acromioclavicular stability. J Shoulder Elbow Surg. 2009;18:237–244.

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CHAPTER 36  Shoulder Anatomy and Biomechanics 82. Ebraheim N, Whitehead J, Alla S, et al. The suprascapular nerve and its articular branch to the acromioclavicular joint: an anatomic study. J Shoulder Elbow Surg. 2010;20(3):e13–e17. 83. Debski R, Fenwick J, Vangura A, et al. Effect of arthroscopic procedures on the acromioclavicular joint. Clin Orthop. 2006;406:89–96. 84. Klimkiewicz J, Williams G, Sher J, et al. The acromioclavicular capsule as a restraint to posterior translation of the clavicle: a biomechanical analysis. J Shoulder Elbow Surg. 1999;8: 119–124. 85. Spencer E, Kuhn J, Huston L, et al. Ligamentous restraints to anterior and posterior translation of the sternoclavicular joint. J Shoulder Elbow Surg. 2002;11(1):43–47. 86. Ludewig P, Behrens S, Meyer S, et al. Three-dimensional clavicular motion during arm elevation: reliability and descriptive data. J Orthop Sports Phys Ther. 2004;4(3): 140–149. 87. Ludewig P, Phadke V, Braman J, et al. Motion of the shoulder complex during multiplanar humeral elevation. J Bone Joint Surg Am. 2009;91(2):378–389. 88. Schmeling A, Schulz R, Reisinger W, et al. Studies on the time frame for ossification of the medial clavicular epiphyseal cartilage in conventional radiography. Int J Legal Med. 2004;118(1):5–8. 89. Bagg S, Forrest W, et al. Electromyographic study of the scapular rotators during arm abduction in the scapular plane. Am J Phys Med. 1986;65(3):111–124. 90. Dugas J, Campbell D, Warren R, et al. Anatomy and dimensions of rotator cuff insertions. J Shoulder Elbow Surg. 2002;11(5):498–503. 91. Howell S, Imobersteg A, Seger D, et al. Clarification of the role of the supraspinatus muscle in shoulder function. J Bone Joint Surg Am. 1986;68(3):398–404. 92. Gerber C, Blumenthal S, Curt A, et al. Effect of selective experimental suprascapular nerve block on abduction and external rotation strength of the shoulder. J Shoulder Elbow Surg. 2007;16(6):815–820. 93. Gates J, Gilliland J, McGarry M, et al. Influence of distinct anatomic subregions of the supraspinatus on humeral rotation. J Orthop Res. 2010;28(1):12–17. 94. Fallon J, Blevins F, Vogel K, et al. Functional morphology of the supraspinatus tendon. J Orthop Res. 2002;20(5):920–926. 95. Clark J, Harryman D. Tendons, ligaments and capsule of the rotator cuff: gross and microscopic anatomy. J Bone Joint Surg Am. 1992;74:713–725. 96. Brooks C, Revell W, Heatley F. A quantitative histological study of the vascularity of the rotator cuff tendon. J Bone Joint Surg Br. 1992;74:151–153. 97. Lohr J, Uhthoff H. The microvascular pattern of the supraspinatus tendon. Clin Orthop. 1990;254:35–38. 98. Rathbun J, Macnab I. The microvascular pattern of the rotator cuff. J Bone Joint Surg Br. 1970;2:540–553. 99. Fukuda H, Hamada K, Yamanaka K. Pathology and pathogenesis of bursal-sided rotator cuff tears viewed from en bloc histologic sections. Clin Orthop. 1990;254:75–80. 100. Nakajima T, Rokuuma N, Hamada K, et al. Histologic and biomechanical characteristics of the supraspinatus tendon: reference to rotator cuff tearing. J Shoulder Elbow Surg. 1994;3(2):79–87.

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101. Richards D, Burkhart S, Tehrany A, et al. The subscapularis footprint: an anatomic description of its insertion site. Arthroscopy. 2007;23(3):251–254. 102. Richards D, Burkhart S, Campbell S. Relation between narrowed coracohumeral distance and subscapularis tears. Arthroscopy. 2005;21(10):1223–1228. 103. Wuelker N, Korell M, Thren K. Dynamic glenohumeral joint stability. J Shoulder Elbow Surg. 1998;7(1):43–52. 104. Sharkey N, Marder R. The rotator cuff opposes superior translation of the humeral head. Am J Sports Med. 1995;23: 270–275. 105. Burkhart S. Fluoroscopic comparison of kinematic patterns in massive rotator cuff tear. A suspension bridge model. Clin Orthop. 1992;84:144–152. 106. Kibler W. The role of the scapula in athletic shoulder function. Am J Sports Med. 1998;26(2):325–337. 107. Burkhead W, Scheinberg R, Box G. Surgical anatomy of the axillary nerve. J Shoulder Elbow Surg. 1992;1:31–36. 108. Flatow E, Bigliani L, April E. An anatomic study of the musculocutaneous nerve and its relationship to the coracoid process. Clin Orthop. 1989;244:166–171. 109. Inman V, Saunders J, Abbott L. Observations on the function of the shoulder joint. J Bone Joint Surg. 1944;27:1–30. 110. An K, Browne A, Korinek S, et al. Three-dimensional kinematics of glenohumeral elevation. J Orthop Res. 1991;9: 143–149. 111. Braman J, Engel S, LaPrade R, et al. In vivo assessment of scapulohumeral rhythm during unconstrained overhead reaching in asymptomatic subjects. J Shoulder Elbow Surg. 2009;18(6):960–967. 112. Dayanidhi S, Orlin M, Kozin S, et al. Scapular kinematics during humeral elevation in adults and children. Clin Biomech (Bristol, Avon). 2005;20(6):600–606. 113. Ebaugh D, McClure P, Karduna A. Three-dimensional scapulothoracic motion during active and passive arm elevation. Clin Biomech (Bristol, Avon). 2005;20(7):700–709. 114. Ludewig P, Cool T, Nawoczenski D. Three-dimensional scapular orientation and muscle activity at selected positions of humeral elevation. J Orthop Sports Phys Ther. 1996;24(2):57–65. 115. McClure P, Michener L, Sennett B, et al. Direct 3-dimensional measurement of scapular kinematics during dynamic movements in vivo. J Shoulder Elbow Surg. 2001;10(3):269–277. 116. McClure P, Michener L, Karduna A. Shoulder function and 3-dimensional scapular kinematics in people with and without shoulder impingement syndrome. Physical Ther. 2006;86(8): 1075–1090. 117. Bagg S, Forrest W. A biomechanical analysis of scapular rotation during arm abduction in the scapular plane. Am J Phys Med Rehabil. 1988;67(6):238–245. 118. Jobe C, Iannotti J. Limits imposed on glenohumeral motion by joint geometry. J Shoulder Elbow Surg. 1995;4:281–285. 119. Warner J, Micheli L, Arslanian L, et al. Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impingement syndrome. Clin Orthop. 1992;285:191–199. 120. Hallstrom E, Kärrholm J. Shoulder kinematics in 25 patients with impingement and 12 controls. Clin Orthop. 2006;448:22–27.

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37  Shoulder Diagnosis and Decision-Making Thomas J. Gill

Perhaps more than any other joint in the body, the shoulder can present a complex diagnostic challenge to the examining physician. There are a variety of anatomic and clinical reasons for this challenge. First, the “shoulder” is actually a functional complex of four distinct and separate articulations: the sternoclavicular joint, acromioclavicular joint, glenohumeral joint, and scapulothoracic joint. These joints all function together to allow a strong, stable platform with a wide arc of motion through multiple geometric planes. Thus it is not uncommon for patients to present with periscapular pain, for instance, which is actually secondary to a primary glenohumeral problem such as adhesive capsulitis or a large rotator cuff tear. “Shoulder pain” can also be due to referred pain from the neck. Cervical radiculopathies, paracervical muscle strains, “whiplash,” and other neck-related pathologies can all cause patients to present to the clinician with a subjective feeling of pain in their “shoulder.” There are also vascular etiologies for shoulder pain, peripheral neuropathies and nerve entrapments, intrathoracic pathologies, and malignancies whose presenting symptoms are often shoulder pain or instability. As a result of the diagnostic challenge presented by patients with shoulder-related symptoms, it is important to take a detailed history, perform a truly regimented and comprehensive physical examination, order and review appropriate diagnostic imaging, and carefully correlate all relevant findings prior to arriving at a final “diagnosis.” In some instances, the selective use of injections can often confirm the etiology of the patient’s pain much more accurately than high-cost advanced imaging techniques. The clinician cannot simply “get an MRI” (magnetic resonance imaging) to arrive at the correct source of the patient’s symptoms, as might be done with other types of musculoskeletal pathologies. In fact, a shoulder MRI may show four or five structural “abnormalities,” none of which have anything to do with the cause of the patient’s presenting symptoms. No part of the diagnostic workup can be taken in isolation. It is only after careful consideration of all the clinical data that a diagnosis and treatment plan can be decided. The goal of this chapter is to present a practical approach to the patient with shoulder-related symptoms. It will present the diagnostic clues that can be obtained from taking a focused, detailed history, the specific parts of the physical examination that lead to a specific diagnosis, the indications for advanced imaging techniques, the use of selective diagnostic and therapeutic 402

injections that can confirm the etiology of the patient’s shoulder complaints, and how these decisions can be made. For most patients with shoulder complaints, it is helpful to divide the possible etiologies and diagnoses into the most likely diagnostic categories. These include (1) referred pain from the cervical spine, (2) acromioclavicular (AC) joint pathology, (3) rotator cuff–related pathology, (4) biceps-related pathology, (5) glenohumeral instability, and (6) glenohumeral arthritis. Although pathologies such as occult tumors, traumatic fractures, vascular disease, and peripheral nerve entrapments can also cause shoulder symptoms, they are not the primary focus of this chapter.

HISTORY The most important parts of a patient’s history are the patient’s age and whether or not there was a specific trauma or incident involved in the onset of symptoms. For patients younger than 25 years of age, the most likely diagnosis is glenohumeral instability or AC joint–related pain. For patients older than 40 years, rotator cuff–related pathology, with or without biceps tendon involvement, is most common. The next part of the history should be a precise determination of the patient’s chief complaint. Is the reason for the patient’s visit pain, instability, loss of motion, or weakness? Patients can often tell the clinician their own diagnosis if proper questioning is performed in this manner. Loss of motion indicates adhesive capsulitis, large rotator cuff tears, or glenohumeral arthrosis. Weakness is typically due to rotator cuff tears or, less likely, suprascapular nerve entrapment. Instability symptoms are typically related to glenohumeral labral tears or capsular redundancy. “Pain” is less specific but is most commonly due to subacromial impingement (specifically bursitis, rotator cuff tendinitis), biceps tendinitis, partial- or full-thickness rotator cuff tears, and AC joint arthritis. Glenohumeral instability can also present as pain, which is when the patient’s age should also be considered. If “pain” is the chief complaint, the question of referred pain must be considered. It is helpful to ask the patient to “put one finger where it hurts the most.” If the patient points to his or her AC joint, the diagnosis is typically made. If specific localization is made to the biceps groove, then biceps pathology with or without rotator cuff involvement is common. Pointing to the lateral shoulder near the insertion of the lateral deltoid is indicative of rotator cuff–related pain. However, if the patient cannot

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CHAPTER 37  Shoulder Diagnosis and Decision-Making

Abstract

Keywords

As a result of the diagnostic challenge presented by patients with shoulder-related symptoms, it is important to take a detailed history, perform a truly regimented and comprehensive physical examination, order and review appropriate diagnostic imaging, and carefully correlate all relevant findings prior to arriving at a final “diagnosis.” In some instances, the selective use of injections can often confirm the etiology of the patient’s pain much more accurately than high-cost advanced imaging techniques. The clinician cannot simply “get an MRI” (magnetic resonance imaging) to arrive at the correct source of the patient’s symptoms, as might be done with other types of musculoskeletal pathologies. In fact, a shoulder MRI may show four or five structural “abnormalities,” none of which have anything to do with the cause of the patient’s presenting symptoms. No part of the diagnostic workup can be taken in isolation. It is only after careful consideration of all the clinical data that a diagnosis and treatment plan can be decided. The goal of this chapter is to present a practical approach to the patient with shoulder-related symptoms. It will present the diagnostic clues that can be obtained from taking a focused, detailed history, the specific parts of the physical examination that lead to a specific diagnosis, the indications for advanced imaging techniques, the use of selective diagnostic and therapeutic injections that can confirm the etiology of the patient’s shoulder complaints, and how these decisions can be made.

shoulder diagnosis physical examination history management

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CHAPTER 37  Shoulder Diagnosis and Decision-Making

“localize” the pain, the question of referred pain should be considered. When asked to localize the “shoulder” pain that is actually being referred from a cervical spine etiology, patients cannot use one specific finger to localize the pain. Instead, they use their palm to rub over their trapezius and upper arm. As a general rule, truly shoulder-related pain does not radiate below the elbow. If the patient indicates that symptoms travel below the elbow into the hand, then cervical stenosis or cervical disc herniation should be considered. After the chief complaint is ascertained, the patient should be questioned about any history of trauma or inciting event. If there is no history of trauma, repetitive overuse injuries, tendinopathies and AC joint or glenohumeral arthrosis are most common. If there is a history of trauma, the question of fracture, labral tear, or rotator cuff tear becomes more important. It is helpful to then ask what position the patient’s arm was in when the trauma occurred. If the patient fell with his or her arm at his or her side, an AC joint or clavicular injury is most common. In contrast, falling on an outstretched arm can lead to rotator cuff tears, superior labral tears, and traumatic glenohumeral instability episodes. Patients should then be asked what position of their arm brings on their symptoms or worsens their pain. Symptoms that worsen when reaching overhead or at night indicate rotator cuff and/or bursal inflammation. Abduction and external rotation worsens symptoms of anterior instability, whereas pain reaching out to the side is often an indicator of biceps-related pain. If reaching across the body is problematic, AC joint arthritis should be considered.

PHYSICAL EXAMINATION When assessing a patient with “shoulder pain,” the examination should begin with a focused evaluation of the cervical spine to rule out an etiology of referred pain from the neck. First, the patient should be asked to fully flex, extend, and rotate his or her neck from side to side. Restrictions in motion may indicate the presence of cervical spondylosis. The presence of any tenderness along the cervical midline, paraspinal muscles, and trapezius should be assessed. Next, the “Lhermitte sign”1 is tested, in which there is a generalized electric shock sensation associated with axial compression of the cervical spine. The “Spurling test”2 is the most sensitive examination maneuver, in which radicular pain is exacerbated by extension and lateral bending of the neck toward the side of the lesion, which causes further neuroforaminal compromise. A detailed neurologic examination should also be performed to rule out a focal cervical radiculopathy. The assessment of the shoulder itself is then performed. The patient’s shirt must be removed to permit a thorough inspection of the entire affected shoulder girdle and to compare it with the opposite side. The evaluation begins by inspecting the sternoclavicular joint, clavicle, and acromioclavicular joint for evidence of prominence, swelling, deformity, or discoloration. Previous surgical incisions should be noted, as well as traumatic skin lesions, bruising, and muscular asymmetry. The pectoralis major muscles should be assessed for any asymmetry in their contours, which could indicate a rupture. The biceps muscle is inspected

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for any evidence of a Popeye deformity, indicating a torn long head of biceps tendon. Next, any evidence of atrophy in the deltoid muscle is noted, which could indicate a C5 radiculopathy or axillary neuropathy. It is important to also inspect the posterior aspect of the shoulder girdle. The presence of any atrophy in the supraspinatus and infraspinatus fossae can be diagnostic. For example, if there is evidence of muscle atrophy in the supraspinatus fossa alone, it may indicate the presence of a chronic tear of the supraspinatus tendon. If there is atrophy in both the supraspinatus and infraspinatus fossae, it could indicate a chronic tear of both the supraspinatus and infraspinatus tendons or entrapment of the suprascapular nerve at the level of the suprascapular notch. Isolated atrophy is in the infraspinatus fossa alone can indicate entrapment of the suprascapular nerve at the spinoglenoid notch, often from a paralabral cyst.3 Periscapular pathology is best assessed by asking the patient to actively raise his or her arms overhead while observing from behind. Evidence of scapular dyskinesis should be noted, as should evidence of scapular winging.4 If the medial border of the scapula becomes prominent with either forward elevation or doing a “push up against the wall,” the examiner should consider an injury to the spinal accessory nerve. Such an injury typically occurs during cervical lymph node biopsies. If the inferior border becomes prominent, injury to the long thoracic nerve is considered. Scapular winging can also contribute to symptoms of glenohumeral pain and instability. The examiner can confirm the contribution of the scapular dyskinesis to the patient’s presenting symptoms by compressing/stabilizing the scapula against the chest wall and asking the patient to again elevate the arm. If this maneuver diminishes the patient’s symptoms or improves active motion, it confirms the scapula as an etiology in the patient’s diagnosis. Next, palpation of the shoulder girdle should be performed in a systematic manner. The sternoclavicular joint should be palpated for evidence of tenderness or dislocation, followed by the clavicle and acromioclavicular joint. The biceps groove is then palpated just distal to the coracoid process with the arm in neutral rotation. The presence of tenderness typically indicates pathology of the long head of the biceps tendon or attachment of the subscapularis tendon to the lesser tuberosity. Posterior periscapular tenderness can be associated with muscle spasm (“trigger points”) and occasionally cervical radiculopathy. Medial periscapular and trapezial spasms are not uncommon in patients with large rotator cuff tears, adhesive capsulitis, glenohumeral arthrosis, and instability for whom scapulothoracic motion is often used to achieve forward elevation of the arm. Crepitance at the superomedial border of the scapula during active shoulder elevation is seen with scapulothoracic bursitis. An assessment of the patient’s active and passive range of motion (ROM) is then performed. Specifically, notation should be made of forward elevation, internal rotation, and external rotation. In throwing athletes, it is important to check external rotation at both 90 degrees of glenohumeral abduction, as well as adduction. The “total arc of motion” should then be compared with the opposite shoulder, noting the presence of deficits in elevation or rotation.

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Differences between active and passive motion can also indicate a potential diagnosis. If the patient has full passive motion but limited active motion, the presence of a large rotator cuff tear should be considered. If there is limited active and passive motion with a “firm end point,” adhesive capsulitis is often the etiology. If there is limited active and passive motion in the presence of glenohumeral crepitus or a “gear shifting” sensation, glenohumeral arthrosis is typically present. Excess passive external rotation is seen when there is a rupture of the subscapularis tendon. Strength testing is the next step in the examination of the shoulder. It is used to investigate the integrity of the rotator cuff or the presence of neurologic pathology. The neurologic motor examination of the upper extremity should be completed during the assessment of the cervical spine. At this stage, the supraspinatus muscle function is isolated by performing the “Jobe test” or “empty can” test.5 The shoulder is tested in the scapular plane with the elbow extended and with the shoulder in a position of 90 degrees abduction, 30 degrees flexion, and full internal rotation. The patient is asked to resist downward pressure on the forearm by the examiner. Especially in athletes, it is helpful to assess both arms at the same time to identify often subtle differences in strength. The more posterior rotator cuff muscles are tested by resisted external rotation with the arm adducted and in neutral rotation. Weakness in this position is often present with injury to the infraspinatus, whereas weakness in external rotation with the shoulder abducted and externally rotated indicates injury to the teres minor. It is important not to forget to examine the subscapularis while examining the rotator cuff and its strength. This is performed by the “lift-off,” “belly-press,” and “bear-hug” tests.6 The lift-off test is performed by placing the dorsum of the patient’s hand on his or her back and asking him or her to “lift it off.” The result can be difficult to interpret because patients will often use their triceps to perform this task. It can be more reliable for the examiner to lift the hand/arm away from the patient’s back instead, and ask the patient to hold it in that position. The bellypress test is performed by having patients place their hand on their abdomen, wrists in neutral position, and instructing the patients to keep their elbows forward as they press against their abdomen. Gentle pressure can be applied to the elbows to further assess strength. With this maneuver, the latissimus dorsi can substitute for the subscapularis function. The bear-hug test was developed to help isolate testing of the subscapularis.7 In this maneuver, patients are asked to place their hand on their opposite shoulder and resist the examiner as he or she starts to pull the elbow anteriorly. When the elbow is lowered, the upper subscapularis is tested. When the elbow is initially elevated, the lower subscapularis is tested. Lag signs were initially described by Hertel et al.8 They are used to help quantify the degree of rotator cuff tearing or dysfunction. The “external rotation lag sign” is performed by asking patients to maintain their arm in a position of maximal passive external rotation with their arm by their side. Any change in position of the arm after it is released by the examiner is then noted and typically indicates a large tear or atrophy of the infraspinatus. The same test is then performed with the shoulder

in a position of 90 degrees of abduction. This is called “hornblower’s sign” and is used to assess injury to the teres minor.9 The lift-off test is also considered a lag sign when testing the subscapularis. After strength has been tested, specialty tests are performed to narrow the diagnosis further. It is helpful to group the exam maneuvers by shoulder pathology. First, the subacromial space and rotator cuff are further assessed by the “Neer” and “Hawkins” impingement signs. The Neer test10 is performed by forward flexing the patient’s arm with the elbow extending and hand pronated. The presence of pain at maximal forward elevation is a sign of subacromial impingement, as seen with bursitis and rotator cuff tendinopathy. Hawkins test11 is sensitive for the presence of subacromial impingement and is tested by the examiner internally rotating the arm after placing it in 90 degrees of glenohumeral and elbow flexion. Shoulder instability is the next diagnostic category to be considered. The examiner needs to perform multiple specialty tests when evaluating for shoulder instability, given the large spectrum of pathology that can be present in patients with an unstable shoulder. Perhaps the most sensitive and pathognomonic test for anterior shoulder instability is the “apprehension test.” This test is best performed with the patient lying supine. In this position, patients tend to be less tense and relax their shoulder musculature to a greater extent. Once supine, the patient’s arm is abducted to 90 degrees and slowly externally rotated while the examiner also exerts a gentle and steady anteriorly directed pressure on the posterior aspect of the shoulder. A positive test is when the patient indicates a feeling of “apprehension” that his or her shoulder may dislocate if external rotation and anterior pressure continues. It is important to differentiate between an expression of true “apprehension” versus “pain,” because pain can be experienced in this position with other shoulder pathologies besides shoulder instability alone. The apprehension test is one of the most specific tests around the shoulder. It is difficult to assign a diagnosis of anterior instability in the absence of a positive apprehension sign. The “relocation test” can support the diagnosis of anterior instability. In this test, the examiner applies a posteriorly directed “relocation/reduction” pressure to the anterior aspect of the shoulder, which decreases the patient’s apprehension and often allows the arm to be further rotated without issue. The “posterior apprehension test” is performed with the patient supine or seated. The arm is forward flexed to 90 degrees and maximally adducted while the examiner applies a slight posteriorly directed axial load. The test is positive if the patient describes apprehension that the shoulder will dislocated. However, unlike the anterior apprehension test, the posterior apprehension test is much less sensitive for the presence of posterior instability. Because most patients with posterior instability seldom actually dislocate their shoulders posteriorly, there is typically not a learned “apprehensive” response to this position as is seen in anterior instability. Instead, a posterior “jerk test” is more sensitive to identify the presence of posterior instability. The examiner applies a posteriorly directed axial load to the arm in 90 degrees of flexion and full internal rotation while the arm is steadily adducted. A positive test is noted if the humeral head slides or

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“jerks” over the posterior glenoid rim. A jerk can also be noted upon reduction of the subluxated humeral head. The “load and shift test” is used to assess and describe both anterior and posterior humeral head translation in the glenoid fossa. The examiner should note whether the humeral head can be translated to the anterior glenoid rim or over the glenoid rim with the patient supine and the arm at 90 degrees of abduction. The test should be repeated with the arm at both 45 and 90 degrees of abduction. The examiner should then apply a posterior load and note the degree of posterior translation. It is important that the load and shift test also be performed on the contralateral shoulder, because findings can be subtle and difficult to interpret in isolation. The “sulcus sign” is performed to assess the degree of inferior instability and the integrity of the superior glenohumeral ligament and rotator interval. The examiner exerts an inferiorly directed pull on the arm with it placed at the patient’s side. The presence and size of a dimple or “sulcus” at the edge of the acromion is then noted. The sulcus should be eliminated when the test is repeated with the arm in a position of adduction and external rotation. A persistent sulcus indicates a greater degree of shoulder laxity, especially in the rotator interval. The presence and extent of labral tearing is further assessed by examining for injuries to the superior labrum. Although multiple tests have been described, the active compression test (“O’Brien test”) is typically regarded as the most sensitive and specific for a torn superior labrum.12 In this maneuver, the arm is placed in a position of 90 degrees forward flexion, 10 degrees adduction, maximum internal rotation, and elbow extension. The examiner exerts a downward pressure on the patient’s arm, and the presence of pain and/or weakness is assessed. The test is repeated with the hand and forearm maximally supinated. The test is positive if the patient describes feeling a “deep” pain that is relieved or eliminated when the hand is supinated. If pain persists with the hand fully supinated, it often is a sign of AC joint arthritis. AC joint pain can be confirmed by performing a “cross-body adduction test” in which the arm is then maximally adducted across the body and pain is elicited at the AC joint. The biceps tendon itself is tested by the “Speed test” and “Yergason test.”13 The Speed test is performed when the examiner exerts a downward pressure with the patient’s arm extended in 90 degrees of forward flexion and fully supinated. A painful response is indicative of pathology in the biceps groove. Less commonly, it can be positive in the setting of a superior labral tear. The Yergason test is performed with the patient’s arm by his or her side, the elbow flexed 90 degrees, and the forearm pronated. The patient is then asked to supinate the arm against resistance. Although this test is more sensitive for biceps pathology at the elbow, it can elicit pain in the biceps groove for patients with long head biceps tendon pathology as well.

DECISION-MAKING Referred Pain From the Neck The most common source of referred pain to the shoulder is cervical spine pathology. Of the various different anatomic diagnoses, the most commonly encountered are cervical strains,

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whiplash, cervical stenosis/spondylosis, cervical disc herniation, and “burners/stingers.”

Cervical Strain Cervical strains are typically the result of repetitive overuse or mild trauma. The patient can present with “shoulder pain,” which, upon further questioning, localizes to the trapezius and paracervical area posteriorly. The mechanism of injury is generally a forced motion or trauma that causes an eccentric contraction of the neck, such as a sudden twist or turn. Important to the history is a lack of true radicular or arm symptoms. On physical examination, there is tenderness over the paraspinal muscles and trapezius and an absence of positive provocative neurologic tests such as the Lhermitte sign or Spurling test. Diagnostic testing should include plain x-rays if there is a significant trauma, including lateral flexion/extension views. There is often a loss of cervical lordosis in the acute stage from paracervical spasm. MRI is seldom indicated in the absence of true radicular complaints, and symptomatic treatment can progress as tolerated. Whiplash A whiplash injury is a subset of cervical strains. The patient typically complains of posterior shoulder and neck pain but no arm pain. There is a history of forced flexion and extension of the cervical spine, typically following a motor vehicle accident. In this situation, a careful neurologic examination should be performed to rule out an acute radiculopathy from a herniated cervical disc or instability. Lateral flexion/extension views of the cervical spine should be obtained to rule out ligamentous instability. If present, advanced imaging including an MRI is indicated. Cervical Spondylosis/Stenosis Degenerative changes of the cervical spine can lead to symptoms of shoulder pain. There is seldom a recent history of trauma, although one may exist in the distant past. Unlike cervical strain injuries, patients with spondylosis often complain of both neck/ shoulder pain and radicular complaints that are worse with extremes of neck motion. On physical examination, the patient will have pain with cervical extension. There can be a positive Lhermitte sign, often with a generalized electric shock sensation associated with axial compression of the cervical spine. The Spurling test is the most sensitive examination maneuver, in which radicular pain is exacerbated by extension and lateral bending of the neck toward the side of the lesion, which causes further neuroforaminal compromise. A detailed neurologic examination should be performed, looking for dermatomal loss of sensation or motor weakness; and decreased biceps, triceps, or brachioradialis reflexes. Plain x-rays show hypertrophy of facet joints that cause central stenosis or foraminal encroachment. MRI is indicated when localizing neurologic signs are obtained on exam, such as dermatomal loss of sensation and weakness in the setting of radicular complaints. Cervical Disc Herniation Acute cervical disc herniations presenting as “shoulder pain” are relatively uncommon but do exist. The patient typically presents

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with a history of trauma that caused an acute hyperflexion of the cervical spine, followed by true radicular complaints. Less commonly, the disc herniation can cause a feeling of posterior shoulder pain and muscle spasm. Both the Lhermitte sign and Spurling test are generally positive, and an MRI is indicated for further treatment decision analysis.

Burners/Stingers A burner is an upper cervical root neurapraxia (reduction or block of conduction across a segment of nerve with conservation of underlying nerve function) most common at C5/C6. In sports such as football, the diagnosis of a burner or stinger often leads to the chief complaint of shoulder pain and weakness. The player’s head is forced to one side (lateral bend), and the contralateral shoulder is forced downwards; it is also seen with falls from a height. The player will give a history that “my arm went dead.” On examination, there is often weakness of shoulder abduction due to axillary nerve involvement at C5 and, less commonly, biceps or triceps weakness. What differentiates this injury from a disc herniation is that the symptoms typically clear after several seconds to minutes, with a complete return of sensation and strength. Plain x-rays are recommended to rule out fracture or instability. MRI is not usually indicated acutely, unless motor weakness does not improve after 24 hours.

Referred Pain From an Intrathoracic Source A rare but serious source of “shoulder pain” can be due to an intrathoracic etiology such as a hemothorax or pleural effusion. In this setting, there is irritation of the phrenic nerve, which has contributions from C3, C4, and C5 nerve roots. The C3 dermatome is located on the superior aspect of the shoulder. As a result, these patients can present with acute “shoulder pain.”

COMMON SHOULDER PATHOLOGIES Acromioclavicular Joint Pathology Patients with shoulder pain due to AC joint pathology present with a typical history and physical examination. The history should include whether or not there was a history of trauma, and if so, how did it occur? The AC joint is typically injured by a direct blow to the lateral aspect of the shoulder. The patient should then be asked to “place one finger where you feel the pain the most.” The patient will almost invariably point directly to the AC joint. On physical examination, there is tenderness at the AC joint, and pain can be elicited by cross-body adduction. If there is any question about whether the AC is the cause of the pain, a selective injection to the AC joint can be performed. Plain films are indicated in the presence of a traumatic injury to rule out fracture, AC joint widening, or dislocation. Weighted stress views are not typically needed. The x-rays will also help to classify an AC joint dislocation, which will have a direct effect on management decisions.14 Rockwood type 1 and 2 injuries are usually managed nonoperatively. Types 4, 5, and 6 are indications for surgery, whereas type 3 management can be operative or nonoperative. If the type of AC dislocation cannot be made on plain x-ray alone, a computed tomography (CT) scan may be considered.

Rotator Cuff Pathology Impingement Syndrome Impingement syndrome is one of the most common causes of shoulder pain. Anatomically, impingement syndrome includes pain caused by rotator cuff tendinitis, subacromial bursitis, and biceps tendinitis. Acromioclavicular arthritis also can contribute to symptoms of impingement in the presence of hypertrophic bone spurs. When considering the diagnosis of impingement syndrome, the most important question to ask the patient is their age. Primary impingement is seldom seen in patients less than 30 years of age. The patient should be asked if they have pain at night or with overhead activity, the primary complaints of patients with rotator cuff–related pain. There is usually a history of repetitive overhead activity; such as seen with throwers, tennis players, swimmers, painters, or electricians. On physical examination, there is a positive Neer sign and Hawkins sign. The patient may or may not have weakness on the “empty can test.” In this situation, an injection test is helpful to differentiate between simple impingement syndrome and a full-thickness rotator cuff tear. An injection test can be performed using a 25-gauge, 1.5′′ needle with 9 cc 1% lidocaine and with or without 1 cc steroid. A posterior approach is recommended, approximately 2 cm distal to posterolateral corner of the acromion. If the patient had pain and weakness prior to the injection but no pain or weakness afterwards, then there is not likely to be a torn rotator cuff. Plain x-rays alone are indicated to rule out arthritis or calcific tendinitis. On the other hand, if the patient’s pain is gone but he or she still has weakness, then an MRI is indicated to investigate a torn rotator cuff. Rotator Cuff Tear Continuing along the spectrum of rotator cuff pathology are rotator cuff tears. The tear can be partial thickness or full thickness, with size and chronicity of the tear playing a major role in the decision-making of the clinician. Classically, the patient has a history of pain at night and with overhead use. There is often a history of trauma but not always. On physical examination, Neer and Hawkins impingement signs are usually positive and there is weakness with supraspinatus (“empty can”) or external rotation resistance. There is a discrepancy between active and passive ROM for large and massive tears. In this setting, plain x-rays and an MRI are indicated. The MRI in particular is useful to help differentiate between partial- and full-thickness tears, labral tears, the presence of associated biceps lesions, the size of the tear, and whether any fatty atrophy of the rotator cuff is present. MRI also allows visualization of the subscapularis, which is often overlooked when evaluating patients with shoulder pain and weakness. Shoulder instability.  Shoulder instability is most commonly seen in patients younger than 25 years of age. It can result from both traumatic and atraumatic etiologies. Patients may present with a history of a single instability episode following an injury, or multiple subluxation events from a positional or even voluntary etiology. Shoulder instability occurs along a spectrum of severity. In fact, chief complaints of shoulder “pain” are more

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CHAPTER 37  Shoulder Diagnosis and Decision-Making

common than “instability.” To help make the diagnosis of shoulder instability, several specific questions are helpful. For example, “Does your shoulder feel loose?” or “Have you ever dislocated your shoulder?” can lead to an immediate diagnosis. In addition, “Do you avoid placing your arm in certain positions?” and “Do you have difficulty reaching behind you, throwing, or pushing open a heavy door?” can also help to determine if anterior or posterior instability is present. “Is it difficult to lift a heavy bag or suitcase?” also indicates whether an inferior or multidirectional component are present. On physical examination, the apprehension test is pathognomonic for anterior instability. The relocation test, in which the aforementioned apprehensive sensation is eliminated with posteriorly directed pressure on the joint by the examiner, helps to confirm the diagnosis. An anterior and posterior load test is similar to the Lachman test in the knee, in which a manual attempt to translate joint is performed. This test can be difficult to interpret, and a comparison to the contralateral shoulder can be helpful. Lastly, a “sulcus sign” can be performed. Imaging tests are mandatory when considering the diagnosis of shoulder instability. Plain radiographs are first performed to assess for osseous lesions of the humeral head and glenoid and to confirm that the joint is reduced following a trauma. Specific x-ray views should be considered. First, actual reduction of the glenohumeral joint can only be confirmed by obtaining an axillary view or transscapular Y-view. An anteroposterior (AP) view alone is not acceptable. A Stryker notch view will help to assess for the presence of a Hill-Sachs deformity, whereas a West Point view will identify a bony Bankart lesion. MRI is useful to identify labral tears, capsular tears, or subscapularis tears that are contributing to the instability problem. If bony lesions are present, the physician may consider a CT scan with or without threedimensional reconstructions to help determine whether an arthroscopic versus open approach to a shoulder stabilization is optimal. Adhesive capsulitis.  Adhesive capsulitis is most commonly seen in diabetic patients. Typically, there is an insidious onset of motion loss following a period of pain or “tendonitis.” Patients have a chief complaint of pain and restricted motion. Early in its course, the pain is often more severe than that seen in patients with rotator cuff tears, arthritis, or simple impingement. The natural history is typically 18 to 24 months to restore motion and decrease pain, if untreated. On physical examination, patients have restricted active and passive motion, as opposed to patients with a torn rotator cuff who have restricted active motion but full passive motion. A true AP x-ray and axillary view should be obtained to rule out osteoarthritis and calcific tendinitis. Superior Labrum, Anterior to Posterior tears. Superior Labrum, Anterior to Posterior (SLAP) tears typically occur after a history of an eccentric contraction of the biceps muscle. This mechanism is typically caused by a fall on an outstretched arm, or during the deceleration phase of throwing. Patients will present with a history of either anterior or posterior shoulder pain, “rotator cuff symptoms” such as pain at night and with overhead

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activity, and classically pain when reaching out to the side. There are multiple tests that have been described to test for a SLAP tear, but the active compression test (O’Brien test) is the most sensitive.15 MRI with or without contrast helps to confirm the diagnosis, while ruling out confounding pathology such as a torn rotator cuff. Glenohumeral arthritis. The shoulder is typically not a “weight-bearing joint.” Therefore shoulder arthritis is not as common as hip or knee arthritis. Patients with glenohumeral arthritis typically present with complaints of posterior shoulder pain, limited motion, and difficulty sleeping. On physical examination, patients have glenohumeral crepitus, with limited ROM. The diagnosis is confirmed by plain radiographs. Specifically, a true AP x-ray of the glenohumeral joint (“Grashey view”) is important, and an axillary view helps to confirm the diagnosis and assess for joint subluxation. “Shoulder pain” can be a complex complaint to evaluate. It should be remembered that shoulder pathologies can be present in tandem, with a multifactorial basis for the patient’s presenting complaints of pain and disability. An accurate diagnosis following injury to the shoulder requires a careful, focused history, a comprehensive physical examination, and judicious use of appropriate imaging modalities. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Neer CS. Impingement lesions. Clin Orthop Relat Res. 1983;173:70–77.

Level of Evidence: IV

Summary: Classic article describing the clinical and anatomic basis for impingement syndrome.

Citation: Hertel R, Ballmer FT, Lombert SM, et al. Lag signs in the diagnosis of rotator cuff rupture. J Shoulder Elbow Surg. 1996;5(4):307–313.

Level of Evidence: V

Summary: Original description of lag signs in the diagnosis of rotator cuff tears.

Citation: Lee S, Savin DD, Shah NR, et al. Scapular winging: evaluation and treatment: AAOS exhibit selection. J Bone Joint Surg Am. 2015;21(97):1708–1716.

Level of Evidence: V

Summary: Reviews the evaluation of different types of scapular winging and their treatment options.

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REFERENCES 1. Kempster PA, Rollinson RD. The Lhermitte phenomenon: variant forms and their significance. J Clin Neurosci. 2008;15:379–381. 2. Tong HC, Haig AJ, Yamakawa K. The Spurling test and cervical radiculopathy. Spine. 2002;27:156–159. 3. Freehill MT, Shi LL, Tompson JD, et al. Suprascapular neuropathy: diagnosis and management. Phys Sportsmed. 2012;40:72–83. 4. Lee S, Savin DD, Shah NR, et al. Scapular winging: evaluation and treatment: AAOS exhibit selection. J Bone Joint Surg Am. 2015;97:1708–1716. 5. Jobe FW, Jobe CM. Painful athletic injuries of the shoulder. Clin Orthop Relat Res. 1983;173:117–124. 6. Gerber C, Hersche O, Farron A. Isolated rupture of the subscapularis tendon. J Bone Joint Surg Am. 1996;78:1015–1023. 7. Barth JR, Burkhart SS, De Beer JF. The bear-hug test: a new and sensitive test for diagnosing a subscapularis tear. Arthroscopy. 2006;22(10):1076–1084. 8. Hertel R, Ballmer FT, Lombert SM, et al. Lag signs in the diagnosis of rotator cuff rupture. J Shoulder Elbow Surg. 1996;5(4):307–313.

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9. Walch G, Boulahia A, Calderone S, et al. The ‘dropping’ and ‘hornblower’s’ signs in evaluation of rotator cuff tears. J Bone Joint Surg. 1998;80:624–628. 10. Neer CS. Impingement lesions. Clin Orthop Relat Res. 1983;173:70–77. 11. Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med. 1980;8:151–158. 12. O’Brien SJ, Pagnani MJ, Fealy S, et al. The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med. 1998;26(5):610–613. 13. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231–236. 14. Rockwood C. AC joint injury: Rockwood classification. In: Rockwood CA, ed. Fractures in Adults. Lippincott-Raven; 1996:1341–1414. 15. McFarland EG, Kim TK, Savino RM. Clinical assessment of three common tests for superior labral anterior-posterior lesions. Am J Sports Med. 2002;30(6):810–815.

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38  Glenohumeral Joint Imaging Alissa J. Burge, Gabrielle P. Konin

CONVENTIONAL RADIOGRAPHY Conventional radiography is and should be the initial imaging examination performed for a patient presenting with shoulder pain. Although radiographs provide limited evaluation of the rotator cuff and glenoid labrum, they can offer important information about the source of the patient’s symptoms. Radiographs depict an assortment of osseous abnormalities, including fracture, arthritis, soft tissue calcifications, postsurgical changes, and tumor, and they are frequently complementary to more advanced imaging modalities, such as computed tomography (CT) and magnetic resonance imaging (MRI). A wide variety of radiographic views are available to aid in the evaluation of the glenohumeral joint. Knowledge about the advantages and disadvantages of each view will assist in optimizing imaging protocols, depending on the clinical presentation (Box 38.1).1–3

Anteroposterior View The anteroposterior (AP) view (Fig. 38.1A) is obtained with the patient in either the upright or the supine position. The beam is directed in a true AP direction relative to the body. The glenoid rim is normally tilted anteriorly about 40 degrees, which results in overlap of the humeral head and glenoid rim in the AP view. This view can be obtained with the humeral head in the neutral position, internal rotation, or external rotation. When compared with other radiographic views of the shoulder, the AP view provides the best overview of the osseous structures of the shoulder girdle because the projection allows for relatively uniform distribution of soft tissue density across the entire shoulder. As a result, one or more of the AP views is nearly always included in the standard radiographic evaluation of the shoulder. These projections allow for adequate evaluation of the humeral head, glenoid, and body of the scapula, as well as the acromioclavicular (AC) joint and coracoid process. The AP projection is very helpful in the evaluation after acute trauma for evidence of fracture or dislocation and is also of value in assessing the cause of chronic pain from arthritis, impingement, calcific tendinitis/bursitis, tumor, or infection.

Grashey View The Grashey view is a true or neutral AP view (see Fig. 38.1B), and differs from the standard AP view in that the patient is rotated posteriorly 35 to 40 degrees, thus providing a tangential view of the glenohumeral joint. The advantage of the Grashey 408

view is that it provides a superior evaluation of the glenohumeral joint. This view can demonstrate subtle subluxation in the superior or inferior direction and will show subtle joint space narrowing associated with glenohumeral arthritis. The disadvantage of this view is that a rapid change in soft tissue density occurs from medial to lateral, and as a result, the lateral aspect of the shoulder, including the acromion and AC joint, is difficult to evaluate because of a rapid change in density on the radiograph and loss of anatomic detail laterally. This loss can be decreased with use of a boomerang-shaped filter draped along the lateral shoulder.

Axillary Lateral View Variations of the axillary lateral view exist, but the projection is most commonly obtained with the patient supine and with the arm abducted 90 degrees (see Fig. 38.1C). The beam is then directed from distal to proximal while tilted 15 to 30 degrees toward the spine. This projection is best suited for evaluation of the joint space as well as anterior or posterior subluxation or dislocation. Bankart fractures of the anterior glenoid rim may also be detected. Numerous variations of this projection have been developed, some with the goal of decreasing movement of the arm in the setting of acute trauma (Velpeau view), and others with the intention of accentuating certain anatomic features. The West Point view is a variation of the axillary view developed to optimize visualization of an osseous Bankart lesion. It is obtained by placing the patient in the prone position on the x-ray table with the arm abducted 90 degrees from the long axis of the body and with the forearm draped over the edge of the top of the table. The beam is directed 15 to 20 degrees in an inferior-to-superior direction and tilted 25 degrees toward the spine. This projection improves the detection of osseous Bankart lesions but is very difficult to obtain in the setting of acute trauma and is best reserved for the patient in the setting of subacute or chronic instability.4

Scapular Y View The scapular Y view is easily obtained in the setting of acute trauma because it can be obtained with the arm immobilized by the side, and little or no movement of the arm is required (see Fig. 38.1D). This view can be very helpful in the setting of acute trauma to evaluate for anterior or posterior dislocation. The projection is obtained with the patient upright or prone and rotated approximately 30 to 45 degrees toward the cassette.

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CHAPTER 38  Glenohumeral Joint Imaging

Abstract

Keywords

Various imaging modalities, including conventional radiography, arthrography, magnetic resonance imaging, multidetector computed tomography, and ultrasound, are readily available for the musculoskeletal radiologist and clinician to evaluate, diagnose, and ultimately manage shoulder pain. Advances in imaging and overall improvements in quality allow for more accurate characterization of various shoulder pathology, thereby ultimately improving patient outcome.

imaging magnetic resonance imaging multidetector computed tomography ultrasound conventional radiography

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CHAPTER 38  Glenohumeral Joint Imaging

BOX 38.1  Common Radiographic Views of

the Shoulder

Anteroposterior (AP) view (external and internal rotation views) Grashey view (true or neutral AP view of the glenohumeral joint) Axillary view Scapular Y view Stryker notch view Zanca view

409

The beam is directed down the body of the scapula and results in a projection in which the body of the scapula is seen in tangent and the glenoid fossa en face as a Y-shaped intersection of the scapular body, coracoid process, and acromion process. It is also the projection commonly used when classifying the acromial morphology.

Stryker Notch View The Stryker notch view is best suited for viewing the posterolateral aspect of the humeral head and is an excellent radiographic

Clavicle Clavicle

Acromioclavicular joint Acromion process

Acromion process

Coracoid process

Coracoid process

Greater tuberosity Lesser tuberosity

Glenohumeral joint

Glenoid rim

A

B Clavicle

Clavicle

Coracoid Acromioclavicular joint

Acromion process

Glenoid rim Coracoid process Acromion

Humeral head

C Acromion process Scapular body Clavicle

Coracoid process

D Humeral head

Glenoid rim

E Fig. 38.1  (A) An anteroposterior (AP) view of the shoulder in external rotation. (B) An AP view of the glenohumeral joint (Grashey view). (C) An axillary view of the shoulder. (D) A scapular Y view of the shoulder. (E) A Stryker notch view of the shoulder.

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view for detecting a Hill-Sach’s defects when the patient has sustained a translational event (see Fig. 38.1E). However, it is very limited in its evaluation of the glenoid rim for osseous Bankart lesions. The Stryker notch view is obtained with the patient in either the upright or supine position. The arm is positioned vertically overhead with the elbow flexed and the hand supported on the back of the head. The beam is directed toward the mid axilla and is tilted about 10 degrees cephalad.

tissue contrast, multiplanar capabilities provided by MRI, and lack of exposure to ionizing radiation. MRI allows a global assessment of the painful shoulder, including the rotator cuff, labrum and capsular structures, osseous outlet, acromion, and articular surfaces. Bone marrow and muscle quality are readily evaluated with MRI without exposure to ionizing radiation. However, CTA is an effective alternative for patients who have contraindications to MRI.8–14

Acromioclavicular Articulation Views

Arthrography Technique

AC pathology is best evaluated with the patient either sitting or standing with the back flat against the cassette. The arms are usually freely hanging by the sides of the body. A Zanca view is the most accurate view to look at the AC joint, which is obtained by tilting the beam 10 to 15 degrees cephalad and centered over the AC joint with 50% of the standard shoulder AP penetration strength.5 The standard axial radiographic view of the shoulder is valuable to assess for a type III versus a type IV AC joint separation. The patient is infrequently asked to hold weights or sandbags to accentuate AC joint separation, and the value of this measure is questioned.6 Comparison with the contralateral AC joint can be helpful in detecting subtle abnormalities.

Although many variations in technique exist, a method for performing arthrography prior to MRI or CT begins with a review of prior radiographs and/or scout films to ensure identification of pertinent abnormalities. The patient is then placed supine on the fluoroscopic table with the arm positioned next to the body in slight external rotation and a point is chosen with fluoroscopic guidance overlying the lower third of the humeral head about 0.5 cm lateral to the medial cortex of the humeral head. An alternative anterior approach is through the rotator interval15 or a posterior approach.16 Knowledge of all three approaches allows for tailored techniques based on the clinical situation; for example, a posterior approach may permit more consistent visualization of the anterior capsular structures. The skin is prepared and draped in sterile fashion and the subcutaneous tissues are anesthetized with 1% lidocaine (Xylocaine) using a 25-gauge needle, which can be advanced into the joint. Rarely, a 22-gauge, 3.5-inch spinal needle is required in order to access the joint. A small amount of radiopaque contrast material is initially injected, which will outline the medial surface of the humeral head and spill into the subscapularis recess and axillary pouch (see Fig. 38.2B). A total injection volume of 12 to 14 mL provides adequate distention of the shoulder joint without undue discomfort. Most practices use an iodinated contrast agent for CTA and a dilute gadolinium solution for MRA. The contrast agent can be mixed with 0.1 to 0.3 mL of 1 : 1000 epinephrine

SHOULDER ARTHROGRAPHY Historically, conventional arthrography of the shoulder (Fig. 38.2) was considered the gold standard for diagnosis of tears of the rotator cuff.7 Conventional arthrography was then replaced with CT arthrography (CTA) and this technique provided a tool for assessing labral injuries associated with instability as well as cuff tears to a limited degree. Subsequently, CTA was largely replaced by MRI and magnetic resonance arthrography (MRA). The primary factors contributing to the shift from conventional arthrography and CTA to MRI/MRA are the superb soft

Su

Bi Ax

A

B Fig. 38.2  Normal shoulder arthrography. (A) Contrast material is seen within the glenohumeral joint. (B) Early contrast filling in a joint during an arthrogram. Note the absence of contrast material near the needle tip and the normal contour of the axillary pouch. This procedure was performed from an anterior approach over the lower third of the joint. Ax, Axillary recess; Bi, bicipital tendon sleeve; Su, subscapularis recess.

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CHAPTER 38  Glenohumeral Joint Imaging

to prolong retention of the contrast agent within the joint, thus allowing adequate time for transportation of the patient to the CT or MRI scanner and for imaging, which should be performed as soon as possible.

COMPUTED TOMOGRAPHY CT imaging of the shoulder is performed primarily as a means of evaluating the osseous structures after trauma. Multidetector CT utilizing isotropic data sets and post-processing techniques can accurately detect the extent of displacement and angulation of fracture fragments involving the humeral head and neck. The

A

C

411

scapula is a complex anatomic structure composed of the body, coracoid and acromion processes, and the glenoid with its articular surface. Following a glenohumeral translational event, CT and three-dimensional volume rendered imaging are useful for presurgical planning in order to accurately depict the extent of glenoid bone loss of an osseous Bankart and the magnitude of a Hill–Sachs defect (Fig. 38.3).17–20

ULTRASONOGRAPHY Sonography of the shoulder (Fig. 38.4) is a noninvasive, accurate and cost-effective method for a dynamic evaluation of the

B

Fig. 38.3  An osseous Bankart lesion demonstrated on a computed tomography scan of the shoulder. (A) An axial computed tomographic image shows a large osseous Bankart lesion with a slightly displaced and comminuted fracture fragment (arrow) involving the inferior glenoid rim. (B) Sagittal reconstruction shows the size of the osseous defect (arrows) of the inferior glenoid rim. (C) A three-dimensional reconstruction shows the relationship of the fracture fragment (short arrows) with the glenoid rim osseous defect (long arrows).

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A

C

B

Fig. 38.4  Paired ultrasound and magnetic resonance images. (A) A short axis ultrasound image of the normal long head of the biceps tendon (B) and subscapularis tendon (SSc) with corresponding axial fast spin echo (FSE) image. (B) A long axis ultrasound image of the supraspinatus tendon (SSp) and acromion (A) with corresponding oblique coronal FSE image. (C) A short axis ultrasound image in the sagittal plane depicting the infraspinatus (Isp), supraspinatus and biceps tendons with corresponding oblique sagittal FSE image. D, Deltoid.

rotator cuff and is a superb means for guided injections about the shoulder.21–25 Ultrasound examination of the shoulder requires a high-resolution linear transducer (6 to 15 MHz) and is performed with the patient in the sitting position. The tendons of the rotator cuff and the long head of the biceps should be evaluated in both the long and short axes. The examination begins with the arm positioned by the side and externally rotated for evaluation of the biceps long head tendon. In this position, the subscapularis can be evaluated with the elbow flexed 90 degrees and externally rotated. The infraspinatus is imaged with the arm adducted and the hand on the opposite shoulder. For evaluation of the supraspinatus, the shoulder is rotated internally, and the arm is placed behind the back, which allows the critical portion of the supraspinatus tendon to glide from beneath the acromion, allowing maximal visualization of this portion of the rotator cuff.26 The normal rotator cuff is sharp and uniform in its fibrillar echotexture. It measures 4 to 6 mm in thickness anteriorly, and is normally somewhat thinner posteriorly.22 A thin echogenic band paralleling the upper surface of the cuff reflects the subacromial– subdeltoid bursa. The overlying deltoid is characterized by the typical striated/marbled echogenicity of muscle that is distinct from the normal overlying tendons (Table 38.1). Although sonography of the rotator cuff has been shown to be as accurate as MRI in the evaluation of the rotator cuff tendons,27–29 sonographic evaluation of the shoulder has a steep learning curve and is operator dependent.30 MRI has, in its favor, a more global evaluation of the shoulder, including the labrum and osseous structures, which has led to the use of MRI in most practices.

TABLE 38.1  Sonographic Imaging Signs of

Rotator Cuff Disease Type of Disease

Imaging Signs

Tendinosis

Heterogeneous echogenicity of the tendon with loss of fibrillar architecture; may be thickened or thinned Difficult, but may see focal thinning of tendon Focal full-thickness discontinuity/absence of the cuff Band of anechoic/hypoechoic fluid superficial to cuff ± power Doppler hyperemia

Partial-thickness tear Full-thickness tear Subacromial subdeltoid bursitis

MAGNETIC RESONANCE IMAGING MRI provides comprehensive evaluation of the shoulder, combining superior soft tissue depiction with the ability to simultaneously evaluate osseous pathology. MRI of the shoulder is best performed at 1.5 or 3.0 Tesla (T) utilizing a dedicated surface coil, and images are typically obtained in the axial, oblique coronal, and oblique sagittal planes relative to the anatomic axis of the shoulder (Fig. 38.5). Specific protocols vary by institution, but optimally should include a combination of pulse sequences allowing for both sensitive detection of mobile water and highresolution evaluation of anatomy. At the authors’ institution, routine shoulder imaging sequences consist of a single oblique coronal fat suppressed image (inversion recovery [IR] or T2 with fat saturation), followed by oblique coronal, axial, and oblique sagittal moderate echo time fast spin echo (FSE) images in the axial, oblique coronal, and oblique sagittal planes (Table 38.2).

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CHAPTER 38  Glenohumeral Joint Imaging

A

B

C

D

413

Fig. 38.5  Sample routine shoulder magnetic resonance imaging protocol, consisting of (A) oblique coronal T2 with fat saturation, (B) oblique coronal proton density, (C) axial proton density, and (D) oblique sagittal proton density.

TABLE 38.2  Sample Acquisition

Parameters for Routine Clinical Imaging of the Shoulder at 1.5 Tesla

Parameter

Coronal Fast IR

Oblique Coronal FSE

Oblique Sagittal FSE

Axial FSE

TR (ms) TE (ms) TI (ms) BW (kHz) ETL NEX FOV (cm) Matrix Slice/gap (mm) NPW Frequency

5000 17 150 31.25 7 2 16 256 × 192 3/D Yes R/L

4000 34 na 31.25 10 2 16 512 × 3S4 3/0 Yes R/L

4000 34 na 31.25 10 2 16 512 × 224 4/0.5 Yes A/P

4000 34 na 31.25 9 2 15 512 × 384 3.5/0 Yes R/L

A/P, Anterior to posterior; BW, receiver bandwidth; ETL, echo train length; FOV, field of view; FSE, fast spin echo; IR, inversion recovery; na, not applicable; NEX, number of excitations; NPW, no phase wrap; R/L, right to left; TE, echo time; TI, time to inversion; TR, repetition time.

Specialized MRI techniques may be useful for certain applications. For reduction of motion artifact in patients who are unable to remain still during pulse acquisition, the periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) pulse sequence, utilizing radial sampling of parallel data lines rotating about the center of K space, reduces the severity of motion artifact, thereby improving image quality and diagnostic yield.31 MRI of the postoperative shoulder requires knowledge of the surgical intervention performed, in order to allow the implementation of proper pulse parameter modifications if necessary, such as in the presence of extensive metallic hardware. When utilizing conventional pulse sequences in the presence of metal, techniques that may be used to decrease artifact include widening the receiver bandwidth, aligning the frequency encoding axis along the long axis of the implant, and oversampling in the frequency direction. Additional improvement in image quality may be obtained by decreasing the voxel size and increasing the number of excitations. Because the artifact generated by a particular metal implant increases with field strength, imaging at higher field strengths, such as 3.0T, should be avoided. Additionally,

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frequency selective fat suppression methods should be avoided in favor of methods that are less frequency dependent (e.g., short tau inversion recovery [STIR]) and therefore more robust in the presence of field inhomogeneities that occur in the vicinity of metal hardware.32,33 In the setting of large metallic implants, specialized pulse sequences designed to significantly reduce metal artifact may be employed. These include multiple acquisition variable resonance image combination (MAVRIC) and slice encoding metal artifact correction (SEMAC). MAVRIC utilizes multiple acquisitions at varying off-resonance spectral frequency bins, which are subsequently postprocessed to create images with significantly reduced susceptibility artifact. SEMAC utilizes view angle tilting plus the addition of a phase encoding step in the Z axis, resulting in extremely robust spatial encoding which diminishes the amount of artifact.32,34 Evaluation of early chondral degeneration may be performed using quantitative parametric MRI techniques, which have been demonstrated to correlate to early changes in chondral matrix elements, including proteoglycan and collagen, prior to the development of gross morphologic changes visible on routine conventional imaging sequences. These techniques include T2 mapping, which is sensitive to changes in collagen orientation and free water content, and spin lattice relaxation in the rotating frame (T1 rho), which is sensitive to depletion of proteoglycan. Delayed gadolinium enhanced MRI of cartilage (dGEMRIC) is an additional biomarker for proteoglycan depletion, though requires the intravenous administration of gadolinium-based contrast material.35,36 While CT remains the gold standard for high resolution evaluation of mineralized bone, newer “silent” magnetic resonance (MR) techniques, such as zero TE imaging, allow evaluation of bone with CT-like contrast concurrently with the acquisition of routine clinical MR sequences, obviating the need for a separate imaging study and a dose of ionizing radiation, though these sequences are not yet in widespread clinical use.37 MRA: While some authors have described an advantage in detecting chondral and labral pathology following the intraarticular administration of gadolinium contrast material, others have achieved statistically equivalent or superior sensitivity and specificity utilizing optimized high resolution noncontrast techniques.38 The accuracy of MRA versus noncontrast MRI depends largely upon the experience and preference of the interpreting radiologist, and therefore the viewpoint of which technique is optimal in a given situation will often depend on the convention of a particular institution. At the authors’ institution, high resolution noncontrast imaging is preferred, given its ability to reliably detect chondral and labral lesions while simultaneously allowing direct visualization of the synovium and evaluation of chondral signal changes in the setting of early degeneration without a frank chondral defect.

IMAGING OF SPECIFIC SHOULDER ABNORMALITIES

various pulse sequences. The following sections provide a systematic approach for MRI evaluation as the imaging basis for recognizing common pathologic processes; when appropriate, complementary imaging modalities are discussed. The important structures that must be thoroughly evaluated on each MRI examination include the osseous structures (outlet and acromion), the rotator cuff muscles and tendons, the biceps tendon and rotator interval, and the labrum (capsular structures and articular surfaces).

Osseous Outlet and Acromion The clinical syndrome of shoulder impingement refers to a painful compression of the soft tissues of the anterior shoulder (i.e., the rotator cuff, subacromial bursa, and bicipital tendon) between the humeral head and the coracoacromial arch (i.e., the coracoid process, acromion, coracoacromial ligament and AC joint).39–41 Pain occurs when the arm is elevated forward and internally rotated or placed in the position of abduction and external rotation.40 In the normal shoulder, the upward pull of the deltoid on the proximal humerus is resisted by an intact rotator cuff so that the humeral head remains centered on the glenoid in all ranges of motion. If this stabilizing mechanism becomes weakened as a result of trauma, overuse or age, the humeral head is pulled upward under the structures of the coracoacromial arch. Impingement is initially followed by subacromial bursitis and rotator cuff tendinopathy. Over time, irreversible cuff trauma occurs with fibrosis and degeneration. In the latter stages, subacromial enthesophyte tends to form at the anteroinferior margin of the acromion where the coracoacromial ligament attaches (Fig. 38.6). Tears of the rotator cuff are frequent in this stage, undoubtedly in part because of direct cuff trauma from the spur. After massive tears of the rotator cuff, the humeral head typically migrates anterosuperiorly and chronic impaction with the undersurface of the anterior acromion results in sclerosis and proliferative changes—acetabularization. Neer (1983) introduced the term impingement syndrome and described three stages with the rotator cuff disorder.41 The

A

Interpretation of a shoulder MRI examination requires the evaluation of images obtained in several imaging planes and with

B

Fig. 38.6  Subacromial spur. (A) Grashey and (B) scapular Y views of the shoulder. The arrowheads point to the spur emanating off the anteroinferior acromion.

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diagnosis of impingement syndrome is usually made clinically on the basis of appropriate historical and physical examination findings. A thorough history and physical examination by an experienced physician have an 84% to 90% sensitivity and a 75% to 95% specificity for diagnosis of a tear of the rotator cuff.42–44 Many imaging modalities are available to assist in the evaluation of the progressively painful shoulder, and their role is both to assess the extent of abnormality of the rotator cuff and to identify configurations of the osseous outlet that may predispose to rotator cuff impingement. The osseous changes that occur with impingement are seen late and thus offer little in establishing an early diagnosis and preventing progression of the associated soft tissue injuries. The following osseous abnormalities may be associated with the clinical syndrome of impingement40,45–47: • Enthesophyte formation on the anteroinferior aspect of the acromion • A long anterior portion of the acromion with downward sloping of the acromion • An os acromiale that is not fused • AC joint arthrosis with hypertrophy Optimal conventional radiographic views have been described for identifying these variations of the osseous outlet.48,49 The AP radiograph at a 30-degree caudal angle is helpful in visualizing the anterior aspect of the acromion and in detecting inferiorly directed enthesophytes. A modified transcapular lateral view obtained with 10 to 15 degrees of caudal angulation (the supraspinatus outlet view) helps further identify the anteroinferior aspect of the acromion (see Fig. 38.6). A high-riding humeral head with remodeling of the undersurface of the acromion and sclerosis of the greater tuberosity are conventional radiographic findings (Fig. 38.7) that are pathognomonic of a chronic rotator cuff insufficiency.

Magnetic Resonance Imaging of the Osseous Outlet and Acromion The multiplanar capabilities of MRI and its ability to demonstrate the relationship of the entire osseous outlet to the underlying rotator cuff allow excellent assessment of the outlet. Bigliani45 described three different radiographic acromial shapes (Fig. 38.8) and related the configuration of the undersurface of the acromion to the presence of rotator cuff tears. A type I acromion (see Fig. 38.8A) has a flat undersurface, a type II acromion (see Fig. 38.8B) has a curved undersurface, and a type III acromion (see Fig. 38.8C) has an anterior hook. The acromial types II and III have an increased association with rotator cuff tears.45,47 A type IV acromion with a convex undersurface has been described, but no definite correlation has been shown to exist between type IV acromion and impingement (see Fig. 38.8D).50 On MRI, the shape of the acromion is best assessed on the oblique sagittal view just lateral to the AC joint. However, one study suggests poor correlation of acromial arch shape between conventional radiography and MRI.51 Another study found no association between rotator cuff tears and the acromial structure.52 A third study reported poor interobserver agreement between radiographs and MRI scans at the categorization of the acromial shape.53

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Fig. 38.7  Acromiohumeral interval. Frontal radiograph demonstrates superior migration of the humeral head and loss of the acromiohumeral interval with early acetabularization of the acromion indicating rotator cuff insufficiency. Mild glenohumeral osteoarthritis is evident.

Downward sloping of the acromion can also narrow the supraspinatus outlet and potentially result in impingement,54,55 and is best seen on the oblique coronal images (Fig. 38.9). An enthesophyte (Fig. 38.10) extending off the anteroinferior aspect of the acromion also can be clearly demonstrated on MRI. It typically appears as a marrow-containing osseous excrescence. Potential pitfalls include the attachment of the coracoacromial ligament and the anterolateral acromial attachment of the deltoid (see Fig. 38.10). These structures may mimic an osseous excrescence, but they can be differentiated from enthesophytes by correlating with concurrent radiographs and because they lack marrow signal and appear dark on all pulse sequences. The acromion should also be evaluated for an os acromiale, which is an accessory ossification center along the outer edge of the anterior acromion. It is normally fused by 25 years of age. An association exists between persistent os acromiale and impingement of the rotator cuff.56–59 The deltoid muscle attaches to the inferior aspect of the accessory ossicle, and contraction of the deltoid results in a downward motion of the unstable segment, potentially leading to impingement of the underlying rotator cuff (Fig. 38.11). Os acromiale are demonstrated best on axial MR images.60 MRI signs of instability of the os acromiale include fluid signal within the synchondrosis as well as sclerosis, cystic change, and marrow edema on either side of the synchondrosis (Box 38.2). Hypertrophic changes of the AC joint capsule and inferiorly directed osteophyte formation (Fig. 38.12) can also be associated with impingement.40 MRI is useful to evaluate for mass effect

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A

B

C

D

Fig. 38.8  Acromial morphology. Oblique sagittal fast spin echo images of the acromion lateral to the acromioclavicular joint. (A) A type I acromion demonstrates a flat undersurface (arrow). (B) A type II acromion has a gentle curvature to the undersurface of the acromion (arrows). (C) A type III acromion demonstrates a hook (arrow) extending off the anterior aspect of the acromion. (D) A type IV acromion demonstrates a curved acromial undersurface (arrow).

Fig. 38.9  Acromial downward sloping. An oblique coronal fast spin echo image demonstrates anterolateral downward sloping of the acromion (black arrowhead) resulting in mild mass effect upon the underlying supraspinatus muscle (arrow), which shows mild increased signal intensity. Anterolateral acromial origin of the deltoid (white arrowhead).

Fig. 38.10  Subacromial enthesophyte. Sagittal oblique fast spin echo (FSE) image demonstrates a marrow containing osseous excrescence extending off the anterior acromion (arrowhead). Note that an enthesophyte contains marrow signal that is high to intermediate in signal on FSE images, which differs from the coracoacromial ligament attachment, which is of low signal intensity on all pulse sequences.

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A

417

B

C Fig. 38.11  (A) Axillary radiograph depicts an os acromiale and its synchondrosis with the acromion. (B) Axial fat-suppressed T2-weighted image demonstrates an os acromiale with degeneration at the synchondrosis and increased signal on either side of the synchondrosis suggesting instability. Note the chondral denudation over the acromioclavicular (AC) joint and effusion. (C) Oblique coronal fast spin echo image shows severe narrowing of the acromiohumeral interval and a chronic full-thickness supraspinatus tendon tear with retraction of the tendon medial to the glenoid. Os acromiale (*), synchondrosis (arrows), AC joint (arrowheads).

BOX 38.2  Magnetic Resonance Imaging

Findings of the Acromion Associated With Extrinsic Impingement Acromion type—assessed on the oblique sagittal sequences on the image immediately lateral to the acromioclavicular joint: • Type I: Flat undersurface • Type II: Curved undersurface • Type III: Anterior hook • Type IV: Convex undersurface Downward sloping—assessed on sagittal and coronal oblique sequences Acromial spur—assessed on sagittal and coronal oblique fast spin echo sequences (fatty marrow signal within the bony excrescence differentiates a spur from the deltoid tendon slip or coracoacromial ligament) Unfused os acromiale—best assessed on axial images (fluid signal within the synchondrosis suggests instability)

on the underlying rotator cuff. The coracoacromial ligament (Fig. 38.13), a soft tissue structure that forms part of the coracoacromial arch extends from the coracoid to the acromion and is well seen on oblique sagittal MR images. It normally measures less than 2 mm in thickness and extends across the rotator interval and anterior aspect of the supraspinatus tendon. The role of the coracoacromial ligament in impingement remains controversial; some believe that thickening or ossification of the ligament may

be a potential cause of impingement, whereas others believe that thickening results from impingement.61,62 Coracohumeral impingement, also referred to as subcoracoid or coracoid impingement, is an uncommon cause of extrinsic impingement that results from a narrowed distance between the coracoid process and the underlying humeral head (Fig. 38.14). Lo and Burkhart63 suggested using an interval less than 6 mm to make the diagnosis at arthroscopy. On axial images, the normal interval is approximately 10 mm. A narrowed coracohumeral distance may result in entrapment of the subscapularis tendon between the coracoid process and the humeral head, and can lead to isolated tendinosis and disruption of the subscapularis tendon. Abnormalities isolated to the subscapularis tendon should prompt an investigation of the coracohumeral distance and consideration of this diagnosis.64,65 However, after reporting on a small series of patients with subcoracoid impingement at arthroscopy and control subjects, Giaroli et al.65 concluded that subcoracoid impingement is primarily a clinical diagnosis that may be supported with imaging.

Rotator Cuff The rotator cuff is composed of four tendons: the supraspinatus superiorly, the subscapularis anteriorly, and the infraspinatus and teres minor posteriorly. These tendons are important dynamic stabilizers of the glenohumeral joint. Most cuff failures originate

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Fig. 38.12  Osteoarthritis of the acromioclavicular joint. A sagittal oblique fast spin echo image shows bony and capsular hypertrophy with an inferiorly directed spur resulting in mass effect upon the supraspinatus muscle tendon junction (arrowhead).

in the supraspinatus tendon at or near its insertion onto the greater tuberosity of the humeral head. The supraspinatus tendon receives its arterial supply from the anterior humeral circumflex, subscapular, suprascapular, and posterior humeral circumflex arteries.66–68 A zone of relative avascularity has been described in the tendon proximal to its attachment site and may represent a “critical zone” for cuff failure.66,67 Other authors have found this zone to be vascularized by anastomosing vessels from the tendon and humeral tuberosity.69 Arterial filling of the cuff vessels in the critical zone depends on the position of the arm; poor filling is present when the arm is adducted.67 A high correlation also has been shown to exist between rotator cuff tears and subacromial impingement.41 It is probably a combination of avascularity and subacromial impingement that leads to most rotator cuff abnormalities originating in the critical zone of the supraspinatus tendon. Conventional radiography only plays a limited role in the direct evaluation of the rotator cuff, although it is frequently the initial imaging study performed for patients with the clinical syndrome of impingement. Radiographs allow identification of associated pathologic change, especially of the osseous outlet and acromion. Conventional radiography findings associated with cuff pathology include the following3,70: • Enthesopathic changes at the cuff footprint on the humeral head • Calcific tendinopathy/bursitis

Fig. 38.13  Coracoacromial ligament. An oblique sagittal fast spin echo image demonstrates a normal coracoacromial ligament (arrowhead) extending from the coracoid process to the anterior acromion. The normal ligament measures less than 2 mm in thickness.

Fig. 38.14  Subcoracoid impingement. An axial fast spin echo image at the level of the coracoid process (white arrowhead) demonstrates narrowing of the coracohumeral interval with attenuation of the superior fibers of the subscapularis. Lesser tuberosity (*).

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• A high-riding humeral head with an acromiohumeral interval less than 7 mm is associated with rotator cuff insufficiency • Remodeling of the acromial undersurface to frank acetabularization

TABLE 38.3  Magnetic Resonance Imaging

Magnetic Resonance Evaluation of the Rotator Cuff The normal anatomy of the rotator cuff is accurately depicted with MRI. The subscapularis is located anteriorly and has multiple tendon slips. It has a broad origin along the anterior aspect of the scapula and attaches to the lesser tuberosity on the anterior aspect of the humeral head. An extension of the subscapularis tendon known as the transverse ligament extends across the intertubercular groove and helps to stabilize the long head of the biceps tendon within the intertubercular groove. The subscapularis muscle and tendon are best evaluated on axial and oblique sagittal MRI. The supraspinatus muscle originates along the posterosuperior portion of the scapula above the level of the scapular spine. A single tendon arises out of the muscle and extends superiorly above the humeral head to insert onto the greater tuberosity of the humeral head. The supraspinatus tendon is best evaluated in the oblique coronal and oblique sagittal MRI planes. The infraspinatus is located posterosuperiorly and has a broad origin along the posterior aspect of the scapula inferior to the scapular spine. The teres minor is located posteroinferiorly, below the level of the infraspinatus, originating along the axillary surface of the scapula and inserting on the most inferior aspect of the greater tuberosity of the humeral head. The infraspinatus and teres minor are best evaluated on oblique coronal and oblique sagittal images. The normal tendons demonstrate a uniformly dark signal intensity on all pulse sequences; increased signal on FSE sequences is a nonspecific finding that may represent a wide array of conditions ranging from artifact to a complete tear. T2-weighted images with fat suppression have a lower signal/noise ratio and provide less anatomic detail, but they are both sensitive and specific for depicting the full range of rotator cuff abnormalities. When increased signal is identified on FSE images, the morphologic features of the tendon and the T2-weighted images should be evaluated.42 A normal appearance of the tendon and normal signal intensity on T2-weighted images suggest that the tendon is probably normal. It is important to be aware of the magic angle effect, an MRI artifact likely to occur in the critical zone of the supraspinatus tendon, occasionally causing confusion about the tendon integrity. This MRI artifact results in increased signal in normal tendons that are angled 55 degrees relative to the direction of the main magnetic field. It occurs primarily on short TE sequences (proton density, T1 and GRE), and as echo time lengthens with T2 weighting, the signal intensity decreases. A wide spectrum of rotator cuff pathology can be accurately depicted on MRI, ranging from tendinosis to a full-thickness tear of the rotator cuff (Table 38.3). Tendinosis is noted as intermediate to high signal on FSE sequences, which does not reach the same brightness as fluid signal (Fig. 38.15). The tendon may demonstrate attritional wear or diffuse or focal thickening, but no evidence of tendon disruption will be seen. Tendinosis represents a degenerative process of the tendon, which histologically represents a combination of inflammation

Normal tendon Tendinopathy

Appearance of Rotator Cuff Pathology Cuff Pathology

Calcific tendinosis

Partial-thickness tear Full-thickness tear

Musculotendinous retraction Fatty atrophy

Magnetic Resonance Imaging Appearance Low signal on all pulse sequences Intermediate signal on fast spin echo sequences Thickening or attenuation of the tendon Globular low signal on all pulse sequences within the tendon Surrounding edema signal Fluid signal extending partially through the thickness of the tendon Intramuscular cyst Fluid signal extending completely through tendon superior to inferior Discontinuity of the tendon, often with a gap and retraction of the tendon Measured as the length of the medial-to-lateral tendon gap Graded as mild, moderate, or severe Streaks of high signal on fast spin echo sequences and low signal on fat suppressed images: irreversible Loss of muscle bulk: reversible

Fig. 38.15  Supraspinatus tendinosis. An oblique coronal fast spin echo image reveals mild thickening of the supraspinatus tendon, as well as increased signal intensity (arrowhead) arising from the tendon adjacent to its attachment site on the greater tuberosity, but without fluid signal intensity.

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and mucoid degeneration.71 On arthroscopic examination, the tendon may appear to be edematous and hyperemic, with occasional fraying, roughening, or degeneration of the surface of the tendon. At times, it may be difficult to differentiate tendinosis from early partial-thickness tearing both at arthroscopy and on MRI; however, with quality improvements in image acquisition protocols and scanners, the performance of detecting rotator cuff injuries by radiologists is improved.72 Partial-thickness tears (Figs. 38.16–38.18) can occur on either the articular or bursal surface or within the substance of the tendon. A partial-thickness tear is seen on MRI as fluid signal intensity, which extends only partially through the thickness of the tendon from superior to inferior. Tendon tears may partially

A

B

Fig. 38.16  Articular-sided tear. (A) Coronal oblique T2-weighted fatsuppressed and (B) coronal oblique fast spin echo images demonstrate a high-grade partial-thickness, articular-sided supraspinatus tendon tear with mild retraction of tendon slips. Overlying subacromial bursitis is present.

A

B

heal with granulation tissue resulting in scar continuity, making them difficult to distinguish from tendinosis on MRI as they demonstrate intermediate to high signal as opposed to fluid signal. It has been suggested that the detection of partial-thickness articular-sided tears can be improved by adding an abduction external rotation view.73 Articular surface tears are the most common type to occur (see Fig. 38.16). A partial articular-sided supraspinatus tendon avulsion lesion is a subset of partial-thickness tears (PASTA).74 The tear represents a partial-thickness articular-sided avulsion of the supraspinatus tendon, typically at its most anterior attachment site and deserves special attention as one study demonstrated the progression of this type of tear in 80% of the patients, suggesting that early surgical treatment should be considered.75,76

B

A

Fig. 38.17  Bursal-sided tear. (A) Coronal oblique T2-weighted fat-suppressed and (B) coronal oblique fast spin echo images show a bursal-sided, partial-thickness tear involving the superficial fibers of the supraspinatus tendon (arrowhead).

C

Fig. 38.18  Intrasubstance tear. (A) and (B) Coronal oblique T2-weighted fat-suppressed and fast spin echo (FSE) images show a small fluid signal partial interstitial attachment tear in the supraspinatus tendon. (C) Coronal oblique FSE image in a different patient demonstrates medial delamination of a small intrasubstance tear. Note that both the articular- and bursal-sided fibers are intact in both patients.

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Fig. 38.20  Full-thickness tear. (A) Coronal fast spin echo and (B) axial fast spin echo images demonstrate a full-thickness tear of the subscapularis tendon allowing for medial intra-articular destabilization of the long head of the biceps tendon (arrowhead).

Fig. 38.19  Full-thickness tear. A coronal oblique fast spin echo image shows a full-thickness supraspinatus tendon tear at the critical zone with a stump of tendon remaining attached to the greater tuberosity and without medial retraction of the torn fibers. Note also the prominent subacromial spur with thickening of the coracoacromial ligament attachment (low in signal intensity) and a lateral downslope of the acromion.

On MRI, an articular-sided avulsion is seen as fluid signal at the footprint with extension along the articular surface of the supraspinatus tendon. Bursal tears affect the superficial fibers of the tendon (see Fig. 38.17). Intrasubstance tears of the rotator cuff do not involve the bursal or the articular surface (see Fig. 38.18) and appear as a linear fluid signal contained within the substance of the tendon, which typically occurs at the footprint. A full-thickness tear of the rotator cuff tendon is defined as a tear that extends through the complete thickness of the tendon from superior to inferior. This tear allows communication between the joint space and the subacromial-subdeltoid bursa. MRI criteria for establishing the diagnosis of a full-thickness tear include high signal to fluid signal completely traversing the tendon from superior to inferior on FSE images, a gap or absence of the tendon, and retraction of the musculotendinous junction (Fig. 38.19). Many cuff tears originate in the supraspinatus tendon and large tears may extend into either the infraspinatus or subscapularis tendon. An isolated tear of the infraspinatus tendon is usually associated with the internal impingement syndrome (discussed further in the section on glenohumeral instability). An isolated tear of the subscapularis (Fig. 38.20 and Fig. 38.21) tendon may result from shoulder dislocation or in association with coracohumeral impingement,77 and is best demonstrated on axial MRI as high signal traversing the tendon with medial retraction of the tendon from the lesser tuberosity. An extension of the subscapularis tendon, known as the transverse ligament, holds the long head of the biceps tendon in the intertubercular groove;

Fig. 38.21  Intrasubstance tear. Axial fast spin echo image demonstrates an intrasubstance tear of the subscapularis tendon allowing for medial destabilization of the biceps tendon into the substance of the subscapularis.

disruption of these fibers can lead to medial destabilization of the long head of the biceps tendon.78 Depending on the type of subscapularis tendon tear, the biceps tendon may be displaced superficial to, deep to, or within the substance of the tendon. An intramuscular cyst within the rotator cuff (Fig. 38.22) has been described as a finding associated with small full-thickness or partial-thickness tears of the rotator cuff.79 Intramuscular cysts are similar to paralabral cysts of the shoulder or meniscal cysts of the knee. Fluid leaks through a defect in the cuff and tracks in a delaminating fashion along the fibers of the tendon, resulting in a fluid collection contained within either the muscle or fascia of the rotator cuff. They appear as lobulated fluid collections within the rotator cuff and should prompt a thorough search for a small associated cuff tear. Calcific tendinitis (hydroxyapatite crystal deposition disease) can be diagnosed with MRI (Fig. 38.23). The crystalline deposits are typically within the critical zone of the rotator cuff and appear as areas of low signal intensity on all MR pulse sequences. Calcific deposits within the rotator cuff may be difficult to identify on MRI because both the tendon and the calcific deposit appear

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Fig. 38.22  Intramuscular cyst. Coronal oblique T2-weighted fat-suppressed image demonstrates a small intramuscular cyst, which has dissected medially into the muscle tendon junction of the infraspinatus. These intramuscular cysts typically indicate a prior delaminating tendon tear, which may not always be identified due to interval healing.

dark on all pulse sequences. Ancillary MRI findings that may aid in the identification of calcific tendinitis include globular thickening of the involved tendon, and high signal within the tendon and surrounding tissues as a result of associated inflammation. Gradient-echo imaging, although infrequently performed, may improve conspicuity of the deposits as a result of the “blooming” artifact associated with local magnetic field heterogeneity. More often, correlation with conventional radiographs will improve the likelihood of detecting calcific tendinitis. Rotator cuff muscles can undergo atrophy after tendon tears or denervation. Denervation results in muscle edema followed by progressive fatty infiltration. Chronic rotator cuff tendon tears also result in muscle atrophy even if no nerve injury is present. The terminology with regard to atrophy of the rotator cuff musculature is confusing. The term fatty infiltration is typically used to describe actual fatty infiltration or replacement of the muscle, whereas muscle atrophy is used to describe a loss of muscle bulk. Muscle atrophy is seen on MRI as loss of muscle bulk, whereas fatty infiltration is seen as streaks of high signal within the substance of the muscle (Fig. 38.24). Goutallier and colleagues reported a system for grading fatty infiltration of the cuff musculature on the basis of CT imaging,80 and is frequently adapted for use with MRI, as it is at our institution. Fatty infiltration is typically graded as mild, moderate, or severe based on the extent of fatty infiltration (high signal on FSE sequences and low signal on sequences with fat suppression) within the belly of the muscle. Muscle atrophy can be graded separately as mild, moderate, or severe on the basis of muscle bulk depicted on sagittal images at the level of the supraspinatus fossa.81 At times, the muscle tendon junction will be retracted far medially

and the degree of atrophy will be overestimated. It is therefore important to confirm the degree of atrophy with another imaging plane. Regardless of the terms used to describe muscle atrophy and fatty infiltration, they are associated with poor functional outcomes after rotator cuff tendon repair and increased risk of a recurrent tear81; therefore assessment of preoperative MRI scans should include the degree of muscle atrophy and fatty infiltration. Denervation of a rotator cuff muscle can result from either a compressive neuropathy or an acute traumatic injury of a nerve. Compressive neuropathies most commonly result from a paralabral cyst associated with a labral tear, but they also can be caused by fractures or other masses in the area of the shoulder. Paralabral cysts (Fig. 38.25) most commonly arise in association with a superior labrum, anterior, and posterior (SLAP) tear or a posterior labral tear. These cysts may extend into either the spinoglenoid or suprascapular notches and can result in entrapment of the suprascapular nerve, which innervates the supraspinatus and infraspinatus muscles.82 Paralabral cysts arising from an anteroinferior labral tear are less common, but they may compress the axillary nerve as it traverses the quadrilateral space.83 Compression of the axillary nerve can also result from adhesive bands in the quadrilateral space in athletes, such as pitchers, who participate in repetitive overhead activities.84 The axillary nerve innervates both the teres minor and deltoid muscles. Anterior dislocation can result in a stretching injury of the axillary nerve and give rise to a temporary or permanent denervation of the teres minor and deltoid muscles and can occasionally mimic a rotator cuff tear on clinical examination in a person with previous anterior dislocation. Parsonage Turner syndrome, also referred to as idiopathic brachial plexopathy or neuralgic amyotrophy, remains elusive in etiology (various etiologies reported in the literature include postoperative, post-infectious, posttraumatic and post-vaccination) and demonstrates a characteristic diffuse denervation edema pattern (Fig. 38.26).85 On MRI, subacute denervation edema signal appears as homogeneous high signal on all pulse sequences within the affected muscle and is associated with reversible muscle atrophy (see Fig. 38.25). The more chronic and irreversible form of fatty atrophy appears as decreased muscle bulk and hyperintense streaks (representing the fat) within the muscles on FSE sequences (see Fig. 38.26) and low signal on fat suppressed images.

Rotator Interval, Biceps, and the Biceps Pulley The rotator cuff interval is the gap between the supraspinatus and infraspinatus tendons at the anterior aspect of the shoulder, which is traversed by multiple structures, including the biceps tendon, coracohumeral ligament (CHL), and superior glenohumeral ligament (SGHL) (Box 38.3). Formed largely by contributions from the coracohumeral and SGHLs, with lesser contributions from the supraspinatus and subscapularis tendons, the biceps pulley is a sling-like confluence of predominantly ligamentous structures that supports the distal aspect of the proximal biceps tendon as it exits the joint (Fig. 38.27).86–88 The biceps pulley may be conceptualized as two functional units: (1) a medial unit located along the inferomedial aspect of the biceps tendon and composed of fibers arising from the SGHL, capsule, and CHL;

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D

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E

Fig. 38.23  Calcific tendinosis. (A) A globular focus of hydroxyapatite is seen within the infraspinatus bursal fibers/overlying bursa on this frontal radiograph. (B) Coronal oblique fast spin echo and (C) coronal oblique T2-weighted fat-suppressed images show the low signal intensity foci of calcium within the bursal fibers of the infraspinatus tendon and overlying bursa. Extensive edema signal is seen within the regional soft tissues representing associated inflammation. (D) Ultrasound-guided lavage aspiration of the calcium, and (E) a followup radiograph demonstrating near complete resolution of the calcium.

BOX 38.3  Rotator Interval: Anatomy,

Function, and Pathologic Entities

Normal Anatomy A gap within the rotator cuff formed by the interposition of the coracoid process Superior border—anterior margin of the supraspinatus tendon Inferior border—superior leading edge of subscapularis tendon Roof—coracohumeral ligament (bursal surface); superior glenohumeral ligament (articular surface) Contains the long head of the biceps tendon

A

B

Fig. 38.24  Fatty infiltration. (A) Sagittal oblique and (B) coronal oblique fast spin echo images demonstrate severe fatty infiltration of the chronically torn and retracted supraspinatus and superior infraspinatus. It is important to triangulate with an additional view to confirm the degree of fatty infiltration, as medial retraction on the sagittal view may be misleading.

Function Limits excessive external rotation of the humeral head Prevents superior migration of the humeral head Pathologic Conditions Traumatic disruption Inflammatory arthritis Adhesive capsulitis

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Fig. 38.25  Paralabral cyst. (A) Coronal oblique T2-weighted fat suppressed (B) axial fast spin echo and (C) oblique sagittal fast spin echo images demonstrate a lobulated paralabral cyst arising from a torn posterosuperior labrum, which extends into the spinoglenoid notch. There is mild homogenous increased signal within the infraspinatus indicating denervation.

A

B

C

Fig. 38.26  Parsonage Turner syndrome. (A) Oblique sagittal fast spin echo and (B) and (C) coronal oblique fat-suppressed T2-weighted images demonstrates fatty infiltration as well as high-signal intensity within the supraspinatus and infraspinatus tendons, along with loss of supraspinatus muscle bulk.

and (2) a lateral unit, with contributions from the CHL, rotator cuff, and SGHL.87 Disruption of the structures within the rotator interval may contribute to instability of the long head of the biceps tendon; however, injury to the pulley structures may be difficult if not impossible to visualize directly, both at arthroscopy and on imaging studies.86 Ancillary signs of pulley injury may be more easily visualized; these include tears of the superior subscapularis and anterior supraspinatus tendons, focal chondral wear adjacent to the bicipital groove, and medial subluxation of the biceps tendon (Fig. 38.28).87,89,90

Adhesive Capsulitis Adhesive capsulitis is an idiopathic condition characterized by inflammation and subsequent fibrosis involving the soft tissues about the glenohumeral joint; in particular, the capsule and rotator interval (Box 38.4). Clinically, onset is typically insidious,

with progressive pain and limited range of motion (ROM), most commonly affecting women over the age of 40. The imaging characteristics of adhesive capsulitis evolve with the clinical stage of the disease; capsular hyperintensity and thickening tends to be most pronounced in the earlier inflammatory stages (particularly stage 2), while later fibrotic stages demonstrate less overt inflammation. Features observed at all stages include some degree of capsular thickening, scarring of the rotator interval, and decompression of synovitis into extracapsular recesses such as the biceps tendon sheath and the subscapularis recess. Autodecompression of synovitis may also result in a degree of local extracapsular edema (Fig. 38.29).91

Long Head of the Biceps Tendon The long head of the biceps tendon takes origin at the superior aspect of the glenoid and labrum, with variation in the degree to which it originates from osseous versus labral tissue. The

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labral origin of the long head of the biceps tendon is referred to as the biceps anchor or biceps labral complex (Figs. 38.27 and 38.30). The tendon origin may vary in terms of both the anteriorposterior location of the tendon origin upon the superior labrum, as well as in the morphology of the attachment of the bicepslabral complex to the subjacent glenoid rim.92,93 Accessory tendon origins have also been described; these arise most commonly from the anterior margin of the supraspinatus.87,94

The biceps tendon enters the biceps tendon sheath within the bicipital groove of the humerus upon exiting the glenohumeral joint (see Figs. 38.27 and 38.30). A structure that has been referred to as the transverse humeral ligament forms the soft tissue roof of the osseous groove, though this structure is thought to represent not a distinct ligament, but a confluence of fibers BOX 38.4  Adhesive Capsulitis: Clinical and

Imaging Findings

Risk Factors Female 40 to 70 years of age Minor trauma Rheumatologic disorders Diabetes Clinical Presentation Insidious onset pain, stiffness Decreased range of motion Misdiagnosed as impingement Arthrography Decreased joint volume (4 mm) Pericapsular edema and enhancement Synovitis in rotator interval Thickened coracohumeral ligament

Fig. 38.27  Anatomy of the rotator interval and biceps pulley.

A

B

425

C

Fig. 38.28  Axial (A), oblique coronal (B), and oblique sagittal (C) fast spin echo proton density images of the shoulder demonstrate an intrasubstance tear of the subscapularis (white arrowheads) allowing for medial subluxation of the degenerated and chronically torn biceps tendon (black arrowheads).

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C

Fig. 38.29  Coronal inversion recovery (A) and fast spin echo (FSE) proton density (PD) (B) images demonstrate hyperintensity and thickening of the joint capsule (white arrowheads), and (C) infiltration of the rotator interval (black arrowhead) on sagittal FSE PD image, in a patient with adhesive capsulitis.

Fig. 38.30  Anatomy of the glenoid, labrum, and capsule.

arising from multiple structures, including the supraspinatus and infraspinatus tendons, with a possible fascial contribution from the pectoralis major tendon.87 A small synovial band termed the vincula may be present within the biceps tendon sheath, traversing the interval between the anterior aspect of the tendon to the tendon sheath. Because the biceps tendon sheath communicates with the glenohumeral joint space, synovial fluid from the joint may decompress into the tendon sheath. Given the complex course of the proximal biceps tendon, it is best evaluated in multiple planes, though axial images provide cross-sectional evaluation of a majority of the more distal tendon.

On most routine clinical MR sequences, tendinosis manifests as hyperintensity and thickening of tendon fibers; ancillary findings of impingement or tendon instability may also be observed.87 Tendinosis may predispose the biceps tendon to partial tears, which often manifest as longitudinal splits, or to complete tendon rupture (Fig. 38.31). Spontaneous proximal biceps rupture occurs most commonly in the setting of a chronically degenerated tendon in an older patient, manifesting as discontinuity of the tendon, often with distal retraction of the torn tendon yielding a gap, with an empty tendon sheath more proximally. Fluid distention of the biceps tendon sheath may result from decompression of

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A

B C Fig. 38.31  Axial fast spin echo (FSE) proton density (PD) (A), inversion recovery (B) and sagittal FSE PD (C) images of the shoulder and upper arm demonstrate complete proximal biceps rupture, as manifest by empty biceps tendon sheath proximally (black arrowhead), with prominent intramuscular hemorrhage (white arrows), and retraction of the distal tendon stump (white arrowhead).

synovial fluid from the glenohumeral joint, though it may also be related to tenosynovitis. Longstanding inflammation may result in associated tenosynovial adhesions. Hydroxyapatite depositional disease (HADD), also known as calcific tendonitis, may involve the biceps tendon, and, as with HADD involving the rotator cuff, is amenable to ultrasound-guided lavage (Fig. 38.32).

Labrum and Capsular Structures Anatomy The rather shallow osseous articulation between the glenoid and humeral head allows a relatively large ROM, with a great deal of the stability of the joint being conferred by peri-articular soft tissue structures. The glenoid labrum and capsular structures act as static stabilizers, whereas the rotator cuff provides dynamic stabilization of the glenohumeral joint. The glenoid labrum is a rim of fibrous and fibrocartilaginous tissue that extends along the circumference of the glenoid, adding depth to the glenoid fossa, thereby augmenting joint stability, as well as serving as a point of attachment for the glenohumeral ligaments and biceps tendon. Normal labral tissue is uniformly dark on routine clinical MRI sequences, being composed of fibrous tissue and fibrocartilage, and the normal labrum is

typically roughly triangular in cross section. Location of labral pathology is often described in terms of clock position, with 12:00 being superior and 3:00 being anterior, as imaged in the sagittal plane. Alternately, the various portions of the labrum may be described simply by their relative anatomic position: direct superior, anterosuperior, anteroinferior, direct inferior, posteroinferior, and posterosuperior (see Fig. 38.30).95 Anatomic variants are commonly described within the labrum, with variants most commonly involving the anterosuperior portion of the labrum. Common labral variants include the sublabral foramen and sublabral sulcus, focal defects confined to the anterosuperior labrum, as well as the Buford complex, which refers to a hypoplastic anterosuperior labrum with compensatory thickening of the middle glenohumeral ligament (MGHL). These labral variants may be mistaken for tears, and familiarity with their appearance may help prevent their being misinterpreted as pathology.92,93 Three glenohumeral ligaments, which represent thickenings of the capsule, also serve to improve stability of the shoulder. The inferior glenohumeral ligament (see Fig. 38.30) is the most important of the three thickenings and functions primarily to improve glenohumeral stability with the arm in abduction and external rotation.96

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C A

B Fig. 38.32  Coronal inversion recovery (A) and fast spin echo proton density (B) images of the shoulder demonstrate a large focus of mineralization (white arrows) within the biceps tendon sheath, consistent with hydroxyapatite deposition. Long axis ultrasound images (C) re-demonstrate the mineralized focus (white arrow), with subsequent ultrasound-guided lavage performed (black arrowheads indicate needle).

It is composed of three separate components: the anterior band, the posterior band, and the axillary pouch.97,98 The origin of the inferior glenohumeral ligament is somewhat variable; it arises from either the inferior glenoid labrum or adjacent osseous glenoid. It then inserts in a collar-like fashion along the medial aspect of the humeral neck. It is lax when the arm is in the neutral position and appears redundant when the arm is imaged in the standard planes on MRI (see Fig. 38.30). The MGHL (see Fig. 38.30) is less important as a stabilizer, but it is responsible for preventing external rotation of the arm during abduction between 60 and 90 degrees.99 In terms of size, it is the most variable of the three ligaments, ranging from a thick cordlike ligament to complete absence.100 It arises from the superior glenoid tubercle adjacent to the origin of the biceps tendon and the SGHL, and then courses obliquely in an inferolateral direction to merge with the deep fibers of the subscapularis tendon just before attaching to the humeral neck. It is typically seen on axial MRI deep to the subscapularis muscle and superficial to the anterior labrum, occasionally mimicking an avulsed fragment of the anterior labrum. The SGHL (see Fig. 38.30) contributes to shoulder stability, although a report suggests that it provides some degree of restraint, preventing inferior subluxation of the humeral head when the arm is in 0 degrees of abduction.101,102 It arises from the superior glenoid tubercle adjacent to the attachment of the biceps tendon and then courses obliquely and anteriorly to merge with the CHL before its attachment on the humeral head. The SGHL forms the floor of the rotator interval and also plays a role in stability of the long head of the biceps tendon, merging with the CHL to form the biceps pulley.103–105 It is consistently visualized on axial MRA images as a thick band-like structure arising from the glenoid tubercle and paralleling the coracoid process.98

Instability The anatomic configuration, which permits a wide ROM at the glenohumeral joint, also predisposes the articulation to a degree of instability, with the potential for subluxation and dislocation. While radiographs are often the first line of imaging in instability, with specific views allowing the visualization of osseous pathology, such as Hills-Sachs and osseous Bankart lesions, injury tends to largely involve the periarticular soft tissue stabilizers; therefore MRI is often the main modality for definitive assessment of the degree and extent of injury in the setting of instability. Anterior The humeral head most commonly dislocates anteroinferiorly relative to the glenoid, often as a result of a fall on an outstretched hand or traumatic stress while the extremity is in the abducted externally rotated position. In younger patients, this results in a classic constellation of findings, including a Hill–Sachs lesion of the humeral head plus some degree of capsulolabral injury, commonly a Bankart lesion or variant. Capsular injury may occur at various attachment sites, often resulting in stripping along the scapula, or the classically described humeral avulsion of the glenohumeral ligaments (HAGL) lesion, which tends to warrant a change in the surgical approach.106–108 Hill–Sachs and osseous Bankart lesions are typically visible on radiographs, with MR evaluation in the acute setting demonstrating associated local marrow edema along the humeral head and anteroinferior glenoid impaction sites. Nonosseous Bankart lesions manifest as a tear of the anteroinferior labrum, which may be displaced or nondisplaced, and which may manifest as a discrete defect through the substance of the labrum, or as an irregular/amorphous appearance. A variety of Bankart variants

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have been described, with the configuration of the Bankart lesion having potential therapeutic implications in terms of surgical planning. A Perthes lesion is a nondisplaced Bankart in which the medial scapular periosteum remains intact, tethering the torn labrum to the glenoid, such that the tear may be difficult to visualize both on imaging and at arthroscopy. A displaced variant of the Perthes lesion is termed an anterior labral periosteal sleeve avulsion (ALPSA), with an anteroinferior labral tear and stripping of the medial scapular periosteum, allowing for medial displacement of the torn labrum, which may scar down in this abnormal medialized position if not properly reduced. In an osseous Bankart lesion, impaction results in some degree of anteroinferior glenoid rim fracture, yielding an ossific fragment with attached labral tissue. The size of this fragment is important in terms of treatment planning, with large fragments warranting surgical fixation. Excessive loss of glenoid bone stock may require some type of osseous augmentation, such as coracoid transfer. In older patients with rotator cuff pathology, anterior glenohumeral dislocation often results in a different constellation of imaging findings, including rotator cuff tears and avulsion fractures of the greater tuberosity (Figs. 38.33–38.36).106–108

Posterior Posterior glenohumeral dislocation is much less common than anterior dislocation, and tends to occur in the setting of activities that result in specific injury patterns; for example, football linemen who incur repetitive forceful posteriorly directed forces at the glenohumeral joint. Certain anatomic anomalies, such as glenoid dysplasia, also contribute to a predisposition for posterior dislocation. Imaging findings in the setting of posterior dislocation are analogous to those observed in anterior dislocation, with reverse Hill-Sachs lesions occurring along the anterior aspect of the humeral head, and reverse Bankart lesions and variants occurring along the posterior glenoid (Box 38.5). Posterior HAGL lesions may also occur along the posterior capsular attachments at the humerus (Fig. 38.37).107,108

A

Fig. 38.34  Axial fast spin echo proton density image in a patient status post recent glenohumeral dislocation demonstrates anterior labral periosteal sleeve avulsion lesion, with anteroinferior labral tear, which is slightly medially retracted and tethered to a band of stripped periosteum (white arrowhead).

B

Fig. 38.33  Coronal inversion recovery (A) and sagittal fast spin echo proton density (B) images in a patient status post recent anterior glenohumeral dislocation demonstrates acute Hill-Sachs lesion (white arrowheads) and osseous Bankart lesion (black arrowheads).

Fig. 38.35  Axial fast spin echo proton density image demonstrates anteroinferior labral tear (white arrowhead), with adjacent focal area of chondral loss (black arrowhead), consistent with glenoid labral articular defect lesion.

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A A

B

Fig. 38.36  Coronal inversion recovery (A) and fast spin echo proton density (B) images in an older patient status post glenohumeral dislocation demonstrates avulsion fracture of the greater tuberosity (white arrowheads) and humeral avulsion of the glenohumeral ligaments (black arrowheads).

B

Fig. 38.38  Oblique coronal (A) and axial (B) fast spin echo proton density images demonstrate pronounced capsular remodeling with marked thickening anteriorly (white arrowheads) in a swimmer with multidirectional instability.

BOX 38.5  Posterior Shoulder Dislocation:

Radiographic Findings

Positive rim sign (widening of glenohumeral joint >6 mm) Humeral head appears in same position on internal and external rotation anteroposterior views “Trough line,” or reverse Hill-Sachs defect Reverse Bankart lesion Fracture of lesser tuberosity

A

B

Fig. 38.37  Axial (A) and oblique sagittal (B) fast spin echo proton density images demonstrate posterior humeral avulsion of the glenohumeral ligaments (white arrowheads) in a patient status post recent posterior glenohumeral dislocation.

Multidirectional Multidirectional instability occurs in the setting of generalized capsular laxity, which predisposes patients to subluxations and dislocations in at least two directions. This entity is often atraumatic, though it may develop in athletes with recurrent injuries and/or repetitive strain. Imaging findings in these patients may be nonspecific, though they may include a remodeled, patulous joint capsule as well as sequelae of recurrent dislocations (Fig. 38.38).107,108

A

B

Fig. 38.39  Oblique coronal (A) and axial (B) fast spin echo images of the shoulder demonstrate a tear across the base of the superior labrum (white arrow, A), extending to the anterosuperior labrum (white arrow, B).

Superior Labrum, Anterior, and Posterior Tears The term SLAP tear refers to any superior labral tear that propagates anteroposteriorly to some degree, and which may also propagate along various adjacent structures. Originally described in throwing athletes by Andrews et al. (1985),109 with the term “SLAP” coined and the original four tear subtypes described by Snyder et al. (1990),110 the initial classification of these tears has been expanded to include at least 10 types (Table 38.4). A type I SLAP tear is described as superior labral fraying without involvement of the biceps tendon, and appears as intrasubstance signal hyperintensity without a defined intrasubstance tear on MRI. The remainder of SLAP injuries involve defined superior labral tears, manifesting as intrasubstance linear signal hyperintensity and/or labral detachment, with variable degrees and directions of extension. Type II SLAP tears are reportedly the most common, consisting of a superior labral tear with involvement of the biceps (Fig. 38.39).111 Classification of SLAP tears may provide insight into the type of injury, the probable mechanism, and the therapeutic options; however, precise classification of these lesions may not always be possible, and the classification system cannot be assumed to be universally known or accepted. Therefore when reporting these types of injuries, rather than providing a numeric classification,

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TABLE 38.4  Classification of Superior Labrum, Anterior and Posterior (SLAP) Tears SLAP

Location

Description

Management

I

11-1

Superior labral fraying with intact biceps tendon

II

11-1

Superior labral tear with involvement of biceps tendon

III

11-1

IV

11-1

V

11-5

VI

11-1

VII

11-3

VIII

7-1

IX

7-5

X

11-1

Bucket handle tear of superior labrum with intact biceps Bucket handle tear of superior labrum with involvement of biceps Bankart lesion with extension to superior labrum and involvement of biceps tendon Anterior or posterior superior labral flap tear with involvement of biceps Superior labral tear with involvement of biceps tendon and middle glenohumeral ligament Superior labral tear with posteroinferior extension Superior labral tear with extensive anterior and posterior extension Superior labral tear with extension to rotator interval

Associated with repetitive overhead motion, also seen in the setting of degeneration Associated with repetitive overhead motion; may have extension anteriorly, posteriorly, or both Most common type Associated with fall on outstretched hand Associated with fall on outstretched hand Associated with anterior glenohumeral dislocation Associated with fall on outstretched hand Associated with anterior glenohumeral dislocation

Conservative vs. débridement

Associated with posterior shoulder dislocation Typically associated with severe trauma. Typically associated with severe trauma

Capsulolabral reconstruction

Débridement and repair

Excision of bucket handle fragment Excision of bucket handle fragment, repair of biceps Labral repair and biceps tenodesis Labral repair and biceps tenodesis Labral repair, biceps tenodesis, middle glenohumeral ligament repair

Labral débridement and glenohumeral stabilization Labral débridement and glenohumeral stabilization

it is generally more important to provide an accurate description of the injury, including location and extent, the involvement of adjacent structures, the morphology of the tear including displacement, and any associated injuries.95

Posterior Impingement, Glenohumeral Internal Rotational Deficit Athletes who perform repetitive overhead motions in the abducted externally rotated position, such as pitchers, are at risk for the development of impingement of the structures along the posterosuperior aspect of the glenohumeral joint, including the rotator cuff tendons and labrum. These athletes often develop a characteristic articular-sided tear centered along the junction of the supraspinatus and infraspinatus tendons, as well as degeneration and/or tearing of the posterosuperior labrum. Skeletally immature patients may develop chronic remodeling of the posterosuperior glenoid due to repetitive impaction in this region, resulting in relative glenoid retroversion. Remodeling of the joint capsule may also occur, with patulous anterior capsule and contracted posterior capsule resulting in a relative loss of internal rotation, a clinical condition referred to as glenohumeral internal rotational deficit (GIRD).112

Articular Surfaces Normal hyaline articular cartilage consists of multiple layers, and therefore has a consistent laminar appearance on high resolution cartilage-sensitive imaging sequences. The deepest layer of articular cartilage, the tidemark, is mineralized and therefore is uniformly hypointense on typical clinical sequences. The next

Fig. 38.40  Fast spin echo proton density image demonstrating the normal layered appearance of hyaline articular cartilage (the patella is shown for ease of visualization), with the tidemark being the deepest layer of cartilage, and the lamina splendens the most superficial.

deepest layer consists largely of radially oriented collagen fibers, conferring a shortened T2 relaxation time relative to adjacent superficial layer, in which the collagen fibers are organized in arcades. The most superficial layer, the lamina splendens, is a thin layer consisting of parallel horizontally oriented fibers, and is therefore hypointense (Fig. 38.40). Early chondral wear is often evident as a loss of typical greyscale stratification, chondral hyperintensity, and surface fibrillation, often involving the medial aspect of the humeral head. As wear progresses, cartilage may delaminate and form flaps (Fig. 38.41). While typical osteoarthritis often first affects the superomedial humeral head, patients who develop osteoarthritis secondary to rotator cuff pathology often display a characteristic pattern of chondral wear, typically affecting the anterosuperior glenoid, in

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SECTION 4  Shoulder

A

B

Fig. 38.42  Oblique coronal (A) and axial (B) fast spin echo proton density images demonstrate features of rotator cuff arthropathy, with superior migration of the humeral head in the setting of massive rotator cuff tear (white arrowhead), and associated arthrosis preferentially affecting the anterosuperior aspect of the glenoid (black arrowheads).

Level of Evidence: V, expert opinion

Summary: Fig. 38.41  Oblique coronal fast spin echo proton density image demonstrates chondral delamination and flap formation (white arrowhead) over the superomedial humeral head.

the setting of massive rotator cuff tear and resultant superior migration of the humeral head (Fig. 38.42).113 For a complete list of references, go to ExpertConsult.com.

This article covers imaging artifacts and normal variations that can affect interpretation of shoulder magnetic resonance images.

Citation: Sanders TG, Jersey SL. Conventional radiography of the shoulder. Semin Roentgenol. 2005;40(3):207–222.

Level of Evidence: V, expert opinion

Summary:

SELECTED READING Citation: Dunham KS, Bencardino JT, Rokito AS. Anatomic variants and pitfalls of the labrum, glenoid cartilage, and glenohumeral ligaments. Magn Reson Imaging Clin North Am. 2012;20(2):213–228.

Level of Evidence:

This article covers conventional radiography of the shoulder. Views are discussed along with their strengths and role in diagnosing sources of shoulder pain.

Citation: Sanders TG, Miller MD. Systematic approach to magnetic resonance imaging interpretation of sports medicine injuries of the shoulder. Am J Sports Med. 2005;33:1088–1105.

Level of Evidence:

V, expert opinion

V, expert opinion

Summary: The authors of this review article discuss normal anatomy and variants in the shoulder labrum, glenohumeral ligaments, and cartilage.

Summary: The authors of this article present a systematic approach to reading shoulder magnetic resonance imaging examinations.

Citation: Fitzpatrick D, Walz DM. Shoulder MR imaging normal variants and imaging artifacts. Magn Reson Imaging Clin North Am. 2012;18(4):615–632.

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CHAPTER 38  Glenohumeral Joint Imaging

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CHAPTER 38  Glenohumeral Joint Imaging 85. Feinberg JH, Radecki J. Parsonage-Turner syndrome. HSS J. 2010;6(2):199–205. 86. Hunt SA, Kwon YW, Zuckerman JD. The rotator interval: anatomy, pathology, and strategies for treatment. J Am Acad Orthop Surg. 2007;15(4):218–227. 87. Morag Y, Bedi A, Jamadar DA. The rotator interval and long head biceps tendon: anatomy, function, pathology, and magnetic resonance imaging. Magn Reson Imaging Clin N Am. 2012;20(2):229–259, x. 88. Nakata W, Katou S, Fujita A, et al. Biceps pulley: normal anatomy and associated lesions at MRA. Radiographics. 2011;31(3):791–810. 89. Bennett WF. Correlation of the SLAP lesion with lesions of the medial sheath of the biceps tendon and intra-articular subscapularis tendon. Indian J Orthop. 2009;43(4):342–346. 90. Braun S, Horan MP, Elser F, et al. Lesions of the biceps pulley. Am J Sports Med. 2011;39(4):790–795. 91. Sofka CM, Ciavarra GA, Hannafin JA, et al. Magnetic resonance imaging of adhesive capsulitis: correlation with clinical staging. HSS J. 2008;4(2):164–169. 92. Dunham KS, Bencardino JT, Rokito AS. Anatomic variants and pitfalls of the labrum, glenoid cartilage, and glenohumeral ligaments. Magn Reson Imaging Clin N Am. 2012;20(2): 213–228, x. 93. Fitzpatrick D, Walz DM. Shoulder MRI normal variants and imaging artifacts. Magn Reson Imaging Clin N Am. 2010;18(4): 615–632. 94. Dierickx C, Ceccarelli E, Conti M, et al. Variations of the intra-articular portion of the long head of the biceps tendon: a classification of embryologically explained variations. J Shoulder Elbow Surg. 2009;18(4):556–565. 95. Chang D, Mohana-Borges A, Borso M, et al. SLAP lesions: anatomy, clinical presentation, MRI diagnosis and characterization. Eur J Radiol. 2008;68(1):72–87. 96. Bigliani LU, Pollock RG, Soslowsky LJ, et al. Tensile properties of the inferior glenohumeral ligament. J Orthop Res. 1992; 10(2):187–197. 97. O’Brien SJ, Neves MC, Arnoczky SP, et al. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med. 1990;18(5):449–456. 98. Palmer WE, Caslowitz PL, Chew FS. MRA of the shoulder: normal intraarticular structures and common abnormalities. AJR Am J Roentgenol. 1995;164(1):141–146.

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99. Ferrari DA. Capsular ligaments of the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sports Med. 1990;18(1):20–24. 100. Tirman PF, Feller JF, Palmer WE, et al. The Buford complex–a variation of normal shoulder anatomy: MR arthrographic imaging features. AJR Am J Roentgenol. 1996;166(4):869–873. 101. O’Connell PW, Nuber GW, Mileski RA, et al. The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med. 1990;18(6):579–584. 102. Turkel SJ, Panio MW, Marshall JL, et al. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am. 1981;63(8):1208–1217. 103. Kask K, Poldoja E, Lont T, et al. Anatomy of the superior glenohumeral ligament. J Shoulder Elbow Surg. 2010;19(6): 908–916. 104. Kumar VP, Satku K, Balasubramaniam P. The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop Relat Res. 1989;244:172–175. 105. Vinson EN, Major NM, Higgins LD. Magnetic resonance imaging findings associated with surgically proven rotator interval lesions. Skeletal Radiol. 2007;36(5):405–410. 106. Bencardino JT, Gyftopoulos S, Palmer WE. Imaging in anterior glenohumeral instability. Radiology. 2013;269(2):323–337. 107. Omoumi P, Teixeira P, Lecouvet F, et al. Glenohumeral joint instability. J Magn Reson Imaging. 2011;33(1):2–16. 108. Walz DM, Burge AJ, Steinbach L. Imaging of shoulder instability. Semin Musculoskelet Radiol. 2015;19(3):254–268. 109. Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337–341. 110. Snyder SJ, Karzel RP, Del Pizzo W, et al. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274–279. 111. Modarresi S, Motamedi D, Jude CM. Superior labral anteroposterior lesions of the shoulder: part 2, mechanisms and classification. AJR Am J Roentgenol. 2011;197(3): 604–611. 112. Chang IY, Polster JM. Pathomechanics and magnetic resonance imaging of the thrower’s shoulder. Radiol Clin North Am. 2016;54(5):801–815. 113. Eajazi A, Kussman S, LeBedis C, et al. Rotator cuff tear arthropathy: pathophysiology, imaging characteristics, and treatment options. AJR Am J Roentgenol. 2015;205(5):W502–W511.

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39  Shoulder Arthroscopy Thomas M. DeBerardino, Laura W. Scordino

BACKGROUND Shoulder arthroscopy was first described in the 1930s by Burman,1 who learned how to perform arthroscopy on cadaveric joints. Remarkably, shoulder arthroscopy has been used regularly only for the past 30 years. The use of shoulder arthroscopy has continued to grow, and today it is one of the most commonly performed orthopedic procedures. It is the second most common procedure performed by persons taking Part II of the American Board of Orthopaedic Surgery certification examination.2

INDICATIONS AND CONTRAINDICATIONS Shoulder arthroscopy allows excellent visualization of the glenohumeral joint, periarticular structures, and subacromial space, and thus facilitates both the diagnosis and treatment of intraarticular and periarticular pathology of the shoulder joint. Shoulder arthroscopy is indicated for, but not limited to, rotator cuff repair, revision rotator cuff repair, glenohumeral instability,3 labral repair or débridement, removal of loose bodies, synovectomy or synovial biopsy, irrigation and débridement of a septic shoulder, repair of a glenoid fracture, bicep tenodesis or tenotomy, subacromial decompression, and distal clavicle excision. Contraindications include medical problems that preclude a patient from undergoing elective surgery, and infection of the shoulder joint or overlying tissue if surgery is being performed for a reason other than to eradicate the infection. In a 2003 survey of 908 members of the Arthroscopy Association of North America, of the 700 members who responded, 24% stated that they repair rotator cuff injuries via an allarthroscopic technique; however, 5 years earlier, only 5% reported using an all-arthroscopic technique.4 Only 2 years later, in 2005, an electronic poll of 167 orthopedic surgeons attending the annual American Academy of Orthopaedic Surgeons meeting showed that 67% would fix a mobile, 3-cm rotator cuff tear.5 The percentage of surgeons performing arthroscopic rotator cuff repairs continues to grow, and surgeons today not only feel confident about using arthroscopy for massive rotator cuff repairs, but also have even had good results for revision rotator cuff repairs.6

ARTHROSCOPIC VERSUS OPEN PROCEDURES Reported benefits of shoulder arthroscopy compared with open shoulder procedures include limited damage to the surrounding

structures, particularly the deltoid muscle and the area of insertion. Furthermore, with regard to rotator cuff repair, some surgeons believe that arthroscopy provides a more complete evaluation of both intra-articular and bursal anatomy. Many surgeons believe that arthroscopy allows easier mobilization of potential retracted cuff musculature. The main downside to arthroscopy is its large learning curve, which can result in longer operative times, iatrogenic injuries during the learning process, and potentially inferior repair compared with open techniques. With regard to rotator cuff repair, many studies have shown that all-arthroscopic compared with mini-open rotator cuff repair has yielded comparable short-term and mid-term results.7-10 Other studies have shown that pain, strength, motion, and strength may be improved with all-arthroscopic repair.

PREOPERATIVE IMAGING In our practice we obtain a standard set of four radiographs preoperatively, including a true anteroposterior radiograph of the shoulder, the supraspinatus outlet view (SOV), an axillary view, and a bilateral Zanca view. These images allow us to evaluate a large number of pathologic shoulder conditions and to make preoperative plans. The SOV provides a look at the acromion for classification according to the system proposed by Bigliani and colleagues11: type 1, flat acromion; type 2, gently curved acromion; and type 3, “beaked” or sharp, inferiorly pointed acromion. The SOV radiograph also allows us to determine the amount of acromion that needs to be taken down if we are planning a subacromial decompression, based on how thick it is, and to confirm that there is no os acromiale, which may result in pain and instability if a decompression is performed. The Zanca view allows for evaluation of the acromioclavicular joints for pathology.12 Magnetic resonance imaging (MRI) without contrast provides visualization of the rotator cuff musculature. MRI with an arthrogram is an excellent imaging modality for patients with instability or when concern exists about the possibility of labral pathology, because intra-articular anatomy is more clearly defined with this procedure. Many institutions and surgeons use ultrasound for the evaluation of shoulder joint pathology. This method of evaluation has proven to be both sensitive and specific for the radiologists and orthopedic surgeons who use ultrasound in their own office.13-15 In direct comparison with arthroscopy as the standard, MRI and

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CHAPTER 39  Shoulder Arthroscopy

Abstract

Keywords

Shoulder arthroscopy was first described in the 1930s by Burman, who learned how to perform arthroscopy on cadaveric joints. Remarkably, shoulder arthroscopy has been used regularly only for the past 30 years. The use of shoulder arthroscopy has continued to grow, and today it is one of the most commonly performed orthopedic procedures. It is the second most common procedure performed by persons taking Part II of the American Board of Orthopedic Surgery certification examination.

shoulder arthroscopy beach chair lateral decubitus

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ultrasound have shown no significant difference in diagnostic accuracy.15 Ultrasound also has the benefit of providing a dynamic evaluation. However, this imaging modality relies heavily on the experience of the person performing the examination.15

PATIENT POSITIONING As depicted in Fig. 39.1, two main options exist for patient positioning: lateral decubitus and beach chair. Positioning is based on surgeon preference. Advantages and disadvantages of each position are described in this section. Lateral positioning of the patient occurs after the patient is intubated while supine on a standard operating room table with the bean bag already underneath him/her, but uninflated (see Fig. 39.1A). The patient is then turned to the lateral position with the operative arm up and the torso posteriorly tilted approximately 20 degrees to position the glenoid parallel with the floor. An axillary roll is placed and the legs are positioned with adequate pillows and cushioning to protect bony prominences and the peroneal nerve as it passes around the fibular neck. The bean bag is then inflated, warm blankets are placed over the patient, and a belt is secured over as opposed to under the blankets so it is always clear that the belt is in place. The arm undergoing surgery is then positioned in approximately 70 degrees of abduction and 20 degrees of forward flexion. One cadaveric study showed that positioning the arm in 45 degrees of flexion with arm abduction of either 0 or 90 degrees allowed for the best visualization with the least amount of strain placed on the brachial plexus.16 To distend the joint, 10 to 15 lb of traction is applied to a device set up at the foot of the bed. The arm is prepared and draped so that the entire shoulder and part of the arm is sterile and the distal extent of the arm that is hooked up to traction is not sterile and is draped out of the field. Some surgeons believe that the lateral position allows better visualization of the joint because of the traction. Lateral positioning has been reported to have a 10% rate of neurapraxia; most cases resolve in 48 hours. The neurapraxia is thought to be a result

A

of traction on the brachial plexus, with biomechanical studies showing a 100% incidence of abnormal somatosensory evoked potentials in the musculoskeletal nerve.17,18 Beach chair positioning often entails the use of a specialized operating table that bends to create a semiseated, or beach chair, position (see Fig. 39.1B). The patient is anesthetized while supine and then positioned. The anesthesiologist stabilizes the head while the surgeon and assistant move the patient cephalad on the table and the head holder attachment is positioned on the bed. A padded face mask is placed over the patient’s face to hold the head against the head rest. A padded side post is placed on each side of the patient to hold him or her in position on the middle of the bed, and a pillow is placed under the knees to prop the patient up and prevent him or her from sliding down the beach chair. The heels are padded. Unlike with the lateral position, no traction is necessary when the beach chair position is used. The entire operative arm is prepped and draped so it is free for manipulation and movement throughout the operation. Some surgeons find it helpful to use a device that holds the operative arm in various adjustable positions, to free up the hands of their assistants so they can help with the case. The beach chair position facilitates an easy transition to an open procedure because the patient is already in a suitable position for an open procedure. Risks relating to head position do accompany the use of the beach chair position, and neurapraxia of cutaneous nerves in the cervical plexus related to the headrest itself has been reported, and thus a padded head rest should be carefully positioned and neck flexion should be avoided.18 Also unique to beach chair positioning is the risk of hypoperfusion to the brain. Although the use of hypotensive anesthetic has been well supported in the literature for patients in the supine or lateral decubitus position to decrease operative blood loss and to improve visualization, concern exists about relative hypotension to the brain as a result of hydrostatic pressure. The literature includes rare case reports of patients who have sustained ischemic brain and spinal cord injury while receiving hypotensive anesthesia in the beach chair position.18 Therefore it has been recommended that blood pressure

B Fig. 39.1  (A) A patient with the right shoulder prepped in the lateral decubitus position with a distal forearm holder and longitudinal traction in place. (B) A patient with the left shoulder prepped in the beach chair position.

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CHAPTER 39  Shoulder Arthroscopy

be measured in the contralateral arm and that attempts be made to keep systolic blood pressure and subacromial pressure (pump pressure) within 49 mm Hg of each other.17,18

ARTHROSCOPY SETUP Arthroscopy is an equipment-intensive procedure. It involves the use of an arthroscope, which is a small fiber-optic camera that is usually 4 mm in size when used for the shoulder. The arthroscope projects images onto a television that can be seen by all the surgical team members. Arthroscopes come with varying degrees of angulation of the lens, but most commonly the 30-degree arthroscope is used for shoulder arthroscopy. It is advisable to have both 30- and 70-degree scopes available because each scope allows improved visualization depending on the procedure to be performed. Arthroscopy involves the inflow of fluid through the joint both to distend the joint and to decrease bleeding. The best fluid to use with arthroscopy is a topic of debate. Some studies have shown that epinephrine allows better visualization, likely by decreasing bleeding without associated cardiovascular adverse effects19; however, other in vitro studies have suggested that epinephrine may damage articular cartilage.20 Therefore we prefer to use the most diluted epinephrine in saline solution for our irrigation fluid. Surgeon preference also determines the use of gravity versus a pressure-controlled pump to manage irrigation inflow. Outflow of fluid from the shoulder joint occurs through suction tubing attached to the motorized burr, which is a rotating blade within a smooth sheath. The suction of fluid through the burr allows debris and other tissue to be sucked into the shaver and removed from the joint. Thermal heat in the form of monopolar devices are used for anticoagulation. Cartilage is sensitive to heat, with chondrocyte death being shown to occur with exposure to temperatures as low as 45°C, whereas devices provide heat at temperatures greater than 100°C.21,22 Furthermore, previous use of thermal heat for capsulorrhaphy resulted in multiple complications, including chondrolysis, which will be discussed later. Therefore intraarticular devices providing thermal heat are used sparingly for débridement and mainly for anticoagulation to provide good visualization.

OPTIMIZING VISUALIZATION One of the potentially limiting factors of arthroscopy is bleeding that compromises the ability to visualize pathology. Burkhart and Lo23 describe four main factors to consider when attempting to control bleeding. First, the patient’s systolic blood pressure should be kept between 90 and 100 mm Hg in the absence of medical contraindications. Second, arthroscopic pump pressure should be kept at around 60 mm Hg, with intermittent increases to 75 mm Hg as needed for visualization (for only 10 to 15 minutes at a time). If the pump pressure is not regulated and is too high, the shoulder will swell, which compromises the surgical technique. Third, if possible, a separate 8-mm inflow cannula should be used to maximize fluid flow. Surgical instrumentation

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through this portal should be limited because it may increase turbulence. Finally, turbulence within the system must be minimized. Turbulence occurs as a result of rapid flow of fluid out of the shoulder, such as through a skin portal without a cannula. As Burkhart and Lo23 indicate, the Bernoulli effect creates forces at right angles of the many capillaries in the subacromial space, increasing the bleeding into the operative field. Digital pressure over skin portals can obstruct the outflow of fluid and in effect decrease turbulence.24

ANATOMY AND PORTAL PLACEMENT Having a thorough understanding of basic shoulder anatomy is essential to developing good shoulder arthroscopic technique. We will first address the superficial anatomy, which is the guide to adequate portal placement and thus facilitates maneuverability about the shoulder joint (Fig. 39.2). We start by palpating the bony anatomy. It is important to mark not only the superficial edge of the bone but also the depth of the bone because trocar placement must be directed inferior to the edge of the bone. The clavicle and the anterolateral and posterolateral acromion are outlined. A soft triangle that is often palpable just medial to the acromion serves as a guide. Anteriorly the clavicle can be palpated, moving laterally to where it meets the acromion at the acromioclavicular joint. The coracoid is another important anterior landmark that can be palpated and should be drawn out as well. The posterolateral acromion is a key landmark that can be felt even in larger patients. Once the superficial anatomy is appreciated for each individual patient, portal placement sites are marked on the skin. We start with the posterior portal first. This portal is made 2 cm inferior and 1 to 2 cm medial to the posterolateral edge of the acromion. A sharp scalpel is used to make a deep incision. The trocar is then slowly advanced; it is aimed superior, anterior, and medial, toward the coracoid process anteriorly. The trocar is advanced through soft tissue, and often a soft gap can be gently appreciated between the glenoid and humeral head. In addition, the arm can be internally or externally rotated, and if this movement is felt with the trocar, it is on the humeral head and should be directed to a greater degree medially. If no movement is felt, the trocar may be on the glenoid and needs to be directed to a greater degree laterally. The trocar is advanced until it is felt to “pop” through the capsule of the glenohumeral joint. One way to tell if the trocar is in the shoulder joint instead of the subacromial space is to judge the ease of movement of the trocar superiorly and inferiorly, as would be suggested by the proper location in the shoulder joint. Furthermore, if synovial fluid drips out of the cannula when the trocar is removed, proper placement in the glenohumeral joint is likely. The camera is then introduced into this portal, and one can either proceed with a diagnostic examination or place the anterior portal. We prefer to evaluate the rotator interval and then place the anterior portal as the next step. The anterior portal is ideally placed lateral to the coracoid process through the rotator interval. The portal should never be placed in a position that is inferior or medial to the coracoid process because that would place neurovascular structures at

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SECTION 4  Shoulder Anterior superior

Anterior inferior

Lateral

Neviaser Wilmington

Anterior superior

Posterior

Anterior inferior Lateral

Wilmington

Neviaser

Posterior

7 o’clock

7 o’clock

Fig. 39.2  A right shoulder demonstrating portal positions for the more standard posterior, anterior superior, anterior inferior, and lateral portals. Other common accessory portals shown include the Neviaser portal, the portal of Wilmington, and the 7 o’clock portal. (From Thompson S, Choi L, Brockmeier S, Miller MD. Shoulder and arm. In: Miller M, Cdhhabra A, Park J, Shen F, Weiss D, Browne J, eds. Orthopaedic Surgical Approaches. 2nd ed. Philadelphia: Elsevier Saunders; 2015:41, figure 2-52.)

risk. We prefer to visualize the anterior portal as it is placed from an outside-in technique. Therefore the arthroscope is kept in the posterior portal and moved anteriorly to view the rotator interval between the biceps tendon and the subscapularis tendon. A finger depresses the skin from the anterior side and is viewed on the arthroscope to be within the rotator interval. A spinal needle is then advanced into this area. If we are satisfied with this position for the anterior portal, a superficial skin incision is made (a deeper incision may create bleeding that will obscure visualization). The anterior portal is used mainly for instruments, but often surgeons alternate between portals depending on the procedure being performed. To access the subacromial space, the same initial posterior portal is used, but the trocar is directed more superiorly. The trocar and cannula are advanced so that they hit the acromion and slide just inferior to it. The surgeon’s other hand is used to palpate the anterior acromion and the trocar is advanced until it too can be palpated interiorly just inferior to the acromion. Often the coracoacromial ligament can be palpated with the trocar anteriorly, giving a good indication that the trocar is in the subacromial space. Medial to lateral movement of the trocar clears off some of the bursa that is often found with chronic impingement and is often located more posteriorly. Next, a lateral portal is established. This portal is made just inferior to the lateral border of the acromion, at the anterior third to middle third of the acromion, often 1 to 2 cm posterior to the anterolateral border of the acromion. We like to use a spinal needle to judge our position before creating the portal because we try to

position the portal so it is as parallel to the acromion as possible to make the decompression easier. Accessory portals can be made depending on the procedure to be performed. Often additional portals are useful for instability procedures for anchor placement.

DIAGNOSTIC EXAMINATION We perform a standard diagnostic examination for each patient regardless of the planned procedure or diagnosis to ensure that no possible lesions are overlooked. We start with the arthroscope in the posterior portal and orient our position with the glenoid and humeral head in an upright position to go along with the patient in a beach chair position (Fig. 39.3A–D). The glenoid and humeral head are evaluated for signs of cartilage damage or the presence of osteoarthritis. The superior labrum–biceps tendon complex is a good landmark to find early because the biceps is seen traversing the glenohumeral joint from the labrum to its exit out of the glenohumeral joint. The labrum is evaluated for tears or degenerative fraying (Fig. 39.4). A probe can be used to check the stability of the labrum by pulling it away from the glenoid. Having a small foramen between the anterior–superior labrum and the glenoid is a normal variant that is often associated with a cordlike middle glenohumeral ligament.22 The biceps is followed out to where it exits the glenohumeral joint, and a probe can be used to pull the biceps into the joint to look for signs of inflammation. The superior glenohumeral ligament is seen within the rotator interval, between the biceps tendon and

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CHAPTER 39  Shoulder Arthroscopy

A

B

C

D

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Fig. 39.3  A diagnostic shoulder scope. (A) The initial view of the glenohumeral joint viewed from the posterior portal. The glenoid is on the left and the humeral head is on the right. The labrum can be faintly visualized around the periphery of the glenoid. (B) Looking slightly superior, the insertion of the long head of the biceps into the superior labrum and superior glenoid can be visualized at the upper right. Again, the glenoid is on the left and the humeral head is on the right. (C) The biceps is followed from the mid-left portion of the picture as it exits the glenohumeral joint. An intact supraspinatus is visualized as it inserts at the articular margin of the humeral head at the middle to right portion of this figure. (D) An intact inferior labrum and glenohumeral ligament are visualized at the inferior portion of this figure. The glenoid is on the left and the humeral head is on the right.

subscapularis, and can be evaluated for thickening associated with frozen shoulder or looseness associated with laxity. If the arthroscope is turned inferiorly, the superior border of the subscapularis tendon can be visualized and followed laterally to its insertion onto the lesser tuberosity of the humerus. The anterior labrum is evaluated, and moving more inferiorly, the anterior and posterior labrum and glenohumeral ligaments are evaluated. The anterior-inferior glenohumeral ligament and labral complex makes up the classic Bankart lesion that is seen in anterior shoulder instability (Fig. 39.5). To evaluate posterior portions of the rotator cuff, the anterior edge of the supraspinatus is visualized just lateral to the biceps tendon exit point and can be evaluated throughout its tendinous portion, moving posteriorly both by moving the camera

posteriorly and by abducting the arm and externally rotating the arm. Posteriorly the supraspinatus insertion on the greater tuberosity ends and a bare area is seen because a gap exists between the edge of the articular surface and the infraspinatus insertion. Pitting is commonly seen in this area and represents vascular channels. Continuing posteriorly, the posterolateral humeral head can be seen, and the presence or absence of a Hill-Sachs lesion is confirmed. Moving more inferiorly, the axillary pouch is examined to ensure that no loose bodies are present.25 Finally, the posterior labrum and capsule are examined by slowly backing the arthroscope out of the posterior portal until they come into view, taking care not to pull the scope out completely. The posterior anatomy can be evaluated further by switching the arthroscope to the anterior portal as well.25

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A

B

C Fig. 39.4  A superior labral anterior to posterior (SLAP) tear. (A) Fraying of the superior glenoid labrum, a SLAP lesion. (B) A SLAP lesion as it is being prepared for repair. It has been separated from the glenoid, and the glenoid surface has been roughened to prepare a good healing bed for repair. (C) A SLAP lesion after repair with three suture anchors (which cannot be seen) and sutures passing around the superior labrum.

Fig. 39.5  A Bankart lesion. A traumatic Bankart lesion can be visualized with separation of the inferior glenohumeral ligament/labral complex from the anterior inferior glenoid. This lesion was repaired in a similar manner as the superior labral anterior to posterior lesion in Fig. 39.4, with glenoid bone preparation for a good healing bed, and then suture anchor placement and sutures to hold the Bankart complex down (not shown).

Often a diagnostic scope of the subacromial space also should be performed. The camera is inserted as previously described, with management of bursal tissue being the key to good visualization. To begin the examination, the anterior acromion and coracoacromial ligament are evaluated for impingement. The subacromial space also can be used to evaluate the bursal side of the rotator cuff. To evaluate the rotator cuff, the scope is then turned to look inferiorly so that the top or bursal side of the rotator cuff can be evaluated. Signs of impingement are suggested by the presence of fraying, inflammation, or partial bursal-sided rotator cuff tears. If partialthickness articular-sided tears of the rotator cuff are suspected, a Prolene suture can be passed from the joint side through the rotator cuff and evaluated as it exits the cuff on the subacromial side. If a rent is visualized at the point where the suture comes through, then the tear is actually full thickness.

COMPLICATIONS As with all surgeries, shoulder arthroscopy is not without risk, which includes bleeding, although this is minimal, and infection, which can be both superficial and deep.

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CHAPTER 39  Shoulder Arthroscopy

As mentioned in the “Patient Positioning” section, neurapraxia is also a risk with shoulder arthroscopy, and patient positioning must be performed diligently to avoid this complication in both the beach chair and the lateral decubitus positions. Although the risk of deep venous thrombosis (DVT) and pulmonary embolism is very low (a 0.08% risk of DVT with shoulder arthroscopy, which is only one-tenth of the risk of developing DVT after shoulder arthroplasty), the risk still exists, and no definitive recommendation is provided in the literature for postoperative anticoagulation.26 For our patients, we prescribe enteric coated aspirin, 325 mg for 2 weeks after surgery. Chondrolysis is a complication of shoulder arthroscopy that is characterized by the dissolution of the articular cartilage of the humeral head and glenoid. It presents with the onset of pain and loss of range of motion weeks to months after surgery, and joint space narrowing and subchondral cysts in the absence of osteophytes are noted on imaging.27-32 Chondrolysis has been reported after use of intra-articular thermal energy, after intraarticular injection of radiopaque contrast medium, and most notably, after intra-articular postoperative infusion of a local anesthetic.27-33 In one retrospective review of 375 shoulder arthroscopies, a 13% incidence of chondrolysis was found. It was more common in young patients when one or more suture anchors were used in the glenoid, and in each case a postoperative infusion of local anesthetic was used.27 It is recommended that a postoperative infusion of local anesthetic not be administered to avoid this devastating complication.

Level of Evidence:

CONCLUSION

Level of Evidence:

Shoulder arthroscopy is commonly performed and has many potential indications. It is an equipment-intense procedure that involves two main patient positioning options, each of which has its own advantages and disadvantages. A systematic diagnostic examination should be performed at the start of each procedure so that pathology is not missed. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Youm T, Murray DH, Kubiak EN, et al. Arthroscopic versus mini-open rotator cuff repair: a comparison of clinical outcomes and patient satisfaction. J Shoulder Elbow Surg. 2005;14:455–459.

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III

Summary: In this retrospective review, the outcomes 53 patients who had either an arthroscopic or mini-open rotator cuff repair were examined. Patients were followed up for an average of 19 months (for the arthroscopic procedure) or 33 months (for the mini-open procedure), and results were similar for function and patient reported outcomes.

Citation: Verma NN, Dunn W, Alder RS, et al. All-arthroscopic versus mini-open rotator cuff repair: a retrospective review with minimum 2-year follow-up. Arthroscopy. 2006;22:587–594.

Level of Evidence: III

Summary: In this retrospective review, the outcomes of 71 patients who were treated with either an arthroscopic or mini-open rotator cuff repair were examined. Patients were followed up for an average of 2 years with ultrasound to evaluate the repair. Results for function and patient-reported outcomes were similar, and patients had similar rates of rerupture, which was seven times more likely if the original tear was greater than 3 cm.

Citation: Pearsall AW, Ibrahim KA. Madanagopal SG. The results of arthroscopic versus mini-open repair for rotator cuff tears at mid-term follow-up. J Orthop Surg. 2007;2:1–8. III

Summary: In this study, 52 patients were treated with either a mini-open or arthroscopic rotator cuff repair for a small to large full-thickness rotator cuff tear. Results were similar for both function and patient reported outcomes, suggesting that either treatment option is acceptable at midterm follow-up.

Citation: Teefey SA, Rubin DA, Middleton WD, et al. Detection and quantification of rotator cuff tears: comparison of ultrasonographic, magnetic resonance imaging, and arthroscopic findings in seventy-one consecutive cases. J Bone Joint Surg Am. 2004;86:708–716.

Level of Evidence: Diagnostic study

Level of Evidence: III

Summary:

Summary: In this study, the outcomes of at least 2 years were compared for 40 patients who underwent arthroscopic rotator cuff repair and 40 patients who underwent mini-open rotator cuff repair. Results suggested similar outcomes and patient satisfaction scores for small-, medium-, and massive-sized cuff tears.

Seventy-four patients underwent ultrasound and magnetic resonance imaging (MRI) of their partial- or full-thickness rotator cuff, and then arthroscopy was used for a gold standard comparison. Ultrasonography and MRI had comparable accuracy rates in the identification and measurement of full- and partial-thickness rotator cuff tears.

Citation: Sauerbrey AM, Getz CL, Piancastelli M, et al. Arthroscopic versus mini-open rotator cuff repair: a comparison of clinical outcome. Arthroscopy. 2005;21:1415–1420.

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CHAPTER 39  Shoulder Arthroscopy

REFERENCES 1. Burman MS. Arthroscopy or the direct visualization of joints: An experimental cadaver study. J Bone Joint Surg. 1931;13:669–695. 2. Garret WE, Swiontkowski MF, Weinstein JN, et al. American Board of Orthopaedic Surgery Practice of the Orthopaedic Surgeon: Part II, certification examination case mix. J Bone Joint Surg Am. 2006;88:660–667. 3. Lintner SA, Speer KP. Traumatic anterior glenohumeral instability: the role of arthroscopy. J Am Acad Orthop Surg. 1997;5:233–239. 4. Fineberg M, Wind W, Stoeckl A, et al. Current Practices and Opinions in Shoulder Surgery: Results of a survey of members of the American Orthopaedic Society for Sports Medicine and the Arthroscopy Association of North America. 22nd Annual Meeting Abstracts of Podium Presentations. Phoenix: Arthroscopy Association of North America; 2003:19. 5. Abrams JS, Savoie III. Arthroscopic Rotator Cuff Repair: Is It the New Gold Standard? 72nd Annual Meeting Proceedings. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2005:71. 6. Denard P, Burkart S. Arthroscopic revision rotator cuff repair. J Am Acad Orthop Surg. 2011;19:657–666. 7. Verma NN, Dunn W, Alder RS, et al. All-arthroscopic versus mini-open rotator cuff repair: A retrospective review with minimum 2-year follow-up. Arthroscopy. 2006;22:587–594. 8. Sauerbrey AM, Getz CL, Piancastelli M, et al. Arthroscopic versus mini-open rotator cuff repair: A comparison of clinical outcome. Arthroscopy. 2005;21:1415–1420. 9. Youm T, Murray DH, Kubiak EN, et al. Arthroscopic versus mini-open rotator cuff repair: A comparison of clinical outcomes and patient satisfaction. J Shoulder Elbow Surg. 2005;14:455–459. 10. Pearsall AW, Ibrahim KA. Madanagopal SG: The results of arthroscopic versus mini-open repair for rotator cuff tears at mid-term follow-up. J Orthop Surg. 2007;2:1–8. 11. Bigliani LU, Morrison DS, April EW. The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans. 1986;10:216. 12. Zanca P. Shoulder pain: Involvement of the acromioclavicular joint. (Analysis of 1000 cases). Am J Roentgenol Radium Ther Nucl Med. 1971;112:493–506. 13. Jeyam M, Funk L, Harris J. Are shoulder surgeons any good at diagnosing rotator cuff tears using ultrasound? A comparative analysis of surgeon vs radiologist. Int J Shoulder Surg. 2008; 2:4–6. 14. Ziegler DW. The use of in-office, orthopaedist-performed ultrasound of the shoulder to evaluate and manage rotator cuff disorders. J Shoulder Elbow Surg. 2004;13:291–297. 15. Teefey SA, Rubin DA, Middleton WD, et al. Detection and quantification of rotator cuff tears. comparison of ultrasonographic, magnetic resonance imaging, and arthroscopic findings in seventy-one consecutive cases. J Bone Joint Surg Am. 2004;86:708–716.

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16. Klein AH, France JF, Mutschler TA, et al. Measurement of brachial plexus strain in arthroscopy of the shoulder. Arthroscopy. 1987;3:45–52. 17. Rains DD, Rooke GA, Wahl CJ. Pathomechanisms and complications related to patient positioning and anesthesia during shoulder arthroscopy. Arthroscopy. 2011. 18. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth. 2005;17:463–469. 19. Jensen KH, Werther K, Stryger V, et al. Arthroscopic shoulder surgery with epinephrine saline irrigation. Arthroscopy. 2001;17:578–581. 20. Dang AB, McCarthy MB, Dang AB. Effects of adding epinephrine to arthroscopic irrigation fluid on cultured chondrocyte survival in vitro. Arthroscopy. 2011;27:1118–1122. 21. Lu Y, Edwards RD 3rd, Cole BJ, et al. Thermal chondroplasty with radiofrequency energy. An in vitro comparison of bipolar and monopolar radiofrequency devices. Am J Sports Med. 2001;29:42–49. 22. Good CR, Shindle MK, Griffith MH. Effect of Radiofrequency energy on glenohumeral fluid temperature during shoulder arthroscopy. J Bone Joint Surg Am. 2009;91:429–434. 23. Burkhart S, Lo I. Arthroscopic rotator cuff repair. J Am Acad Orthop Surg. 2006;14:333–346. 24. Burkart SS, Danaceau SM, Athanasiou KA. Turbulence control as a factor in improving visualization during subacromial shoulder arthroscopy. Arthroscopy. 2001;17:209–212. 25. Gartsman G. Shoulder Arthroscopy. Philadelphia: Saunders; 2003:48–78. 26. Ojike N, Bhadra A, Giannoudis P, et al. Venous thromboembolism in shoulder surgery: A systematic review. Acta Orthop Belg. 2011;77:281–289. 27. Wiater B, Neradilek MB, Polissar NL, et al. Risk factors for chondrolysis of the glenohumeral joint. J Bone Joint Surg Am. 2011;93:615–623. 28. Levy JC, Virani NA, Frankie MA, et al. Young patients with shoulder chondrolysis following arthroscopic shoulder surgery treated with total shoulder arthroplasty. J Shoulder Elbow Surg. 2008;17:380–388. 29. Athwal GS, Shridharani SM, O’Driscoll SW. Osteolysis and arthropathy of the shoulder after use of bioabsorbable knotless suture anchors. A report of four cases. J Bone Joint Surg Am. 2006;88:1840–1845. 30. Tamai K, Higashi A, Cho S, et al. Chondrolysis of the shoulder following a “color test” assisted rotator cuff repair—a report of 2 cases. Acta Orthop Scand. 1997;68:401–402. 31. Hansen BP, Beck CL, Beck EP, et al. Postarthroscopic glenohumeral. Chondrolysis. Am J Sports Med. 2007;35: 1628–1634. 32. Petty DH, Jazrawi LM, Estrada LS, et al. Glenohumeral chondrolysis after shoulder arthroscopy; case reports and review of the literature. Am J Sports Med. 2004;32:509–515. 33. Levine WN, Clark AM Jr, D’Alessandro DF, et al. Chondrolysis following arthroscopic thermal capsulorrhaphy to treat shoulder instability. A report of two cases. J Bone Joint Surg Am. 2005;87: 616–621.

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40  Anterior Shoulder Instability Stephen R. Thompson, Heather Menzer, Stephen F. Brockmeier

Anterior shoulder instability is the most common type of shoulder instability. It is typically the result of a traumatic event with dislocation of the glenohumeral joint. However, instability also may present as subluxation, a condition in which the joint symptomatically translates but does not completely dislocate. The estimated incidence of shoulder dislocations in the United States in 23.9 per 100,000.1 Patients of any age may sustain a shoulder dislocation; however, 48% of the patients reported were between the ages of 20 and 29 years. The prevalence of shoulder dislocations in high and collegiate school athletes is reported to be 2.04 and 2.58 respectively per 100,000 athletic exposures.2 Football was reported to have the highest shoulder dislocation rate compared with other sports at each competition level. Dislocation occurred more frequently in competition than in practice, and direct contact was the most common mechanism. Ice hockey, wrestling, and basketball all had higher rates of dislocation compared with other sports, though soccer and baseball had increased rates of noncontact injury. This chapter discusses the anatomy, clinical features, and treatment of anterior shoulder instability. Posterior and multidirectional instability may involve a component of anterior patholaxity; these topics are addressed separately in subsequent chapters. This chapter first reviews the anatomy and pathoanatomy of shoulder instability. The “History and Physical Examination” sections provide an evidence-based approach and assume a general knowledge of shoulder examination. The “Decision-Making Principles and Treatment Options” sections discuss acute shoulder reduction and immobilization, timing of surgery, arthroscopic versus open surgery, unique clinical scenarios, and the approach to bone loss. Our preferred technique for the treatment of shoulder instability is arthroscopic Bankart repair. For revision situations, or in cases of significant bone loss, we prefer the Latarjet procedure. Methods for both of these scenarios are outlined, along with postoperative management. Lastly, the results of treatment and complications are discussed, along with future directions of research.

ANATOMY The glenohumeral joint is a unique diarthrodial joint. More than any other joint in the body, it must carefully balance function and stability. Because of its role in positioning the arm in space, it has 6 degrees of freedom and is the most mobile of the 440

diarthrodial joints. However, to achieve this range of motion (ROM), stability is sacrificed. When discussing the stabilizing anatomy of the shoulder, it has become common to dichotomize the stabilizers as static or dynamic. We recognize that this approach is an oversimplification3 and that the entire system functions in a coordinated fashion, but we believe it serves as a useful pedagogic instrument, and thus we will retain it for the purposes of this discussion. Static stabilizers of the shoulder may be considered as the structures that provide a unidirectional limitation to translation. The three principle groups of static stabilizers are bony, ligamentous, and labral. Dynamic stabilizers are primarily musculotendinous and include the rotator cuff, biceps, deltoid, pectoralis major, and latissimus dorsi. The bony anatomy of the glenohumeral joint has been compared with a golf ball on a tee. The humeral head is significantly larger than the overall size of the glenoid, with only 25% to 30% of the humeral head in contact with the glenoid at any given anatomic position. The bony glenoid concavity is quite shallow, with a depth of only a few millimeters. To confer some degree of stability, the glenoid concavity is deepened by the articular cartilage and the labrum. The articular cartilage is thinner in the center of the glenoid and progressively thickens toward the periphery, thus increasing the functional depth of the glenoid (Fig. 40.1). Loss of the articular cartilage has been found to decrease stability by nearly 50%.4 The glenoid labrum is a critical structure for the stability of the glenohumeral joint. It encircles the glenoid to both increase the depth of the glenoid concavity and the overall surface area of the glenoid in contact with the humeral head by approximately 50%.5 Although it is commonly referred to as a fibrocartilaginous structure, anatomic studies have demonstrated that the glenoid labrum has a structure similar to a tendon, with dense fibrous connective tissue that is devoid of chondrocytes.6–8 The labrum has a predominantly triangular cross-sectional shape and, consequently, functions as a “chock block” that prevents translation of the humeral head outside the articular surface of the glenoid. However, the stabilizing mechanism of the labrum is much more complex than this simple mechanical function. The labrum has a complex anatomic structure and attachment to the glenoid. It is typically more adherent in the inferior half of the glenoid and quite variably attached in the anterior superior quadrant. The labrum serves as an attachment site for the glenohumeral joint capsule and the long head of the biceps tendon,

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CHAPTER 40  Anterior Shoulder Instability

441

Biceps tendon

Depth

MGHL

Anterior band IGHL

SGHL Posterior band Labrum Labrum Cartilage Glenoid

Fig. 40.1  Glenoid concavity is deepened by both the articular cartilage and labrum.

which helps create a suction seal that leads to a negative intraarticular pressure and aids in the creation of the concavitycompression effect of glenohumeral stability. The glenohumeral capsule that attaches to the glenoid labrum has four distinct thickenings that have been termed the glenohumeral ligaments (GHLs): the superior, middle, and anterior band of the inferior and the posterior band of the inferior (Fig. 40.2). Of these ligaments, the inferior glenohumeral ligament (IGHL) is the most important for providing stability to the shoulder. The GHLs are not as strong as the knee ligaments; for example, the IGHL possesses an ultimate stress capability that is only 15% of that reported for the anterior cruciate ligament.9 This characteristic underscores the importance of the entire relationship between the static and dynamic components that provide stability to the glenohumeral joint. The IGHL should be considered a complex rather than an individual structure. Within the IGHL structure, an anterior band originates at the 3-o’clock position of the glenoid, a posterior band originates at the 8-o’clock position of the glenoid, and an intervening capsule exists that is termed the “axillary pouch.” This complex is likened to a hammock. When the arm is brought into the “apprehension position” of abduction and external rotation, the axillary pouch becomes more taut as the anterior band is placed under tension from being pulled superiorly and anteriorly to span the midportion of the glenohumeral joint (Fig. 40.3).10 In this position, the anterior band of the IGHL functions to prevent anterior translation of the humeral head while the taut axillary pouch prevents anteroinferior translation. If the arm is brought into 45 degrees of abduction, the middle GHL becomes taut and prevents anterior displacement.11 In 0 degrees of abduction, the superior GHL has a minor function in preventing anterior displacement and an accessory role in preventing inferior displacement along with the supraspinatus, deltoid, and coracohumeral ligament.10,12

Fig. 40.2  Anatomy of the glenohumeral ligaments: superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament (IGHL). The view is from the posterior aspect, as traditionally seen in lateral-position arthroscopy.

The dynamic stabilizers of the shoulder provide stability by providing compression of the humeral head into the glenoid and coracoacromial arch concavities, which is termed the “concavity-compression effect.”13 The deltoid and the rotator cuff function to dynamically compress and center the humeral head within these concavities during shoulder motion, thereby enhancing (or perhaps providing primary restraint to)14 glenohumeral stability. In a review of anatomy relating to anterior shoulder instability, it is important to note two relatively common anatomic variants that should not be mistaken for pathology. The anterosuperior aspect of the capsulolabral complex is the most variable in the shoulder. A sublabral foramen (or sublabral hole) is the complete separation or absence of the labrum from the glenoid. It is the most common variant, with an incidence between 3% and 18%.15–17 A Buford complex18 is the combination of an absent anterosuperior labrum with an associated “cordlike” middle GHL that attaches to the superior labrum near the base of the biceps tendon. The incidence varies between 1.5% and 6%.15–17 Other less common variants exist as well. Overall, recognition of variant anatomy both on magnetic resonance imaging (MRI) and at arthroscopy is vital to avoid inappropriate diagnosis or treatment.

PATHOANATOMY When A. S. Blundell Bankart described the pathology and treatment of recurrent dislocation of the shoulder, he emphasized

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SECTION 4  Shoulder

3-o’clock position on glenoid

SGHL MGHL

IGHL anterior band

8-o’clock position on glenoid

IGHL posterior band

Anterior

Posterior

A 3-o’clock position on glenoid

SGHL MGHL

8-o’clock position on glenoid

IGHL posterior band

Anterior

IGHL anterior band

Posterior

B Fig. 40.3  The glenohumeral ligaments are dynamic structures. (A) In 0 degree of abduction, the superior glenohumeral ligament (SGHL) is taut. (B) As the arm is brought into the “apprehension position” of abduction and external rotation, the anterior band of the inferior glenohumeral ligament (IGHL) is pulled superiorly and anteriorly to span the midportion of the glenohumeral joint, thus providing anterior stability. MGHL, Middle glenohumeral ligament.

the importance of understanding the pathoanatomy to guide treatment. To him, the “essential lesion” occurred when the “[humeral] head shears off the fibrous or fibrocartilaginous glenoid ligament from its attachment to the bone.”19,20 His original description was based on his work with only four patients, and

his subsequent description 15 years later was based on work with a further 23 patients. Bankart believed that the essential lesion occurred in 100% of cases and that “no one who has ever seen this typical lesion exposed at operation could possibly doubt that the only rational treatment is to reattach the

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CHAPTER 40  Anterior Shoulder Instability Pathogenesis of Bankart lesion

TABLE 40.1  Capsulolabral Lesions Lesion

Description

Tensile force on anterior band

Labral avulsion

Associated With Anterior Instability Perthes Avulsion of the anterior-inferior glenolabral complex with preservation of the medial scapular neck periosteum Bankart Complete avulsion of the anterior-inferior glenolabral complex along with a piece of scapular neck periosteum Bony Bankart Osseous avulsion fracture of the anterior-inferior glenolabral complex ALSPA Avulsion of the anterior-inferior glenolabral complex with stripping of the medial scapular neck periosteum but preservation of a medial hinge; the loose fragment subsequently scars medially down the scapular neck HAGL Avulsion of the glenohumeral ligaments from their humeral-sided attachment Not Associated With Instability Glenolabral A superficial tear of the anterior-inferior labrum with articular associated cartilage injury but preservation of the disruption162 anterior-inferior glenolabral complex; presents with a painful shoulder but is not a cause of shoulder instability SLAP163 Disruption of the superior labrum, originally described to stop at the midglenoid notch; recent descriptions have associated SLAP tears with Bankart lesions, but SLAP lesions alone are not a cause of shoulder instability ALSPA, Anterior labroligamentous periosteal sleeve avulsion; HAGL, humeral avulsion of the glenohumeral ligaments; SLAP, superior labrum anterior posterior.

glenoid ligament (or the capsule) to the bone from which it has been torn.”20 Since Bankart provided this description, a more nuanced understanding of the pathoanatomy of recurrent anterior shoulder instability has been developed. Fundamentally, the pathoanatomy can be capsulolabral, osseous, or both. The capsulolabral lesions are typically related to the glenoid labrum and the anterior band of the IGHL. The nomenclature of these lesions has evolved into a mixture of eponymous terms and acronyms that can confuse even the most experienced clinician. The nomenclature includes the Perthes lesion, Bankart lesion (or “anterior labral tear”), bony Bankart lesion, anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion, and humeral avulsion of the glenohumeral ligaments (HAGL) lesion (Table 40.1). Despite this confusing jargon, the Bankart lesion remains an “essential lesion” and has been found to occur in approximately 90% of patients with recurrent anterior instability.21,22 A Bankart lesion can be arbitrarily defined as an avulsion of the anterior-inferior capsulolabral complex with extension into the scapular periosteum and rupture of the periosteal tissue (Fig. 40.4A). Acutely, the avulsed tissue is free to move about the shoulder. As such, the stabilizing function of the labrum is lost and the anterior band of the IGHL can no longer resist anterior translation in abduction and external rotation.23 A bony Bankart lesion occurs when the capsulolabral complex is avulsed along with a variably sized fragment of bone (see Fig. 40.4B), which can create a significant osseous injury that can contribute to the

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Periosteum

A

B

Fig. 40.4  (A) A Bankart lesion, which is defined as avulsion of the anterior-inferior capsulolabral complex with extension into the scapular periosteum and rupture of the periosteal tissue. (B) A bony Bankart lesion occurs when the capsulolabral complex is avulsed along with a variably sized fragment of bone.

pathogenesis of shoulder instability in a manner more severe than that of a soft-tissue Bankart lesion (discussed later). A Perthes lesion and an ALPSA lesion are variants of the Bankart lesion (Fig. 40.5). A Perthes lesion24 can be thought of as representing the initial stages of a Bankart lesion. The capsulolabral complex is avulsed from the anterior-inferior aspect of the glenoid, but the medial scapular periosteum remains intact. In essence, it is a nondisplaced Bankart lesion. An ALPSA lesion25 occurs when the capsulolabral complex is avulsed and the medial scapular periosteum is stripped (but not detached as in a Bankart lesion) and subsequently displaced down the denuded anterior glenoid neck. In essence, it can be conceptualized as a medialized Bankart lesion. In either lesion, the capsulolabral function is lost and recurrent instability ensues. Although the most common site of injury relating to anterior instability is at the glenoid, rupture of the GHLs can also occur on the humeral side. This rupture has been termed an HAGL lesion and has an incidence between 1% and 9%.26 Similar to that which occurs on the glenoid, the rupture of the humeral insertion, along with a bony avulsion, is coined a bony HAGL or B-HAGL (pronounced “bagel” lesion). Although loss of the GHL tension mechanism results in either case, it is important to recognize this lesion and thus perform the correct surgery. In addition to capsulolabral injury, some degree of bony injury occurs in virtually every patient with anterior shoulder instability. Osseous glenoid lesions are thought to occur as the humeral head either passes over the glenoid rim or as the posterior superior aspect of the humeral head has an impact on the anterior glenoid rim upon dislocation. Conversely, osseous injury to the posterior superior humeral head occurs via an impression-impaction fracture of the soft humeral head bone against the less giving, sclerotic anterior rim of the glenoid when subluxation or dislocation occurs. The existence of this lesion was popularized by two radiologists, Hill and Sachs, in 1940 and has since been termed a Hill-Sachs lesion.27,28 Glenoid bone injury is common and predominately occurs in two configurations. A visible bone fragment with its attached

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SECTION 4  Shoulder

Bankart

Normal

Perthes

ALPSA (close-up acute)

AGHL failure

ALPSA (acute)

HAGL lesion

ALPSA (close-up chronic)

ALPSA (chronic)

Fig. 40.5  Variants of the Bankart lesion. A Perthes lesion represents avulsion of the capsulolabral complex, but the scapular periosteum remains intact. An anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion occurs when the periosteum is stripped and displaced down the anterior glenoid neck. Failure of the glenohumeral ligaments on the humeral side is termed a humeral avulsion of the glenohumeral ligaments (HAGL) lesion. AGHL, Anterior glenohumeral ligaments.

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CHAPTER 40  Anterior Shoulder Instability

capsulolabral structures may fracture from the anterior glenoid rim and is termed a bony Bankart lesion. Alternatively, the anterior glenoid rim may be impacted or eroded from the force of the humeral head during subluxation or dislocation. In a threedimensional (3D) computed tomography (CT) scan of 100 consecutive shoulders with recurrent anterior instability, only 10% were found to have normal glenoid morphology29; 50% of patients had some degree of bony fragment, and 40% presented with erosion or a compression fracture of the glenoid. A subsequent CT study found similar results, with 40% of persons with first-time dislocations and 85% of persons with recurrent dislocations sustaining a degree of glenoid bone loss.30 These noninvasive studies corroborate Rowe’s observations that 73% of his patients undergoing open Bankart surgery had glenoid rim damage.31 Hill-Sachs lesions are common, but until recently, they were less regarded in the pathogenesis of recurrent instability. These lesions occur in approximately 40% of patients with recurrent subluxation but no dislocation, in 70% to 90% of patients with a single dislocation, and in virtually 100% of patients with recurrent dislocations.32–35 The majority of these lesions are small, and in general, they are clinically insignificant. However, a minority have been termed “engaging,” which means the Hill-Sachs lesion is oriented in such a manner that placing the shoulder in abduction and external rotation results in the humeral head losing contact with the glenoid and subsequent subluxation or dislocation of the glenohumeral joint.36 If we return to the analogy of the glenohumeral joint as a golf ball on a tee, it becomes apparent that if either the tee (glenoid) or golf ball (humeral head) is damaged, the stability is altered or even lost. But what degree of injury will result in instability? It is easiest to first consider the glenoid. In a classic biomechanical study by Itoi and colleagues,37 a series of glenoid osteotomies were performed to determine the effect of glenoid bone loss on the glenoid concavity mechanism of shoulder stability. Using the stability ratio,38 these investigators found a significant loss of stability after the creation of a 6-mm defect, which is roughly equivalent to 28% of the total glenoid width. Practically speaking, however, it is difficult to measure the total glenoid width because this bone may be lost due to impaction or erosion. The glenoid length, defined as the superior to inferior distance of the glenoid (i.e., from 12 o’clock to 6 o’clock), can be used as a surrogate if some geometric assumptions and transformations are used. Accordingly, this critical defect size corresponded to 20% of the glenoid length. When the study was repeated with the soft tissue structures retained, the authors confirmed their original findings but also demonstrated that repair of the Bankart lesion failed to confer added stability. Stability was restored only after a coracoid bone graft was placed. Clinically, these results have been supported by numerous studies that have found significant bone loss to be a risk factor for failure after a Bankart repair.39–41 Burkhart and De Beer36 described their clinical experience with bony glenoid loss. If the glenoid is viewed en face, it has an appearance similar to that of a pear. When anterior glenoid bone loss occurs, Burkhart and De Beer indicated that the glenoid has an “inverted pear”

445

appearance and hypothesized that this arthroscopically viewable appearance is an indicator of clinically significant bone loss. When patients were dichotomized into a normal glenoid or inverted pear glenoid group, the recurrent dislocation rate after arthroscopic Bankart repair was 4% for the normal glenoid group but 61% for the inverted pear glenoid group. Lo, Parten, and Burkhart then reexamined these data and compared them with a cadaveric model, demonstrating that approximately 6.5 mm of glenoid bone loss (or 29% of the glenoid width) was necessary to achieve an inverted pear glenoid configuration.42 This led to a common acceptance that glenoid bone loss of 20% to 27% was “critical” bone loss and the surgeon should consider performing an open bone grafting procedure, such as a Latarjet, in these patients. However, a recent cohort study by Shaha and colleagues43 of military recruits has questioned this dogma. In their population with high levels of mandatory activity, they found glenoid bone loss of 13.5% was associated with worse patient reported outcomes and higher failure rates following arthroscopic Bakhart repair. In those patients with bone loss less than 13.5%, the failure rate was 5% compared with 22% in the group with more than 13.5% bone loss. A subsequent biomechanical study has supported this, finding that glenoid bone loss more than 15% resulted in an inability of a soft tissue procedure to restore stability.44 The significance of humeral bone loss via Hill-Sachs lesions has been more difficult to characterize. Numerous authors have proposed classification schemes in an attempt to guide clinical decision-making. They have variably defined the size according to length and depth,45 percentage of humeral head involvement at arthroscopy,33 percentage of humeral head involvement on a Notch View radiograph,46 and circular degree involvement and location on axillary MRI.47 Regardless of classification, it has been recognized that persons with large Hill-Sachs lesions are at risk for recurrent dislocation.36,45 Small lesions have conversely been viewed as clinically insignificant. Intermediate lesions have represented something of a management quandary. Due to the multiple variables associated with Hill-Sachs lesions, many of these classification schemes are not useful. Recent interest in how both glenoid and humeral osseous defects can contribute to the pathogenesis of instability has increased and resulted in the concept of the “glenoid track.”48 This concept has been gaining significant traction in the classification and treatment paradigm of shoulder instability. The glenoid track is defined as the zone of contact between the glenoid and the humeral head when the humerus is in maximal external rotation and horizontal extension and the arm is elevated and depressed (Fig. 40.6A). If a Hill-Sachs lesion is entirely contained by the glenoid track, regardless of its length, depth, or percentage of the humeral head, then it never has the ability to engage the glenoid and dislocate (see Fig. 40.6B). If the Hill-Sachs lesion does not engage with the glenoid defect, it is considered an “on-track” lesion.49 Conversely, a small and shallow Hill-Sachs lesion can become an “off-track” symptomatic defect if its location is medial to the glenoid track (see Fig. 40.6C). It is also vital to understand that, by definition, any glenoid-side bone loss will decrease the width of the glenoid track (see Fig. 40.6D).

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SECTION 4  Shoulder

Hill-Sachs lesion

A

B

Hill-Sachs lesion

True glenoid track width 84%

C

D Fig. 40.6  Glenoid track. (A) The glenoid track is defined as the zone of contact between the glenoid and the humeral head when the humerus is in maximal external rotation and horizontal extension and the arm is elevated and depressed. (B) If the Hill-Sachs lesion is entirely within the glenoid track, then it will not dislocate. (C) A lesion outside the glenoid track can result in instability, even if it is small. (D) Any glenoid bone loss functionally decreases the width of the glenoid track.

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CHAPTER 40  Anterior Shoulder Instability

Although the glenoid track is a recently proposed concept, its application was reported superior at predicting postoperative stability in a cohort of patients who underwent arthroscopic Bankart reconstruction.50 It provides an excellent framework for considering the interaction and importance of both glenoid and humeral bone loss in the pathogenesis of shoulder instability. Given the high incidence of osseous injury in persons with either acute or recurrent anterior instability, it is vital for the clinical evaluation to account for potential osseous causes of instability to avoid the risk of treatment failure.50

HISTORY The purpose of the history is both to establish the diagnosis of shoulder instability and to obtain information that will guide treatment. Often the diagnosis of shoulder instability is not in question after a traumatic dislocation and a physician-assisted reduction. Conversely, some persons present with more subtle forms of instability and require differentiation from patients with posterior or multidirectional instability. Information to guide treatment must include data that will allow the surgeon to identify the risk of recurrence, the risk of failure of arthroscopic surgery, and the risk of associated pathology. When first approaching a patient who reports shoulder instability, it is useful to classify the patient as either having sustained or not having sustained a dislocation. If the patient has experienced a dislocation, the details should be ascertained, including the mechanism of injury, the use of radiographs, the need for reduction (as well as who performed the required reduction), and the length of disability resulting from the dislocation. What arm position aggravates the sense of instability? If the patient has experienced multiple dislocations, it is useful to proceed in chronologic order to evaluate how the mechanism of injury may have evolved. Are the dislocations becoming more frequent? Are they occurring with less traumatic force? Lastly, it is vital to document the age of the patient when the first dislocation occurred and his or her age at the time of subsequent dislocations, because age is a significant prognostic indicator for recurrence. Symptoms of shoulder subluxation without dislocation are vague, difficult to evaluate, and difficult to distinguish from the symptoms of patients with multidirectional instability.51 Typically the symptoms have an insidious onset and include a sense of looseness, shoulder achiness, and possibly transient neurologic deficits. The activities causing symptoms are often random and, in contrast to the cases of patients with traumatic instability, may occur with activities of daily living. To distinguish patients with anterior instability from patients with posterior and multidirectional instability, identifying the arm position that aggravates symptoms is occasionally useful. Classically, anterior instability presents with discomfort when the shoulder is abducted and externally rotated (such as when throwing a ball). Posterior instability presents with discomfort when the shoulder is internally rotated, adducted, and forward elevated, such as when pushing a door open. Multidirectional instability presents with symptoms in a variety of positions, but by definition, symptomatic inferior translation is part of the spectrum of complaints.

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Once the history of the present illness is concluded, a comprehensive social history is obtained. In which sport (or sports) does the patient participate? Are these sports competitive or recreational? Is the activity a contact sport? Which way does the patient typically shoot, throw, or swing? What is the patient’s occupation? Does the patient’s occupation require forced overhead activity? This vital information will guide treatment. A small number of patients present with the ability to voluntarily dislocate their shoulder. A classic study by Rowe and colleagues52 found that a substantial proportion of patients who could voluntarily dislocate their shoulder had an associated psychiatric condition and did very poorly after surgical stabilization. However, these investigators acknowledged that the majority of persons who could voluntarily dislocate their shoulder had no cognitive disturbance. Nevertheless, the association between persons who can voluntarily dislocate their shoulder and psychopathology has persisted. The astute clinician should screen for psychopathology but recall that the majority of these patients warrant more than cognitive and physical therapy. It is important to differentiate “voluntary” from positional instability. “Voluntary” suggests a muscular contraction and a volitional component, whereas patients with positional instability (commonly posterior) can reproduce the instability by positioning their hand in space. It is very common for patients with posterior instability to demonstrate their instability in forward elevation. From the history alone, it is possible to estimate the risk for the presence and size of a glenoid bony defect. Milano and colleagues53 demonstrated that the presence of a defect was significantly associated with multiple dislocations, male gender, and type of sport. The size of the defect was significantly associated with recurrent dislocation, an increasing number of dislocations, timing from first dislocation, and manual labor. Presence of a 20% defect of the glenoid width was significantly associated with the number of dislocations and age at first dislocation.

PHYSICAL EXAMINATION As with the history, the physical examination must be goal directed. Goals of the examination are to: • Either narrow the differential diagnosis or confirm the suspected diagnosis after the history is taken • Rule out possible associated pathology • Obtain information that will influence management The standard systematic orthopedic approach of “look, feel, move,” which was popularized by A. Graham Apley, should be used on a routine basis. First, a general impression of the patient is obtained. For example, unlike a 15-year-old underweight swimmer, a 22-year-old muscular football player is likely to have anterior instability. If the patient is older than 40 years, a rotator cuff tear should be considered, whereas if the patient is older than 60 years, a rotator cuff tear, axillary nerve injury, or brachial plexus palsy should be considered. After inspection, palpation, and ROM testing, the examination proceeds to strength testing (see Chapter 43). All components of the rotator cuff musculature should be evaluated with great care. Massive subscapularis ruptures may manifest as anterior

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instability, whereas associated supraspinatus tears are not uncommon in older patients after shoulder dislocations.54 Once a generalized appreciation of both shoulders has been obtained, special tests are performed to confirm the diagnosis of anterior shoulder instability. It is important to note that instability is a subjective complaint of the patient and not a physical examination finding. By definition, instability is “symptomatic translation,” not merely the presence of larger magnitudes of translation upon physical examination. A multitude of tests has been described for instability, but within the literature, the most accurate test is the apprehensionrelocation test.55 To perform this test, the patient is placed supine at the edge of the examination table and the affected shoulder is brought into an abducted/externally rotated position. This arm position is considered to be the apprehension position because it maximizes the tension on the IGHL. If the patient has anterior instability with an incompetent IGHL, the restraints to anterior translation are lost and the patient feels a sense of apprehension that the shoulder will dislocate. The patient may alternatively experience pain, but pain is considered to be a less accurate criterion for a positive apprehension sign.56 The relocation test, or Fowler sign, is a continuation of the apprehension test that entails placing a posterior force on the arm to relieve the symptoms of apprehension (Fig. 40.7). Without warning, the examiner may remove his or her hand, thus reproducing the symptoms of the apprehension test. This maneuver is termed the surprise test or anterior release test. The sensitivity of these tests is moderate, but they have high associated specificities, and the positive likelihood ratios for these examinations vary between 6 and 20.56–58

After the apprehension tests are used to diagnose anterior shoulder instability,59 the examination turns to ruling out associated pathology. The most important concomitant pathology is a rotator cuff tear, which should have been detected with muscle strength testing. The belly-press test and lift-off test can be used to diagnose subscapularis insufficiency, the Jobe empty can test evaluates supraspinatus integrity, and massive cuff tears can be identified with the dropping sign and horn blower’s sign (signe de Clarion).60 Other commonly associated lesions include superior labral anterior to posterior (SLAP) tears, posterior or circumferential labral tears, and incompetence of the rotator interval. SLAP tears are notoriously difficult to diagnose with physical examination.61 Anecdotally, we have found that O’Brien’s test works best to diagnose SLAP tears when combined pathology is present, but the significance of concomitant SLAP lesions is unclear. Posterior labral pathology can be detected with the posterior apprehension test and jerk test. Competency of the rotator interval can be evaluated by performing the sulcus test in 30 degrees of external rotation. Lastly, but very certainly not of least importance, is the evaluation of laxity. Several tests are used to gain comprehensive knowledge of the various ligamentous structures. Anterior shoulder laxity is determined by performing external rotation with the arm at the side (Fig. 40.8A). More than 85 degrees of external rotation is considered to be lax. Inferior hyperlaxity is evaluated with the Gagey hyperabduction test, which is performed with the patient in the seated position and the examiner standing behind the patient. The examiner’s arm is forcefully placed on the shoulder to prevent scapular movement (see Fig. 40.8B). The shoulder is passively abducted and the amount of glenohumeral abduction, prior to the initiation of scapulothoracic movement, is noted. More than 105 degrees of abduction is consistent with inferior laxity. The examination is concluded with an assessment of generalized ligamentous laxity, using the Beighton criteria (see Fig. 40.8C).

IMAGING

Fig. 40.7  The relocation test, or Fowler sign, is a continuation of the apprehension test, in which the examiner places a posterior force on the arm to relieve the symptoms of apprehension. It is useful to use a small stool on which the left leg is rested to provide stability to the elbow.

Imaging is vital in the diagnostic process of anterior shoulder instability. Imaging is obtained for several purposes; the foremost reason is to ensure that the joint is not currently dislocated. Imaging also allows for determination of glenoid or humeral bone loss, identification of the pathoanatomy, and detection of associated pathology. Plain radiographs, CT, and MRI all have a role in diagnosing anterior shoulder instability. Plain radiographs are obtained initially and should include anteroposterior (AP) shoulder views in internal and external rotation, a true AP Grashey view, and an axillary view. The AP view in internal rotation allows for a generalized assessment of the joint and surrounding structures. Unexpected pathology, such as abnormal calcifications and tumors, can be detected with radiographs. Radiographs also should be carefully inspected for the presence of a Hill-Sachs lesion. The external rotation AP view is also examined for presence of a Hill-Sachs lesion, because only large lesions are typically visualized with this view. The Grashey view is used to assess the glenohumeral joint and the presence of subtle subluxation or joint space narrowing consistent

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A B Joint Left little (fifth) finger Right little (fifth) finger Left thumb

Right thumb

Left elbow Right elbow Left knee Right knee Forward flexion of trunk with knees full extended

C

Finding Passive dorsiflexion beyond 90° Passive dorsiflexion ≤90° Passive dorsiflexion beyond 90° Passive dorsiflexion ≤90° Passive dorsiflexion to the flexor aspect of the forearm

Points 1 0 1 0 1

Cannot passively dorsiflex thumb to flexor aspect of the forearm

0

Passive dorsiflexion to the flexor aspect of the forearm

1

Cannot passively dorsiflex thumb to flexor aspect of the forearm

0

Hyperextends beyond 10° Extends ≤10° Hyperextends beyond 10° Extends ≤10° Hyperextends beyond 10° Extends ≤10° Hyperextends beyond 10° Extends ≤10° Palms and hands can rest flat on the floor

1 0 1 0 1 0 1 0 1

Palms and hands cannot rest flat on the floor

0

Fig. 40.8  Evaluation of laxity. (A) Anterior shoulder laxity is determined by performing external rotation with the arm at the side. More than 85 degrees of rotation (for the patient’s right arm) is considered lax. (B) The Gagey hyperabduction test. More than 105 degrees of glenohumeral abduction prior to initiation of scapulothoracic movement is considered abnormal. (C) Beighton criteria of generalized ligamentous laxity.

with a cartilage defect or dislocation arthropathy. The axillary view is key in detecting dislocation of the joint and can also be used to visualize a Hill-Sachs lesion. All patients should have an axillary radiograph performed before leaving an emergency department setting to confirm glenohumeral reduction. Standard views are extremely helpful, but because of the anatomy of the shoulder, overlap of the humeral head and the glenoid on other structures is often significant. As such, a specialized view should be obtained to examine for the presence and severity of glenoid and humeral bone loss. Glenoid bone

loss can be detected using the West Point view or Bernageau view. Hill-Sachs lesions are easily identified with use of the Stryker Notch view or Didiée view. The apical oblique view (Garth view) is useful, as it adequately visualizes both glenoid bone loss and Hill-Sachs lesions with minimal patient positioning (Fig. 40.9). Advanced imaging is dictated by the history, physical examination, and radiographic findings. CT is commonly used for the determination of bony anatomy, whereas MRI is more often used to detect occult soft tissue pathology. Recent studies show that glenoid bone loss can be accurately measured on MRI alone,

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X-

ra

y

45° Bare area

B 45°

A

y

ra

X-

Percentage bone loss = Fig. 40.9  Garth’s apical oblique view adequately visualizes both glenoid bone loss and a Hill-Sachs lesion.

thereby avoiding the need for a CT scan, although the accuracy of the measurement correlates with level of experience and training of the persons reading the study.62 Either scan can be performed in association with arthrography to increase the overall sensitivity of the examination. Detection of bony pathology is important prior to standard arthroscopic stabilization. Indications for obtaining advanced imaging include multiple dislocations, increasing ease of dislocations and/or reductions, apprehension on physical examination with the arm in less than 75 degrees of abduction, and radiographic evidence of glenoid bone loss. Quantitative evaluation of glenoid bone loss is best performed using 3D CT.63 Use of this imaging modality permits the humerus to be subtracted and the glenoid to be viewed en face. Numerous methods have been described to quantify bone loss, and currently no standard has been agreed upon. Perhaps the most straightforward technique is based on the observation that the inferior aspect of the glenoid is a true circle, with the bare spot located in the exact center.64 As such, the simple mathematical principle that the diameter of the circle is twice the radius can be used to determine the percentage of bone loss. This quantification method has been termed the perfect circle technique50 in the literature (Fig. 40.10). To quantify bone loss, the 3D CT scan is used with the humerus subtracted. The first goal is to estimate the bare area. To do so, a vertical line from the supraglenoid tubercle at the most superior aspect is drawn. Next, a horizontal line at the widest AP distance is drawn. At the intersection of these two lines is the approximated bare area. The next goal is to draw a best-fit circle, which is centered about the bare area. The distance from the bare area to the posterior

Distance to anterior rim

Distance to posterior rim

(B – A) 2×B

Fig. 40.10  Determining glenoid bone loss using the anteroposterior distance from bare area method.

glenoid rim is measured. The distance from the bare area to the remaining anterior glenoid rim is also measured. The percentage of bone loss can be calculated as [(posterior distance) − (anterior distance)]/(2 × posterior distance).63,65 Significant instability that is not amenable to standard arthroscopic techniques has been described as low as 13.5% of glenoid width loss.44 If the diagnosis of shoulder instability is in question or an associated rotator cuff tear is suspected, an MR arthrogram is obtained. MRI is able to accurately detect a variety of soft tissue pathologies, but sensitivity is approximately 70%. Intraarticular injection of gadolinium contrast dye results in distention of the joint, thus enabling better anatomic resolution, as well as permitting T1 imaging with a higher signal-to-noise ratio compared with T2 imaging. This use of contrast dye improves the sensitivity into the mid-90% range.66 In addition, placing the arm into the abducted and externally rotated position results in increased tension on the IGHL and can accentuate subtle pathology, thus further improving sensitivity.67 The various soft tissue pathologies are demonstrated in Fig. 40.11. MRI is also accurate in identifying the HAGL lesion (Fig. 40.12), which has traditionally been treated in an open fashion and, as such, is key to identifying preoperatively if arthroscopic repair is typically performed.68 Recent literature has suggested that CT arthrography is equal, if not superior, to MR arthrography in identifying HAGL lesions.69

DECISION-MAKING PRINCIPLES Fundamentally, the most important decision in patients with anterior shoulder instability is operative versus nonoperative management. If surgical treatment is elected, the type of procedure must be determined. Options include open or arthroscopic

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CHAPTER 40  Anterior Shoulder Instability Bankart Lesion Avulsed anteroinferior labrum

Distrupted medial scapular periosteum

Osseous Bankart Lesion Cortical distruption inferior glenoid rim

Hill-Sachs lesion with marrow edema

Perthes Lesion Intact medial Anterior labrum scapular periosteum

Nondisplaced anteroinferior labral tear

Displaced osseous Bankart lesion Perthes Lesion in ABER View Anteroinferior labrum

Triangular-shaped contrast collection between labrum and glenoid indicates a nondisplaced labral tear

Intact medial scapular periosteum

ALPSA Lesion

Torn and medialized anteroinferior labrum

Glenoid rim

Reverse Bankart Lesion

Posterior labral tear

Fig. 40.11  Magnetic resonance imaging appearance of the various soft tissue pathologies associated with shoulder instability. ABER, Abduction external rotation; ALPSA, anterior labroligamentous periosteal sleeve avulsion. (Modified from Morrison WB, Sanders TG. Problem Solving in Musculoskeletal Imaging. St Louis: Elsevier; 2008.)

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A

B

Fig. 40.12  Magnetic resonance imaging appearance of a humeral avulsion of the glenohumeral ligaments lesion. A coronal magnetic resonance T1-weighted (A) arthrogram anterior to a T2-weighted (B) image shows the humeral avulsion of the anterior band of the inferior glenohumeral ligament (arrowhead). The attachment of the axillary recess capsule to the humerus is too distal, the so-called J sign (arrows). (Modified from Pope TL, Bloem HL, Beltran J, et al. Imaging of the Musculoskeletal System. Philadelphia: Elsevier; 2008.)

stabilization or the Latarjet (coracoid transfer) procedure. The goals of treatment, regardless of method, are to provide the patient with a stable, durable shoulder that permits the patient to perform his or her desired activities without a loss in quality of life. To achieve these goals, a variety of factors are important to consider when making this decision. These factors include age at initial dislocation, first-time versus recurrent instability, in-season versus off-season with regard to sports activity, sporting activity level, and associated injuries.

Age at Initial Dislocation Age at the time of the initial dislocation is the single most important factor for predicting recurrent instability. McLaughlin and Cavallaro70 first discovered that the incidence of recurrence is approximately 90% in patients younger than 20 years and that the incidence of recurrence decreases to only 10% in persons older than 40 years. In a study spanning 20 years of admissions to the Massachusetts General Hospital, Rowe71 observed an 83% recurrence rate in persons younger than 20 years. The largest prospective study with a 25-year follow-up was published in 2008 by Hovelius and colleagues.72 They also found that age was the most important predictive factor, with a 72% recurrence rate in patients younger than 20 years. Recurrence decreased with age, with a 56% rate of recurrence in persons aged 23 to 29 years and a 27% rate in persons between 30 and 40 years of age. Investigators have also examined recurrence rates in groups of patients on either end of the age spectrum. Marans and colleagues73 found a 100% recurrence rate in children with open physes at the time of initial dislocation with a mean time to redislocation of 8 months. A systematic review by Olds et al.74 observed an overall 73% rate of recurrent instability in children 18 years and under. Pooled data from this study reported a 94% recurrent in children with a closed proximal humerus physis, compared with 61% recurrence with an open physis, suggesting a child with a closed physis is 14 times more likely to experience recurrent instability. In addition, males were found to be 3.4 times more likely for recurrent episodes than females. The rate

of recurrence does not decrease to a negligible level in elderly patients, however. Gumina and Postacchini75 found a recurrence rate of 22% in patients older than 60 years. Many other studies have been published that have indirectly found associations between age and recurrent instability.74,76–80 The results of these studies can be broadly summarized as observing a high rate in young patients and a lower rate in older patients. Recurrence occurs in 70% to 95% of persons younger than 20 years, 60% to 80% in persons aged 20 to 30 years, and 15% to 20% in persons older than 40 years at the time of the initial dislocation. Age may also play a role in recurrent instability after arthroscopic stabilization procedures.81–84 Voos and colleages81 reported an 18% rate of recurrent instability following arthroscopic stabilization. Patients under the age of 25 with ligamentous laxity and large Hill-Sachs lesions were at greatest risk for recurrent instability. Cho et al.83 performed open stabilization after recurrent instability following arthroscopic treatment in 26 patients with a mean age of 24 years. Identifying age as a predictor of recurrence instability helps council patients and facilitates discussion about risk for revision procedures, including open stabilization.81

First-Time Versus Recurrent Instability The decision to proceed with surgical stabilization after a firsttime shoulder dislocation is controversial.85,86 Four randomized controlled trials87–90 and two meta-analyses91,92 have been published to guide this decision. Three of the four randomized trials compare arthroscopic Bankart repair with conservative care, whereas the fourth compared open Bankart repair with use of a sling. The meta-analyses of these studies demonstrate that Bankart repair results in a significant reduction in the risk of recurrent instability over a 2- to 10-year period compared with the use of a sling or arthroscopic lavage. Furthermore, with the use of the Western Ontario Shoulder Instability Index93 as a disease-specific quality of life measurement tool, Bankart repair is associated

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with improved quality of life over a 2- to 5-year period. However, global patient satisfaction was no different between conservative treatment and operative groups. These trials and meta-analyses have significant limitations that render the conclusions somewhat speculative. Two of the four studies use operative techniques that are no longer performed. Activity levels were poorly defined, different rehabilitation protocols were used, and the length of follow-up was highly variable. The present literature supports use of the Bankart repair in young persons with a first-time dislocation as a method of reducing recurrent dislocation and improving quality of life. Two recent Markov decision models have further supported this claim.94,95 A retrospective analysis comparing the results of repair after initial dislocation with repair after recurrent instability also supports surgical intervention for first-time dislocators.96 Further primary research is required to better substantiate these claims.

In-Season Management Anterior shoulder instability frequently occurs in athletes, with most traumatic events occurring during competition.97 Approximately half of instability events lead to more than 10 days lost to sport,97,98 despite the typical pressure on the athlete to return as quickly as possible. As such, the management of anterior shoulder instability during the sporting season is difficult. Ultimately, the goals of treatment remain the same, but in the competitive athlete, additional goals include minimizing time away from sport, preventing additional injury and ensuring the safe return to full activity.99 In a study of 30 athletes who sustained an in-season dislocation across a variety of sports, 90% were able to return to their sport in the same season using a supervised physical therapy program and no period of immobilization.98 Seventyfive percent of patients returned to sport wearing either a Duke Wyre or Sully brace, and 37% had recurrent in-season instability episodes. Ultimately, 53% of all patients underwent surgical stabilization. A multicenter trial at the military academies followed 45 contact intercollegiate athletes for two seasons who had sustained an in-season dislocation or subluxation.100,101 Following a standardized rehabilitation protocol, 73% of individuals were able to return to play (RTP) that same season with a mean time to return of 5 days.100 However, only 27% completed the season without further instability episodes. In a subsequent study following this same cohort into the following season, 74% of patients had elected arthroscopic Bankart repair while 26% continued with rehabilitation.101 The operative group had a 90% successful completion of the subsequent season, while the rehabilitation group had only a 40% success rate. These results suggest that that a highly competitive athlete who sustains an in-season shoulder instability event has the potential to be treated nonoperatively, but that surgical intervention should also be strongly considered. The algorithm developed by Owens and colleagues99 is particularly helpful in identifying patients who are appropriate for a trial of nonoperative management and early return to sport. After a complete physical examination and radiographic evaluation, players with an initial

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instability episode who do not have significant osseous defects of the glenoid or humeral head and are at the beginning of the season with time to appropriately rehabilitate are most suitable for physical therapy and sport-specific training. Criteria for RTP include full ROM and normal strength. A brace should be used RTP when possible.

Athletes in Contact Sports Athletes who compete in contact sports are particularly prone to anterior shoulder instability. Achieving return to sport is much more difficult for them, as evidenced by a study of professional rugby players whose mean absence from competition after a shoulder dislocation was 81 days.102 In this cohort of athletes, the decision to proceed with surgical stabilization is typically not difficult. However, deciding between an open or arthroscopic technique can be problematic. Athletes in contact sports have typically been treated with an open Bankart stabilization, based on its historical gold standard status103 and early reports of increased failure rates after arthroscopic stabilization.104,105 Pagnani and Dome106 reported no postoperative dislocations and 3% postoperative subluxation in American football players after open Bankart stabilization, whereas Uhorchak and colleagues107 reported a 3% recurrent dislocation rate and a 19% subluxation rate in contact athletes after open Bankart stabilization and anterior capsulorrhaphy. Despite the low rates of recurrence after open Bankart stabilization, more sophisticated arthroscopic techniques have recently been developed, and arthroscopic stabilization is being increasingly recommended to avoid the morbidity associated with open Bankart stabilization.99,108 Recent reports of long-term outcome at 13-year follow-up after arthroscopic stabilization are comparable to reported results after open Bankart repair.109 In addition, in National Collegiate Athletic Association (NCAA) Division I football, the RTP following arthroscopic Bankart repair has been demonstrated to be as high as 90%.110 Open stabilization using the Latarjet technique has also been reported in rugby players. Neyton and colleagues111 reported no postoperative dislocations or subluxations with a mean 12-year follow-up. Considering these results, in our clinical practice, we recommend the Latarjet procedure or arthroscopic Bankart repair for athletes participating in contact sports.

Associated Injuries A variety of associated injuries may occur after an anterior shoulder dislocation, including rotator cuff tear, greater tuberosity fracture, brachial plexus palsy, axillary nerve palsy, and axillary artery injury. Associated injuries occur predominately in the older population, with 40% sustaining some form of injury after dislocation.112 Dislocation with associated greater tuberosity fracture is most common and occurs in approximately 15% of older patients. Rotator cuff tears, which are the second most common associated injury, occur in 10% of older patients. Neurologic deficit, primarily involving the axillary nerve, occurs in 5% of older patients. Identifying these associated injuries is critically important because they can significantly influence management. Patients with an associated greater tuberosity fracture are generally viewed

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as having a better prognosis than patients who have an associated rotator cuff tear. Associated greater tuberosity fracture decreased the odds of recurrent instability by 3.8 times after nonsurgical management of shoulder dislocation.113 Hovelius and colleagues114 found a 32% rate of redislocation in patients with isolated anterior dislocation but no redislocations in patients with an associated greater tuberosity fracture. Few studies have been performed to guide parameters for operative fixation of associated greater tuberosity fractures, but given the biomechanical disadvantage of small amounts of displacement of the greater tuberosity, the current consensus in the literature is fixation of fractures with more than 5 mm of displacement.115,116 Rotator cuff function must be carefully evaluated in the older patient. It is not uncommon for rotator cuff dysfunction to be confused with axillary nerve palsy,117 and any patient with suspected axillary nerve palsy after anterior dislocation should undergo ultrasonographic or MRI evaluation to rule out a rotator cuff tear. Furthermore, given the prevalence of rotator cuff tears in the older population, any history of preexisting shoulder dysfunction should be obtained. As with greater tuberosity fractures, few studies are available in the literature to support management.118 Older patients who sustain an anterior shoulder dislocation should be carefully monitored. Patients who experience significant dysfunction or pain should be considered for operative management. When diagnostic imaging shows that patients with suspected axillary nerve palsies do not have rotator cuff tears, electrodiagnostic studies may be obtained. The prognosis for recovery is excellent, with one study demonstrating a 100% recovery rate.75

Synthesis Should surgery be elected, the aforementioned considerations must be synthesized into a comprehensive view of the patient. Balg and Boileau119 have developed the Instability Severity Index Score (ISIS) as a way to determine which patients would ultimately benefit most from arthroscopic Bankart repair or the Latarjet procedure. In a prospective case-control study, these investigators identified six risk factors that, when combined as a scoring system, resulted in unacceptably high rates of failure after arthroscopic stabilization (Table 40.2). Patients with more than 6 points had a recurrence risk of 70%, whereas patients with a score of 6 or less had a recurrence risk of 10%. Accordingly, patients with an ISIS greater than 6 should undergo an open Latarjet procedure, whereas patients with 6 points or fewer are acceptable candidates for arthroscopic Bankart repair.120 A similar case-control study had a similar failure risk of 70% if ISIS was 4 or greater compared with 4% if ISIS was less than 4.121 Currently, competitive athletes younger than 20 years who are involved in a contact or forced overhead sport should be counseled regarding the risks, benefits, and alternatives regarding Latarjet and arthroscopic Bankart reconstruction.

TREATMENT OPTIONS Treatment options may be categorized into acute reduction on the field, reduction in the emergency department, nonoperative sling immobilization and rehabilitation, and surgery.

TABLE 40.2  Instability Severity Index

Score

Prognostic Factor

Points/Type of Procedure

Age at Surgery (year) ≤20 >20

2 0

Preoperative Sport Participation Competitive Recreational or none

2 0

Preoperative Sporting Activity Contact or forced overhead Other

1 0

Shoulder Hyperlaxity Anterior or inferior Normal laxity

1 0

Hill-Sachs on Anteroposterior Radiograph Visible in external rotation Not visible in external rotation

2 0

Glenoid Loss of Contour on Anteroposterior Radiograph Loss of contour 2 No lesion 0 Total Score ≤4 4–6 >6

Arthroscopic Bankart procedure Current research suggests open procedure, but not definitive Open Latarjet procedure

From Balg F, Boileau P. The instability severity index score. A simple pre-operative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Sur Br. 2007;89:1470–1477.

On-Field Management Despite the frequency with which traumatic shoulder dislocation occurs during sporting activity, surprisingly little literature exists to guide initial treatment. Fundamentally, on-field management can be dichotomized into an attempted reduction or direct transfer to an emergency department. Based on experience, a brief window of time exists during which significant pain is associated with the dislocation but muscular spasm has not yet occurred. In this scenario and assuming a compliant and willing patient, on-field reduction is attempted. A focused neurovascular examination is performed prior to the reduction attempt. A single reduction attempt is performed. Reduction is accomplished via longitudinal traction with gentle forward elevation. If an immediate on-field reduction could not be performed with ease, the athlete can be escorted to the training room and placed in a prone position, with the shoulder hanging at approximately 90 degrees of forward flexion. A weight can be held by the athlete, if available. Gentle traction with slight external rotation of the arm and scapular manipulation is often a successful reduction technique without use of sedatives or analgesics.122 If reduction is achieved, pain relief can be dramatic and the patient can be referred to the team

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CHAPTER 40  Anterior Shoulder Instability

physician for subacute radiographs to rule out bony injury. If reduction cannot be achieved, the patient should be transported to the emergency department.

Management in the Emergency Department Patients who present to the emergency department with suspected anterior shoulder dislocation must undergo a comprehensive evaluation, including a history, complete physical examination, and radiographs, prior to any reduction attempt. Radiographs must include orthogonal views and should include an AP and axillary view. A scapular Y view is insufficient to diagnose a located shoulder. If the patient is unable to tolerate an axillary view, a modified axillary view, termed a Velpeau view, should be obtained.123 This view does not require abduction of the injured shoulder and can be obtained in any patient without a spine injury. After radiographic documentation of an anterior shoulder dislocation is performed, the clinician must decide on the analgesia/sedation to be administered and the reduction technique. Options for analgesia/sedation include no analgesia or sedation,124 intraarticular injection of 20 mL of 1% lidocaine, or intravenous analgesics with or without sedatives. A Cochrane review suggests no difference between intraarticular injection of lidocaine and intravenous sedation with regard to the success rate of reduction, pain during reduction, or postprocedural pain.125 The use of intraarticular lidocaine may require fewer resources, be more cost effective, and result in a faster discharge from the emergency department.126 A multitude of reduction maneuvers have been described for anterior shoulder dislocation. Despite reports, no one technique is 100% effective, and as such, it is important for the clinician to be familiar with several different maneuvers to ensure rapid reduction.127 Recently, several nonrandomized and randomized trials from multiple institutions have demonstrated improved rates of success and time to achieve reduction with the use of the Milch technique.128,129 Importantly, the Milch technique does not require any form of sedation or intraarticular injection, and as such, it is our preferred initial technique for shoulder reduction.130 This technique is performed by slowly abducting and externally rotating the shoulder over a period of 5 to 15 minutes. Once the arm has reached 90 degrees of abduction and 90 degrees of external rotation, the joint has usually spontaneously reduced. If it has not spontaneously reduced, a modification of the maneuver can be performed that involves pulling gentle longitudinal traction in line with the humerus using one hand and manipulating the humeral head laterally and superiorly with the other to effect reduction.124

Nonoperative Sling Immobilization and Rehabilitation Traditionally, after reduction, the shoulder is immobilized for a period and a course of physiotherapy may be prescribed. However, this basic principle of nonoperative management has recently come into question because of a wide range of recommendations on the duration of immobilization but seemingly similar rates of recurrence. To date, five level I studies and one level II study have been performed to investigate the duration of immobilization and the rate of recurrent instability.131 A cohort of Swedish patients

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in a study by Hovelius and colleagues has been followed up for 25 years and constitutes four of the five level I studies.72,114,132,133 When comparing patients who were immobilized for 1 week or less with those who were immobilized for 3 to 4 weeks, no statistically significant effect could be detected on the rate of recurrent dislocation or the need for surgery at any of the four analyzed time points. Similar conclusions have been drawn in the remaining studies.77,134 The position of immobilization has also been challenged, based on findings of MRI135 and cadaveric136 studies that demonstrate a decreased degree of displacement and increased contact force between the Bankart lesion and glenoid with the arm in external rotation. Itoi and colleagues137 were the first to report results of a randomized controlled trial comparing immobilization in internal rotation to external rotation; they found reduced rates of recurrent instability in patients immobilized 3 weeks in external rotation. However, this study had many limitations, and a larger trial was later conducted. Again, Itoi and colleagues138 were able to demonstrate a reduced rate of recurrent instability using an intention-to-treat analysis. Compliance with treatment in external rotation was notably and significantly worse. An independent but smaller study also investigated the same question with patients who were 100% compliant with treatment.139 Recurrence rates were not significantly different at a mean followup of 30 months. Abduction of the shoulder with 30 degrees external rotation during immobilization improves reduction of a Bankart lesion on MRI evaluation, which may help reduce recurrence rate after initial dislocation.140 Meta-analysis of these data has failed to demonstrate a significant difference between immobilization in internal and external rotation.141 Currently, at our clinic, we opt for simple immobilization in a sling for approximately 1 week or until the patient is comfortable using the shoulder again.

Surgical Management Should surgical intervention be elected, a variety of options exist; indeed, more than 300 different techniques have been described. Although the vast majority of these techniques are now historic in nature, many are still in use. Options include open, arthroscopic, and adjunctive techniques, salvage operations, and techniques used in a revision setting (Box 40.1). Open anatomic repair of the detached capsulolabral complex to the anterior glenoid rim, known as the Bankart procedure,19 is considered the historic gold standard. However, the procedure is technically demanding and violates the subscapularis, and rehabilitation proceeds slowly. Arthroscopic techniques of the Bankart procedure have been refined over the years, and with the introduction of suture anchors to fixate the repair to the glenoid, the arthroscopic technique is becoming recognized as equivalent to open surgical repair.142–144 A number of treatment options are available to address Hill-Sachs, including benign neglect, arthroscopic remplissage, retrograde disimpaction, and placement of an osteochondral allograft.145,146 Wolf and colleagues discuss remplissage as the arthroscopic treatment to engaging defects.147 Increased stability is achieved by performing a posterior capsulodesis and infraspinatus tenodesis into the bony defect to increase. Aside from

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BOX 40.1  Surgical Options for Anterior Shoulder Instability Open Bankart Repair19 • A Bankart repair is performed to reattach the labrum to the anterior articular margin of the glenoid. • This repair is often combined with a capsular shift (Neer capsulorrhaphy) to restore tension to the capsulolabral complex.164

Supplementary Procedures Remplissage173 • Remplissage means “to fill” in French. • Remplissage is performed in patients with a large Hill-Sachs lesion. • The infraspinatus and posterior capsule are fixated into the Hill-Sachs lesion arthroscopically using suture anchors.

Coracoid Transfer • A coracoid transfer procedure is performed to transfer a portion of the coracoid, along with the conjoint tendon, to the anterior glenoid neck. They are secured to the glenoid with one or two screws.

Humeral Head Allograft174 • A humeral head allograft is performed in patients with a large Hill-Sachs lesion. • An osteoarticular allograft is inserted into the lesion to prevent engagement. • A humeral head allograft is typically performed with an open technique, but arthroscopic techniques have been developed.

Bristow165 • The Bristow procedure is performed to transfer the most distal 1 cm of coracoid. • The CA ligament is preserved. • The coracoid is secured to the glenoid with one screw. Latarjet149 (with Patte modification)150 • The Latarjet procedure is performed to transfer the distal 2–3 cm of coracoid. • The CA ligament is divided with a 1-cm stump. • The inferior portion of coracoid is secured to the glenoid with two screws. • The CA ligament is attached to the anterior glenohumeral capsule. Latarjet (with congruent-arc modification)36 • The Latarjet procedure is performed to transfer the distal 2–3 cm of coracoid. • The medial portion of the coracoid is secured to the glenoid with two screws. • The CA ligament is not reattached. Anterior Capsulolabral Reconstruction166 • Anterior capsulolabral reconstruction was designed by Jobe to address instability in athletes who frequently use overhead maneuvers. • Anterior capsulolabral reconstruction is a glenoid-based capsular shift. • Anterior capsulolabral reconstruction may be performed as an adjunct to Bankart repair.167 Arthroscopic Bankart Repair • A Bankart repair is performed to reattach the labrum to the anterior articular margin of the glenoid with the use of suture anchors.168 • Arthroscopic use of tacks or transglenoid sutures (known as the Caspari technique) is no longer considered modern practice because of high failure rates.169 Coracoid Transfer • When a coracoid transfer is performed, highly specialized instruments are used to transfer the distal 2–3 cm of coracoid.170 • The CA ligament is not reattached. • The coracoid transfer procedure can be combined with a Bankart repair.171 Anterior Capsular Plication172 • Anterior capsular plication is the arthroscopic version of an anterior capsulolabral reconstruction.

Partial Humeral Head Resurfacing175 • Partial humeral head resurfacing is performed in patients with a large HillSachs lesion. • Partial humeral head resurfacing is an alternative to a humeral head allograft. • A cobalt-chrome articular component is inserted into the Hill-Sachs lesion. • Reported techniques are performed in conjunction with a Latarjet procedure. Rotator Interval Closure176 • Rotator interval closure provides superior capsular shift of the MGHL to the SGHL. • Rotator interval closure can be performed open or arthroscopically to limit external rotation. Revision or Salvage Procedures Iliac Crest Bone Grafting of the Glenoid41 • Iliac crest bone grafting of the glenoid is performed in patients with severe anterior glenoid bone loss. • An autogenous iliac crest bone graft is contoured to match the concavity of the glenoid and secured with cannulated screws. Humeral Hemiarthroplasty177 • Humeral hemiarthroplasty traditionally has been indicated for older patients with more than 45% of humeral head bone loss and preexisting degenerative arthritis. • The humeral component must be retroverted up to 50 degrees to achieve stability. Rotational Humeral Osteotomy178 • A rotational humeral osteotomy is performed in patients with severe Hill-Sachs lesions. • A subcapital external rotational osteotomy of the humerus is performed to rotate the Hill-Sachs lesion outside of the glenoid track. Allograft Anterior Capsulolabral Reconstruction179 • Allograft anterior capsulolabral reconstruction is performed in patients with severe capsular deficiency as a result of systemic soft tissue disorders, electrothermal capsular necrosis, or repeated surgical procedures without bone loss. • Allograft anterior capsulolabral reconstruction is performed via an open technique; allograft tendon is used to reconstruct the anterior band of the IGHL and MGHL, with bioabsorbable screws used in the humerus and suture fixation performed in the glenoid.

CA, Coracoacromial; IGHL, inferior glenohumeral ligament; MGHL, middle glenohumeral ligament; SGHL, superior glenohumeral ligament.

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recurrent traumatic dislocation in 4% of the included patients, there were no other complications at the 2- to 10-year follow-up. Many studies support remplissage and an arthroscopic solution to engaging defects.146,148 Coracoid bone block transfers represent an alternative to the anatomic reconstruction of the Bankart procedure. The most commonly used coracoid bone block transfer is the Latarjet.149 Originally described in 1954, it has subsequently been modified by Patte150 into the procedure performed today. Although transferring a block of bone is advantageous in cases of bony glenoid deficiency, Patte recognized that the so-called bone block effect only partially contributes to the efficacy of the Latarjet procedure to prevent recurrent instability. He described the mechanism as a triple effect: (1) a sling effect of the conjoint tendon that

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supplements the anteroinferior capsule and inferior aspect of the subscapularis tendon, particularly in abduction and external rotation; (2) a bony effect that increases the overall dimension of the glenoid; and (3) a ligamentous effect of the repaired anterior capsule to the stump of the coracoacromial ligament.151 Two viewpoints exist regarding the utility of the Latarjet procedure.152 In the English-speaking world, it is primarily used as a revision procedure or a procedure that is used when significant bony glenoid loss is detected preoperatively.36 In the Frenchspeaking world, however, the Latarjet procedure is used as a primary procedure, even in the absence of glenoid bony loss.153 Allograft glenoid augmentation is another consideration for stabilization in patients with large glenoid defects or in revision cases (see Chapter 43).

Authors’ Preferred Technique Arthroscopic Bankart Repair (Fig. 40.13) Patient Positioning and Setup • The patient is anesthetized and an examination is performed. • The patient is placed in the lateral decubitus position. • A commercially available shoulder distraction device with lateral overhead distraction is used. The arm holder is angled at 45 degrees of abduction and 15 degrees of forward elevation, and 5 to 7 lb of longitudinal traction and 5 lb of lateral traction are used. • The bed is rotated approximately 50 degrees to allow better access to the anterior shoulder. • Osseous landmarks are drawn on the shoulder. Portal Placement and Diagnostic Arthroscopy • A standard posterior viewing portal is established. The portal is created blindly using the “Romeo three-finger-shuck”154 to identify the soft spot that corresponds to the interval between the infraspinatus and teres minor. The joint line can then be palpated using a shucking maneuver. It is critical to be in line with the joint. • The arthroscope is introduced into the joint and the rotator interval is immediately identified. With assistance from the transillumination of the arthroscope, an 18-gauge spinal needle is inserted and its obturator is removed. The needle is used both for outflow and as a probe. • Diagnostic arthroscopy is undertaken, first evaluating the biceps anchor. The biceps is followed up into its grove and, using the needle, is pulled into the joint to examine for pathology. The arthroscope is then directed toward the insertion site of the supraspinatus, followed by the infraspinatus and posterolateral humeral head. A Hill-Sachs lesion may be identified at this point. Next, the inferior axillary recess is examined for the presence of a HAGL lesion or any loose bodies. The 5-o’clock position of the glenoid can often be examined at this juncture, and the glenolabral junction is followed posteriorly and superiorly. The articular cartilage of the glenoid and humeral head are next inspected. Finally, the arthroscope is advanced into the anterior aspect of the joint where the anterior labrum is identified, often detached or scarred as observed in an ALPSA lesion. Inspection of the subscapularis tendon completes the diagnostic evaluation. • Once the Bankart lesion is identified, two portals are established with use of an outside-in technique. A 5.5-mm threaded cannula is placed at the most superior aspect of the rotator interval. It is also slightly medialized. An 8.5-mm threaded cannula is placed immediately off the rolled edge of the superior border of the subscapularis tendon. This cannula is slightly lateralized to permit the proper angle for anchor insertion.

Glenolabral Preparation • With use of a knife-rasp instrument inserted from the high interval portal, the labrum is freed from the glenoid neck. This maneuver can make up a significant portion of the procedure and is vital to a successful operation. Alternatively, if a significantly scarred ALPSA lesion is encountered, a hook cautery probe can be used, but only with extreme caution. • It can be difficult to ascertain when the labrum is sufficiently mobilized. A useful test is to insert the shaver into the joint, open the window, and turn the suction on. If the labrum floats up to an anatomic position, mobilization is complete. • Next, the shaver is placed against the glenoid neck and used to roughen the bone and create a bleeding surface. Anchor Insertion • The tear configuration is carefully evaluated, and a plan is established for suture anchor placement. Typically a three- or four-anchor configuration is used. • Using the insertion technique specific to the anchor being used, a single-loaded suture anchor is placed through the low-interval cannula at approximately the 5-o’clock position. It should be placed at a 45-degree angle to the glenoid face and just up on the glenoid face. • The anterior suture limb (i.e., the limb closest to the labrum) is identified, and using a claw grasper inserted from the high-interval portal, the suture is grasped to shuttle it out through the portal. Labral Repair • A suture-relay technique with creation of a simple suture is used to achieve labral repair. • An arthroscopic suture passer, such as the Spectrum suture hook (ConMed Linvatec, Largo, FL), is loaded with a 90-cm-long No. 0 polydioxanone (PDS) suture and inserted into the low-interval cannula. • The claw grasper is inserted into the high-interval portal. • The claw grasper is used to grasp the labrum and advance it superiorly. The Spectrum then penetrates the capsulolabral tissue 5- to 10-mm inferior to the level of the suture anchor and 1 cm lateral to the labral edge. The PDS suture is then advanced into the joint. The claw grasper is released and then used to retrieve the PDS suture out through the high-interval portal. • Once the PDS suture is out of the cannula, an incomplete simple knot is tied. Through the open loop, the docked anterior suture limb is passed, and then the simple knot is completed. The Spectrum suture passer is rotated to Continued

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Authors’ Preferred Technique Arthroscopic Bankart Repair (Fig. 40.13)—cont’d

A

B

C

D

E

F

G

H

I

J

K

L

Fig. 40.13  Arthroscopic Bankart repair. (A) The patient is placed in the lateral decubitus position. “High” and “low” portals are established in the rotator interval. (B) A knife-rasp is used to free the labrum from the glenoid neck. (C) A suture anchor is inserted at a 45-degree angle to the glenoid face. (D) The anterior suture limb is identified and, using a claw grasper, is docked in the high portal. (E) An arthroscopic suture passer is used to penetrate the capsulolabral tissue while the claw grasper advances the labrum superiorly. A polydioxanone (PDS) suture is passed into the joint. (F) The PDS suture is retrieved out the high portal. (G) An incomplete knot is tied and the anterior suture limb is placed through to perform a suture relay. (H) The suture passer is withdrawn to accomplish the suture relay. (I) The suture relay is complete, and the passed suture is now the postsuture. (J) A sliding Duncan loop is tied and passed with the use of a knot pusher. (K) Sequential anchors are placed to create a three- to four-anchor configuration construct. (L) The repair is now complete.

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Authors’ Preferred Technique Arthroscopic Bankart Repair (Fig. 40.13)—cont’d disengage from the labral tissue, and the Spectrum suture passer is pulled out of the low-interval cannula, along with the PDS suture. The remaining PDS is pulled out through the low-interval cannula, thus completing the suture relay. Knot Tying • The passed suture is now the postsuture to ensure the knot is tied away from the articular surface. We prefer to use a sliding Duncan loop arthroscopic knot, but any arthroscopic knot can be used. • The Duncan loop is tied, dressed, and passed with the use of a knot pusher. An assistant can use the claw grasper through the high-interval portal to aid in accurate placement of the knot. Four additional alternating post half-hitches are then tied to secure the knot. The sutures are then cut with an arthroscopic suture cutter.

Complete the Repair • Following the plan established prior to the first anchor insertion, sequential anchors are placed in identical fashion. • The capsulolabral tissue should be continually advanced superiorly to retension the capsulolabral complex. Closure • The completed repair is carefully evaluated with use of a hook probe. • Additional procedures such as remplissage or rotator interval closure may be performed, if desired. • The cannulae are removed from the shoulder. • Portals are closed with interrupted 3-0 absorbable monofilament suture. • Twenty milliliters of bupivacaine with epinephrine is injected around the portals. • The arm is placed into a sling with a bolster.

ALPSA, Anterior labroligamentous periosteal sleeve avulsion; HAGL, humeral avulsion of the glenohumeral ligaments.

Authors’ Preferred Technique Latarjet-Patte Coracoid Transfer (Fig. 40.14) Patient Positioning and Setup • A towel is placed behind the scapula to make the coracoid process more prominent. • The patient is placed into a 30-degree modified beach chair position. • The patient is anesthetized, and an examination is performed. • The arm is draped free and placed into a pneumatic arm positioner.

• A 90-degree angled microsagittal saw is used to osteotomize the base of the coracoid, which is identified as the elbow, approximately 2 cm posterior to the coracoid tip, in a medial to lateral fashion. • The coracohumeral ligament is released at the lateral base of the coracoid. • The coracoid should now be completely mobile, and it is brought out of the wound inferiorly. It is placed onto a Darrach retractor overlying the skin.

Initial Exposure • Landmarks for surgery include the coracoid process and axillary fold. • A 5-cm incision is made from the coracoid, directed inferiorly toward the axillary fold. • A deltopectoral approach is used. • The plane between the deltoid and pectoralis major is identified by the cephalic vein. The cephalic vein is typically retracted laterally with the deltoid using a Taylor retractor and dissection is continued medially. A Richardson retractor is used medially. • Typically a crossing vein from the cephalic vein can be identified at the superior pole of the incision. This vein should be suture ligated to prevent a postoperative hematoma. • The conjoint tendon is identified, and a Hohmann retractor is inserted immediately above the coracoid to provide superior retraction. • The arm is placed into 45-degree of external rotation and 30 degrees of abduction to aid in the visualization of the coracoacromial ligament (CI).

Coracoid Preparation • The CI stump is identified and protected by placing an Allis clamp on the stump. A towel clip is placed around the coracoid. • The undersurface of the coracoid is decorticated using a high-speed burr. • The 3.5-mm drill from the small fragment set is used to make drill holes in the coracoid. The drill should be angled in such a way that the drill holes are angled a few degrees away from the joint once the coracoid has been positioned against the glenoid. • The coracoid is then returned to the wound and tucked into the medial aspect of the incision.

Coracoid Mobilization • The lateral aspect of the conjoint tendon is sharply dissected. • The CI is divided 1 cm lateral to its insertion into the coracoid. This ligament is tagged for later repair. • The arm is then brought into a neutral position. • The insertion of the pectoralis minor into the coracoid is identified and sharply removed. Coracoid Osteotomy • A forked retractor or Darrach retractor is used to retract the pectoralis minor and expose the base of the coracoid.

Glenoid Exposure • The subscapularis is identified and split horizontally in line with its fibers at the midportion of the muscle belly. • The subscapularis is elevated from the anterior scapula by packing a sponge in a superior direction into the subscapularis fossa. • A large Steinmann pin is inserted into the superior aspect of the scapular neck to provide retraction of the superior portion of subscapularis. • A 1-cm vertical capsulotomy is performed adjacent to the glenoid rim. • A humeral head retractor may then be inserted through the capsulotomy to retract the humerus. • Medially, an anterior glenoid neck retractor is inserted for further visualization. • The anterior inferior capsule and labrum are excised, and the periosteum of the anterior inferior glenoid neck is elevated. An osteotome may be required to remove a loose bony fragment. Coracoid Transfer • The anterior inferior glenoid neck is decorticated with an osteotome in preparation for the coracoid transfer. Continued

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Authors’ Preferred Technique Latarjet-Patte Coracoid Transfer (Fig. 40.14)—cont’d

A

Cut lines for coracoid mobilization

B

Coracoid osteotomy

D

Glenoid neck decortified

F

Closure

Subscapularis muscle split

C

Glenoid exposure

Coracoacromial ligament

Anterior inferior joint capsule

E

Coracoid transfer

Fig. 40.14  Latarjet-Patte coracoid transfer technique. (A) Following a modified deltopectoral approach, the coracoacromial ligament is divided 1 cm lateral to its insertion into the coracoid. The insertion of pectoralis major is sharply released along the coracoid. (B) A 90-degree angled microsagittal saw is used to osteotomize the base of the coracoid, approximately 2 cm posterior to the coracoid tip. (C) The subscapularis is split horizontally. (D) After a vertical capsulotomy is performed, the anterior inferior capsule and labrum are excised and the periosteum of the anterior inferior glenoid neck is elevated to expose bone. (E) The coracoid is transferred and screwed into place with 4.0-mm cannulated screws. (F) The retained stump of the coracoacromial ligament is attached to the anterior inferior joint capsule.

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Authors’ Preferred Technique Latarjet-Patte Coracoid Transfer (Fig. 40.14)—cont’d • The coracoid is retrieved from the wound. A 30-mm-long 4.0-mm cannulated screw is placed into the superior hole of the coracoid only. This screw acts as a joystick to allow reduction of the coracoid onto the glenoid neck. The proposed placement is carefully evaluated to ensure it is neither too far medial nor too far lateral, resulting in coracoid overhang. • A 1.25-mm guidewire is then inserted through the inferior hole of the coracoid to hold the reduction. This wire should be inserted approximately 10 degrees away from the joint to avoid intraarticular penetration. However, excessive medial angulation will displace the graft and put the suprascapular nerve at risk. • The reduction is evaluated. If it is acceptable, a second 1.25-mm guidewire is then inserted through the cannulated screw in the superior hole. The reduction is again evaluated. If it is acceptable, the superior cannulated screw is removed.

• The 2.7-mm cannulated drill bit is then used to drill bicortical holes in the glenoid. • The 30-mm cannulated screw is typically reused in the superior hole. The inferior hole is measured for length, and a length-appropriate 4.0-mm cannulated screw is inserted. Closure • The arm is placed into external rotation. The CI is reattached to the anterior inferior joint capsule, and the remaining CI stump with No. 1 Vicryl. • A horizontal capsulotomy will allow for a north–south capsular shift if one is desired, but this procedure is not normally done. • The subscapularis split is not repaired. • The remainder of the wound is closed in a layered fashion.

Postoperative Management Arthroscopic Bankart repair.  The patient is discharged home with a sling and bolster to be worn at all times. Immediate goals after surgery are primarily to protect the repair, initiate gentle passive and active assisted ROM, and achieve pain control. Active external rotation, extension, and abduction are avoided in the first 2 weeks. ROM goals are flexion to 90 degrees, abduction to 90 degrees, and external rotation to 15 degrees by 3 to 4 weeks. At 4 weeks, use of the sling is typically discontinued for daytime use, but it may continue to be used while sleeping if concerns exist. Gentle ROM is continued with progression to flexion of 130 degrees and external rotation to 30 degrees. Stretching exercises and proprioceptive activities may begin, along with scapular strengthening. By 8 to 10 weeks, ROM should progress to full ROM, and strengthening activities may begin. At 4 months, strengthening continues and sport-specific physiotherapy is initiated. RTP criteria include full ROM, satisfactory muscular strength and endurance, and absence of subjective and objective instability. In general, noncontact athletes may return to sport at 4 months, whereas contact athletes are permitted to resume play at 6 months. Latarjet-Patte coracoid transfer. Rehabilitation after the Latarjet-Patte procedure is considerably different from that after a Bankart repair.153 The patient is discharged home with his or her arm in a simple sling. The sling is used for the first 2 weeks continuously. After 2 weeks, the use of the shoulder, out of the sling, is permitted for all typical activities of daily living. At 1 month, ROM exercises, without limitation, are initiated. Return to sport criteria are the same as for Bankart repair, but also include radiographic evidence of healing of the coracoid graft. Athletes participating in contact sports are typically permitted to return at the 3-month mark.

Recurrent instability is the most common complication after surgical management. The rate of recurrent instability is difficult to estimate, however, based on many different definitions in the literature.156 Preoperative risk factors also make instability difficult to predict. Aboalata and colleagues109 reported overall redislocation rate of 18% after arthroscopic stabilization at 13-year followup. Marshall et al.157 reported postoperative instability in 29% of patients treated after first-time dislocation and 62% of patients treated after multiples episodes at 51 months. A systematic review reported redislocation rates in collision athletes between 5.9% and 38.5% compared with 0% and 18.5% in noncollision athletes.158 Infection and nerve palsy are less common but may occur. After coracoid bone block surgery, specific risks include hardware breakage or pain as a result of the hardware.159 The coracoid graft may achieve a fibrous union, may fail to unite, or may migrate. Coracoid graft osteolysis is also being increasingly recognized.160

Results

FUTURE CONSIDERATIONS

Based on the results of several systematic reviews and metaanalyses, the best available current evidence suggests the following:

Despite the multiple studies investigating the many facets of anterior shoulder instability, high-level evidence remains scarce.

• Duration of sling immobilization after primary anterior shoulder dislocation does not influence the rate of recurrent instability.131 • Immobilization of the arm in internal or external rotation does not influence the rate of recurrent instability.131 • Arthroscopic Bankart repair after primary anterior shoulder dislocation reduces the rate of recurrent instability compared with sling immobilization and may improve short-term quality of life.91 • Arthroscopic Bankart repair after recurrent anterior shoulder instability demonstrates equivalent rates of recurrent instability, return to work, and function outcomes compared with open Bankart repair.143,155,156 • Arthroscopic Bankart repair after recurrent anterior shoulder instability results in slightly improved ROM compared with open Bankart repair.155,156

Complications

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Further research must continue to define the best imaging modality for diagnosis and as a guide for management.161 The question of position of immobilization has not been fully answered because of less than ideal trial design. The contentious question of whether to offer surgery to a patient with a first-time shoulder dislocation requires a rigorous randomized controlled trial using modern suture-anchor fixation, standardized physiotherapy, and stratification of age and gender. Similarly, open versus arthroscopic management, particularly in athletes who participate in contact sports, has yet to be defined. For a complete list of references, go to ExpertConsult.com.

Level of Evidence:

SELECTED READINGS

Level of Evidence:

I

Summary: In this study, patients with first-time dislocations were randomly assigned to arthroscopic stabilization or sling immobilization. A significant improvement in Western Ontario Shoulder Instability Index Score and a reduction in redislocation risk were demonstrated.

Citation: Balg F, Boileau P. The Instability Severity Index Score. A simple pre-operative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Surg Br. 2007;89B(11):1470. III

Citation: Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649.

Level of Evidence:

Summary: In this prospective case-control study, important risk factors for failure of arthroscopic Bankart repair were identified. A simple score was devised to determine which patients would benefit from the Latarjet versus the arthroscopic Bankart procedure.

Citation:

Biomechanical study

Summary: This article introduces the concept of the “glenoid track,” which informs the discussion of how to manage glenoid and humeral bone loss.

Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677.

Level of Evidence:

Citation: Kirkley A, Griffin S, Richards C, et al. Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder. Arthroscopy. 1999;15(5):507.

IV

Summary: In this retrospective study, causes of failure of arthroscopic Bankart repair were examined. Burkhart and De Beer recognized that significant bony defects were associated with a high rate of failure.

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CHAPTER 40  Anterior Shoulder Instability

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arthroplasty for the management of humeral bone defects in shoulder instability: systematic review and quantitative synthesis of the literature. Arthroscopy. 2014;30:1650–1666. Wolf EM, Arianjam A. Hill-Sachs remplissage, an arthroscopic solution for the engaging Hill-Sachs lesion: 2- to 10-year follow-up and incidence of recurrence. J Shoulder Elbow Surg. 2014;23:814–820. Buza JA III, Iyengar JJ, Anakwenze OA, et al. Arthroscopic Hill-Sachs remplissage: a systematic review. J Bone Joint Surg Am. 2014;96:549–555. Latarjet M. Treatment of recurrent dislocation of the shoulder. Lyon Chir. 1954;49:994–997. Patte D. Instabilité antérieure de l’épaule. Cahier des enseignements de la Sofcot. 1981;55. Giles JW, Boons HW, Elkinson I, et al. Does the dynamic sling effect of the Latarjet procedure improve shoulder stability? A biomechanical evaluation. J Shoulder Elbow Surg. 2013;22:821–827. Abboud JA, Armstrong AD. Management of anterior shoulder instability: ask the experts. J Shoulder Elbow Surg. 2011;20:173–182. Edwards TB, Walch G. The Latarjet procedure for recurrent anterior shoulder instability: rationale and technique. Oper Tech Sports Med. 2002;10:25–32. Seroyer ST, Nho SJ, Provencher MT, et al. Four-quadrant approach to capsulolabral repair: an arthroscopic road map to the glenoid. Arthroscopy. 2010;26:555–562. Godin J, Sekiya JK. Systematic review of arthroscopic versus open repair for recurrent anterior shoulder dislocations. Sports Health. 2011;3:396–404. Litchfield R, Shannon F. Open versus arthroscopic repair for shoulder instability: what’s best? In: James G, James G, Wright M, eds. Evidence-Based Orthopaedics. Philadelphia: Elsevier; 2009:667. Marshall T, Vega J, Siqueira M, et al. Outcomes after arthroscopic Bankart repair: patients with first-time versus recurrent dislocations. Am J Sports Med. 2017;363546517698692. Alkaduhimi H, van der Linde JA, Willigenburg NW, et al. Redislocation risk after an arthroscopic Bankart procedure in collision athletes: a systematic review. J Shoulder Elbow Surg. 2016;25:1549–1558. Butt U, Charalambous CP. Complications associated with open coracoid transfer procedures for shoulder instability. J Shoulder Elbow Surg. 2012;21:1110–1119. Gupta Ashish, Delaney Ruth, Petkin Kalojan, et al. Complications of the Latarjet procedure. Curr Rev Musculoskelet Med. 2015;8:59–66. Thompson SR. One-stop shopping: CT arthrography outperforms MR arthrography in preoperative identification of both osseous and soft-tissue pathology in patients with anterior shoulder instability. JBJS Orthop Highlights. Sports Med. 2012;2:e6. Neviaser TJ. The GLAD lesion: another cause of anterior shoulder pain. Arthroscopy. 1993;9:22–23. Snyder SJ, Karzel RP, Del Pizzo W, et al. SLAP lesions of the shoulder. Arthroscopy. 1990;6:274–279.

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164. Neer CS 2nd, Foster CR. Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am. 1980;62: 897–908. 165. Helfet AJ. Coracoid transplantation for recurring dislocation of the shoulder. J Bone Joint Surg Br. 1958;40-B:198–202. 166. Jobe FW, Giangarra CE, Kvitne RS, et al. Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med. 1991;19:428–434. 167. Rokito AS, Birdzell MG, Cuomo F, et al. Recovery of shoulder strength and proprioception after open surgery for recurrent anterior instability: a comparison of two surgical techniques. J Shoulder Elbow Surg. 2010;19:564–569. 168. Wolf EM, Wilk RM, Richmond JC. Arthroscopic Bankart repair using suture anchors. Operative techniques in orthopaedics. 1991;1:184–191. 169. Freedman KB, Smith AP, Romeo AA, et al. Open Bankart repair versus arthroscopic repair with transglenoid sutures or bioabsorbable tacks for recurrent anterior instability of the shoulder: a meta-analysis. Am J Sports Med. 2004;32: 1520–1527. 170. Lafosse L, Boyle S, Gutierrez-Aramberri M, et al. Arthroscopic latarjet procedure. Orthop Clin North Am. 2010;41:393–405. 171. Boileau P, Mercier N, Roussanne Y, et al. Arthroscopic Bankart-Bristow-Latarjet procedure: the development and early results of a safe and reproducible technique. Arthroscopy. 2010;26:1434–1450. 172. Jones KJ, Kahlenberg CA, Dodson CC, et al. Arthroscopic capsular plication for microtraumatic anterior shoulder instability in overhead athletes. Am J Sports Med. 2012;40: 2009–2014. 173. Purchase RJ, Wolf EM, Hobgood ER, et al. Hill-sachs “remplissage”: an arthroscopic solution for the engaging hill-sachs lesion. Arthroscopy. 2008;24:723–726. 174. Miniaci A, Gish MW. Management of anterior glenohumeral instability associated with large Hill–Sachs defects. Techniques in Shoulder & Elbow Surgery. 2004;5:170–175. 175. Moros C, Ahmad CS. Partial humeral head resurfacing and Latarjet coracoid transfer for treatment of recurrent anterior glenohumeral instability. Orthopedics. 2009;32. 176. Mologne TS, Zhao K, Hongo M, et al. The addition of rotator interval closure after arthroscopic repair of either anterior or posterior shoulder instability effect on glenohumeral translation and range of motion. Am J Sports Med. 2008;36: 1123–1131. 177. Pritchett JW, Clark JM. Prosthetic replacement for chronic unreduced dislocations of the shoulder. Clin Orthop Relat Res. 1987;89–93. 178. Weber BG, Simpson LA, Hardegger F. Rotational humeral osteotomy for recurrent anterior dislocation of the shoulder associated with a large Hill-Sachs lesion. J Bone Joint Surg Am. 1984;66:1443–1450. 179. Braun S, Horan MP, Millett PJ. Open reconstruction of the anterior glenohumeral capsulolabral structures with tendon allograft in chronic shoulder instability. Oper Orthop Traumatol. 2011;23:29–36.

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41  Posterior Shoulder Instability James Bradley, Fotios P. Tjoumakaris

Posterior shoulder instability is a unique condition that not only represents a spectrum of instability, but can also be difficult to diagnose and technically challenging to treat. Although less common than anterior shoulder instability, accounting for only 2% to 10% of cases, this condition is becoming increasingly recognized in the athletic population.1–4 Mclaughlin et al. first recognized the wide clinical spectrum of posterior shoulder instability ranging from the locked posterior shoulder dislocation to recurrent posterior subluxation (RPS).2 The causes are multifactorial and include acute traumatic injury, repetitive microtrauma, and atraumatic or ligamentous laxity.5 In the general population, seizures and electrocution are rare causes of posterior shoulder dislocation. More commonly in the traumatic setting, a posterior direct blow to an adducted, internally rotated and forward flexed upper extremity such as a fall on an outstretched arm is the mechanism of injury.6 In the athletic population, however, instability results from repetitive microtrauma, which can occur in a variety of loading conditions and multiple arm positions.2,7 Management of patients with posterior shoulder instability is challenging in recognition of the diagnosis and underlying pathology. Treatment includes both conservative and operative management. Surgeries for posterior instability include both open and arthroscopic procedures, with arthroscopic procedures recently gaining more popularity with advances in surgical techniques and decreased morbidity.

Background RPS has been observed in overhead athletes, baseball hitters, golfers, tennis players, butterfly and freestyle swimmers, weightlifters, rugby players, and football linemen.8–10 Other activities where RPS may be present include archery, riflery, and wheelchair use.11 Distinct from the acute traumatic dislocation, the etiology of RPS is due to repetitive microtrauma to the posterior capsule leading to capsular attenuation and labral tears. In the overhead athlete, adaptive and structural changes in combination with the high forces across the glenohumeral joint result in posterior capsular contracture and posterosuperior labral tear, which is a distinct mechanism from other entities. Diagnosis and workup of athletes with RPS is often challenging when determining the underlying pathology. These patients present with complaints of vague and diffuse shoulder pain and fatigue without a specific injury. A thorough history and physical and examination in combination with specific imaging studies are required to determine the pathogenesis and treatment for

patients with RPS. Provocative clinical examination tests in addition to advanced imaging such as the MR arthrogram have aided in identifying RPS in the athletic population. A thorough history should include the mechanism of injury, which can consist of a true posterior shoulder dislocation, repetitive microtrauma, acute, or chronic subluxation. Specific direction of instability, meaning posterosuperior, directly posterior, posteroinferior as well as pattern of instability, including unidirectional or multidirectional, should be identified. All of these factors should be documented and considered, as they will ultimately affect treatment and outcome.12 Structural abnormalities of the shoulder, to include any combination of the labrum, capsule, supporting ligaments, or rotator cuff, also must be taken in account to maximize optimal treatment outcome. Posterior glenohumeral stabilization has evolved from various open procedures to an all arthroscopic approach.13 This has allowed for enhanced identification of repair of intraarticular pathology.14 As outcomes have been improving, clinical and biomechanical studies continue to refine our approach to RPS.

Pathogenesis The posterior labrum, capsule, and posterior band of the inferior glenohumeral ligament (IGHL) are the primary stabilizers to posterior translation of the humeral head between 45 and 90 degrees of abduction.15 The posterior capsule is identified by the area between the intra-articular potion of the biceps tendon and the posterior band of the IGHL. This area is the thinnest segment of the shoulder capsule and also does not contain any supporting ligamentous structures, making it susceptible to attenuation from repetitive stresses.16 The pathogenesis of RPS shares a direct relationship to the specific repetitive stresses placed onto the glenohumeral joint. This differs from the pathogenesis in a traumatic setting where the patient may sustain an acute capsulolabral detachment or reverse Bankart tear (Figs. 41.1 and 41.2).17 In RPS, specific activities such as the tennis backhand, golf or baseball backswing, follow-through phase of throwing, and pull-through phase in swimming all can result in RPS. Activities such as push-ups, bench press, and blocking in football also place a direct posterior stress on the posterior capsulolabral complex of the shoulder. Due to the various positions athletes use in contact and noncontact sport, many other mechanisms likely exist that are continuously being identified.

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Abstract

Keywords

Posterior shoulder instability is a unique condition that not only represents a spectrum of instability, but can also be difficult to diagnose and technically challenging to treat. Although less common than anterior shoulder instability, accounting for only 2% to 10% of cases, this condition is becoming increasingly recognized in the athletic population.1-4 Mclaughlin et al. first recognized the wide clinical spectrum of posterior shoulder instability ranging from the locked posterior shoulder dislocation to recurrent posterior subluxation (RPS).2 The causes are multifactorial and include acute traumatic injury, repetitive microtrauma, and atraumatic or ligamentous laxity.5 In the general population, seizures and electrocution are rare causes of posterior shoulder dislocation. More commonly in the traumatic setting, a posterior direct blow to an adducted, internally rotated and forward flexed upper extremity such as a fall on an outstretched arm is the mechanism of injury.6 In the athletic population, however, instability results from repetitive microtrauma, which can occur in a variety of loading conditions and multiple arm positions.2,7 Management of patients with posterior shoulder instability is challenging in recognition of the diagnosis and underlying pathology. Treatment includes both conservative and operative management. Surgeries for posterior instability include both open and arthroscopic procedures, with arthroscopic procedures recently gaining more popularity with advances in surgical techniques and decreased morbidity.

posterior shoulder instability posterior shoulder instability reconstruction posterior shoulder instability repair arthroscopic posterior capsulolabral reconstruction recurrent posterior shoulder instability

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Fig. 41.1  A posterior labral tear from the glenoid (right shoulder, viewed from the anterior portal).

Fig. 41.2  Posterior labral splitting and tear (right shoulder, viewed from the posterior portal). Placing the patient in the lateral decubitus position facilitates posterior labral visualization and repair.

One proposed mechanism of RPS in overhead athletes, throwers, and swimmers is due to the progressive laxity of the posterior capsule and fatigue of static and dynamic stabilizers.18 RPS can lead to deformation of the posterior capsule, resulting in a patulous posteroinferior capsular pouch that can be seen on both magnetic resonance arthrogram (MRA) and arthroscopically. Cadaveric studies have examined position and applied force in relation to posterior instability. Pagnani et al. placed the arm into the position of flexion and internal rotation and found that transection of the infraspinatus, teres minor, and entire posterior capsule was sufficient to produce a dislocation.16 When the anterosuperior capsule and superior glenohumeral ligament (SHGL) were transected, a posterior dislocation would occur. These studies validated the “circle concept,” where a dislocation in one direction would require capsular damage on both the same and opposite side of the joint. A different study by Cole et al. found that with the arm in an adducted position, the rotator interval and SGHL provided static glenohumeral stability limiting inferior and posterior joint translations.19 Wellmann et al. found in their cadaveric study that a lesion of the rotator interval contributes to increased glenohumeral translation.20 However,

Provencher and colleagues demonstrated that rotator interval closure, while causing loss of external rotation, did not have an effect on reducing posterior instability.21 Other anatomic studies have questioned the concept of injury to anterior structures, including the rotator interval in a posteriorly dislocated shoulder altogether.22,23 This work, alongside others, suggests that in an overhead athlete, interval closure may not be clinically indicated and may in fact have an undesired effect on throwing athletes who function with their arm in the abduction and external rotation (ABER) position. The muscles around the shoulder also significantly contribute to the dynamic cavity compression effect of the humeral head within the glenoid.24 Of the rotator cuff muscles, the subscapularis provides the most resistance to posterior translation, acting as a dynamic supporter of the action of the posterior band of the IGHL.25,26 In one cadaveric study, decreased subscapularis muscle strength in the late cocking phase of throwing motion resulted in increased maximum glenohumeral external rotation and increased glenohumeral contact pressure.27 Therefore overhead throwers with subscapularis fatigue would be more susceptible to these forces, resulting in a type II superior labral anterior posterior (SLAP) tear. In some instances these tears can propagate posteroinferiorly around the glenoid resulting in type VIII SLAP tear and symptomatic RPS.27,28 From an anatomic standpoint, the humeral head possesses an oblong shape. In the ABER position the anterior band of the IGHL becomes taut as it is draped over the anteroinferior aspect of the eccentrically positioned humeral head, providing a check-rein against excessive external rotation.29,30 Pitchers that have increased external rotation at the expense of internal rotation will have more rapid internal humeral rotation in their follow through and pitch velocity. Chronic use of the shoulder in this manner will result in a posterior capsular contracture and glenohumeral rotation deficit. Burkhart suggested that the oblong (cam) effect of the humerus is counteracted by the development of posterior capsular tightness, thus shifting the rotational fulcrum posterosuperiorly.30 This shift allows the shoulder to clear the anteroinferior labroligamentous restraints while leading them to be susceptible to posterior and posterosuperior microtrauma events.4,18,31 This occurs during the followthrough phase with the shoulder in a flexed, adducted, and internally rotated position. The posteroinferior capsular thickening associated with glenohumeral internal rotation deficit (GIRD) has been visualized on magnetic resonance imaging (MRIs) of throwing athletes.32 Dynamic MRA with the arm in the ABER position has shown a phenomenon known as posterosuperior labral “peel-back.” On MRA with the arm in the ABER position, the detached posterosuperior labral tissue separates and moves medially toward the glenoid rim. This can also be visualized arthroscopically (Fig. 41.3).28 It has been observed that some adaptive changes can occur in the shoulder without negative consequence, whereas other athletes may go on to become symptomatic. Studies have demonstrated that after approximately 25 degrees of GIRD, the posterosuperior shift in the glenohumeral center of rotation progresses from adaptive to pathologic shearing forces on the

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of posterior shoulder instability and subacromial impingement. An initial treatment in these patients should include a periscapular muscle strengthening program, which should be incorporated into the physical therapy protocol.

HISTORY

Fig. 41.3  Complete detachment of the posterosuperior labrum from the glenoid in an overhead thrower, as localized by the spinal needle (right shoulder, viewed from the posterior portal).

posterosuperior labrum and rotator cuff.33 Excessive external rotation in the ABER position exposes the posterosuperior labrum, longhead of the biceps tendon, and undersurface rotator cuff tendons to excessive rotary forces resulting in peel-back phenomenon.34 Posterior shift of the humeral head in the ABER position also results in a relative redundancy of the anteroinferior capsuloligamentous complex due to a decreased cam effect. Although not the primary pathology of a tight posteroinferior capsule, this secondary anterior pseudolaxity may have clinical implications in the pathophysiology of the disabled throwing shoulder. The presentation of a posterosuperior labral tear in combination with posteroinferior capsular contracture in throwing athletes differs from the spectrum of pathology in lifters, offensive lineman, and athletes who receive repetitive high loads with the arm in the forward flexed and adducted position.9 The pathogenesis of these conditions is important because initial treatment may differ based on the underlying etiology. Initial treatment in overhead athletes with GIRD and RPS is conservative with posteroinferior capsular contracture stretching, “sleeper stretches” is a more appropriate initial treatment.30,35 Subscapularis treatment may also play a role. If the thrower remains symptomatic, arthroscopic posterior labral repair with optional capsular release can then be performed. “Batter’s shoulder” is another cause of RPS in baseball hitters where this syndrome affects the lead shoulder during the baseball swing.36,37 As the dynamic pulling forces approach 500 Newtons, a posterior labral tear results. It has been inferred that golfers may experience a similar mechanism of injury along with any athlete with a similar follow through type motion during swinging. Identification and treatment of scapular dyskinesia is also of importance when identifying the pathogenesis of RPS. Scapular winging can act as a compensatory mechanism to prevent posterior subluxation of the humeral head. In other patients, winging is thought to be the primary etiology of subluxation.4 A study in golfers with posterior shoulder instability found that fatigue developed in the serratus anterior muscle.38 This possibly contributing to scapulothoracic asynchrony and the combination

Patients with RPS often have vague and nonspecific complaints and symptoms that make clinical diagnosis difficult to elucidate. Symptoms can include any combination of activity related pain, crepitus, perceived weakness, and episodes of intermittent subluxation. If capsular contracture has developed, a complaint of loss of motion may also be present. One study by Pollock et al. noted that two-thirds of athletes who ultimately required surgery presented with difficulty using the shoulder outside of sports with use of the arm above the horizontal.39 Another study found that 90% of patients with RPS note clicking or crepitation with motion.

PHYSICAL EXAMINATION A thorough physical examination of the shoulder includes initial inspection focusing on shoulder asymmetry, muscular atrophy, or scapular dysrhythmia. A skin dimple over the posteromedial deltoid of both shoulders has been found to be 62% sensitive and 92% specific in correlating with posterior instability.40 On palpation, tenderness is assessed at the posterior glenohumeral joint line, greater tuberosity, and biceps tendon. In patients with RPS, posterior joint line tenderness is likely a result of posterior synovitis or posterior rotator cuff tendinosis secondary to multiple episodes of instability.39 Shoulder range of motion (ROM) should also be assessed in both shoulders. Record measurements of forward elevation, abduction in the scapular plane, external rotation with the arm at the side, and internal rotation with the hand behind the back to the highest vertebral level. Shoulder measurements while the patient is in the supine position should also be recorded. While supine, the arm is abducted 90 degrees, the scapula is stabilized, and glenohumeral external and internal rotation are measured. Total arc of rotation is calculated by adding total external plus total internal rotation, and GIRD is assessed by assessing the side to side difference in internal rotation. Crepitus can oftentimes be reproduced during ROM examination as well. Strength testing is performed bilaterally, with a focus on the rotator cuff. Grading is performed on a five-point scale (Table 41.1). The majority of athletes with RPS will demonstrate grade 4 or 5 strength. Supraspinatus strength is tested with a downward force while the arm is abducted 90 degrees in the scapular plane, otherwise known as the “empty can” test. Infraspinatus and teres minor muscles are assessed with resisted external rotation, with the arm adducted and the elbow flexed 90 degrees. If the posterior cuff has been damaged, subtle differences can be detected. Subscapularis strength testing is performed with the lumbar lift-off, belly press, and bear hug tests.41–43 Glenohumeral stability is assessed in both shoulders with the patient supine. The load and shift maneuver is performed with the arm held in 90 degrees of abduction and neutral rotation.

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TABLE 41.1  Muscle Grading Scale

TABLE 41.3  Sulcus Test

0 1

1+ 2+ 3+

2 3 4 5

No muscle contraction is detectable A contraction can be seen or palpated but strength is insufficient to move the joint at all The muscle can move the joint if the limb is oriented so that the force of gravity is eliminated The muscle can move the joint against the force of gravity, but not against any additional applied force The muscle can move the joint against the force of gravity and additional applied force but is not believed to be normal The muscle strength is considered normal

Acromiohumeral distance 2 cm

A 3+ sulcus sign that remains 2+ or greater in 30 degrees of external rotation is considered pathognomonic for multidirectional instability.

TABLE 41.4  Beighton Score for Joint

Hypermobility (9 Points) Joint Ability to hyperextend the elbows beyond 10 degrees Ability to passively touch the thumb to the adjacent forearm with the wrist in flexion Ability to passively hyperextend the small finger metacarpophalyngeal joint more than 90 degrees Ability to hyperextend the knees beyond 10 degrees Ability to touch the palms to the floor with feet together

Negative

Unilateral

Bilateral

0

1

2

0

1

2

0

1

2

0

1

2

0

1

1

Patients who score 5 points or more on the Beighton scale are considered ligamentously lax.44

Fig. 41.4  The load-and-shift test is performed to assess anterior and posterior glenohumeral stability.

TABLE 41.2  Grading of Anterior and

Posterior Laxity 0 1+ 2+ 3+

A humeral head that does not translate to the glenoid rim A humeral head that translates to but does not translate over the glenoid rim A humeral head that translates over the glenoid rim but spontaneously reduces A humeral head that translates over the glenoid rim and does not spontaneously reduce

Axial load is applied to the glenohumeral joint with an anteriordirected force applied then a posterior directed force (Fig. 41.4). Translation of the humeral head over the anterior glenoid rim is quantified from 0 to 3+ (Table 41.2). The sulcus test is performed to asses for excessive IGHL and SGHL laxity. With the patient in a seated position, longitudinal traction is applied with the arm adducted and in neutral rotation. The test is repeated in 30 degrees of external rotation. Laxity is quantified based on the acromial humeral distance (Table 41.3). A sulcus sign that remains 2+ or greater in 30 degrees of external rotation is considered pathognomonic for multidirectional instability (MDI). Patients who present with RPS and concomitant MDI may need to have the rotator interval

addressed at the time of surgery, in addition to the posterior capsulolabral complex for successful stabilization. Generalized ligamentous laxity is also important to examine, as this may contribute to MDI. The Beighton scale assesses the spectrum of ligamentous laxity based on a 9-point scale (Table 41.4).44 Patients with a score of 5 or more are considered ligamentously lax. Special tests have also been applied to further identify capsulolabral pathology in the shoulder. The jerk test is used to assess posterior instability while in the seated position. The medial border of the scapula is stabilized with one hand while the other hand applies a posterior directed force to the 90 degree forward flexed, adducted, and internally rotated arm. The test is positive if posterior subluxation, dislocation, or pain and apprehension are present.7,45 The Kim test assesses posteroinferior shoulder instability.46 With the patient seated, the arm is placed into 90 degrees of abduction in the scapular plane and an axial load is applied. The arm is then forward elevated an additional 45 degrees, and a posteroinferior vector is placed across the glenohumeral joint. A sudden onset of posterior subluxation with pain is positive, with 97% sensitivity in eliciting a posteroinferior labral lesion.46 The circumduction test is performed to assess patients with higher grades of chronic posterior instability. With the elbow in full extension, the arm is placed into 90 degrees of forward elevation and slight adduction. A posterior load is then applied, which subluxes or possibly dislocates the humeral head posteriorly. The arm is then circumducted with a combination of abduction and extension until the head reduces in the glenoid. A palpable

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clunk as the head reduces into the glenoid is significant for a positive test. In patients with chronic posterior instability, this test can often be performed without pain or guarding. In some cases of RPS, and primarily involving overhead throwers, a posterior labral tear is seen in combination with a superior labral tear resulting in a type VIII SLAP tear.28 The active compression (O’Brien) test for superior labral pathology should also be performed. With the patient seated, the arm is forward elevated 90 degrees, adducted 10 degrees, and internally rotated with the elbow extended; a downward force is placed on the arm. A positive test is when deep pain within the shoulder joint is elicited when the arm is in this position compared with when the arm is externally rotated and the same force is applied. It is important to note that deep pain in the shoulder joint is suggestive of superior labral pathology, and is different than pain at the acromioclavicular joint, which can result in a false positive result. Impingement signs may also be present on physical examination. This impingement is typically due to underlying scapular dyskinesia. Stress-related changes in the posterior rotator cuff can manifest as a secondary impingement syndrome.

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Fig. 41.5  An axial magnetic resonance imaging arthrogram image (left shoulder) demonstrating a posterior capsulolabral avulsion from the glenoid with associated posterior translation of the humeral head relative to the glenoid (arrow).

IMAGING Initial radiographs of the shoulder should be obtained in the workup of RPS. Radiographs should consist of an anteroposterior view in the plane of the scapula, an axillary view, and a scapular Y lateral view. In most patients with RPS, these radiographic images are normal. In some cases, a posterior glenoid lesion or impaction of the anterior humeral head (reverse Hill-Sachs lesion) can be seen.44,45 The axillary view is particularly useful in assessing glenoid version. A West Point radiographic view can be useful detecting fractures of the glenoid rim or subtle ectopic bone formation around the glenoid.47,48 CT Scan can also be useful in providing osseous detail in posttraumatic or chronic cases. MRA is the most sensitive diagnostic test for identifying lesions of the posterior labrum and capsule.49 MRA findings indicative of posterior shoulder instability include posterior translation of the humeral head relative to the glenoid, posterior labrocapsular avulsion, posterior labral tear or splitting, discrete posterior capsular tears or rents, reverse humeral avulsion of the glenohumeral ligaments, posterior labrum periosteal sleeve avulsion, and subscapularis tendon avulsion (Fig. 41.5).50,51 The Kim classification is used to describe posterior labral tear morphology (Figs. 41.6–41.8; Table 41.5).52 Arthroscopically the Kim lesion appears as a crack at the junction of the posteroinferior glenoid articular cartilage and labrum through which a complete detachment of the deeper labrum from the glenoid rim can be identified. MRA can also be used to identify chondrolabral and glenoid version.53 Kim examined 33 shoulders with atraumatic posterior instability, and when compared with age matched controls, the affected shoulders were found to have a glenoid that was more shallow and also had more osseous and chondrolabral retroversion present in the middle and inferior glenoid (Fig. 41.9).53 Studies performed by Bradley and colleagues have also found in athletes with RPS higher chondrolabral retroversion and glenoid bony retroversion when compared with controls.8,54 Another study by Tung et al. found 24 patients with RPS had MRA findings of

Fig. 41.6  An axial magnetic resonance imaging arthrogram image (left shoulder) demonstrating a type I Kim lesion: a posterior chondrolabral fissure without displacement (arrow).

Fig. 41.7  An axial magnetic resonance imaging arthrogram image (right shoulder) demonstrating a type II Kim lesion: a concealed complete detachment of the posterior labrum from the glenoid (arrow).

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DECISION-MAKING PRINCIPLES

Fig. 41.8  An axial magnetic resonance imaging arthrogram image (left shoulder) demonstrating a type III Kim lesion: posterior chondrolabral erosion with loss of contour (arrow).

TABLE 41.5  Kim Classification of Posterior

Labral Tear Morphology Type I Type II (Kim Lesion) Type III Type IV

Incomplete detachment (Fig. 41.6) Concealed complete detachment (Fig. 41.7) Chondrolabral erosion (Fig. 41.8) Flap tear of the posteroinferior labrum

Fig. 41.9  An axial magnetic resonance imaging arthrogram image (left shoulder) demonstrating the technique used to measure the degree of chondrolabral retroversion, which can be increased in patients with recurrent posterior subluxation (RPS) of the shoulder.

more posterior humeral head translation, posterior labral tears, and posterior labrocapsular avulsions compared with healthier controls.49 Dynamic MRA can also be performed to evaluate for the peel back phenomenon, which is consistent with a posterosuperior labral tear.55 The use of CT is limited to cases in which a significant amount of bony glenoid retroversion is suspected.

Thorough knowledge of an athlete’s sport, position, and training regimen is critical in determining the pathogenesis and specific pathology associated with their shoulder instability. Rehabilitation with an emphasis on strengthening the rotator cuff, posterior deltoid, periscapular muscles is commonly the first line of treatment.7,31,39,56–59 It is recommended that this physical therapy protocol be maintained for a minimum of 6 months to decrease an athlete’s functional disability. A total of 70% of athletes with this protocol can return to sport. Although the RPS is not eliminated, the functional disability is improved for the athlete to participate in play. Therapy has been traditionally more effective in patients with atraumatic RPS, as opposed to those with generalized ligamentous laxity or a discreet traumatic event.31,57 For patients that fail therapy and are not able to return to preinjury levels of competition, surgery should be considered. Treatment options may ultimately include labral débridement, labral repair, posterior capsular release, posterior capsular plication, or a combination of these procedures.

TREATMENT OPTIONS Many operative procedures have been described for the treatment of posterior instability, including both open and arthroscopic procedures. There has been a general trend in the transition from open procedures to arthroscopic repair, and from nonanatomic to an anatomic reconstruction. Open procedures included a reverse Putti-Platt procedure, biceps tendon transfer, subscapularis transfer, infraspinatus advancement, posterior opening glenoid wedge osteotomy, proximal humeral rotational osteotomy, bone block augmentation of the posterior glenoid or acromion, posterior staple capsulorrhaphy, allograft reconstruction, capsulolabral reconstruction, and open capsular shift.2,7,17,18,31,59–62 Posterior bone block repair has been found to have good outcomes, with one study by Scapinelli reporting 100% success at 9.5 year follow-up.63 However, a separate biomechanical study has shown that posterior bone block capsulorrhaphy overcorrects posterior translation and does not restore inferior glenohumeral stability.64 Notable soft tissue tightening procedures include the reverse Putti-Platt and Boyd and Sisk procedures (rerouting the longhead of the biceps tendon to the posterior glenoid).3,65 In 1980 Neer and Foster reported good results in their laterally based posterior capsular shift to tighten a patulous posteroinferior capsule.66 Other studies have attempted a medially based posterior capsular shift for posterior capsular tightening.18,31,59 Misamore et al. reported on 14 patients with traumatic unidirectional posterior instability who were treated with an open posterior capsulorrhaphy. They found excellent results, with 12 of 14 returning to preinjury level of play.59 Other studies by Rhee presented a review of 33 shoulders for which open, deltoid saving posterior capsulolabral reconstruction was performed and reported that at 25 month follow-up, four patients had recurrent instability.67 Another study by Wolf and colleagues presented similar findings in a retrospective review of 44 shoulders after open posterior glenohumeral stabilization.17 The recurrence rate was 19%, poor results in patients older than 37 years, and in those with chondral damage.17

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CHAPTER 41  Posterior Shoulder Instability

Arthroscopic techniques for the treatment of shoulder instability have been implemented and become increasingly popular. Historically, arthroscopic thermal capsulorrhaphy was performed, but results have been fair at best. One study by Bisson presented 14 shoulders without labral detachment who underwent thermal capsulorrhaphy with 2-year follow-up.68 They found that treatment failed in 3 of their 14 patients (21%). In another study, D’Alessandro found that 37% of patients who underwent thermal capsulorrhaphy for anterior, anteroinferior, or multidirectional shoulder instability had unsatisfactory results with American Shoulder and Elbow Surgeons (ASES) scores at 2- to 5-year follow-up.69 Other studies by Miniaci reported 47% recurrent instability in patients being treated for MDI at 9 months post op.70 Due to the variable response patients have demonstrated, thermal capsulorrhaphy for treatment of RPS is not recommended. Arthroscopic capsulolabral repair has evolved over time, providing a minimally invasive approach with less morbidity and faster recovery.13 With advances in arthroscopic techniques, the all-arthroscopic approach to posterior stabilization has the ability to treat a wide array of pathology. With open techniques, anterior pathology of the shoulder (labrum tearing, subscapularis disruption), in addition to superior pathology (supraspinatus, biceps tendon, and superior labrum tearing), is near impossible to address through the same exposure. The arthroscopic approach allows for clear visualization of the entire labrum, rotator cuff, and other pain-generating pathology around the glenohumeral joint, which also allows for adequate treatment. In addition, arthroscopic management of posterior instability allows for complete labrum repair, in addition to capsular plication in an “around the world” fashion. Recent studies evaluating postoperative outcomes of the arthroscopic approach have also surpassed those of open techniques, making the arthroscopic modality the current standard of care for the majority of patients.

Indications Patients are candidates for arthroscopic posterior stabilization if they present with prior episodes of posterior dislocation or RPS of the glenohumeral joint that has not responded favorably to conservative management. After an initial posterior dislocation occurs, a closed reduction is performed and instability is assessed. Once a pain-free shoulder with full ROM is restored, patients are gradually returned to regular activity. If resultant instability or pain persists and physiotherapy is not ameliorative, then the patient is counseled regarding surgical intervention. Patients with RPS may not report an initial traumatic event; however, they may have an insidious course with deep shoulder pain, reduced athletic participation (inability to throw long ball, loss of velocity and control), and pain with cross body and adducted shoulder movements. An initial course of physical therapy can be initiated in addition to a throwing regimen for overhead-throwing athletes. If pain subsides, gradual return to play (RTP) is begun and the patient can be assessed for recurrence of symptoms. If pain or subluxation returns, a MRA can be obtained to confirm the diagnosis. Once confirmed, the specific anatomical

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considerations can be evaluated and the patient can be counseled regarding the need for surgical intervention. Primary indications for surgery include a history consistent with prior dislocation or RPS; physical examination that is positive for any or all of the provocative tests, including the Kim test, Jerk test, posterior load and shift, and pain with cross body adduction with reproduction of symptoms; diagnostic imaging (MRA) demonstrating a patulous posterior capsule, posterior labrum tear, capsular tear or concealed crack (“Kim” lesion); reverse humeral avulsion of the glenohumeral ligaments, reverse Hill-Sachs impaction fracture, reverse osseous Bankart lesion, relative increase in glenoid retroversion with hypoplastic labrum, and chondrolabral retroversion greater than 10 degrees; and patients who failed conservative treatment with a stretching and strengthening rotator cuff rehabilitation program and an inability to return to sport or activity at a preinjury level.

Contraindications As arthroscopic techniques have evolved, so have the relative contraindications to an arthroscopic approach. Contraindications to arthroscopic surgery may include large glenoid (>25%) or reverse Hill-Sachs (>30%) lesions that may be better managed with an open bone grafting technique, capsular tearing with loss of capsular tissue (from prior surgery or thermal modification), excessive glenoid retroversion (type C glenoid), significant osteoarthritis or chondral erosion, neuromuscular abnormality resulting in motor deficit, and patients who have failed a prior arthroscopic procedure (relative contraindication). Patients unable to comply with a postoperative regimen that consists of a brief period of immobilization followed by a structured therapy protocol are not suitable candidates for surgical intervention.

Goals of the Procedure The main purpose of arthroscopic posterior stabilization is to prevent recurrent macro (dislocation) or micro (RPS) posterior instability of the glenohumeral joint. Traditional techniques focused on open capsular plication with labrum repair, bone block, or wedge osteotomy to prevent recurrent posterior instability. Evolving techniques have allowed for better access to the glenohumeral joint with an arthroscopic approach with accompanying superior clinical outcomes in recent years.13 The ultimate goal of arthroscopic management is to restore normal glenohumeral mechanics, prevent recurrent instability or subluxation, and allow for return to normal physiologic function of the joint and athletic participation. The arthroscopic method is also aimed at improving short-term ROM goals and preventing disruption of the deltoid or scapular musculature, which can delay postoperative rehabilitation and may accompany an open technique.

POSTOPERATIVE MANAGEMENT At the completion of the surgery, the shoulder is placed in a shoulder abduction sling, which immobilizes the shoulder in 30 degrees of abduction and prevents internal rotation. An optional cryotherapy device may be used for the first 3 postoperative days to minimize swelling and pain. During the initial postoperative

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Authors’ Preferred Technique Arthroscopic Posterior Shoulder Stabilization Preoperative Preparation and Positioning Preoperative Preparation Prior to surgery, the magnetic resonance arthrogram (MRA) is evaluated for degree of glenoid retroversion, significance of any osseous pathology, and the degree of labrum pathology. Routine radiographs (AP, scapular Y, and axillary view) are also typically obtained prior to MRA to exclude the presence of fracture, subluxation, or frank dislocation. Understanding the needs of each patient is critical to achieving success with this technique. For instance, patients who engage in high-risk contact sports are more likely to have significant labral pathology and require added capsular plication. Patients who are overheadthrowing athletes will have difficulty returning to sports if excessive plication is performed, causing a decrease in ROM and capsular tightness. Patients are given information regarding the risks of surgery, which may include stiffness, infection, neurovascular injury, and recurrence of instability. On the date of the surgery, an interscalene nerve block is routinely used with general anesthesia for both intraoperative muscle relaxation and postoperative pain control. Positioning A lateral decubitus position is preferred; however, a beach-chair position can be utilized for this technique. The lateral decubitus position offers excellent access to the posterior joint and capsule without the use of accessory traction by an assistant. A beanbag positioner is typically used with an axillary roll to protect the nonoperative extremity. The down leg is padded over the peroneal nerve, fibular head, and lateral malleolus. The operative arm is placed in 10 to 15 lbs of balanced arm traction in 45 degrees of abduction and 20 degrees of forward flexion. When the posterior, inferior aspect of the labrum is approached arthroscopically, forward flexion can be increased to gain better exposure. The bed should be angled 45 degrees away from anesthesia, and the visualization tower should be placed across the surgical field and at eye level to the surgeon.

Typical pathology associated with posterior instability includes posterior labral fraying and splitting, posterior labral detachment from the glenoid rim, a patulous posterior capsule, a discrete posterior capsular tear, undersurface partial-thickness rotator cuff tears, and widening of the rotator interval (Fig. 41.10). The surgeon also must be cognizant of the subtle Kim lesion—that is, a concealed incomplete detachment of the posterior labrum.52 Glenoid and Labrum Preparation A meticulous glenoid preparation is critical to achieving success of the repair. An elevator is initially placed through the posterior portal, and the labrum is sharply elevated off the glenoid (Fig. 41.11). The labrum is mobilized until the underside of the capsule edge of the glenoid rim is visualized. Care is taken during labral elevation and mobilization to not transect the labrum. Adequate trajectory through the posterior portal is critical in achieving this goal. If the angle is difficult, the elevator can be brought in through the anterior portal and the labrum visualized posteriorly. Once adequate mobilization is achieved, a hooded burr is used to prepare the glenoid rim (Fig. 41.12). Great care should be used to ensure the labrum is protected during the bony débridement. A shaver is then used to remove any remaining soft tissue debris from the glenoid rim

Operative Technique Portal Placement All bony landmarks are marked with a marking pen (the acromion, coracoid process and acromioclavicular joint). The anterior portal is typically placed in the rotator interval in a trajectory that is diagonal from the coracoid process to the anterolateral edge of the acromion. The posterior portal is created slightly lateral to a traditional posterior arthroscopy portal to allow tangential access to the posterior glenoid for anchor placement. The posterior portal is created first after insufflation of the joint with 30 cc of normal saline. This facilitates safe insertion of the arthroscope cannula and blunt trochar. The anterior portal is created in the rotator interval either using an “inside out” technique with a switching stick, or an “outside in” technique with a spinal needle. Once portals are created, a clear cannula is placed in the anterior portal using a traditional dilation technique. Either a 5.75 mm or 8.25 mm clear cannula (distally threaded) can be used for the anterior portal. Diagnostic Arthroscopy A 30-degree arthroscope placed through a posterior viewing portal is used to perform an initial diagnostic arthroscopy (see Figs. 41.2, 41.3). The joint is assessed for concomitant pathology such as superior labral tears, rotator cuff tears, and osteochondral injury. Débridement of the joint can be carried out with a 4.5 mm shaver through the anterior portal as needed. Following an initial diagnostic arthroscopy, the camera is placed into the anterior cannula, and inflow is placed on the side port on the cannula. A switching stick is placed in the posterior portal, and this portal is dilated to 8 mm. An 8.25-mm cannula (Arthrex, Naples, FL) is then placed in the posterior portal. The arthroscope can be switched to a 70-degree arthroscope, which allows better visualization of the posterior and inferior capsule and posterior inferior band of the inferior glenohumeral ligament.

Fig. 41.10  A discrete posterior capsular tear in an athlete with recurrent posterior subluxation of the shoulder (right shoulder, viewed from the anterior portal).

Fig. 41.11  An arthroscopic chisel used to elevate the torn labrum, which is scarred medially, away from the glenoid rim. In this case, a split in the labrum is used to access the scarred tissue (right shoulder, viewed from the anterior portal).

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CHAPTER 41  Posterior Shoulder Instability

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Authors’ Preferred Technique Arthroscopic Posterior Shoulder Stabilization—cont’d

Fig. 41.12  A motorized shaver is used at the posterosuperior extent of the labral tear to decorticate the glenoid rim and abrade the labral undersurface (right shoulder, viewed from the posterior portal). To complete the abrasion posteroinferiorly, the shaver is switched to the posterior portal and the arthroscope is placed in the anterior portal.

Fig. 41.13  Arthroscopic view from the posterior portal looking inferiorly along the glenoid after labrum mobilization and glenoid preparation is complete.

followed by rasping to create a fresh, bleeding surface conducive to soft tissue healing (Fig. 41.13). Suture Passing and Labral Repair A knotless anchor system is employed (2.4 mm biocomposite short PushLock anchors [Arthrex, Naples, FL] for patients with smaller glenoids [subequatorial width 60; stability FQuads

FPT < FQuads

Fig. 89.26  The mechanical function of the patella as a lever and as a spacer to increase the patellar tendon moment arm. Left, With the knee near the extended position, the levering action of the patellar mechanism produces greater force values in the patellar tendon (FPT) in comparison with those developed by quadriceps contraction (FQuads). Right, With the knee in the flexed position, the levering action of the patella is decreased, and the force values developed in the patellar tendon are less than those developed by the quadriceps. (From Huberti HH, Hayes WC, Stone JL, et al. Force ratios in the quadriceps tendon and ligamentous patellae. J Orthop Res. 1984;2:49.)

the large isokinetic or isometric knee moments with the knee in positions between extension and 45 degrees should be avoided. In this flexion range, quadriceps activity actually produces forces of greater magnitude in the patellar tendon. This finding has been demonstrated by the work of Huberti and colleagues,233 who showed that the FPT/FQuads ratio is greater than 1.0 for knee positions between extension and 45 degrees (see Fig. 89.25). It may be advisable to restrict rehabilitation programs for patellar tendinitis to flexion angles between 45 and 120 degrees, in which the FPT/FQuads ratio is less than 1.0. This constraint prevents an amplification of FPT. This restriction would not apply to normal gait, in which the bending moments and therefore FQuads are not high. Because of the changing relationship between developed FQuads and resulting FPT as the knee courses from extension through full flexion, the effectiveness of the quadriceps in developing an extension moment becomes substantially smaller at larger knee flexion angles, which also prevents the amplification of FPT. These studies also have important implications in the rehabilitation and surgical treatment of patellofemoral pain syndromes. Rehabilitation programs designed to minimize the PFJR but not the FQuads should avoid large isokinetic, isotonic, or isometric moments with the knee positioned between 60 and 120 degrees of flexion. In this range, the predicted PFJR force is equal to the FQuads (see Fig. 89.26).238 With the requirement of minimizing the PFJR force, it may be advisable to restrict knee

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Force Ratio: FPFJR

1

FQuads

0.5

0 0

20

80 40 60 Knee flexion angle

100

120

Fig. 89.27  The predicted force ratio patellofemoral joint reaction force/quadriceps force (FPFJR/FQuads) for the knee positioned between 0 and 120 degrees of flexion. Between 0 and 70 degrees, FPFJR is less than that developed by quadriceps contraction, whereas from 70 to 120 degrees, FPFJR is equal to FQuads. (From van Eijden TM, Kouwenhoven E, Verburg J, et al. A mathematical model of the patellofemoral joint. J Biomech. 1986;19:219–288.)

rehabilitation to range between the limits of extension, when the PFJR is about 50% of the FQuads, and 40 degrees, when the PFJR is 90% of the FQuads.238 Maquet212 has investigated the surgical treatment of patellofemoral pain, demonstrating that by increasing the extensor moment arm by a 2-cm elevation of the tibial tubercle, a 50% reduction in the PFJR force occurred when the knee is flexed to 45 degrees. Ferguson and associates239 investigated the effect of anterior displacement of the tibial tubercle on patellofemoral contact stress. In this study, the patella-trochlea interfaces of human cadaver specimens were instrumented with miniature force sensors to monitor the patellofemoral contact stress. They revealed that anterior displacement of the tibial tubercle decreased the patellofemoral contact stress between 0 and 90 degrees of flexion.239 The largest decrease in contact stress was achieved with a 12.5-mm elevation of the tubercle; further elevation produced only a minimal decrease in contact stress.239 This finding demonstrates the importance of the anteroposterior position of the patellar tendon and its role in controlling the extensor moment arm. In addition, the proximal-distal location of the patellofemoral contact point is critical to the function of the patella as a lever (as explained earlier). In the frontal plane, the axis of the FQuads forms an angle with the patellar tendon. This angle has been defined as the Q angle and is measured as the intersection of the center line of the patellar tendon and the line from the center of the patella to the anterior superior iliac spine.237 The normal Q angle is reported to range between 10 and 15 degrees with the knee in full extension.240,241 With knee flexion, the Q angle decreases because a coupled internal rotation of the tibia occurs relative to the femur.214 Contraction of the quadriceps creates a bowstring effect that displaces the patella in a lateral direction, producing a contact force against the lateral margin of the femoral trochlear groove. Abnormal tracking of the patella, which allows lateral subluxation of only a few millimeters, markedly decreases the contact area, greatly increasing the local stress (force per unit area; Fig. 89.28).

R5

RM

R5

RL

R5

Fig. 89.28  Patellofemoral joint reaction forces for the normal knee (left). The joint reaction force (R5) is resisted by the lateral (RL) and medial (RM) components. In the knee with a lateralized patella (right), the joint reaction force is resisted by the lateral component only (R5). (From Maquet P. Mechanics and osteoarthritis of the patellofemoral joint. Clin Orthop. 1979;144:70.)

This mechanism may contribute to patellofemoral pain and degeneration of the patellar articular cartilage (chondromalacia). Other anatomic conditions can also contribute to abnormal patellar tracking. These conditions include hypoplasia of the trochlear groove, abnormal patellar articular configuration, underdevelopment of the vastus medialis, transverse plane rotational malalignment of the proximal tibia relative to the distal femur, and an abnormally high Q angle. Huberti and Hayes220 studied the effect of different Q angles by simulating the squatting activity in human cadaver specimens while measuring patellofemoral contact pressure with pressure-sensitive film. They demonstrated that either an increase or a decrease in Q angle developed an increased peak patellofemoral pressure and the

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CHAPTER 89  Knee Anatomy and Biomechanics of the Knee

associated unpredictable patterns of cartilage loading. Cox242 has presented a retrospective study of the Roux-Elmslie-Trillat procedure for realignment of the knee extensor mechanism and prevention of recurrent subluxation of the patella. An evaluation of 116 patients observed for at least 1 year demonstrated that this procedure is a satisfactory method for the prevention of lateral subluxation, with recurrence in only 7% of the cases. Careful attention to the medial transfer of the tibial tuberosity without a posterior displacement was emphasized as the key to successful long-term results.242 Procedures resulting in some posterior transfer of the tibial tuberosity, such as that described by Hauser, decrease the patellar tendon moment arm and consequently increase the patellofemoral contact stress. Fulkerson and Hungerford243 have reviewed the clinical and radiologic outcomes of the Hauser procedure and have presented evidence of progressive knee joint degeneration. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Farrow LD, Chen MR, Cooperman DR, et al. Morphology of the femoral intercondylar notch. J Bone Joint Surg Am. 2007;89A(10):2150–2155.

Level of Evidence: V

Summary: In this study the morphologic features of the femoral intercondylar notch are described. The posterolateral rim of the intercondylar notch is not well defined. Accurate placement of commercial femoral tunnel aiming guides may be difficult.

Citation: Warren LF, Marshall JL. The supporting structures and layers on the medial side of the knee: an anatomical analysis. J Bone Joint Surg Am. 1979;61A:56–62.

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Level of Evidence: V

Summary: In this study an anatomic description of the medial aspect of the knee is provided.

Citation: Beynnon BD, Fleming BC. Anterior cruciate ligament strain in vivo: a review of previous work. J Biomech. 1998;31:519–525.

Level of Evidence: IV

Summary: The strain behavior of the anterior cruciate ligament (ACL) has been measured by arthroscopic implantation of the differential variable reluctance transducer while subjects are experiencing local anesthesia. Movement of the knee from a flexed to an extended position, either passively or through contraction of the leg muscles, produces an increase in ACL strain values. Isolated contraction of the dominant quadriceps with the knee between 50 degrees and extension creates substantial increases in strain. In contrast, isolated contraction of the hamstrings at any knee position does not increase ACL strain. With the knee unweighted, the protective strain shielding effect of a functional knee brace decreases as the magnitude of anterior shear load applied to the tibia increases. The approach used in this study is novel in that it can be used to measure an important portion of the ACL’s strain distribution while clinically relevant loads are applied to the knee, subjects perform rehabilitation exercises, or in the presence of different orthoses such as functional knee braces.

Citation: Beynnon BD, Fleming BC, Labovitch R. Chronic anterior-cruciate ligament deficiency is associated with increased anterior translation of the tibia during the transition from non-weightbearing to weightbearing. J Orthop Res. 2002;20:332–337.

Level of Evidence: III

Level of Evidence: V

Summary:

Summary: In this study the anatomic structures in the medial side of the knee are described. This study is one of the most important works describing the medial side of the knee. Only minor variations in the overall anatomic pattern are found.

Citation: LaPrade RF, Morgan PM, Wentorf FA, et al. The anatomy of the posterior aspect of the knee. An anatomic study. J Bone Joint Surg Am. 2007;89A:758–764.

Level of Evidence: V

Translation of the tibia relative to the femur was measured while a group of subjects with normal knees and a group with anterior cruciate ligament (ACL) tears underwent transition from non–weight-bearing to weight-bearing stance. A fourfold increase in anterior translation of the tibia for the knees with ACL tears compared with the contralateral side is a concern because it is substantially greater than the 95% confidence limits of the side-to-side differences in anteroposterior knee laxity measured from subjects with normal knees. This observation could explain, at least in part, one of the mechanisms that initiates damage to the meniscus and articular cartilage in subjects who have sustained an ACL tear.

Citation:

Summary: In this study an anatomic detailed description of the posterior aspect of the knee is provided.

Citation: LaPrade RF, Engebretsen AH, Ly TV, et al. The anatomy of the medial part of the knee. J Bone Joint Surg Am. 2007;89A:2000–2010.

Beynnon BD, Johnson RJ, Naud S, et al. Accelerated versus nonaccelerated rehabilitation after anterior cruciate ligament reconstruction: a prospective, double-blind investigation evaluating knee joint laxity using roentgen stereophotogrammetric analysis. Am J Sports Med. 2011;39(12):2536–2548.

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Level of Evidence: I

Summary: Rehabilitation with the accelerated and nonaccelerated programs administered in this study produced the same increase in the envelope of knee laxity. Most of the increase in the envelope of

knee laxity occurred during healing when exercises were advanced and activity level increased. Patients in both programs had the same clinical assessment, functional performance, proprioception, and thigh muscle strength, which returned to normal levels after healing was complete. For participants in both treatment programs, the Knee Injury and Osteoarthritis Outcome Score assessment of quality of life did not return to preinjury levels.

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REFERENCES 1. Espregueira-Mendes M, da Silva V. Anatomy of the lateral collateral ligament: a cadaver and histological study. Knee Surg Sports Traumatol Arthrosc. 2006;14:221–228. 2. Fu FH, Jordan SS. The lateral intercondylar ridge a key to anatomic anterior cruciate ligament reconstruction. J Bone Joint Surg Am. 2007;89(10):2103–2104. 3. Farrow LD, Chen MR, Cooperman DR, et al. Morphology of the femoral intercondylar notch. J Bone Joint Surg Am. 2007;89(10):2150–2155. 4. Ferretti M, Ekdahl M, Shen W, et al. Osseous landmarks of the femoral attachment of the anterior cruciate ligament: an anatomic study. Arthroscopy. 2007;23(11):1218–1225. 5. Hutchinson MR, Ash SA. Resident’s ridge: assessing the cortical thickness of the lateral wall and roof of the intercondylar notch. Arthroscopy. 2003;19(9):931–935. 6. Farrow LD, Gillespie RJ, Victoroff BN, et al. Radiographic location of the lateral intercondylar ridge: its relationship to Blumensaat’s line. Am J Sports Med. 2008;36(10):2002–2006. 7. Shino K, Suzuki T, Iwahashi T, et al. The resident’s ridge as an arthroscopic landmark for anatomical femoral tunnel drilling in ACL reconstruction. Knee Surg Sports Traumatol Arthrosc. 2010;18(9):1164–1168. 8. Beltran J, Matityahu A, Hwang K, et al. The distal semimembranosus complex: normal MR anatomy, variants, biomechanics and pathology. Skeletal Radiol. 2003;32: 435–445. 9. Warren LF, Marshall JL. The supporting structures and layers on the medial side of the knee: an anatomical analysis. J Bone Joint Surg Am. 1979;61:56–62. 10. Ullrich K, Krudwing WK, Witzel U. Posterolateral aspect and stability of the knee joint. I. Anatomy and function of the popliteus muscle-tendon unit: an anatomical and biomechanical study. Knee Surg Sports Traumatol Arthrosc. 2002;10(2):86–90. 11. LaPrade RF, Morgan PM, Wentorf FA, et al. The anatomy of the posterior aspect of the knee. An anatomic study. J Bone Joint Surg Am. 2007;89:758–764. 12. Pagnani MJ, Warner JJP, O’Brien SJ, et al. Anatomic considerations in harvesting the semitendinosus and gracilis tendons and a technique of harvest. Am J Sports Med. 1993;21:565–571. 13. LaPrade RF, Engebretsen AH, Ly TV, et al. The anatomy of the medial part of the knee. J Bone Joint Surg Am. 2007;89: 2000–2010. 14. Solman CG, Pagnani MJ. Hamstring tendon harvesting. Reviewing anatomic relationships and avoiding pitfalls. Orthop Clin North Am. 2003;34:1–8. 15. Fritschy D, Fasel J, Imbert JC, et al. The popliteal cyst. Knee Surg Sports Traumatol Arthrosc. 2006;14:623–628. 16. Zivanovic S. Menisco-meniscal ligaments of the human knee joint. Anat Anz. 1974;135:35–42. 17. Aydingoz U, Kaya A, Atay OA, et al. MR imaging of the anterior intermeniscal ligament: classification according to insertion sites. Eur Radiol. 2002;12:824–829. 18. de Abreu MR, Chung CB, Trudell D, et al. Anterior transverse ligament of the knee: MR imaging and anatomic study using clinical and cadaveric material with emphasis on its contribution to meniscal tears. Clin Imaging. 2007;31:194–201. 19. Kapandji IA. The Physiology of the Joints. Vol 2. 5th ed. Edinburgh: Livingstone; 1987.

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20. Thompson WO, Thaete FL, Fu FH, et al. Tibial meniscal dynamics using three-dimensional reconstruction of magnetic resonance images. Am J Sports Med. 1991;19:210–216. 21. Kohn D, Moreno B. Meniscus insertion anatomy as a basis for meniscus replacement: a morphological cadaveric study. Arthroscopy. 1995;11:96–103. 22. Poynton AR, Javadpour SM, Finegan PJ, et al. The meniscofemoral ligaments of the knee. J Bone Joint Surg Br. 1997;79:327–330. 23. Messner K, Gao J. The menisci of the knee joint. Anatomical and functional characteristics, and a rationale for clinical treatment. J Anat. 1998;193:161–178. 24. Gupte CM, Smith A, McDermott ID, et al. Meniscofemoral ligaments revisited: anatomical study, age correlation and clinical implications. J Bone Joint Surg Br. 2002;84:846–851. 25. Wan ACT, Felle P. The menisco-femoral ligaments. Clin Anat. 1995;8:323–326. 26. Krause WR, Pope MH, Johnson RJ, et al. Mechanical changes in the knee after meniscectomy. J Bone Joint Surg Am. 1976;58(5):599–604. 27. Freutel M, Seitz AM, Ignatius A, et al. Influence of partial meniscectomy on attachment forces, superficial strain and contact mechanics in porcine knee joints. Knee Surg Sports Traumatol Arthrosc. 2015;23:74–82. 28. Ihn JC, Kim SJ, Park IH. In vitro study of contact area and pressure distribution in the human knee after partial and total meniscectomy. Int Orthop. 1993;17:214–218. 29. Kraeutler MJ, Mitchell JJ, Chahla J, et al. Intra-articular implantation of mesenchymal stem cells, Part 1: A review of the literature for prevention of postmeniscectomy osteoarthritis. Orthop J Sports Med. 2017;5:2325967116680815. 30. Kraeutler MJ, Mitchell JJ, Chahla J, et al. Intra-articular implantation of mesenchymal stem cells, Part 2: A review of the literature for meniscal regeneration. Orthop J Sports Med. 2017;5:2325967116680814. 31. Lee SJ, Aadalen KJ, Malaviya P, et al. Tibiofemoral contact mechanics after serial medial meniscectomies in the human cadaveric knee. Am J Sports Med. 2006;34:1334–1344. 32. Pozzi A, Tonks CA, Ling HY. Femorotibial contact mechanics and meniscal strain after serial meniscectomy. Vet Surg. 2010;39:482–488. 33. Kraeutler MJ, Wolsky RM, Vidal AF, et al. Anatomy and biomechanics of the native and reconstructed anterior cruciate ligament: surgical implications. J Bone Joint Surg Am. 2017;99:438–445. 34. Siebold R, Schuhmacher P, Fernandez F, et al. Flat midsubstance of the anterior cruciate ligament with tibial “C”-shaped insertion site. Knee Surg Sports Traumatol Arthrosc. 2015;23:3136–3142. 35. Siegel L, Vandenakker-Albanese C, Siegel D. Anterior cruciate ligament injuries: anatomy, physiology, biomechanics, and management. Clin J Sport Med. 2012;22:349–355. 36. Fujimaki Y, Thorhauer E, Sasaki Y, et al. Quantitative in situ analysis of the anterior cruciate ligament: length, midsubstance cross-sectional area, and insertion site areas. Am J Sports Med. 2016;44:118–125. 37. Smith PN, Refshauge KM, Scarvell JM. Development of the concepts of knee kinematics. Arch Phys Med Rehabil. 2003;84:1895–1902. 38. Farrow LD, Chen MR, Cooperman DR, et al. Morphology of the femoral intercondylar notch. J Bone Joint Surg Am. 2007;89:2150–2155.

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39. Tsukada S, Fujishiro H, Watanabe K, et al. Anatomic variations of the lateral intercondylar ridge: relationship to the anterior margin of the anterior cruciate ligament. Am J Sports Med. 2014;42:1110–1117. 40. Ferretti M, Ekdahl M, Shen W, et al. Osseous landmarks of the femoral attachment of the anterior cruciate ligament: an anatomic study. Arthroscopy. 2007;23:1218–1225. 41. Ziegler CG, Pietrini SD, Westerhaus BD, et al. Arthroscopically pertinent landmarks for tunnel positioning in single-bundle and double-bundle anterior cruciate ligament reconstructions. Am J Sports Med. 2011;39:743–752. 42. Strocchi R, de Pasquale V, Gubellini P, et al. The human anterior cruciate ligament: histological and ultrastructural observations. J Anat. 1992;180:515–519. 43. Zantop T, Petersen W, Sekiya JK, et al. Anterior cruciate ligament anatomy and function relating to anatomical reconstruction. Knee Surg Sports Traumatol Arthrosc. 2006;14:982–992. 44. Śmigielski R, Zdanowicz U, Drwiega M, et al. Ribbon-like appearance of the midsubstance fibres of the anterior cruciate ligament close to its femoral insertion site: a cadaveric study including 111 knees. Knee Surg Sports Traumatol Arthrosc. 2015;23:3143–3150. 45. Guenther D, Irarrázaval S, Nishizawa Y, et al. Variation in the shape of the tibial insertion site of the anterior cruciate ligament: classification is required. Knee Surg Sports Traumatol Arthrosc. 2017;25(8):2428–2432. 46. Terry GC, LaPrade RF. The posterolateral aspect of the knee. Am J Sports Med. 1996;24:732–739. 47. Sugita T, Amis A. Anatomic and biomechanical study of the lateral collateral and popliteofibular ligaments. Am J Sports Med. 2001;29:466–472. 48. LaPrade CM, Ellman MB, Rasmussen MT, et al. Anatomy of the anterior root attachments of the medial and lateral menisci: a quantitative analysis. Am J Sports Med. 2014;42: 2386–2392. 49. Wright JO, Skelley NW, Schur RP, et al. Microstructural and mechanical properties of the posterior cruciate ligament: a comparison of the anterolateral and posteromedial bundles. J Bone Joint Surg Am. 2016;98:1656–1664. 50. Claes S, Vereecke E, Maes M, et al. Anatomy of the anterolateral ligament of the knee. J Anat. 2013;223:321–328. 51. Cavaignac E, Ancelin D, Chiron P, et al. Historical perspective on the “discovery” of the anterolateral ligament of the knee. Knee Surg Sports Traumatol Arthrosc. 2016;25(4):991–996. 52. Vincent JP, Magnussen RA, Gezmez F, et al. The anterolateral ligament of the human knee: an anatomic and histologic study. Knee Surg Sports Traumatol Arthrosc. 2012;20:147–152. 53. Kennedy MI, Claes S, Fuso FA, et al. The anterolateral ligament: an anatomic, radiographic, and biomechanical analysis. Am J Sports Med. 2015;43:1606–1615. 54. Tavlo M, Eljaja S, Jensen JT, et al. The role of the anterolateral ligament in ACL insufficient and reconstructed knees on rotatory stability: a biomechanical study on human cadavers. Scand J Med Sci Sports. 2016;26:960–966. 55. Helito CP, Demange MK, Bonadio MB, et al. Anatomy and histology of the knee anterolateral ligament. Orthop J Sports Med. 2013;1:2325967113513546. 56. Helito CP, Helito PV, Bonadio MB, et al. Evaluation of the length and isometric pattern of the anterolateral ligament with serial computed tomography. Orthop J Sports Med. 2014;2:2325967114562205.

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101. Markolf KL, Gorek JF, Kabo M, et al. Direct measurement of resultant forces in the anterior cruciate ligament: an in vitro study performed with a new experimental technique. J Bone Joint Surg Am. 1990;72:557–567. 102. Markolf KL, Burchfield DM, Shapiro MM, et al. Combined knee loading states that generate high anterior cruciate ligament forces. J Orthop Res. 1995;13:930–935. 103. Markolf KL, Meusch JS, Amstutz HC. Stiffness and laxity of the knee—the contributions of the supporting structures. J Bone Joint Surg Am. 1976;58:583–594. 104. Markolf KL, Wascher DC, Finerman GA. Direct in vitro measurement of forces in the cruciate ligaments. Part II: The effect of section of the posterolateral structures. J Bone Joint Surg Am. 1993;75:387–394. 105. Markolf KL, O’Neill G, Jackson SR, et al. Effects of applied quadriceps and hamstrings muscle loads on forces in the anterior and posterior cruciate ligaments. Am J Sports Med. 2004;32:1144–1149. 106. Fleming BC, Good L, Peura GD, et al. Calibration and application of an intra-articular force transducer for the measurement of patellar tendon graft forces: an in situ evaluation. J Biomech Eng. 1999;121:393–398. 107. Fleming BC, Peura GD, Beynnon BD. Factors influencing the output of an implantable force transducer. J Biomech. 2000;33:889–893. 108. Beynnon BD, Fleming BC. Anterior cruciate ligament strain in vivo: a review of previous work. J Biomech. 1998;31:519–525. 109. Fleming BC, Beynnon BD, Johnson RJ, et al. Isometric versus tension measurements: a comparison for the reconstruction of the anterior cruciate ligament. Am J Sports Med. 1993;21: 82–88. 110. Arms SA, Pope MH, Johnson RJ, et al. The biomechanics of anterior cruciate ligament rehabilitation and reconstruction. Am J Sports Med. 1984;12:8–18. 111. Brown TD, Sigal L, Njus GO, et al. Dynamic performance characteristics of the liquid metal strain gauge. J Biomech. 1986;19:165–173. 112. Edwards RG, Lafferty JF, Lange KD. Ligament strain in the human knee. J Basic Eng. 1970;92:131–136. 113. Kennedy JC, Haskins RJ, Willis RB. Strain gauge analysis of knee ligaments. Clin Orthop Relat Res. 1977;129:225–229. 114. Renström P, Arms SW, Stanwyck TS, et al. Strain within the anterior cruciate ligament during hamstring and quadriceps activity. Am J Sports Med. 1986;14:83–87. 115. Wang CJ, Walker PS, Wolf B. The effects of flexion and rotation on the length patterns of the ligaments of the knee. J Biomech. 1973;6:587–596. 116. Berns GS, Hull ML, Patterson HA. Strain in the anteromedial bundle of the anterior cruciate ligament under combination loading. J Orthop Res. 1992;10:167–176. 117. Hull ML, Berns GS, Varma H, et al. Strain in the medial collateral ligament of the human knee under single and combined loads. J Biomech. 1996;29:199–206. 118. Henning CE, Lynch MA, Glick KR. An in vitro strain gauge study of elongation of the anterior cruciate ligament. Am J Sports Med. 1985;13:22–26. 119. Butler DL, Grood ES, Zernicke RR, et al. Non-uniform surface strains in young human tendons and fascia. Trans Orthop Res Soc. 1983;8:8. 120. Woo SLY, Gomez MA, Akerson WH. Mechanical properties along the medial collateral ligament. Trans Orthop Res Soc. 1983;8:7.

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121. Butler DL, Grood ES, Noyes FR, et al. On the interpretation of our anterior cruciate ligament data. Clin Orthop Relat Res. 1985;196:26–34. 122. Sidles JA, Larson RV, Garbini JL, et al. Ligament length relationships in the moving knee. J Orthop Res. 1988;6:593–610. 123. Trent PS, Walker PS, Wolf B. Ligament length patterns, strength, and rotational axes of the knee joint. Clin Orthop. 1976;117:263–279. 124. Warren LF, Marshall JL, Girgis F. The prime static stabilizer of the medial side of the knee. J Bone Joint Surg Am. 1974;56: 665–674. 125. Covey DC, Sapega AA, Marshall RC. The effects of varied joint motion and loading conditions on posterior cruciate ligament fiber length behavior. Am J Sports Med. 2004;32:1866–1872. 126. Beynnon BD, Johnson RJ, Fleming BC, et al. The strain behavior of the anterior cruciate ligament during squatting and active flexion-extension: a comparison of an open and a closed kinetic chain exercise. Am J Sports Med. 1997;25:823–829. 127. Fischer RA, Arms SW, Johnson RJ, et al. The functional relationship of the posterior oblique ligament to the medial collateral ligament of the human knee. Am J Sports Med. 1985;13:390–397. 128. Fleming BC, Beynnon BD, Nichols CE, et al. An in vivo comparison between intraoperative isometric measurement and local elongation of the graft after reconstruction of the anterior cruciate ligament. J Bone Joint Surg Am. 1994;76: 511–519. 129. Fleming BC, Beynnon BD, Renstrom PA, et al. The strain behavior of the anterior cruciate ligament during stair climbing: an in vivo study. Arthroscopy. 1999;15: 185–191. 130. Fleming BC, Beynnon BD, Renstrom PA, et al. The strain behavior of the anterior cruciate ligament during bicycling: an in vivo study. Am J Sports Med. 1998;26:109–118. 131. Cooper RR, Misol S. Tendon and ligament insertion: a light and electron microscopic study. J Bone Joint Surg Am. 1970;52:1–20. 132. Noyes FR, Butler DL, Grood ES, et al. Biomechanical analysis of human ligament grafts used in knee ligament repairs and reconstruction. J Bone Joint Surg Am. 1984;66:344–352. 133. Noyes FR, Grood ES. The strength of the anterior cruciate ligament in humans and rhesus monkeys: age-related and species-related changes. J Bone Joint Surg Am. 1976;58:1074–1082. 134. Noyes FR, DeLucas JL, Torrik PJ. Biomechanics of ligament failure: an analysis of strain-rate sensitivity and mechanism of failure in primates. J Bone Joint Surg Am. 1974;56:236–253. 135. Noyes FR. Functional properties of knee ligaments and alterations induced by immobilization. Clin Orthop. 1977;123:210–242. 136. Chandrashekar N, Mansouri H, Slauterbeck J, et al. Sex-based differences in the tensile properties of the human anterior cruciate ligament. J Biomech. 2006;39:2943–2950. 137. Hsu WH, Fisk J, Yasmamoto Y, et al. Differences in torsional joint stiffness of the knee between genders: a human cadaver study. Am J Sports Med. 2006;34:765–770. 138. Ameil D, Kleiner JB, Akeson WH. The natural history of the anterior cruciate ligament autograft of patellar tendon origin. Am J Sports Med. 1986;14:449–462. 139. Woo SLY, Hollis JM, Adams DJ, et al. Tensile properties of the human femur-anterior cruciate ligament-tibia complex: the

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CHAPTER 89  Knee Anatomy and Biomechanics of the Knee 156. Daniel D, Malcolm L, Losse G, et al. Instrumented measurement of anterior laxity of the knee. J Bone Joint Surg Am. 1985;67:720–725. 157. Jacob RP. Observations on rotary instability of the lateral compartment of the knee. Acta Orthop Scand Suppl. 1981;52:1–31. 158. Johnson RJ. The anterior cruciate: a dilemma in sports medicine. Int J Sports Med. 1982;3:71–79. 159. Markolf KL, Graff-Radford A, Amstutz HC. In vivo stability—a quantitative assessment using an instrumented clinical testing apparatus. J Bone Joint Surg Am. 1978;60:664–674. 160. Torg J, Conrad W, Kalen V. Clinical diagnosis of ACL instability. Am J Sports Med. 1976;4:84–92. 161. Torzilli P, Greenberg R, Hood R, et al. Measurement of anterior-posterior motion of the knee in injured patients using a biomechanical stress technique. J Bone Joint Surg Am. 1984;66:1438–1442. 162. Bach JM, Hull ML. Strain of the anterior cruciate ligament increases linearly with quadriceps contraction. In: Johnson RJ, ed. Skiing Trauma and Safety. Vol 12. West Conshohocken, PA: American Society for Testing and Materials; 1999. 163. Nisell R, Nemeth G, Ohlsen H. Joint forces in extension of the knee. Acta Orthop Scand. 1986;57:41–46. 164. Fleming BC, Per AR, Goran O, et al. The gastrocnemius muscle is an antagonist of the anterior cruciate ligament. J Orthop Res. 2001;19:1178–1184. 165. Markolf KL, Bargar WL, Shoemaker SC, et al. The role of joint load in knee stability. J Bone Joint Surg Am. 1981;63:570–585. 166. Fleming BC, Ohlén G, Renström PA. The effects of compressive load and knee joint torque on peak anterior cruciate ligament strains. Am J Sports Med. 2003;31:701–707. 167. Heijne A, Fleming BC, Renstrom P. Strain on the anterior cruciate ligament during closed kinetic chain exercises. Med Sci Sports Exerc. 2004;36:935–941. 168. Beynnon BD, Johnson RJ, Naud S, et al. Accelerated versus nonaccelerated rehabilitation after anterior cruciate ligament reconstruction: a prospective, double-blind investigation evaluating knee joint laxity using roentgen stereophotogrammetric analysis. Am J Sports Med. 2011;39(12): 2536–2548. 169. Grood ES, Noyes FR, Butler DL, et al. Ligamentous and capsular restraints preventing straight medial and lateral laxity in intact human cadaver knees. J Bone Joint Surg Am. 1981;63:1257–1269. 170. Ellis BJ, Lujan TJ, Dalton MS, et al. Medial collateral ligament insertion site and contact forces in ACL-deficient knee. J Orthop Res. 2006;24:800–810. 171. Haimes JL, Wroble RR, Grood ES, et al. Role of the medial structures in the intact and anterior cruciate ligament–deficient knee: limits of motion in the human knee. Am J Sports Med. 1994;22:402–409. 172. Shrine N. The weight-bearing role of the menisci of the knee. J Bone Joint Surg Br. 1974;56:381. 173. Höher J, Vogrin TM, Woo SL, et al. In situ forces in the human posterior cruciate ligament in response to muscle loads: a cadaveric study. J Orthop Res. 1999;17:763–768. 174. Sonne-Holm S, Fledelius I, Ahn N. Results after meniscectomy in 147 athletes. Acta Orthop Scand. 1980;51:303–309. 175. King D. The function of semilunar cartilage. J Bone Joint Surg Am. 1936;18:1069–1076. 176. Campbell WC. Operative Orthopaedics. St. Louis: CV Mosby; 1939.

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177. Dandy DJ, Jackson RW. Meniscectomy and chondromalacia of the femoral condyle. J Bone Joint Surg Am. 1975;57:1116–1119. 178. Dandy DJ, Jackson RW. The diagnosis of problems after meniscectomy. J Bone Joint Surg Br. 1975;57:349–352. 179. Quigley TB. Knee injuries incurred in sports. JAMA. 1959;171:1666. 180. Smillie JS. Injuries to the Knee Joint. 4th ed. Edinburgh: Churchill Livingstone.; 1971:68. 181. Fairbank TJ. Knee changes after meniscectomy. J Bone Joint Surg Br. 1948;30:664. 182. Huckle JR. Is meniscectomy a benign procedure? A long-term follow-up study. Can J Surg. 1965;8:254. 183. Johnson RJ, Kettelkamp DB, Clark W, et al. Factors affecting late meniscectomy results. J Bone Joint Surg Am. 1974;56: 719–729. 184. Tapper EM, Hoover NW. Late results after meniscectomy. J Bone Joint Surg Am. 1969;51:517. 185. Kettlekamp DB, Jacobs AW. Tibiofemoral contact areas— determination and implications. J Bone Joint Surg Am. 1972;54:349. 186. Krause WR, Pope MH, Johnson RJ, et al. Mechanical changes in the knee after meniscectomy. J Bone Joint Surg Am. 1976;58:599. 187. Maquet PG, Van De Berg AJ, Simonet JC. Femorotibial weight-bearing areas: experimental determination. J Bone Joint Surg Am. 1979;57:766. 188. Seedhom BB. Transmission of the load in the knee joint with special reference to the role of the menisci. Part I. Anatomy, analysis, and apparatus. Eng Med. 1979;8:207. 189. Seedhom BB, Hargreaves DJ. Transmission of load in the knee joint with special reference to the role of the menisci. Part II. Experimental results, discussion, and conclusions. Eng Med. 1979;8:220. 190. Seedhom BB, Dawson D, Wright U. Functions of the menisci—a preliminary study. J Bone Joint Surg Br. 1974; 56:381. 191. Simon WH. Scale effects in animal joints. Arthritis Rheum. 1970;13:244–256. 192. Walker PS, Erkman MJ. The role of the menisci in force transmission across the knee. Clin Orthop. 1975;109:184–192. 193. Zielinska B, Donahue TL. 3D finite element model of meniscectomy: changes in joint contact behavior. J Biomech Eng. 2006;128:115–123. 194. Johnson RJ, Pope MH, American Academy of Orthopaedic Surgeons. Functional anatomy of the meniscus. Symposium on the Athlete’s Knee: Surgical Repair and Reconstruction. St. Louis: Mosby; 1978. 195. Ahmed AM, Burke DL. In vitro measurement of static pressure distribution in synovial joints. Part I. Tibial surface of the knee. J Biomech Eng. 1983;105:216–225. 196. Allen CR, Wong EK, Livesay GA, et al. Importance of the medial meniscus in the anterior cruciate ligament–deficient knee. J Orthop Res. 2000;18:109–115. 197. Baratz ME, Fu FH, Mengato R. Meniscal tears: the effect of meniscectomy and repair in intraarticular contact areas and stress in the human knee. Am J Sports Med. 1986;14:270–275. 198. Bylski-Austrow DI, Ciarelli MJ, Kayner DC, et al. Displacements of the menisci under joint load: an in vitro study in human knees. J Biomech. 1994;27:421–431. 199. Shefelbine SJ, Ma CB, Lee KY, et al. MRI analysis of in vivo meniscal and tibiofemoral kinematics in ACL-deficient and normal knees. J Orthop Res. 2006;24:1208–1217.

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200. Von Eisenhart-Rothe R, Bringmann C, Siebert M, et al. Femorotibial and menisco-tibial translation patterns in patients with unilateral anterior cruciate ligament deficiency—a potential cause of secondary meniscal tears. J Orthop Res. 2004;22:275–282. 201. Hsieh HH, Walker PS. Stabilizing mechanisms of the loaded and unloaded knee joint. J Bone Joint Surg Am. 1976;58:87–93. 202. Beynnon BD, Fleming BC, Labovitch R. Chronic anteriorcruciate ligament deficiency is associated with increased anterior translation of the tibia during the transition from non-weightbearing to weightbearing. J Orthop Res. 2002;20:332–337. 203. Hollis JM, Pearsall AW, Niciforos PG. Change in meniscal strain with anterior cruciate ligament injury and after reconstruction. Am J Sports Med. 2000;28:700–704. 204. Pearsall AW 4th, Hollis JM. The effect of posterior cruciate ligament injury and reconstruction on meniscal strain. Am J Sports Med. 2004;32:1675–1680. 205. Levy MI, Torzilli PA, Warren RF. The effect of medial meniscectomy on anterior-posterior motion of the knee. J Bone Joint Surg Am. 1982;64:883–888. 206. Sullivan D, Levy IM, Shaskier S, et al. Medial restraints to anterior-posterior motion of the knee. J Bone Joint Surg Am. 1984;66:930–936. 207. Tienen TG, Buma P, Scholten JG, et al. Displacement of the medial meniscus within the passive motion characteristics of the human knee joint: an RSA study in human cadaveric knees. J Surg. 2005;13:287–292. 208. Watanabe Y, Scyoc AV, Tsuda E, et al. Biomechanical function of the posterior horn of the medial meniscus: a human cadaveric study. J Orthop Sci. 2004;9:280–284. 209. Levy MI, Torzilli PA, Gould JD, et al. The effect of lateral meniscectomy on motion of the knee. J Bone Joint Surg Am. 1989;71:401–406. 210. Bandi W. Chondromalacia patellae and femora-patellare Arthrose, Atiologie, Klinik, and Therapie. Helv Chir Acta Suppl. 1972;11:3–70. 211. Insall J, Goldberg V, Salvati E. Recurrent dislocation and the high-riding patella. Clin Orthop Relat Res. 1972;88:67–69. 212. Maquet PG. Mechanics and osteoarthritis of the patellofemoral joint. Clin Orthop Relat Res. 1979;144:70–73. 213. Outerbridge RE, Dunlop JAY. The problem of chondromalacia patellae. Clin Orthop Relat Res. 1975;110:177–196. 214. Ficat RP, Hungerford DS. Disorders of the Patellofemoral Joint. Baltimore: Williams & Wilkins; 1977. 215. Hungerford DS, Haynes D. The dynamics of patellar stabilization in knee flexion and rotation. Trans Orthop Res Soc. 1982;7:254. 216. Insall J. Chondromalacia patellae”: patellar malalignment syndrome. Orthop Clin North Am. 1979;10:117–127. 217. Goodfellow J, Hungerford DS, Zindel M. Patellofemoral joint mechanics and pathology. J Bone Joint Surg Br. 1976;58: 287–290. 218. Singerman R, Berilla J, Davy DT. Direct in vitro determination of the patellofemoral contact force for normal knees. J Biomech Eng. 1995;117:8–14. 219. Singerman R, Berilla J, Kotzar G, et al. A six-degree-of-freedom transducer for in vitro measurement of patellofemoral contact forces. J Biomech. 1994;27:233–238. 220. Huberti HH, Hayes WC. Patellofemoral contact pressures, the influence of Q-angle, and tendofemoral contact. J Bone Joint Surg Am. 1984;66:715–724.

221. Von Eisenhart-Rothe R, Siebert M, Bringmann C. A new in vivo technique for determination of 3D kinematics and contact areas of the patello-femoral and tibio-femoral joint. J Biomech. 2004;37:927–934. 222. Van Eijden TMGJ, De Boer W, Weijs WA. The orientation of the distal part of the quadriceps femoris muscle as a function of the knee flexion-extension angle. J Biomech. 1985;18:803–809. 223. Besier TF, Draper CE, Gold GE, et al. Patellofemoral joint contact area increases with knee flexion and weight-bearing. J Orthop Res. 2005;23:345–350. 224. Hungerford DS, Barry M. Biomechanics of the patellofemoral joint. Clin Orthop Relat Res. 1979;144:9–15. 225. Matthews LS, Sonstegard DA, Heuke JA. Load-bearing characteristics of the patellofemoral joint. Acta Orthop Scand. 1977;48:511–516. 226. Morrison JB. The mechanics of the knee joint. J Biomech. 1970;3:51–61. 227. Morrison JB. Function of the knee joint in various activities. Biomed Eng. 1969;4:573–580. 228. Perry J, Antonelli P, Ford W. Analysis of knee joint forces during flexed-knee stance. J Bone Joint Surg Am. 1975;57: 961–967. 229. Reilly DT, Martens M. Experimental analysis of the quadriceps muscle force and patellofemoral joint reaction force for various activities. Acta Orthop Scand. 1972;43:126–137. 230. Smidt GL. Biomechanical analysis of knee flexion and extension. J Biomech. 1973;6:79–92. 231. Maquet PG. Biomechanics of the Knee. New York: SpringerVerlag; 1976. 232. Maquet PG: Biomechanics and osteoarthritis of the knee. 11th Congress, Mexico, Societé Internationale de Chirurgie Orthopédique et de Traumatologie. 1969. 233. Huberti HH, Hayes WC, Stone JL, et al. Force ratios in the quadriceps tendon and ligamentous patellae. J Orthop Res. 1984;2:49–54. 234. Ahmed AM, Burke DL, Hyder A. Force analysis of the patellar mechanism. J Orthop Res. 1987;5:69–85. 235. Bishop RED, Denham RA. A note on the ratio between tensions in the quadriceps tendon and infra-patella ligament. Eng Med. 1977;6:53–54. 236. Buff HU, Jones LC, Hungerford DS. Experimental determination of forces transmitted through the patellofemoral joint. J Biomech. 1988;21:17–23. 237. Ellis MI, Seedhom BB, Wright V, et al. An evaluation of the ratio between the tension along the quadriceps tendon and the patella ligament. Eng Med. 1980;9:189–194. 238. Van Eijden TMGJ, Kouwenhoven E, Verburg J, et al. A mathematical model of the patellofemoral joint. J Biomech. 1986;19:219–229. 239. Ferguson AB, Brown TD, Fu FH, et al. Relief of patellofemoral contact stress by anterior displacement of the tibial tubercle. J Bone Joint Surg Am. 1979;61:159–166. 240. Insall J, Palvoka A, Wise DW. Chondromalacia patellae: a prospective study. J Bone Joint Surg Am. 1976;58:1–8. 241. Pevsner DN, Johnson JRG, Blazina ME. The patellofemoral joint and its implications in rehabilitation of the knee. Phys Ther. 1979;59:869–874. 242. Cox JS. Evaluation of the Roux-Elmslie-Trillat procedure for knee extensor realignment. Am J Sports Med. 1982;10:303. 243. Fulkerson JP, Hungerford DS. Patellar subluxation. In: Fulkerson JP, ed. Disorders of the Patellofemoral Joint. Baltimore: Williams & Wilkins; 1990.

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90  Knee Diagnosis and Decision-Making Andrew J. Riff, Peter N. Chalmers, Bernard R. Bach Jr.

For the experienced practitioner, the history and physical examination remains the most efficient, sensitive, specific, accurate, and cost-effective method of establishing a diagnosis in patients with knee-related complaints. Several investigators have demonstrated that the history and physical examination have equivalent sensitivity and specificity to magnetic resonance imaging (MRI) for a variety of intra-articular pathologies, with an overall accuracy of 93%.1,2 When taking a systematic approach to patients with knee-related concerns, assessing each structure in question sequentially for possible injury is critical.2 Developing an intuitive and comprehensive approach to the physical examination requires a detailed understanding of knee anatomy, in particular the relation of the surface skin to the underlying structures, to be able to relate tenderness to pathology. In-depth knowledge of knee pathology can be helpful so that the history and examination can be dynamically tailored. From an organizational standpoint, it is helpful to stratify knee pathology based on onset (acute injury versus insidious onset) and population affected (adult versus pediatric; Table 90.1). Common acute knee injuries in adults include ligament injuries (including anterior cruciate ligament [ACL] tear, posterior cruciate ligament [PCL] tear, medial and lateral collateral ligament injury, and posterolateral corner [PLC] injury), meniscal tears, patellar dislocation/subluxation, patellar or quadriceps tendon ruptures, and fractures (most commonly patellar or tibial plateau). Additional acute injures that warrant consideration in the pediatric patient include physeal and apophyseal injuries (including tibial eminence avulsion fracture, tibial tuberosity avulsion fracture, or patellar sleeve avulsion fracture). Common causes of insidious knee pain in the adult include patellofemoral pain (including patellofemoral syndrome, lateral patellar tilt, patellar and quadriceps tendinitis/tendinopathy), iliotibial band syndrome, degenerative meniscal tears, pes anserine bursitis, medial plica syndrome, patellofemoral and tibiofemoral chondral and osteochondral defects, and osteoarthritis, rheumatologic conditions, septic arthritis, and pigmented villinodular synovitis. Insidious knee pain in the child may also be secondary to osteochondritis dissecans (OCD), discoid meniscus, Osgood-Schlatter disease, Sinding-Larsen-Johansson syndrome, juvenile rheumatoid arthritis, lyme arthritis, and hip pathology such as Perthes disease or slipped capital femoral epiphysis (SCFE).

HISTORY Eliciting the history starts with the chief or primary complaint that leads the patient to present for an evaluation. We endeavor to record this complaint in the patient’s own words, because he or she provides the first clues regarding the patient’s reason for the office visit. Asking an open-ended question such as “What brings you to the office today?” is very helpful. Giving patients the opportunity to “tell their story” also allows them to develop a more significant and meaningful relationship with their physician. Once the patient has completed his or her initial response, the surgeon can return to the beginning of the story as necessary to fill in gaps and collect more details. In particular, the examiner must determine the duration of symptoms and, if possible, the date of onset. Important details often can be gathered from the patient’s recollection of the inciting event or trauma, should one exist. If the injury occurred during an athletic endeavor, the examiner should obtain a full account of the event, including whether this incident was a contact or noncontact injury and if it occurred during practice or during a competition. These details may provide the first clues as to the underlying pathology. For instance, a valgus stress suggests an injury to the medial collateral ligament (MCL), whereas a high-energy trauma such as a motorcycle accident may suggest a knee dislocation or multiligamentous injury. In comparison, noncontact ACL injuries usually occur in the context of stopping quickly, cutting sharply, and landing and changing direction with the foot planted. The mechanism of ACL injury in skiers is different—when skiers injure the ACL, they are moving out of control with the knee bent or extended. The uphill arm is back, the body is off balance, the hips are lower than the knees, and the weight is placed on the inside edge of the downhill ski. This mechanism of injury has been referred to as the “phantom foot” mechanism.3 Recollection of an auditory pop or a tearing sensation may be present. Up to 66% of patients with an ACL injury describe such a sensation.4,5 Swelling immediately after the event may also occur. Indeed, a hemarthrosis develops in most persons with ACL injuries within 3 hours of the initial tear (Table 90.2). It is often helpful to inquire about foot position during the injury. A fall onto a flexed knee may result in either a patellar fracture (if the ankle is dorsiflexed) or a PCL injury (if the foot is plantar flexed). If no specific event can be recalled, the patient should be asked if he or she has had a recent change in activity, which

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Abstract

Keywords

For the experienced practitioner, the history and physical examination remains the most efficient, sensitive, specific, accurate, and cost-effective method of establishing a diagnosis in patients with knee-related complaints. Developing an intuitive and comprehensive approach to the physical examination requires a detailed understanding of knee anatomy, in particular the relation of the surface skin to the underlying structures, to be able to relate tenderness to pathology. It is helpful to stratify knee pathology based on onset (acute injury versus insidious onset) and population affected (adult versus pediatric). History should focus on timing, mechanism of injury, presence of a pop or effusion and five primary symptoms: (1) pain, (2) instability, (3) mechanical symptoms; (4) swelling, and (5) stiffness. The examination is a multistep process: (1) inspection; (2) palpation; (3) range of motion and strength testing; (4) patellar testing; (5) meniscal testing; (6) ligamentous stability testing; (7) gait assessment; (8) evaluation of muscle weakness and imbalance (e.g., hamstring tightness, quadriceps tightness, or core weakness); and (9) assessment of the back, hip, and feet. After obtaining a history and performing a physical examination, the practitioner must form a working differential diagnosis that is fine-tuned initially with plain radiographs and often further confirmed with advanced imaging. We encourage practitioners to develop a systematic approach when evaluating patients, which is important not only to efficiently arrive at a diagnosis but also to prevent missing conditions that require emergent intervention or associated injuries that can affect treatment decision-making and prognosis.

knee history physical examination differential diagnosis

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TABLE 90.1  Acute and Insidious Causes of

Knee Pain in Adult and Pediatric Patients Adult

Pediatric

Traumatic

Atraumatic

• Ligamentous injury (ACL, PCL, MCL, LCL, PLC) • Meniscal tear • Patellar dislocation • Osteochondral fracture • Extensor mechanism rupture (patellar or quadriceps tendon) • Fracture (most commonly patella or tibial plateau) • Tibial eminence fracture • Tibial tuberosity avulsion • Patellar sleeve avulsion

• Patellofemoral syndrome • Lateral patellar tilt • Tendinitis (patellar/ quadriceps) • Iliotibial band syndrome • Pes anserine bursitis • Degenerative meniscal tear • Osteochondral defect • Osteoarthritis • Rheumatologic condition • Septic arthritis • Pigmented villinodular synovitis • Osteochondritis dissecans (OCD) • Discoid meniscus • Osgood-Schlatter disease • Sinding-Larsen-Johansson syndrome • Juvenile rheumatoid arthritis • Lyme arthritis • Hip pathology (Perthes disease or slipped capital femoral epiphysis [SCFE])

ACL, Anterior cruciate ligament; LCL, lateral collateral ligament; MCL, medial collateral ligament; PCL, posterior cruciate ligament; PLC, posterolateral corner.

TABLE 90.2  Potential Etiologies for a

Hemarthrosis of the Knee Traumatic

Atraumatic

• Anterior cruciate ligament tear • Posterior cruciate ligament injury • Chondral fracture • Patellar dislocation • Meniscal tear • Intra-articular fracture • Tear in the deep portion of the joint capsule

• Pigmented villonodular synovitis • Hemangioma • Hemophilia • Sickle cell anemia • Charcot arthropathy • Pharmacologic coagulopathy • Thrombocytopenia

might suggest overuse. Commonly patients may have changed training techniques (e.g., increased frequency, increased distances, or a change in terrain or surfaces). A recent increase in running, particularly among marathon trainees or military recruits, may suggest a tibial stress fracture, patellofemoral syndrome, or iliotibial band syndrome. Acute changes from inactivity to activity may lead deconditioned patients to subject their knees to nonphysiologic kinetics as a result of loss of neuromuscular control. The major symptoms on which to focus for a patient presenting with knee-related concerns include (1) pain, (2) instability, (3) mechanical symptoms, (4) swelling, and (5) stiffness. As with any patient encounter, the patient should be asked about the characteristics of pain, including onset (acute or insidious), location, duration, severity, quality, and radiation. The patient should be

asked about the continued presence of pain and any change in character or severity of the pain. Use of visual analog scales can be helpful. Pain ratings based on a 0 to 10 scale can be used. It is helpful to hear whether the pain is constant, is only related to activities, or occurs after activity. Pain related to prolonged sitting or linear activities like stair climbing or running suggests a patellofemoral etiology, whereas pain with twisting or rotating activities (e.g., rolling over in bed or getting out of a car) is suggestive of meniscal pathology. Pain that arises at progressively earlier intervals into a run may be suggestive of iliotibial band syndrome. Subjective instability should be explored, with attention paid to determining the frequency and inciting events or activities surrounding each instability event. For example, patients with an ACL tear often state that they experience instability with pivoting, twisting, or cutting activities. They may also describe a sensation of movement with their knees that they often explain by placing two fists together and moving one with respect to the other in what has been called the two-fist sign. In contrast, instability that is experienced linearly, as in walking on level ground or on stairs, is often associated with quadriceps weakness and deconditioning. Side-to-side instability on level ground may suggest valgus or varus laxity, whereas instability when descending a ramp may also be experienced by patients with damage to the PLC. The presence of mechanical symptoms (catching and locking) is suggestive of a displaced intra-articular fragment, most commonly either a displaced meniscal tear or osteochondral loose body. A medial meniscal tear is more likely to promote mechanical symptoms while a lateral meniscal tear is more likely to present as pain in isolation. In addition, the presence of a bucket handle medial meniscal tear is suggestive of underlying ACL insufficiency until proven otherwise. Although not universal, a knee effusion should heighten the examiners suspicion for a structural intra-articular abnormality. A knee effusion following an acute injury may be the result of a ligament injury, meniscal tear, chondral injury, or intra-articular fracture. The timing and size of the effusion are helpful clues to the diagnosis. Rapid onset (within 2 hours) of a large effusion is suggestive of an ACL tear injury or intra-articular fracture (e.g., tibial plateau) while a more gradual onset (24 to 36 hours) is more consistent with a meniscal tear. The presence of an effusion is also helpful in differentiating a patellofemoral chondral injury from patellofemoral syndrome. The patient should be asked about any evaluation or treatment he or she received at the time of the injury or subsequent to the injury. It may also be helpful to know if weight-bearing restrictions were recommended. Knowledge of previous immobilization is also helpful, particularly if the patient has residual loss of range of motion (ROM). For any patient with a prior surgical intervention, the operative report and arthroscopy images can provide valuable information. Finally, the physician should ask which, if any, of these treatments have benefited the patient. These questions help guide the surgeon in creating a treatment plan that avoids the replication of prior failed treatments. Once the history surrounding the present complaint is fully understood, the physician should collect general medical, surgical, and social histories. For athletes, a more complete understanding of their athletic history should be sought, including their current

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and past level of play; the number of hours per week that they play; and their skill level, potential, and athletic goals. These factors all play a role in surgical decision-making.6 In particular, in the patient with an ACL tear who plans to return to category I hard cutting or pivoting sports such as basketball, football, rugby, volleyball, or mogul/black diamond skiing, the risk for reinjury with nonoperative treatment of an ACL tear is high.6 The surgeon should also obtain an occupational history, because a patient who is reliant on the injured extremity for his or her livelihood likely requires a more aggressive treatment regimen. A review of systems should always be collected as well. A particular focus should be placed on pain and swelling in other joints, eye disease, back pain, pain with urination, and skin disorders, all of which may hint at a diagnosis of an inflammatory arthropathy. Similarly, a history of fevers, night sweats, or drainage may lead the physician to suspect infection. A history of atraumatic knee pain with an associated mass with primarily nocturnal or constant pain may lead the physician to a neoplastic diagnosis. Pain out of proportion, hypersensitivity, and color and/or temperature changes to the knee should lead the physician to suspect a complex regional pain syndrome. Finally, the physician must discuss goals and expectations with the patient. Expectations frequently need to be tempered. In athletes and former athletes presenting with a knee injury, it behooves the surgeon to come to a better understanding of whether the athlete would like to return to play (RTP) or simply desires a painless knee for activities of daily living. The patient is most likely to achieve a successful result if he or she understands the goals of the treatment program for the presumed diagnosis.

PHYSICAL EXAMINATION Physical examination of the knee requires an in-depth understanding of the anatomic structures and the function of these structures, because each provocative test seeks to isolate the function of each structure. We often view the examination as a multistep process: (1) inspection; (2) palpation; (3) ROM and strength testing; (4) patellar testing; (5) meniscal testing; (6) ligamentous stability testing; (7) gait assessment; (8) evaluation of muscle weakness and imbalance (e.g., hamstring tightness, quadriceps tightness, or core weakness); and (9) assessment of the back, hip, and feet. We start by examining the noninjured extremity, which may provide important information regarding baseline abnormalities and also helps to relax the patient.

INSPECTION A great deal of information can be gained from inspection of the patient before taking a history or performing a focused physical examination (Box 90.1). If possible, patients should be observed as they enter the examination room or at some other time when they do not know they are being observed.7 Once the patient is in the examination room, the physician can gain insight into the patient’s general mobility by observing his or her transfer from a chair to the examination table. The periarticular skin should be carefully inspected for (1) any surgical scars, which may affect future surgical planning;

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BOX 90.1  Diagnosis by Visualization Atrophy Effusion Ecchymosis Malalignment Gait abnormalities Extensor mechanism disruption

Fig. 90.1  Ecchymoses reflect a subcutaneous hemorrhage and may signal a capsular injury. These posterolateral hemorrhages raise suspicion for a posterolateral corner ligamentous injury.

(2) erythema, which should be demarcated with a skin-marking pen if it is believed to reflect an underlying cellulitis; (3) ecchymoses, which reflect subcutaneous hemorrhage that may signal a capsular injury (Fig. 90.1); and (4) abrasions, which may provide a clue to the direction of the primary trauma. For example, with a dashboard mechanism, a patellar abrasion is concerning for patellar fracture, while an anterior tibial abrasion should raise concern for a PCL injury because of the posteriorly directed force on the anterior tibia at the time of injury (Fig. 90.2). Attention should be directed to the presence or absence of effusion, any localized swelling, and muscle tone within the periarticular muscles—in particular the quadriceps and vastus medialis obliquus. The examiner should examine a patient with a suspected dislocation for the presence of any abnormal skin furrows or dimpling, which could signal buttonholing of the condyles through the capsule and the need for open reduction.8,9 Although general inspection may reveal atrophy, the most sensitive measurement of atrophy is a comparison of thigh circumference with the contralateral knee (typically performed 15 cm proximal to the superior pole of the patella; Fig. 90.3).10 This measurement can be used as a marker for the rehabilitation process after surgery. General inspection may reveal stigmata of other general medical conditions, such as signs of venous stasis, ulcerations, or prior amputations as a result of diabetic neuropathy or vascular insufficiency, as well as signs of chronic infections or abscesses. Predrawn knee schematics may be helpful for recording findings from visual inspection. Alternatively, obtaining a photograph at the time of presentation can be invaluable for comparison at a later date. Photographs can be entered into the electronic medical record. Serial examinations

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this measurement can be affected by a variety of other deformities. Deformities within the foot should also be observed. For instance, pes planus may be a contributing factor to genu valgum or may be a sign of generalized ligamentous laxity. Gluteal strength can also be observed by asking patients to stand on one leg, perform a single-leg squat, or do repetitive single leg jumps. Inability to maintain a level pelvis, increased trunk lean, increased hip adduction, and excessive knee valgus during these activities is indicative of gluteal/core weakness that can indirectly contribute to patellofemoral symptoms. The patient’s gait should be observed. Although gait is a complex process requiring normal function of the foot, ankle, knee, hip, and lumbosacral spine, some gait abnormalities can also be referred to the knee. One should observe for varus and valgus thrusts, an antalgic gait with shortening of the stance phase for the affected limb, and the foot progression angle. Patients with ACL deficiency may exhibit a quadriceps avoidance gait, possibly to prevent excess anterior tibial translation.12 Fig. 90.2  An anterior tibial abrasion is shown with associated posterior subluxation of the tibia, suggesting a posterior cruciate ligament injury.

Fig. 90.3  Thigh circumference, which the examiner should always measure at the same distance proximal to the superior patellar pole, is a sensitive measure of quadriceps atrophy.

can be crucial for the determination of progression, especially in the acutely injured patient. Patients should remove their shoes so that the entire limb can be inspected. Mechanical limb alignment should be visually estimated within the coronal, sagittal, and axial planes. The presence of genu varum, valgum, procurvatum, or recurvatum should be further evaluated radiographically. Specific attention should be directed to malrotation.11 With the patient supine, the examiner should also visually inspect the height level of the patella for alta or baja. The physician may also want to measure limb length. Although the most accurate method for limb length measurement is the placement of sized standing blocks under the short leg until the pelvis is level, a rapid, rough estimation can be gained with a glance at the relative heights of the medial malleoli in the supine patient. The physician can also estimate the Q angle visually and measure it with a goniometer, although

PALPATION It should be noted that many patients in the acute postinjury phase have generalized inflammation with diffuse tenderness that tends to be nondiagnostic; as a result, the patient may need to return at a later date for a repeat examination. The knee should be palpated for the presence or absence of an effusion. The examiner can milk fluid down from the suprapatellar bursa while holding the patella between the thumb and forefinger of the contralateral hand to assess for the ability to ballot the patella. Alternatively, the examiner can feel for swelling at the soft spots medial and lateral to the patellar tendon, where the capsule is fairly subcutaneous. The other area where the surgeon may be able to palpate synovial fluid is in a Baker cyst, which is most commonly posteromedial between the semimembranosus and the medial head of the gastrocnemius. The quadriceps tendon and its patellar insertion can be palpated both for tenderness associated with quadriceps tendonitis and a gap associated with a quadriceps tendon tear. The patella should be palpated for prepatellar tenderness or fullness that may be a sign of prepatellar bursitis. The distal pole of the patella and the patellar tendon origin should be palpated for tenderness associated with patellar tendonitis (or Sinding-Larsen-Johansson syndrome in adolescents; Fig. 90.4), as well as for a gap associated with a patellar tendon tear. The tibial tubercle should be palpated (Fig. 90.5) for bony tenderness, which may be associated with Osgood-Schlatter syndrome. On the medial side of the knee, the entire course of the MCL should be palpated for tenderness. The femoral and patellar attachments of the medial patellofemoral ligament should be evaluated for a palpable gap or tenderness. The medial tibial plateau should be palpated for tenderness because it might be associated with an acute fracture or stress fracture. The region just anteromedial to the patella should be assessed for a palpable tender band from plica syndrome (Fig. 90.6). The distal insertion of the sartorius, semitendinosus, and gracilis tendons should be palpated for pes anserine bursitis. The posteromedial joint line should also be palpated for a possible meniscal tear. Whereas

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Fig. 90.7  Palpation for tenderness at the anterior medial joint line. Fig. 90.4  Tenderness at the inferior pole of the patella suggests patellar tendonitis.

Fig. 90.8  Palpation for tenderness at the posterior lateral joint line.

Fig. 90.5  Tenderness to palpation at the tibial tubercle suggests OsgoodSchlatter syndrome, fracture of the tibial tubercle, or possibly insertional patellar tendonitis.

Fig. 90.6  A tender palpable band, which may snap back and forth over the medial femoral condyle, suggests medial plica syndrome.

anteromedial (Fig. 90.7) and medial joint line tenderness is often associated with plica syndrome or hypertrophic fat pad syndrome, displaced bucket handle meniscal tears characteristically have more tenderness anterior than the classic posteromedial location associated with most meniscal tears. Similarly, the surgeon must also palpate the lateral structures. The lateral collateral ligament is best identified with the knee in the “figure-of-four” position, where varus stress makes the ligament taut and more easily palpable. The other structures of the PLC, such as the popliteus tendon and the popliteofibular ligament, can be more difficult to assess with palpation. The biceps tendon is most easily assessed as a cord at the posterolateral surface of the fibular head. Just anterior to the biceps tendon is the iliotibial band, which can be palpated as it passes over the lateral femoral condyle and at its tibial attachment at the Gerdy tubercle. The fibular head should also be assessed. The lateral tibial plateau should be palpated for tenderness, which might be associated with an acute fracture or stress fracture. The lateral joint line (Fig. 90.8) is palpated for a possible meniscal tear. While medial meniscal tears are more likely to manifest with tenderness over the posteromedial joint line, lateral meniscal tears tend to be more tender over the midbody or anterior horn of the meniscus. Anterolateral joint line tenderness can be associated with hypertrophic fat pad syndrome. Just distal

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to the fibular head, the examiner can commonly palpate the common peroneal nerve. In patients with suspected pathology of the peroneal nerve, the examiner should attempt to elicit a Tinel sign. Pain associated with common peroneal neuritis may be referred to the anterolateral proximal tibial region.

RANGE OF MOTION AND STRENGTH TESTING ROM is a fairly sensitive predictor of intra-articular pathology and is critical for knee function. Normal knee ROM has been described as 0 to 120 degrees,7,13 although the ROM actively used for gait is 10 to 120 degrees.14 However, considerable variation exists. At terminal extension, many persons have up to 5 degrees of hyperextension, which, in combination with range from 0 to 10 degrees of flexion, may be useful for the “screw home” mechanism of internal rotation that tensions the cruciate ligaments and “locks” the knee at full extension. Many persons have additional passive flexion beyond their active range; in men this is commonly 140 degrees and in women it is 143 degrees, although in societies where kneeling is common, such as in Japan, India, and the Middle East, passive flexion to 165 degrees is common.13 One hundred and twenty-five degrees of flexion are necessary to squat, whereas 110 degrees of flexion is required to descend stairs in normal fashion. The loss of as little as 10 degrees of flexion will affect running speed. The loss of as little as 5 degrees of extension can cause a limp with increased quadriceps activation during gait and resultant quadriceps strain and fatigue, as well as patellofemoral pain. Differences between passive and active ROM should be noted. A loss of both is considered a “contracture” and implies a block to motion, whereas a loss of active ROM with preserved passive ROM is considered a “lag” and implies a muscle tightness or imbalance. Several methods may be used to test ROM. A goniometer can be placed on the lateral side of the knee with the proximal end pointed toward the greater trochanter and the distal end pointed toward the lateral malleolus. This method has high interand intraobserver reliability.15 A more sensitive indicator of full extension and flexion is the measurement of the heel-height difference with the patient placed in the prone position (Fig. 90.9). Similarly, the heel-buttock distance can be measured in full flexion in the supine position. One centimeter correlates with approximately 1 degree.14 Restricted knee ROM must be understood in context. Postsurgical motion restriction is almost universally the result of either global or focal arthrofibrosis (e.g., cyclops lesion). Early studies suggested that up to 35% of patients undergoing ACL reconstruction experienced postoperative motion loss16; however, this has decreased to 0% to 4% with appropriate surgical timing, technique, and an accelerated rehabilitation program.17–19 Risk factors for postsurgical motion loss following ACL reconstruction include acute reconstruction (1 cm), displaced, and unstable. Bucket handle tears may frequently cause mechanical symptoms, including locking and the inability to fully extend the knee. They more frequently occur in the medial meniscus because of the limited motion afforded by the strong peripheral meniscocapsular attachments. Smaller, incomplete vertical tears more commonly occur and are frequently identified at the time of arthroscopy. These incomplete tears may not require intervention in the setting of concomitant ACL injury if they are determined to be stable when manually probed.46,47

Vertical/ longitudinal

Oblique

Oblique (parrot beak or flap) tears commonly occur at the junction of the posterior and middle body of the meniscus. These unstable tears frequently cause mechanical symptoms including locking and catching during knee motion that may or may not produce pain. The associated pain has been hypothesized to be associated with irritation of the meniscocapsular junction and surrounding synovium. This tear type is not typically amenable to repair because it most commonly occurs in the white–white meniscal region. Excision of the unstable fragment is effective in addressing the mechanical symptoms. Radial tears are oriented perpendicular to the circumferential fibers and are commonly identified in the lateral meniscus after an acute ACL rupture. Again, variability exists in the length of these tears, which range from small to large tears that extend from the white–white zone through to the periphery. A small radial tear involving less than 60% of the meniscus does not significantly influence compartment biomechanics, whereas a large radial tear that extends through more than 90% of the meniscus to the periphery results in a significant increase in peak compartment pressures.48 Partial tears preserve the crucial peripheral circumferential fibers and thus the load distribution ability of the meniscus. This radial tear subtype can be débrided to a stable edge in most circumstances. Complete tears, on the other hand, result in complete circumferential fiber disruption, which not only compromises the function of the meniscus but also increases the biomechanical tendency for repair diastasis with axial load. Although diastasis significantly impairs healing, repair of this tear type should be attempted, because the only alternative treatment is effectively a near-total meniscectomy. Although further data are required to understand the role of mechanical load on meniscus healing, most recommend an initial period of avoidance of weight-bearing after repair of complete radial tears to reduce the potential for tear diastasis. Horizontal tears often develop from variable shear stress between the superior and inferior meniscal regions in the early stage of meniscal degeneration. This tear type can occur in young patients but is more commonly a degenerative tear and may be associated with meniscal cyst formation that may communicate with the periphery. These latter tears have been commonly identified on MRI; however, their presence is not necessarily linked to clinical symptoms.49 The treatment philosophy of these lesions continues to evolve over time. Some older data suggest that cyst

Degenerative

Transverse (radial)

Horizontal

Fig. 94.6  A descriptive classification of meniscal tears. (Modified from Ciccotti MG, Shields CL, El Attrache NS. Meniscectomy. In: Fu FH, Harner CD, Vince KG, eds. Knee Surgery. Baltimore: Williams & Wilkins; 1994.)

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aspiration and suture repair of the horizontal tear may obviate the need for meniscectomy,50 but for most of the last decade the prevailing philosophy for most horizontal tears, including associated flaps, is treatment with a partial meniscectomy. A recent systematic review51 reports a 78% success rate in repairing these lesions in a young population. Given this high success rate and the benefits of meniscal preservation, repair of such horizontal cleavage tears should be attempted in the younger cohort of patients as this can restore tibiofemoral contact pressures to levels similar to that of the native meniscus.52 If repair is not possible, preserving the superior leaflet of the horizontal tear offers the best preservation of tibiofemoral load sharing.53 In the older cohort of patients with suspected degenerative tears, careful evaluation and exhaustion of conservative measures should be performed before proceeding to surgery as the results of surgery in this patient population may not be durable.54 Complex tears of the meniscus occur in a stellate pattern and propagate through multiple planes, although the horizontal cleavage plane is most common. These tears most commonly occur at the posterior root, are degenerative in nature, and should be treated with partial meniscectomy if surgical management is indicated. A meniscal tear zone classification has been documented and divides each meniscus into three radial and four circumferential zones. This classification system permits improved clinical documentation and comparison of outcomes (Fig. 94.7).55

HISTORY Meniscal tears can be either traumatic or degenerative. Degenerative tears have been closely associated with osteoarthritis. Acute tears are often related to trauma, most frequently as a result of a twisting motion. Early diagnosis and treatment of acute meniscal tears can significantly affect the short-term meniscal viability and subsequent long-term articular chondral protection. This treatment is particularly critical in a younger population

Posterior

F

A

Lateral 0

Medial 1

2

3

3

2

1

0

E

B

D

Anterior

C

Fig. 94.7  Classification of a meniscal tear according to the anatomic position and vascularity. (Modified from Cooper DE, Arnoczky SP, Warren RF. Arthroscopic meniscal repair. Clin Sports Med. 1990;9:589–607.)

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given the high incidence of acute, traumatic meniscal tears, and the importance of joint preservation in younger patients. A carefully completed history, physical examination, and diagnostic imaging evaluation facilitates efficient and accurate diagnosis, and guides appropriate treatment. The aforementioned epidemiology should aid in guiding the patient history with regard to age, mechanism of injury, activity level, concomitant pathology, and previous ipsilateral injury or surgery. Additionally, fundamental questions should also be asked, including the location and duration of symptoms, exacerbating activities, and alleviating mechanisms, including medication and activity modification. Patients may or may not be able to recall a single traumatic event. These events typically include twisting or hyperflexion with or without a mild effusion that may be noticed the day after injury. Notably, this effusion is not specific for meniscal pathology. Pain is often localized to the joint line and is usually intermittent. Constant pain or pain at rest usually indicates separate or additional pathology, such as osteoarthritis. Mechanical symptoms may also herald an unstable flap or bucket handle meniscal tear; these symptoms include catching, locking, popping, pinching, or the feeling of having to move the knee through a specific ROM to “reset” the joint. Locking due to an incarcerated torn meniscal fragment will most often present with an inability to achieve full extension. Unlike traumatic tears, degenerative, chronic meniscal tears are atraumatic and are rarely associated with an acute effusion. Instead, patients may describe mild intermittent effusions, infrequent mechanical symptoms, and generalized joint-line pain. These tears more commonly affect an older, less active population and may exist with concomitant osteoarthrosis.

PHYSICAL EXAMINATION Physical examination of the patient with a possible meniscus tear should include an evaluation of gait, standing alignment, ROM, and strength testing of the hip and knee, ligament stability testing, and a careful inspection and palpation of the knee with particular attention directed to the joint line. Additional specialized tests including the McMurray and Apley grind tests may also be included.56–61 The contralateral extremity also should be examined for comparison because of the variability and patient-specific nature of these physical examination findings. Physical examination may reveal an antalgic gait with varus or valgus alignment. The patient with a medial meniscus tear should be observed for a varus thrust. This alignment may prove to be pertinent to the etiology and treatment of the meniscal tear. Displaced tears may present with a mechanical block to ROM that is also associated with distinct pain at that end point. Pain with deep knee flexion is nonspecific but is common for posterior horn injuries. Cruciate and collateral ligament stability should then be evaluated. A visible knee effusion may also exist that can be exaggerated with “milking” or manipulation of the suprapatellar pouch to maximize the size of the effusion inferiorly. At this time, palpation for point tenderness should be performed with a focus on ligamentous and tendinous origins

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and insertions and the joint line. We prefer to perform the palpation component of the examination with the patient in a supine position with the hip externally rotated and the knee flexed to 90 degrees. Notably, palpable joint-line tenderness has been repeatedly identified as the most sensitive and specific physical examination finding for meniscal pathology.43,56,59,62 However, joint-line tenderness is significantly less accurate for identifying meniscal pathology in the setting of an ACL injury.60 Provocative maneuvers that cause meniscal fragment impingement between the femoral and tibial surfaces have also been described. The McMurray test is performed on the medial meniscus by flexing the knee, creating a varus stress by internally rotating the tibia, and bringing the knee into full extension. Reproducible pain with a palpable mechanical click or pop indicates a positive examination. Conversely, the lateral meniscus is tested with an applied valgus stress and external tibial rotation. Another commonly performed test is the Apley grind test, in which an axial load is created with concurrent internal and external rotation (“grind”) with the patient positioned prone and the affected knee flexed to 90 degrees. A positive examination is defined as pain at the medial and/or lateral joint line. Another test, termed the Thessaly test, has been used to increase the diagnostic accuracy of the physical examination for meniscal tears by dynamically reproducing the load transmission in the knee joint at 5 and 20 degrees of knee flexion. The Thessaly test is performed with the examiner holding the patient’s outstretched hands while he or she performs a single leg stance flat-footed on the affected extremity and axially rotates three times with the knee in 5 degrees and then 20 degrees of flexion. A positive test is documented with the presence of medial or lateral joint-line pain and possible mechanical symptoms. When this test is performed in 20 degrees of flexion, a 94% and 96% accuracy has been documented for medial and lateral meniscal tears, respectively, with low false-positive and false-negative results.61

MRI is the ideal radiographic study for visualizing soft tissue pathology, including injury to the meniscus, capsule, ligaments, and articular cartilage. Arthrography was historically used prior to MRI to identify meniscal tears and may be considered in the setting of a contraindication to MRI. MRI is a noninvasive study that is performed without exposure to ionizing radiation and is able to image in multiple planes, thereby providing a threedimensional depiction of soft tissue and osseous structures. Previous studies have documented a very high accuracy for MRI identification of meniscal abnormalities.63,64 We routinely obtain MRI imaging for the evaluation of meniscal pathology using both fat-suppressed and diffusion-weighted fast spin-echo (cartilage sensitive) axial, coronal, and sagittal images (Fig. 94.8). Normal meniscal architecture is demonstrated by uniform low signal intensity on both fast spin-echo and fatsuppressed images. A high signal within the meniscal substance but not extending to the articular surface frequently exists as a result of intrasubstance degeneration. This signal may lead to an overinterpretation of a meniscal tear. Grading of the meniscal high signal can minimize this overinterpretation (see Fig. 94.8).65 Grade I is characterized by a nonfocal intrasubstance high signal without articular extension. Grade II is a focal linear high-signal region without articular extension. Grade III is a focal linear high-signal region located at the free edge of the meniscus with superior or inferior articular extension. A grade III signal that is identified on two or more MRI images has 90% sensitivity for representing a true meniscal tear.65 Nevertheless, careful evaluation of the surrounding structures, including the meniscofemoral and intermeniscal ligaments and popliteus tendon, should be conducted because they may mimic a meniscal tear. Sagittal meniscal windows may aid in identifying acute, vertical meniscal tears and bucket handle tears, whereas coronal images are most helpful for the identification of horizontal degenerative tears. Axial imaging may further confirm the existence of radial

IMAGING Isolated meniscal pathology can be accurately diagnosed in more than 90% of patients with history and physical examination alone. Nevertheless, diagnostic imaging, including plain radiographs and MRI, is critical to confirm clinical suspicions, evaluate alignment, and identify concomitant pathology. Imaging is particularly useful when concomitant chondral or ligament pathology exists because the history and physical examination are far less accurate in this setting. Plain radiographs should be the first-line radiographic study but are not sensitive or specific to meniscal pathology. Weightbearing anteroposterior, lateral, and 45-degree flexed posteroanterior views should be obtained. A Merchant patellar view allows evaluation of patellofemoral pathology. Standing knee alignment can be assessed and correlated with meniscal pathology and, if a significant concern exists for abnormal alignment, a full-length, standing, long cassette, anteroposterior hip to ankle view of both lower extremities should be obtained. Degenerative joint disease may indicate a degenerative meniscal tear, but acute tears have no specific radiographic findings.

Fig. 94.8  A sagittal fat-suppressed magnetic resonance imaging slice demonstrates a grade III linear signal communicating with joint space through the inferior surface of the meniscus.

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and flap tears. Bucket handle tears should be carefully evaluated at the intercondylar notch with the classic double PCL sign where the displaced medial meniscal tissue may be identified as a second low-signal line parallel and anterior to the PCL. Despite the high sensitivity and noninvasive attributes of MRI, significant limitations exist, including higher cost and technical errors in both imaging technique and interpretation. Multiple studies have shown a high percentage of asymptomatic meniscal tears on MRI examination ranging from 36%66 to 76%.41 This percentage increases significantly with patient age.67 Prior MRI data from asymptomatic patients older than 65 years documented a 67% prevalence of meniscal tears.41 This prevalence increased to 86% in the setting of symptomatic osteoarthritis. For this reason, it is important to correlate MRI findings with the history and physical examination and, when indicated, findings on arthroscopy.

TREATMENT OPTIONS Nonoperative Management Nonoperative management of meniscal tears is not designed to facilitate healing of the tear, but rather is directed at symptom management. Although prior data have documented spontaneous healing of stable, isolated peripheral meniscal tears, this outcome is a rare exception. Most unrepaired meniscal tears will not progress to healing,68 and therefore nonoperative management must be directed at reducing symptoms in carefully selected patients. Our experience suggests that most symptomatic meniscal lesions in the absence of significant concomitant osteoarthrosis do not respond well to nonoperative management, especially in the setting of mechanical symptoms, despite some evidence that symptom resolution may occur with this approach.68 However, nonoperative treatment is frequently used in the setting of associated medial or lateral compartment osteoarthrosis with concomitant meniscal tears and the absence of mechanical symptoms. Nonoperative management should include rest, use of ice and nonsteroidal antiinflammatory medications, and activity modification for 6 to 12 weeks. Intra-articular injections of corticosteroids, analgesic medications (e.g., lidocaine or bupivacaine), and viscosupplementation may also be used if concomitant osteoarthrosis is present. We do not suggest this treatment approach in the absence of osteoarthrosis, and it should be noted that corticosteroids may impair meniscal healing and that bupivacaine may lead to chondral damage.69–71 It is important to note that nonoperative management of an unstable, repairable meniscal tear may also result in tear propagation, thereby producing an irreparable tear that must be excised.

Operative Management Surgical Indications The definitive treatment of meniscal tears involves either repair or excision of the pathologic tissue. Surgery is indicated in patients who have persistent mechanical symptoms and/or pain and have not responded to a course of nonoperative treatment. The indications for arthroscopy include (1) symptoms of meniscal injury that affect activities of daily living, work, and/or sports participation such as instability, locking, effusion, and pain; (2) positive

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physical findings of joint-line tenderness, joint effusion, limitation of motion, and provocative signs such as pain with squatting, a positive pinch test, or a positive McMurray test; (3) failure to respond to nonsurgical treatment, including activity modification, medication, and a rehabilitation program; and (4) ruling out other causes of knee pain identified by patient history, physical examination, plain radiographs, or other imaging studies.72,73 Timing of the injury and surgical management must also be considered. Acute tears have a higher rate of successful healing compared with chronic ones; it is documented that repairs of tears less than 8 weeks old heal more frequently compared with older tears.74 Additionally, patients undergoing repairs of traumatic meniscal tears have better 6-year functional results than do persons with degenerative meniscal tears.75,76 However, the majority of these studies combine traumatic meniscal tear and concomitant injury. Stein et al.77 compared long-term outcomes after arthroscopic meniscal repair versus partial meniscectomy for traumatic meniscal tears and documented no difference in function score. However, the meniscal repair group demonstrated a higher rate of return to preinjury and sporting activity levels. Additionally, only 40% of the meniscal repair group demonstrated osteoarthritic progression at 8-year follow-up compared with 81% of the partial meniscectomy group. For these reasons, a recent traumatic history should be considered a good prognostic factor for meniscal healing within the meniscal repair algorithm. The influence of patient age on meniscal repair outcome has been well documented. Prior data have documented a reduced cellularity and healing response in patients older than 40 years.78 Increased repeat tear rates have also been documented in patients older than 30 years,79 although failure occurred later in older patients.80 The association between increased age and worse outcome seems to be negated in the setting of avascular tears and meniscal tears with concomitant ACL rupture. No difference between younger patients and older patients (>40 years) has been found with regard to clinical success after meniscal repairs performed for tears with relative avascularity.81,82 Kalliakmanis et al.83 documented no difference in repair failure between patients older or younger than 35 years of age in the setting of a concomitant ACL tear. Although prognostic factors, including avascular tears, concomitant ACL rupture, and continued ligamentous instability, seem to play identical roles in younger patients,84 the consequence of postmeniscectomy arthritis remains significantly greater. From the aforementioned variables, one may synthesize surgical indications for meniscal repair that can predict healing prognosis. Contraindications for repair include older or sedentary patients or patients who are unable to perform the necessary postoperative rehabilitation. Additionally, isolated inner third white–white tears with a remaining rim greater than 6 mm should not be repaired. Borderline tears including middle third white– white tears should only be considered for repair if extension exists into the red–white or red–red region. Degenerative or stable longitudinal (35) are all considered contraindications to cartilage restorative procedures unless corrected prior to or during the surgery, if applicable. While tricompartmental arthrosis is considered a strict contraindication, in young patients with intolerable symptoms and no other available treatment options cartilage restoration procedures can still be considered.

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Treatment Algorithm There are multiple factors that interplay to determine what cartilage restoration procedure would be best served to address the patient-specific symptomatic complaints at hand. Having said that, the lesion location and size are the two main considerations when determining a treatment strategy. More commonly, the medial femoral condyle and the patellofemoral joint are the main locations where focal chondral lesions occur. Given the tibiofemoral and patellofemoral compartments see drastically different forces directed throughout their arc of motion, compression versus shear respectively, different surgical treatment modalities should be considered for each.

Osteochondritis Dissecans Lesions Treatment decisions in osteochondritis dissecans (OCD) lesions are based on the presence of open growth plates, size, stability, and displacement of the fragment. Stable OCD lesions in juvenile patients with an open physis should be treated nonoperatively because these lesions have a greater tendency toward resolution and healing. However, if the fragment is displaced, every attempt should be made to reduce and fix the unstable fragment in patients with either open or closed physis. Headless compression screws and bioabsorbable pins can be used for fixation with satisfactory union rates.33 In some cases, fragments are not amenable to fixation due to comminution or inadequate subchondral component of the fragment. Removal of unstable fragments as a sole procedure is reserved for patients with low functional demands or those who are unable to follow rehabilitation protocols after repair. In long-term follow-up studies radiographic evidence of early degenerative joint disease was found in 65% to 71% of patients who underwent excision of OCD without any cartilage repair techniques.34,35 A recently published randomized trial has compared the outcomes of osteochondral allograft transplantation (OAT) and microfracture procedures for the treatment of OCD in young active athletes at an average of 10 years follow-up. The OAT technique allowed for a higher rate of return to and maintenance of sports (75%) at the preinjury level compared with microfracture (37%).36 Another multicenter study revealed functional improvement and pain relief in 85% of patients after ACI despite the complexity and severity of the osteochondral lesions.37 Fresh OAT is another option for treatment for OCD lesions of the femoral condyle with 70% good or excellent results.38

Patient Age and Defect Chronicity The age-dependent outcomes of marrow stimulation techniques are still continuing to be reported today. Cell numbers and their metabolic activity decline over time resulting in poor healing response in older patients. As a result, the clinical success rate of microfracture has been most consistent in patients under the age of 40 years.39,40 However, failure rates of other cartilage restoration techniques in older patients, such as ACI, OATs, and osteochondral allografting, are comparable with rates reported in younger patient groups.41 Depth of injury is also found to be age-related. Adolescents tend to develop osteochondral lesions, whereas adults have a tendency to get pure chondral

lesions, possibly because of the well-developed and matured calcified zone.42 Time since onset of symptoms is an essential variable that should be taken into account because delayed treatment tends to result in less-predictable outcomes whereas significant improvements in the clinical scores were more frequent with a preoperative duration of symptoms of less than 12 months.40,43

TREATMENT OPTIONS Before planning a treatment procedure, patient-specific and lesion-specific variables must be taken into consideration. Physical condition and readiness of the patient for an extended rehabilitation program, concomitant knee pathologies, and limb alignment hold the key for success or failure in cartilage repair.44 There are several techniques described for the management of cartilage lesions. Examples of current attempts at cartilage restoration include marrow stimulating techniques, osteochondral autografts, autologous chondrocyte transplantation, particulated juvenile cartilage allograft, and OAT.45 Débridement and lavage is one of the most basic options and indicated for low-demand older patients with small lesions.46 Although symptomatic relief from this technique is not likely predictable, arthroscopic débridement can reduce pain in more than half of the patients; however, this benefit generally diminishes after 1 year.47 Additionally, unstable chondral flaps and loose bodies that cause mechanical symptoms can be removed with a very short recovery time and can be repeated if needed. Currently this technique is reserved for small lesions found incidentally during arthroscopy or lowdemand patients who could not adjust to activity or weightbearing restrictions postoperatively.

Marrow Stimulation Biological rationale behind marrow stimulation techniques is that direct stimulation of mesenchymal stem cells (MSCs) in the subchondral bone could direct these cells to the chondrogenic pathway to initiate a healing response. Marrow stimulating techniques have been used to treat cartilage defects since 1959 when Pridie introduced subchondral drilling with K-wires.48 Later Johnson described the abrasion of sclerotic lesion with a burr to expose vascularity, providing a tissue bed for blood clot attachment.49 Finally Steadman introduced the microfracture technique to avoid heat necrosis from drilling. In his technique, the bone plate is not completely destroyed in comparison to an abrasion chondroplasty.50 Microfracture involves débridement of loose and unstable cartilage back to a stable rim. Then specially designed awls are used to make multiple perforations, or microfractures, into the subchondral bone plate. Perforation of subchondral bone results in the influx of marrow elements with the formation of blood clot in the defect. It is important to create a well-contained lesion because rims will support the fibrin clot within lesion. As noted it is crucial to breach the calcified cartilage layer to gain better access to the bone marrow stroma.51 This calcified layer appears to be at least 6 mm beneath the surface of the articular cartilage. Thus a routine awl will not be sufficient to breach this calcified layer in most knees, and it has been suggested that nanofracture technique will allow

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for deeper drilling to overcome this obstacle.52 Histologic findings showed that drilling to a depth of 6 mm had superior results in an animal model compared with drilling to 2 mm, without a deleterious effect on the subchondral bone.53,54 Over time this blood clot is slowly remodeled into primarily fibrocartilage rather than normal hyaline articular cartilage. Mature fibrocartilage is predominantly type I collagen with minimal amounts of type II collagen, resulting in a less-durable construct with inferior wear characteristics. The advantages of marrow stimulation techniques include their minimal invasive nature with low technical demands and favorable cost-effectiveness ratio. On the other hand, they require a prolonged restricted weight-bearing period of 4 to 6 weeks and use of a continuous passive motion (CPM) device for 6 to 8 hours per day, for 6 weeks.55

Osteochondral Autograft Transfer Osteochondral autograft transfer technique involves transfer of one or more cylindrical osteochondral plugs into the cartilage defect. The lesions should be small to medium-sized (0.5 to 4 cm2) because the amount of donor tissue available is limited.56,57 Single or multiple small osteochondral plugs can be harvested to match the lesion’s diameter. Traditionally plugs are harvested from less-weight-bearing areas of articular surface, such as the periphery of the trochlea and the intercondylar notch. The lesion is prepared with a punch to create a recipient socket that matches the plugs. Both preparing the socket and harvesting plugs require tubular cutting instruments such as OATS (Arthrex, Naples, FL), mosaicplasty (Smith and Nephew, Andover, MA), or COR (Depuy Mitek, Raynham, MA) to place plugs orthogonal to the articular surface to avoid graft obliquity. Multiple plugs can be used to fill larger defects, but it could be difficult to match the contour of the defective articular surface to the donor plug.58 Elevated angled grafts relative to articular surface result in elevated contact pressures, so it is suggested to leave an edge slightly sunk rather than elevated.59 Thus ideal locations for osteochondral autograft transfer are the convex surfaces of the femoral condyles rather than the patellofemoral joint and tibia with their varying surfaces, which make plugs more difficult to fit in place.60 It is crucial to place grafts in a press-fit fashion for maintaining stability until osseous integration of the plug and socket occurs. This procedure offers several advantages over microfracture or chondrocyte implantation techniques, including the ability to perform the procedure in a single-stage operation, transplanting an autogenous living hyaline cartilage, decreased cost, and relatively brief rehabilitation period.61 Major limitations of this procedure include donor site morbidity and the limited availability of grafts. Residual gaps between plugs may affect the quality of healing and there is an inherent risk for cartilage or bone collapse. The postoperative recovery requires a short period of non-weight bearing and the use of a CPM for up to 6 weeks.

Autologous Chondrocyte Implantation The rationale behind ACI is to cover the cartilage defect with autologous chondrocytes, which have been cultured in vitro. This technique was first described by Brittberg et al. in 1994

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and is one of the first tissue engineering techniques for articular cartilage regeneration.62 ACI is currently a two-stage procedure. First a cartilage biopsy (weight 200 to 300 mg) is taken from a non-weight-bearing area of the affected joint and transferred to a laboratory. The chondrocytes are isolated from the cartilage tissue by enzymatic digestion and then expanded in monolayer culture. The optimal density of the cells during reimplantation remains debated. Generally, a final concentration of 2 to 3 × 107 chondrocytes/mL is recommended for medium-sized defects, but the number of available cells is limited by the amount of cartilage that can be collected.63 This expansion amplifies the total number of cells for implantation, allowing the surgeon to fill the cartilage defect. The cell suspension is returned to the defect during the second stage of the procedure and held in place with a periosteal patch or membrane. ACI can be performed for high-demand patients who have failed arthroscopic débridement or microfracture. The technique is indicated for larger (2 to 10 cm2) symptomatic lesions involving the femoral condyles, trochlea, and the patella.64 The primary theoretical advantage of ACI is to provide hyaline-like cartilage rather than fibrocartilage, resulting in better long-term outcomes and durability of healing tissue. Clinical results are encouraging and overall the patients are satisfied.65,66 This technique is however not without its limitations. These include technical complexity and cost of the two surgical procedures, de-differentiation of chondrocytes during in vitro expansion and periosteal graft delamination, and late periosteal hypertrophy.67–69 Also, previous marrow stimulation techniques have a strong negative effect on outcomes of subsequent cartilage repair with ACI, limiting its use as a salvage procedure.70 Second-generation ACI procedures involve use of collagen sheets to replace periosteal flaps. These collagen matrices avoid graft harvesting and donor site morbidity and using cell-free collagen sheets dramatically eliminated adverse events related to graft hypertrophy and delamination.71 In the third generation of ACI the cultured chondrocyte cells are seeded directly onto a biodegradable porcine type I/III collagen scaffold. Matrix Autologous Chondrocyte Implantation ([MACI] Genzyme, CA) method has been in clinical use for a number of years in Europe and is now approved by the Food and Drug Administration (FDA) and available in the United States.72 This enables three-dimensional (3D) culture of chondrocytes, aiming to prevent de-differentiation and loss of phenotype. Uneven distribution of chondrocytes within the defect and the potential for cell leakage from the defects that often lack intact cartilage rims can be prevented through using scaffolds.73 Additionally, the scaffolds used may act as a barrier to fibroblast invasion.74 Outcomes of these techniques have been promising and are at least equivalent to those achieved with ACI, with reported good clinical medium-term results.72,75 The postoperative treatment is broadly similar to marrow stimulation techniques while time periods are generally extended. Rehabilitation should focus on maintaining muscle function and joint flexibility, with the use of CPM. Full weight bearing is avoided for 8 to 12 weeks.

Particulated Juvenile Cartilage Allograft In the past, allograft transplants were limited to osteochondral grafts because it has been generally accepted that graft

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incorporation to host tissue was only possible at the bone level.76 The concept that cartilage could be transplanted without its underlying bony component is a fairly new and innovative approach. Particulated juvenile cartilage allograft technique DeNovo NT (Zimmer, Warsaw, IN) uses human juvenile allograft articular cartilage minced into small pieces. Mechanical mincing of cartilage into 1- to 2-mm pieces was crucial for successful cartilage repair. This promotes chondrocytes escaping from the extracellular matrix (ECM), multiplying and migrating to surrounding tissues to form a new hyalinelike cartilage tissue matrix that integrates with the surrounding host tissue.77–79 Cartilage is retrieved from the femoral condyle of donors aged 0 to 13 years. Because juvenile chondrocytes are capable of producing greater amounts of ECM compared with mature chondrocytes, these cells also do not stimulate an immunogenic response in vivo.80,81 DeNovo NT has an average 40-day shelf life similar to a fresh osteochondral allograft. During surgery, fragments are mixed with fibrin glue to make a putty-like structure to fill the osteochondral defect so that no sewing of a patch is needed.79 Each package contains 30 to 200 particles and fills defects up to 2.5 cm2, so multiple packets can be used for larger lesions. The use of DeNovo NT has the advantage of being a single-stage procedure and offers unlimited graft material for large lesions. At postoperative period patients are limited in weight-bearing for 2 weeks for small lesions, and 6 weeks for larger lesions.78 Although the preliminary clinical reports show encouraging results, clinical data are still limited.

Osteochondral Allograft Transplantation Fresh OAT entails the transfer of size-matched cadaveric osteochondral graft into the cartilage defect. After standardizations had been established for graft storage in the late 1990s, fresh osteochondral allografts became commercially available from tissue banks and thus accelerated the more widespread use of these tissues.82 This type of transplantation offers some advantages over other cartilage repair techniques for treatment of wide and deep osteochondral lesions given its ability to replace medium to large osteochondral defects in all locations and contours. Additionally, the cartilage defect is replaced with articular cartilage rather than fibrocartilage in a single-stage operation. In most treatment algorithms, OAT is the only current biologic salvage option when previous treatments have failed. Another advantage is that failure does not preclude other reconstructive procedures, such as a second graft procedure or arthroplasty.83 Historically, bulk allografts resulted in collapse at the osseous part of the graft, rather than failure at the articular cartilage itself. The subchondral bone and marrow components of the graft may elicit a strong immune response resulting in incomplete osseous integration due to the slow process of creeping substitution.84 Therefore OAT with cartilage-bone composite thicknesses of only 6 to 8 mm yields the best result in the management of shallow lesions.76 The disadvantages include graft availability, limited shelf life, accurate size matching, technical difficulties, cost, and concerns with possible disease transmission. However, small risk of disease transmission has been minimalized with stringent screening of donors and modern serologic and

microbiologic clearance testing. Postoperative rehabilitation is tailored according to type of surgery and stability of allograft used and includes non-weight bearing for 6 to 8 weeks and the use of a CPM machine.

POSTOPERATIVE MANAGEMENT Rehabilitation is a key factor to achieve greater success regardless of which type of cartilage restoration technique is applied. The primary goal for rehabilitation following cartilage restoration is the provision of an optimal environment for the functional recovery and adaptation of the chondral healing tissue.85 However, treatment goals may differ between professional athletes and recreational players. Considering the short duration of professional careers, athletes desire to return to their previous highdemanding activity level in a very short recovery time whereas pain relief can be adequate for nonathletic patients. Besides biology of repair technique, patient- and lesion-specific variables should be considered when planning a rehabilitation program. Thus an individualized rehabilitation should be performed for every patient.86 In general, current rehabilitation protocols can be divided into three phases aiming at protection of the graft by a gradual increase in weight bearing and active ROM.87 The first phase is a proliferation period that covers the first 6 weeks after the surgical procedure. The main goal in this phase is graft protection and that patients limit their weight bearing during this period. To prevent muscle atrophy and joint stiffness, low-resistance isometric strengthening exercises should be introduced as soon as the patient can tolerate. During this phase, a CPM machine is used for 6 to 8 hours per day to reduce adhesions. Separate rehabilitation protocols are required for the patellofemoral and tibiofemoral joints due to differences in joint kinematics. Generally patellofemoral lesions demonstrate a slow advance in ROM but allow a faster progression of weight bearing when compared to lesions located in femoral condyles.85 Weight bearing can be modified to the type of surgery performed. In contrast to marrow stimulation techniques and ACI, early weight bearing could be tolerated in osteochondral autograft or allografting procedures. Furthermore size of the lesion and stability of graft, as well as the procedures performed for concomitant pathology, such as ligamentous reconstruction, meniscal repair, and osteotomies, govern how early weight bearing can be introduced. After this initial phase, rehabilitation is followed by a transitional phase with increased load bearing and progressive ROM exercises. Together with closed-chain and gentle strengthening exercises, proprioceptive training is introduced in this period as well if the patients tolerate. The final remodeling phase of rehabilitation generally begins 3 months after surgery. In this phase, patients are gradually introduced back to normal daily activities and allowed to perform light sporting activities. However, they need to continue with muscle, proprioceptive, and sports-specific rehabilitation exercises.88 The rehabilitation periods after cell-based therapies such as ACI and microfracture tend to be more conservative and longer than osteochondral transfer and transplant procedures. Recently a randomized study compared the traditional approach (12 weeks) of postoperative weight-bearing rehabilitation with the accelerated approach (8 weeks) in patients who underwent

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MACI to the femoral condyles. While the visual analog scale (VAS) demonstrated significantly less frequent pain at 5 years in the accelerated group, there were no other significant differences between the 2 groups. Outcomes of this randomized trial demonstrate a safe and effective accelerated rehabilitation protocol that provides comparable clinical outcomes.89 Overall, the rehabilitation period is a complex process and requires a multidisciplinary approach to understand postoperative symptoms as they occur and address them in a timely fashion. So, a stepwise and systemic rehabilitation is recommended for an individualized protocol. This allows not only the best chances at recovery and a return to sports at the preinjury level but also to continue professional careers and reduce the risk for reinjury or joint degeneration.86

Return to Play Return to previous levels of athletic activity is the main goal for athletes who undergo cartilage restoration procedures. Before returning to sports participation, athletes should have

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a pain-free and stable extremity with full ROM. Athletes should fully understand that high-impact activities jeopardize the repair tissue. High-impact and pivoting activities should be delayed until a stable, healed tissue is obtained. Return to play (RTP) is generally influenced by several factors such as athlete’s age, preoperative duration of symptoms, level of play, lesion size, and repair tissue morphology.90 Rate for return to sports is higher for younger and more competitive athletes.91 A comprehensive review of 2549 patients, treated with different surgical techniques, revealed an overall 76% return to sport rates at 2 years postoperatively, with the highest rates of return after osteochondral autograft transfer (93%), followed by OAT (88%), ACI (82%), and microfracture (58%). The same study also showed the fastest return to sports was at 5.2 months and was achieved with osteochondral autograft transfer compared to 9.1 months for microfracture, 9.6 months for OAT, and 11.8 months for ACI.92 Age ≥25 years and preoperative duration of symptoms ≥12 months negatively affected the ability to return to athletic activity.93

Authors’ Preferred Method Articular Cartilage Lesion Previous algorithms have been developed that not only take into account patient activity and demand levels, but also guide a decision-making process with regard to the defect size and location in the knee (Fig. 96.1).94 In the following section we discuss five commonly used current techniques for the treatment of chondral and osteochondral lesions in our clinical practice.

for punctate bleeding or fatty marrow content egress is required to ensure an adequate depth has been reached during the procedure (Fig. 96.4). It is the senior author’s recommendation that should this technique be employed, it is recommended to start at the peripheral shoulder edge of the lesion and then work centrally.

Marrow Stimulation Marrow stimulation/microfracture is a prevalent procedure and is performed most commonly through an arthroscopic approach. The setup for a basic knee arthroscopy is performed and the patient is positioned per routine. Should posterior articular lesions be anticipated, then it is important that maximal knee hyperflexion be attainable during the procedure and a knee positioner can be useful.

Wound Closure Routine closure of the arthroscopy portals is performed and full range of motion (ROM) is allowed. Fifty percent partial weight bearing and immediate ROM is instituted, possibly with use of a CPM, to help protect and sculpt the fibrocartilage cap as it formalizes for the first 6 weeks.

Approach and Defect Preparation After completing the diagnostic arthroscopy and confirming the presence of the chondral defect, it is important to débride all loose chondral flaps by shaver or curette while at the same time establishing stable vertical shoulders to the chondral lesion. The importance of this step at creating vertical shoulders cannot be overstated. This can be done with varying curettes or even an 11 blade or Beaver blade (Fig. 96.2). Next, remove the calcified cartilage layer by curette. Marrow Stimulation After thorough preparation of the defect, a microfracture awl or K-wire on power can be used to create multiple holes. It is important to remain orthogonal to the defect surface, either by changing the flexion of the knee, changing portals, using different angled awls, or by creating new portals as needed. It is vital to not place the holes too close to each other to avoid fracturing the subchondral plate and creating an unstable subchondral segment. Doing this properly and routinely allows roughly 3 to 4 holes to be placed in a 1 cm2 area (Fig. 96.3). Placement of holes directly at the shoulder edges improves the fibrocartilage cap transition to the native cartilage. Turning the arthroscopic inflow off and critically evaluating

Osteochondral Autograft Transplantation Osteochondral autograft transplantation can be used as either an open or arthroscopic procedure. Many times this can be dictated based upon the osteochondral lesion location, size, or surgeon’s preference. A basic knee arthroscopic setup is performed with the use of a tourniquet to help with visualization from both the open graft harvest and transplantation. Once again, a knee positioner can be useful to provide adequate hyperflexion of the knee should the articular lesion be in the posterior condyles. Approach, Graft Harvest and Defect Preparation The chondral/osteochondral lesion is identified by arthroscopic visualization. Additional arthroscopic portals are made as needed, after localizing with spinal needle, to ensure the defect preparation and graft placement is orthogonal to the lesion’s surface. An arthroscopic ruler (Fig. 96.5), sizing rod, or probe can be used to measure the defect size, taking into consideration any undermined and delaminated cartilage flaps at the periphery of the lesion that might need to be resected prior to sizing the lesion. Potential donor locations for graft harvest include the lateral or medial trochlea as well as the intercondylar notch. A maximum of three large osteochondral plugs can be obtained, up to 8 mm each, from the far lateral trochlea, which is the senior author’s preferred location (Fig. 96.6). Continued

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Authors’ Preferred Technique Articular Cartilage Lesion—cont’d Lesion Location

Femoro Tibial Joint

Patellofemoral Joint

Concurrent Osteotomy

Malalignment?

Patellofemoral Instability?

Concurrent Stabilization/ Osteotomy Procedure

Concurrent Meniscal Pathology Treatment

Meniscal Deficiency?

Patellofemoral Alignment?

Concurrent Osteotomy

Concurrent Ligament Reconstruction

Ligament Insufficiency?

Size? 2-3 cm2

2-3 cm2

+/− +/− ++ ++ ++

++ Microfracture OC Autograft/AMZ +/− ACI/AMZ ++ DeNovo/AMZ OC Allograft/AMZ

++ ++ ++ +

++ ++

OC Allograft/AMZ ACI/AMZ DeNovo/AMZ OC Allograft/AMZ

+ +/− ++ +

++ ++ ++

Low Demand

High Demand

Fig. 96.1  Knee chondral and osteochondral lesion algorithm addressing location, size and treatment options. (Modified from Alford JW, Cole BJ. Cartilage restoration, part 2: techniques, outcomes, and future directions. Am J Sports Med. 2005;33[3]:443–460.)

Sometimes, arthroscopic harvest of the osteochondral plugs can be performed; however, it is more reproducible to gain access by a small 2- to 3-cm parapatellar incision and arthrotomy in order to visualize the donor site. While many proprietary systems are available, we routinely use a system that has a coring reamer with a serrated tooth at its end. This allows for a clean cut at the end of the transplantation plug and easier retrieval. Each plug is harvested to a depth of at least 10 to 12 mm while remaining completely orthogonal to the articular surface. The definitive size and depth of the osteochondral plug are measured and the graft placed on the back table still in the harvester tube. Next the recipient chondral lesion site is prepared. This can be done arthroscopically if the lesion is in the other compartment of the knee or through the arthrotomy site if it is ipsilateral to the harvest location. Now knowing the size and depth of the autograft plug, the defect is drilled line to line and to the same depth taking into consideration the cartilage cap height (Fig. 96.7). While drilling the lesion, consideration for any slight obliquity of the donor plug can be adjusted for with the drill at that time so that it can be matched to the recipient site articular curvature as best as possible.

The harvester tube with the plug is then inserted at the same angle (either arthroscopic or open), the plug is gently moved into place by a plunger, and final adjustments are made with a size-appropriate tamp (Fig. 96.8). Great care is taken to ensure the graft is flush, if not slightly recessed, and not proud (Fig. 96.9). This process is repeated step by step, with graft harvest, recipient site preparation, and graft placement, until the articular lesion is effectively treated. Multiple smaller plugs can be used for a mosaicplasty or two larger plugs in a “snowman” configuration can be placed to treat more oval shaped defects. The donor site can be either backfilled with synthetic graft, allograft, or left unfilled. Final arthroscopic images are obtained to critically evaluate the overall transplantation construct. Wound Closure Routine closure of arthroscopic portals is performed and the parapatellar arthrotomy is closed in successive layers. Fifty percent partial weight bearing with 0 to 90 degrees ROM is allowed for the first 6 weeks. It is important to monitor for a postoperative hemarthrosis that can significantly limit range of

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Authors’ Preferred Technique Articular Cartilage Lesion—cont’d

Fig. 96.2  Note the vertical shoulders created by the beaver blade at the periphery of the lesion.

Fig. 96.3  Microfracture awl is used to create multiple punctate transsubchondral plate perforations.

Fig. 96.4  Note the marrow element egress from the microfracture perforations.

Fig. 96.5  Arthroscopic measurement of chondral defect.

motion or cause quadriceps inhibition. Sterile serial aspirations can be performed as needed.

Approach and Defect Preparation Compartment-specific paramedian incisions with parapatellar arthrotomies can be used for isolated single lesions; however, a standard utilitarian midline incision with medial parapatellar arthrotomy can be used to gain access to multiple lesions of the knee. Possible fat pad retraction/resection might be necessary for visualization. A bent Homann is placed into the intercondylar notch for patellar retraction. As per any cartilage restoration procedure, it is vital to create a recipient site conducive to healing for the procedure to succeed. Débridement of devitalized tissue and creation of vertical shoulders at the defect’s articular edges is performed. It is the senior author’s recommendation, though, that if excessive resection were to turn a contained lesion into an uncontained lesion,

Autologous Chondrocyte Implantation Once the arthroscopic cartilage biopsy has been completed and the culture finalized, usually taking 6 weeks, the cell suspension is ready for implantation. Standard patient positioning for an open knee procedure can be used; however, a knee positioner can be useful for far posterior lesions, which helps with maintaining deep knee flexion throughout the case. Should the surgeon wish to use a periosteal patch, then it is important to drape out to the level of the mid tibia or to at least include the surgical site of choice.

Continued

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Authors’ Preferred Technique Articular Cartilage Lesion—cont’d

B A Fig. 96.6  (A) and (B), Note the orthogonal position of the harvester to the articular surface, not the extremity.

Fig. 96.7  Lesion is drilled to the same depth as the measured osteochondral plug.

then it would be best served to leave a slight rim of degenerative cartilage tissue present to suture to than to be faced with needing other forms of patch fixation to maintain the implanted cells. It is important to maintain the subchondral plate/bone layer. Should previous failed surgical procedures from OAT or marrow stimulation techniques be present, a sharp curette or burr can be used to gently freshen and decorticate the bone without breaking the subchondral plate. If bleeding from the defect base is encountered, then very minimal amounts of thrombin or fibrin glue can be considered for use. Once the defect has been prepared for implantation, the size is measured with glove paper. Should a periosteal flap be used, this should be oversized by approximately 2 to 3 mm given it will shrink slightly upon its harvesting. This will also allow an adequate suture line to be placed to the

Fig. 96.8  Critical to ensure same angle of insertion as the defect was drilled (see Fig. 96.6) and to monitor the transplanted chondral surface depth in relation to the native cartilage surface so that it is flush or slightly recessed.

articular cartilage, lessening the tension on the repair. Some surgeons prefer to use an artificial membrane or collagen I/III bilayer patch, however, currently this is off-label use in the United States and should always be discussed with the patient preoperatively. Periosteal Harvest Should a periosteal patch be desired, the most reproducible location for harvesting is the proximal medial tibia, just distal to the pes anserinus. The skin incision can either be extended distal past the sartorial attachment or an additional

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Authors’ Preferred Technique Articular Cartilage Lesion—cont’d

B

A

Fig. 96.9  (A) and (B), Note the flush contour of the osteochondral plug placement to native articular chondral curvature.

incision can be made, approximately 3 cm distal to the pes, which can usually be palpated with the hamstring insertions as a landmark or it can be measured roughly at 5 cm distal to the medial joint line. After satisfactory soft tissue dissection to the tibial periosteum, the glove paper template is used to mark and incise the periosteum with a fresh 15 blade. Great care should be used when teasing the patch off the bone and can be done so with a sharp periosteal elevator. Once procured, immediately spread out the patch on a moist ray-tec. This helps to avoid its desiccation and shrinkage. Patch Fixation Once the defect has been prepared, the patch is placed over the lesion with the cambium layer down against the defect and stretched out with nontoothed forceps. Should a collagen patch be used, the glove paper template is used and it is usually cut dry and then hydrated. The collagen patch will sometimes increase in size upon rehydration and so minimal resections might be necessary for final fit and placement. Approximately a 1- to 2-mm rim should still be maintained at the patch periphery to help with the suture placement interface. Using a 6-0 Vicryl or Biosyn on a P-1 cutting needle immersed in mineral oil to help with smooth passage, the sutures are placed through the patch and then the articular cartilage, attempting to exit roughly 3 mm away from the defect’s articular edge. This will nicely evert the edge and provide a better seal against the defect shoulder. Routinely sutures are initially placed at the 3, 6, 9, and 12 o’clock positions and tension is placed so that the patch is centralized. All of these steps limit further trimming, limit suture cut through, and allow the patch to sag into the defect. The knots are tied on the patch side below the articular edge. Additional sutures are placed circumferentially to seal the patch; however, a small defect is left at the most superior aspect to allow an angiocath to be introduced for cell implantation. The seal can be tested prior to cell implantation by injecting saline using a tuberculin syringe and an angiocatheter. Any residual leakage can be corrected with additional suture placement or with fibrin glue if it is small enough. The saline is aspirated by angiocatheter once the seal is confirmed to dry the bone bed for implantation.

Fig. 96.10  Note the completed Matrix Autologous Chondrocyte Implantation method (MACI) procedure with sutured and sealed borders after cell implantation.

Cell Implantation After resuspending the cultured cells, a 16 g needle on a tuberculin syringe is used to aspirate the suspension. Exchanging to at least an 18 g angiocatheter, the tip is inserted into the superior patch defect and placed into the inferior-most aspect of the patch. While retracting the tip, the suspension is injected into the defect and careful watching of the patch fill is performed. Final sutures or fibrin glue are used to seal the superior patch defect once the cells have been implanted (Fig. 96.10). Wound Closure The arthrotomy is closed in successive layers per routine. Given the nature of the procedure, a drain is not recommended as it could potentially damage the recipient site. Protected weight bearing is allowed with 0 to 90 degrees range Continued

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Authors’ Preferred Technique Articular Cartilage Lesion—cont’d of motion for the first 6 weeks; however, for patellofemoral lesions, progressive increases in ROM at 30-degree intervals are allowed every 2 weeks given the more shear-force nature of that cartilage location. Juvenile Particulate Allograft Cartilage Transplantation Approached through an open arthrotomy more commonly than by arthroscopic means, this procedure can be used as either an independent procedure or in combination with a routine diagnostic arthroscopy, where the arthroscopy can better delineate the lesion prior to grafting. Defect Preparation and Graft Application A paramedian incision with parapatellar arthrotomy can be used to gain access to all lesions throughout the knee. Similar to marrow stimulation and ACI, stable vertical shoulders are paramount as well as débriding all devitalized tissue and the calcified cartilage layer by either curette or blade (Fig. 96.11). It is important to resect any undermined or delaminated chondral surface that would “peel away” and not provide a stable transition zone or interface with the graft. While keeping the lesion base dry, a thin layer of fibrin glue is applied. Next, at least 1 vial per 2.5 cm2 is used to layer/fill the defect. Great care is taken to limit excessive filling of the defect so as to not allow a prominence of cartilage irregularity. A final thin coat of fibrin glue is then placed over the defect to seal the allograft cartilage transplant. Again, great care is taken to not place so much graft material and fibrin glue in a single location that there is a gross elevation of the grafted surface relative to the native articular surface curvature (Fig. 96.12). Wound Closure Gentle irrigation of the knee joint is performed after the fibrin glue has cured and the arthrotomy is closed in successive layers per routine. Given the technique employed, a drain is not recommended as it could damage the grafted defect site. Fifty percent partial weight bearing is allowed with 0 to 90 degrees ROM for the first 6 weeks; however, for patellofemoral lesions, progressive increases in ROM at 30-degree intervals are allowed every 2 weeks given the more shearforce nature of that cartilage location.

Fig. 96.11  Note the vertical shoulder of the trochlear lesion once prepared.

Osteochondral Allograft Transplantation OAT is reserved for large, isolated chondral and osteochondral lesions. The patient is positioned supine on a well-padded operating room table with a knee positioner if far posterior condylar work is to be performed, which allows for knee hyperflexion. A tourniquet can be useful for visualization while preparing and reaming the lesion site. A mega-OAT procedure will be described for both cylindrical and oblong-shaped lesions. Approach and Defect Preparation (Mega-Osteochondral Allograft Transplantation) Although a utilitarian midline incision with a medial parapatellar arthrotomy can be used, paramedian skin incisions can also be utilized with a lesion locationcompartment specific arthrotomy performed. Some surgeons prefer a subvastus or mid vastus quadriceps sparing approach given the potential for accelerated postoperative rehabilitation. The senior surgeon recommends using a medial paramedian or a lateral paralateral incision specific to the involved condyle. The patella is retracted with a bent Homann, which is placed carefully into the intercondylar notch. Retraction and/or resection of Hoffa’s fat pad can help with visualization. After identification of the lesion, the abnormal cartilage is measured (Fig. 96.13). It is important to attempt to reconstitute the articular surface congruity with the allograft transplant segment. A cannulated trephine reaming system can be used to size the defect initially. Sometimes this can be accomplished with a single plug, but sometimes two plugs in a “snowman” configuration might be needed to repair the defect if it is oblong in nature. However, more recently, the senior surgeon has been using an oblong-shaped graft procurement system to address these more asymmetric lesions and this will be described below. From a technical perspective, the symmetric cylindrical lesions routinely are prepared first and the graft is then obtained, whereas for the asymmetric oblongshaped lesions, the system requires you to procure the graft first, with measured depth of graft obtained, and then prepare your lesion site. For symmetrically contained lesions within a cylindrical shape, the lesion is measured with a reamer sized to adequately resect the lesion. After placing a

Fig. 96.12  Note the particulate graft material layered into the lesion defect with fibrin glue layer placed superficially.

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Authors’ Preferred Technique Articular Cartilage Lesion—cont’d

Fig. 96.13  Note the more cylindrical-shaped lesion on the lateral femoral condyle. (Courtesy Dr. Eric Carson.)

guidewire in the center of the lesion, a 6- to 8-mm deep recipient socket is usually created with a cannulated reamer (Fig. 96.14). In an attempt to limit thermal necrosis, great care is taken to use irrigant at the lesion site as it is prepared and reamed, especially if there is sclerotic bone. After cylindrically reaming the lesion and confirming the depth of the recipient site, drill holes can be placed in the site’s floor to help promote healing. Should significant cysts be encountered, then it is the senior author’s recommendation to backfill these defects, after débriding the cyst’s walls to healthy bleeding bone, with autologous bone graft. Graft Procurement and Placement After securing the allograft hemicondyle on the back table, the same-sized lineto-line cylindrical coring reamer is selected. It is imperative to recreate the same articular arc, and so the coring reamer is placed directly over the corresponding articular graft segment desired. This is done by direct visualization and palpation. The cylindrical graft is extracted from the reamer and its depth trimmed on the back table to what was measured during the lesion site preparation. This helps to ensure adequate depth upon placement so that the grafted surface is flush with the native articular surface. It is also marked for correct orientation prior to placement. Final preparation of the recipient site with a calibrated dilator can be used as needed and the allograft can then be press-fit with manual pressure and ranging the knee so that the graft reduces. This is completed to satisfaction

Fig. 96.14  Appropriately sized trephine reamer is selected and adequate osteochondral resection performed of the diseased articular segment in Fig. 96.13. (Courtesy Dr. Eric Carson.)

until it is deemed stable and the articular surface is flush (Fig. 96.15). Should additional fixation be needed if concern exists for stability, then absorbable headless screws can be used. For asymmetric lesions contained within an oblong shape, selecting the appropriate oblong sizer to cover the native lesion is performed. It is then used to confirm the location of the correct area on the allograft that will become the procurement donor site. This reproducibly allows the articular congruity and arc of the procured graft segment to match the native articular curvature. Securing the graft to the workstation, the corresponding oblong cutter is used to obtain the graft and oscillating saw with jig is used to cut it at the correct depth transversely. Next the recipient site is prepared by proprietary system techniques of a scoring device, cylindrical reamers, and box cutter to remove final remnants of bone. The site is cleared of debris, a dilator used, the graft is placed by hand, and a tamp is used for gentle, final impaction/adjustments (Fig. 96.16). Should fixation be a concern, then once again headless bioabsorbable screws can be used as needed. Wound Closure Satisfactory irrigation followed by layered arthrotomy closure is to be performed with drain use as per the surgeon’s preference. Protected weight bearing is allowed and 0 to 90 degrees for the first 6 weeks is allowed to protect graft incorporation. Continued

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Authors’ Preferred Technique Articular Cartilage Lesion—cont’d

B A Fig. 96.15  (A) and (B), Note the articular surface congruity with satisfactory placement of the osteochondral allograft segment. (Courtesy Dr. Eric Carson.)

A

B Fig. 96.16  (A) and (B) Oblong defect measured with sizer and final allograft placement after harvest. Again, note the articular congruity and satisfactory placement.

SURGICAL TECHNIQUE RESULTS Marrow Stimulation Marrow stimulation/microfracture techniques result in the formation of an intralesional collection of MSCs and blood products. This has the potential to formalize into a fibromyxoid tissue layer, with the predominant type of cartilage being type I cartilage, or fibrocartilage. Focal contained lesions less than 4 cm2 in athletically active patients less than 40 years of age were found to have demonstrated G/E outcomes in 70% of patients.95 However, long-term follow-up has revealed a decrease in sports participation and decrease in symptom relief associated with this

procedure.95 Recent literature comparing marrow stimulation to autograft OAT procedures in athletes showed a higher rate of return to sporting activity and maintenance of sporting activity compared to preoperative status in OAT patients as well as cost benefit analyses suggesting a lower cost to RTP in patients undergoing OAT procedures over marrow stimulation.36,96 Longerterm 10-year outcome data, reviewed in a meta-analysis recently, have also revealed that the OAT procedure may achieve a higher activity level and a lower risk of failure for lesions even greater than 3 cm2 compared to microfracture and that the risk of failure with microfracture was 2.4 times that seen with OAT.97 Additional study findings have also implicated marrow stimulation procedures with complicating secondary cartilage restoration

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procedures, such as ACI, with inferior clinical results and higher associated failure rates.70,98 Recent reports also highlighted the risks associated with microfracture; that disruption of the subchondral plate could predispose the bone to the development of subchondral cysts and fragile bone subsequently accelerating osteoarthritis.52,99 Optimal outcomes are achieved in the following setting: age less than 40 years old, body mass index less than 30, no prior cartilage surgery, symptom duration less than 12 months, lesion size less than 4 cm2, preoperative Tegner score greater than 4, and postoperative MRI evidence of lesion fill greater than 66%.40,100 The drawback of this technique is the high recurrence rate of symptoms in long-term follow-ups.101 Given the type of cartilage produced at the lesion site with marrow stimulation, the long-term viability and durability is currently the concern with this procedure as is evident in its longerterm outcomes when compared to other cartilage restoration procedures.

Osteochondral Autograft Transfer The osteochondral autograft transfer procedure advantage is that it uses local articular cartilage. Seventeen-year clinical results in an athletic population, with lesions measuring 1 to 4 cm2, reported G/E outcomes in 91% of condylar lesions, 86% in treated tibial lesions, and 74% in trochlear lesions.56,57 Slight deterioration of results was noted at the 9.6-year follow-up time point for this athletic population. Additional long-term reported outcomes at 10- to 14-year follow-up, state 40% poor outcomes, defined as later knee arthroplasty or a Lysholm score of 64 or lower. These poor outcomes were associated with female gender (61%), patient age greater than 40 years (59%), and a defect larger than 3 cm2 (57%).102 Subset analysis of those patients who were younger than 40 years and had an articular cartilage lesion less than 3 cm2 showed a failure rate of only 12.5% and a favorable Lysholm score of at least 82. Conversely, for women over the age of 40 years with a chondral lesion over 3 cm2, the failure rate was 83%.102 Additional prognostic risk factors resulting in a favorable outcome have been reported as male gender, medial femoral condyle defects, OCD, deep, small defects, and the shortest time delay to surgery.103 A prospective randomized study in young active athletes under the age of 40 has also shown significant superiority of mosaicplasty over microfracture for the repair of articular cartilage defects in the knee. At an average of 6.5 months, 93% of OAT patients returned to sports activities at the preinjury level. On the other hand, 52% of microfracture athletes could return to sports at the preinjury level.104 Current evidence suggests that OAT is a viable option to be considered for chondral lesions measuring less than 3 cm2, however, the clinical results do have the potential to start decreasing at roughly the 10-year point and that preoperative risk factors of age, gender, lesion location, lesion size, and chronicity can play a role in longer-term outcomes.

Autologous Chondrocyte Implantation Long-term studies have demonstrated good to excellent results after ACI. Favorable factors for ACI include younger patients with fewer than two previous procedures on the same knee, a less than 2-year history of symptoms, a single defect, and a defect

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on the trochlea or lateral femoral condyle.44 Depth of lesion is also reported as a risk factor for failure. Some authors suggest grafting the bony defect before application of ACI if the depth of the lesion is greater than 8 to 10 mm.105 Long-term outcome studies have shown favorable results for ACI treating condylar lesions with graft survivorship rates of 71% at 10-year followup and nearing 75% improved functional status.106,107 Subgroup analysis revealed that concurrent high tibial osteotomy had a protective effect and increased graft survivorship.107 A recent study with 4-year follow-up data treating patellar lesions with ACI has shown statistically significant improvements in clinically assessed physical outcome scales with 86% rating their knees as G/E at final follow-up.108 A previous randomized controlled trial comparing ACI to microfracture clearly found that while no gross differences existed between the two procedures at 5 years with regard to clinical improvement or progression of radiographic arthrosis, subgroup size analysis did reveal that lesions greater than 4 cm2 did poorly with microfracture and that ACI results demonstrated no correlation with lesion size.109 As alluded to earlier, prior marrow stimulation procedures not only have been found to have a deleterious effect on outcomes, with a markedly higher graft implantation failure rate of 26% in patients undergoing ACI after marrow stimulation compared to an 8% failure rate of ACI as an index procedure, but have also shown inferior clinical outcomes associated with ACI after marrow stimulation procedures.70,98 Ten-year results of a prospective randomized study comparing ACI and OAT for symptomatic articular cartilage lesions, mean size 4 cm2, of the knee reported graft failure in 17% of patients in ACI group and 55% of patients in OAT group. Of note, the functional outcome of those patients with a surviving graft was significantly better in patients who underwent ACI compared with OAT.110 Recent evidence suggests that neither lesion size nor location affects return to low or moderate sport athletic participation or even return to work rates; however, return to high-stress elite-level athletic participation is unlikely following ACI.111 One commonly reported complication found postoperatively at the 7- to 9-month point with the use of a periosteal patch is patch hypertrophy resulting in symptomatic clicking and popping, which can be a cause of subsequent surgery after ACI and which has been reported up to 36%.41,112,113 While using a type I/III collagen patch has dramatically reduced this potential risk for hypertrophy to 5%, this is still off label use for the knee without FDA approval as of yet.114 While still not approved in the United States, MACI has 15-year reported outcome data overseas showing improved and maintained patient reported outcome measures compared to preoperative levels.115 A prospective randomized trial compared the efficacy of MACI with microfracture for patients with symptomatic focal cartilage defects ≥3 cm2. Clinical outcomes from baseline to 2 years were significantly more improved with MACI than with microfracture.116 Additional research has also reported no significant implication of preoperative subchondral edema and MACI outcomes at 5 years with regard to patient outcomes for pain and symptoms or MRI-based cartilage assessments.117 Unfortunately, there is recent literature that still focuses on the potential graft hypertrophy in MACI

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with rates that approach what was seen with periosteal patch ACI use.118

Particulated Juvenile Cartilage Allograft Limited data exist for particulated juvenile cartilage allograft technique because this system was regulated as a minimally manipulated human allograft tissue and no clinical outcome data were provided during the approval process. However, shortterm preliminary clinical reported data show encouraging results.76,119 Recent 2-year follow-up revealed significant improvements in patient-reported outcomes, MRI T2 data showing a return of cartilage signal to near normal articular cartilage, and histologic evaluation detailing a mixture of hyaline and fibrocartilage with more type II collagen than type I with excellent transition zones.120 Improved patient outcomes have also been reported in the treatment of grade IV patellar lesions with corresponding near normalization of cartilage signal as seen on MRI with this treatment modality.121 Further research and longerterm outcome data will be of interest to review as it is presented in the coming years.

Osteochondral Allograft Transplantation Short-term follow-up data have revealed overall patient satisfaction rates of 86% at 58-month follow-up points in patients of a mean age younger than 40 years and a mean lesion of 6.3 cm2 in size.122 Additional studies have reported on the outcomes of OAT as the primary treatment for cartilage injury in patients with no previous surgical treatment. The majority of patients (86%) were extremely satisfied and survivorship was 89.5% at 5 years and 74.7% at 10 years.123 A recent long-term mean 22-year follow-up study reporting on fresh OAT for patients younger than 50 years with unipolar condylar lesions greater than 3 cm2 revealed graft survival at 10, 15, 20, or 25 years of 91%, 84%, 69%, and 59%, respectively.124 Additional studies detailing OAT in the patellofemoral joint have not shown as reliable of graft survivorship, with rates approaching between 50% and 75% in studies reporting on a mean of 8- to 10-year follow-up data.125,126 Overall, poorer results have been reported in older patients, bipolar and patellofemoral lesions, and corticosteroid-induced osteonecrosis when treated with OAT.127–130

COMPLICATIONS Routine knee arthroscopy as well as open knee procedures carry the inherent risks of bleeding and infection, with the potential for their relative increase in risk compounded by comorbidities. With open procedures, an increased risk of infection, arthrofibrosis, and injury to the infrapatellar branch of the saphenous nerve with parapatellar arthrotomy is always of concern. With additional procedures performed either open or arthroscopic, there is the potential for peroneal nerve and popliteal artery injury, although this is rare. Tourniquet-related compression/ ischemia and peripheral regional nerve analgesia also carry an inherent risk with their use. Some previous complications directly attributable to the specific procedure performed have been mentioned already but in general, subchondral plate fracture or subchondral cyst formation with collapse in association with

marrow stimulation procedure, osteochondral autograft and allograft transfer with graft instability potentially requiring additional fixation or failure of union or fragmentation, and juvenile particulate allograft transplantation as well as ACI with the potential for graft hypertrophy and resultant abundance of scar tissue requiring subsequent surgery for resection or lysis of adhesions.

FUTURE CONSIDERATIONS In the attempt to provide histologically normal-appearing cartilage with the hopes that this will translate into functionally viable and durable cartilage in the long term, the advancement of cartilage restoration procedures continues to evolve. Current clinical trials in the United States are under way comparing marrow stimulation techniques to NOVOCART 3D (Aesculap Biologics, Breinigsville, PA). This treatment modality of thirdgeneration matrix-based ACI has been implemented in Europe already with reported follow-up data. These 3D scaffolds are seeded with autologous chondrocytes from a previous operation, where osteochondral plugs were harvested, and ultimately implanted. Bone marrow edema (BME) has been associated with these third-generation ACI techniques with possible influences on clinical outcomes. A recent study reviewing 3-year follow-up data using NOVOCART 3D found overall significant clinical improvements throughout and that the occurrence of BME did not correlate to clinical outcomes.131 An additional short-term follow-up study has also shown the clinical benefits and radiographic improvements of NOVOCART 3D for large focal chondral and osteochondral defects.132 However, just as with other ACI predecessors, graft hypertrophy still is a potential complication, with specific focus detailing NOVOCART 3D in more acute injuries such as acute chondral trauma or OCD, where these etiologies are at risk for developing graft hypertrophy as evidenced with 2-year follow-up data.133 A newer technology is porous osteochondral allograft material Cartiform (Osiris, Columbia, MD). With its cryopreserved, viable chondrocytes, chondrocyte growth factors, ECM, minimal bone thickness, and porosity, this implantable device when combined with a marrow stimulation technique allows for marrow elements to penetrate the graft during formalization of the intralesional mesenchymal clot. No studies have been performed on this implantable allograft material to date and there are no results to report as to its efficacy. Finally, the harvesting of nasal chondrocytes for autologous cartilage tissue implantation into the knee for post-traumatic femoral chondral defects, 2 to 6 cm2 in size, is a novel idea in the continued efforts to address intra-articular chondral lesions of the knee. In 10 patients, these nasal chondrocytes were then embedded into an ECM rich in GAG and type II collagen with frozen section analysis revealing the constructs maintained at least 70% viable chondrocyte cells. Histologic assessments also found viable type II collagen to be present as well as type I collagen at the construct periphery of the implantable tissue. While second look biopsy did not show typical architectural organization of articular cartilage, it did show at least 50% of tissue cells were round, surrounded by lacunae in ECM, which stained significantly for type II collagen

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and GAGs with only faint type I and X collagen. At 24-month follow-up, patient International Knee Documentation Committee (IKDC) scores and Knee Injury and Osteoarthritis Outcome Scores (KOOS) all significantly improved compared to preoperative levels. This study is still ongoing and it will be interesting to see if additional research in the future includes a controlled clinical trial.134

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meet their strict indications. It is paramount to consider the focal nature of the lesion, the overall limb alignment, status of the meniscus and ligament competency, size of the lesion, and the overall patient demand. While taking into account the patient’s expectations is important when weighing which procedure might be of most benefit, it is also of vital importance to have upfront discussions with the patient to help manage overall long-term expectations as well. For a complete list of references, go to ExpertConsult.com.

Cartilage restoration procedures are powerful tools and techniques whose potential benefit can be transformative for patients who

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110. Bentley G, Biant LC, Vijayan S, et al. Minimum ten-year results of a prospective randomised study of autologous chondrocyte implantation versus mosaicplasty for symptomatic articular cartilage lesions of the knee. J Bone Joint Surg Br. 2012;94(4):504–509. 111. Pestka JM, Feucht MJ, Porichis S, et al. Return to sports activity and work after autologous chondrocyte implantation of the knee: which factors influence outcomes? Am J Sports Med. 2016;44(2):370–377. 112. Zaslav K, Cole B, Brewster R, et al. A prospective study of autologous chondrocyte implantation in patients with failed prior treatment for articular cartilage defect of the knee: results of the study of the treatment of articular repair (STAR) clinical trial. Am J Sports Med. 2009;37(1):42–55. 113. Gooding CR, Bartlett W, Bentley G, et al. A prospective, randomised study comparing two techniques of autologous chondrocyte implantation for osteochondral defects in the knee: periosteum covered versus type I/III collagen covered. Knee. 2006;13(3):203–210. 114. Gomoll AH, Probst C, Farr J, et al. Use of a type I/III bilayer collagen membrane decreases reoperation rates for symptomatic hypertrophy after autologous chondrocyte implantation. Am J Sports Med. 2009;37(suppl 1):20s–23s. 115. Gille J, Behrens P, Schulz AP, et al. Matrix-associated autologous chondrocyte implantation: a clinical follow-up at 15 years. Cartilage. 2016;7(4):309–315. 116. Saris D, Price A, Widuchowski W, et al. Matrix-applied characterized autologous cultured chondrocytes versus microfracture: two-year follow-up of a prospective randomized trial. Am J Sports Med. 2014;42(6):1384–1394. 117. Ebert JR, Smith A, Fallon M, et al. Degree of preoperative subchondral bone edema is not associated with pain and graft outcomes after matrix-induced autologous chondrocyte implantation. Am J Sports Med. 2014;42(11):2689–2698. 118. Ebert JR, Smith A, Fallon M, et al. Incidence, degree, and development of graft hypertrophy 24 months after matrixinduced autologous chondrocyte implantation: association with clinical outcomes. Am J Sports Med. 2015;43(9): 2208–2215. 119. Bonner KF, Daner W, Yao JQ. 2-year postoperative evaluation of a patient with a symptomatic full-thickness patellar cartilage defect repaired with particulated juvenile cartilage tissue. J Knee Surg. 2010;23(2):109–114. 120. Farr J, Tabet SK, Margerrison E, et al. Clinical, radiographic, and histological outcomes after cartilage repair with particulated juvenile articular cartilage: a 2-year prospective study. Am J Sports Med. 2014;42(6):1417–1425. 121. Tompkins M, Hamann JC, Diduch DR, et al. Preliminary results of a novel single-stage cartilage restoration technique:

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particulated juvenile articular cartilage allograft for chondral defects of the patella. Arthroscopy. 2013;29(10):1661–1670. Chahal J, Gross AE, Gross C, et al. Outcomes of osteochondral allograft transplantation in the knee. Arthroscopy. 2013;29(3):575–588. Briggs DT, Sadr KN, Pulido PA, et al. The use of osteochondral allograft transplantation for primary treatment of cartilage lesions in the knee. Cartilage. 2015;6(4):203–207. Raz G, Safir OA, Backstein DJ, et al. Distal femoral fresh osteochondral allografts: follow-up at a mean of twenty-two years. J Bone Joint Surg Am. 2014;96(13):1101–1107. Jamali AA, Emmerson BC, Chung C, et al. Fresh osteochondral allografts: results in the patellofemoral joint. Clin Orthop Relat Res. 2005;437:176–185. Torga Spak R, Teitge RA. Fresh osteochondral allografts for patellofemoral arthritis: long-term followup. Clin Orthop Relat Res. 2006;444:193–200. Getgood A, Gelber J, Gortz S, et al. Combined osteochondral allograft and meniscal allograft transplantation: a survivorship analysis. Knee Surg Sports Traumatol Arthrosc. 2015;23(4): 946–953. Gross AE, Shasha N, Aubin P. Long-term followup of the use of fresh osteochondral allografts for posttraumatic knee defects. Clin Orthop Relat Res. 2005;435:79–87. Giannini S, Buda R, Ruffilli A, et al. Failures in bipolar fresh osteochondral allograft for the treatment of end-stage knee osteoarthritis. Knee Surg Sports Traumatol Arthrosc. 2015;23(7):2081–2089. Gracitelli GC, Meric G, Pulido PA, et al. Fresh osteochondral allograft transplantation for isolated patellar cartilage injury. Am J Sports Med. 2015;43(4):879–884. Niethammer TR, Valentin S, Gulecyuz MF, et al. Bone marrow edema in the knee and its influence on clinical outcome after matrix-based autologous chondrocyte implantation: results after 3-year Follow-up. Am J Sports Med. 2015;43(5): 1172–1179. Zak L, Albrecht C, Wondrasch B, et al. Results 2 years after matrix-associated autologous chondrocyte transplantation using the novocart 3D scaffold: an analysis of clinical and radiological data. Am J Sports Med. 2014;42(7):1618–1627. Niethammer TR, Pietschmann MF, Horng A, et al. Graft hypertrophy of matrix-based autologous chondrocyte implantation: a two-year follow-up study of NOVOCART 3D implantation in the knee. Knee Surg Sports Traumatol Arthrosc. 2014;22(6):1329–1336. Mumme M, Barbero A, Miot S, et al. Nasal chondrocyte-based engineered autologous cartilage tissue for repair of articular cartilage defects: an observational first-in-human trial. Lancet (London, England). 2016;388(10055):1985–1994.

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97  Frontiers in Articular Cartilage Treatment Rachel M. Frank, Armando F. Vidal, Eric C. McCarty

Articular cartilage defects in the knee (Fig. 97.1) are common and often result in pain and dysfunction. Over the past several decades, research efforts have focused on better understanding how to diagnose and treat these lesions. Comprised predominately of type II collagen, articular cartilage is relatively avascular, depending on diffusion to obtain nutrients and oxygen, making spontaneous healing of articular cartilage defects exceedingly difficult.1,2 Importantly not all defects are symptomatic, as many are simply incidental in nature, found on diagnostic imaging studies or during diagnostic arthroscopies being performed for other diagnoses, such as anterior cruciate ligament (ACL) tears. In fact, such defects are found in more than 60% of patients undergoing arthroscopy of the knee.3-5 One of the first challenges, therefore, is determining which lesions should be treated, and which can simply be managed with “benign neglect.” For most patients, the combination of a thorough history, focused physical examination, imaging studies, and if necessary, a diagnostic arthroscopy, can determine if a given cartilage injury is symptomatic and warrants treatment. Once the diagnosis is made, a variety of treatment options are available. The optimal management for a given cartilage lesion varies based on lesion location (femoral condyle, tibial plateau, patella, trochlea), size, containment/stability, chronicity, and associated knee pathologies, including meniscus deficiency, ligament insufficiency, and/or malalignment. Bipolar “kissing” lesions (i.e., corresponding lesion on medial femoral condyle and medial tibial plateau, or on the patella and trochlea) are especially difficult to manage. In addition, factors unique to the patient, including age, activity level, expectations, body mass index, history of prior treatment, and ability to comply with rehabilitation, may influence the treatment decision. The goals of the patient are especially important to consider, as these may impact decision-making. For example, treatment for a high-level athlete hoping to return to the same (or better) level of play may differ from treatment for a weekend warrior who has already undergone multiple procedures and is hoping to manage activities of daily living without pain and swelling. Finally, surgeon- and facility-specific factors, including surgeon experience and the availability of treatments/products, will impact clinical decision-making. In most areas within the United States, for example, allograft tissue is readily available and can be considered as part of the treatment algorithm, whereas in many countries around the world, allografts are unavailable, and thus treatment for two very similar patients with two very similar defects can vary simply based on location. 1178

Treatment for articular cartilage defects includes both nonoperative and operative options. Nonoperative options include activity modification, physical therapy with a focus on quadriceps and core strengthening, cryotherapy, oral nonsteroidal antiinflammatory medications, and a variety of injectable agents, including corticosteroids, hyaluronic acid, and more recently, biologics. Biologic therapies have recently emerged as a potential treatment for a wide variety of orthopedic pathologies, including articular cartilage lesions, and can be administered both in the outpatient clinic setting as well as in the operating room. Biologic therapies, including platelet-rich plasma (PRP) and mesenchymal stem cell injections such bone marrow aspirate concentrate (BMAC), can be given either as isolated treatments, or combined with a surgical procedure. Surgical procedures for articular cartilage defects have historically been broken down into palliative (débridement, chondroplasty), reparative (marrow stimulation including microfracture), and restorative (autologous chondrocyte implantation, osteochondral autograft/allograft) procedures.6-23 This chapter will focus on emerging surgical techniques for articular cartilage treatment. The advantages, disadvantages, outcomes, and complications associated with newer reparative techniques, including enhanced/augmented microfracture, as well as emerging reconstructive techniques, including matrixassociated autologous chondrocyte implantation, minced cartilage products, and off-the-shelf osteochondral allograft products, will be discussed in detail.24-49 It should be noted that several of these emerging technologies and products have only recently been introduced in the United States, with many are unavailable unless the patient is enrolled in a clinical trial. The majority of such products have been introduced and studied in Europe and/or Asia prior to becoming available in the United States, and even then, products must be considered “minimally manipulated” or intended for “homologous use” in order to bypass the US Food and Drug Administration approval process.

SURGICAL MANAGEMENT For any patient undergoing surgical management of an articular cartilage defect, it is critical to (1) discuss goals/expectations and (2) treat any associated malalignment, meniscus insufficiency, and/or ligament insufficiency.50 Patients must understand the unclear natural history of articular cartilage lesions and sometimes unpredictable nature of articular cartilage lesion treatment, especially with respect to returning to high-level athletics. In

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Abstract

Keywords

Focal chondral lesions of the knee, particularly those involving the weight-bearing surfaces of the medial or lateral femoral condyles as well as those in the patella and trochlea, often result in pain, effusions, mechanical symptoms, and ultimately dysfunction and disability. In many cases, surgical intervention is helpful in reducing pain, improving function, and restoring normal joint mechanics. “Traditional” techniques include chondroplasty, microfracture, autologous chondrocyte implantation, osteochondral autograft transfer, and osteochondral allograft transplantation. Emerging techniques including augmented microfracture, scaffold and matrix-associated constructs, minced cartilage transplantations, matrix-associated autologous chondrocyte implantation, and off-the-shelf osteochondral allograft transplantations have been described. Additional research on these novel techniques and comparison to more “conventional” techniques is warranted.

cartilage lesion cartilage restoration focal chondral defect stem cells cartilage transplantation

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a quick rehabilitation process and relatively early timeline for return to play.

Reparative

Fig. 97.1  Intraoperative example of a full thickness focal chondral defect of the medial femoral condyle (right knee).

addition, even with the most sophisticated articular cartilage treatments, unaddressed concomitant knee pathology is likely to result in failure of cartilage treatment, particularly in the setting of malalignment, as this may lead to overload of the newly treated cartilage lesion. While beyond the scope of this chapter, in some cases, isolated realignment osteotomy may be the ideal definitive solution for an articular cartilage lesion in a young patient with malalignment.

Palliative Arthroscopic débridement, lavage, and chondroplasty continue to be viable treatment options for many patients with symptomatic, focal chondral defects who have failed nonoperative treatment. This approach is considered palliative as the goals are not to “regenerate” or replace cartilage, but rather to remove any flaps of loose cartilage that may be irritating to the patient and causing mechanical symptoms, and to stabilize the rim of the defect, decreasing the risk of further cartilage delamination. During the procedure, it is critical to débride the lesion down to the level of the subchondral bone, without violating the subchondral bone layer, taking care to maintain vertical walls around the lesion. Similar to a tire rolling over a pothole that is uniform and smooth along its rim, it follows that a well-performed chondroplasty will result in a defect with a uniform and smooth rim that is less likely to cause mechanical symptoms during loading and range of motion. Advantages of this technique include its technical simplicity, ability to be performed arthroscopically for defects in nearly any location (condyle, tibia, trochlea, patella), ability to perform other concomitant procedures such as meniscus surgery or ligament reconstruction, low overall cost, and ease of postoperative rehabilitation.7 The obvious disadvantage is that this procedure does not have any ability to replace the missing cartilage, and thus the patient may remain symptomatic. Chondroplasty has historically been considered an acceptable first-line treatment for low-demand patients with small articular cartilage lesions; however, this may also be appropriate for elite, highdemand patients who seek a minimally invasive approach with

Another viable first-line treatment for patients with focal chondral defects is marrow stimulation. This approach is considered reparative, as the goals are to fill the cartilage defect with actual cartilage, as opposed to débriding the defect and leaving it “empty” as during chondroplasty. Marrow stimulation techniques include drilling/abrasion arthroplasty and microfracture (Fig. 97.2), widely considered the gold-standard surgical procedure for small, isolated focal chondral defects. As reported in a 2014 epidemiology study by McCormick and colleagues,51 surgical procedures for articular cartilage defects in the knee are increasing by approximately 5% on an annual basis in the United States, and of all coded procedures, microfracture remains the most common. The advantages of microfracture are similar to those of chondroplasty, including its technical simplicity, ability to be performed arthroscopically in a single-stage in a minimally invasive fashion, ability to perform other concomitant procedures such as meniscus surgery or ligament reconstruction, low overall cost, and different from chondroplasty, its ability to “fill” the defect with a cartilage product.52-57 From a biologic standpoint, microfracture and other marrow stimulation techniques induce an influx of marrow substrates to “fill” the cartilage defect, ultimately resulting in a fibrocartilage plug composed primarily of type I collagen. Importantly, fibrocartilage repair tissue lacks many of the intrinsic biochemical and viscoelastic properties of normal hyaline cartilage, is more stiff, and thus does not possess same shock absorption and force distribution capabilities as normal hyaline cartilage. When considering the pothole analogy described earlier, while the fibrocartilage produced by microfracture “fills” the defect, and may be superior to leaving the defect empty, the long-term efficacy of microfracture remains unclear due to the lack of hyaline-type cartilage (type II collagen) filling the void. Recently efforts have been made to improve traditional microfracture techniques by using matrices and/or scaffolds to stabilize the mesenchymal clot produced by marrow stimulation, and to improve mesenchymal stem cell (MSC) differentiation into hyaline-type cartilage as opposed to fibrocartilage. Described “augmented microfracture”58,59 techniques include including BioCartilage (Arthrex, Inc., Naples, FL), autologous matrix-induced chondrogenesis (AMIC), BST-CarGel (Smith and Nephew Inc., Andover, MA), GelrinC (Regentis Biomaterials Ltd., Or-Akiva, Israel), and Chondrotissue (BioTissue AG, Zurich, Switzerland). The AMIC technique involves performing microfracture followed by the application of a porcine collagen I/III matrix (ChondroGide, Geistlich, Pharma AG) fixated with either autologous or allogeneic fibrin glue.60-64 The BST-CarGel technique involves performing traditional microfracture followed by the application of the product, which is a bioscaffold containing liquid chitosan and autologous whole blood.65,66 The GelrinC technique involves performing microfracture followed by the application of a hydrogel composed of polyethylene glycol di-acrylate (PEG-DA) and denatured fibrinogen, at which time the materials are exposed to UV light, forming a semisolid biodegradable scaffold for

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A

B

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D

E Fig. 97.2  Intraoperative example of a full thickness focal chondral defect of the lateral femoral condyle (right knee) undergoing microfracture including (A) defect, (B) débridement to stable vertical walls, (C) microfracture with an awl, (D) microfracture holes evenly spaced 3 to 4 mm apart, 3 to 4 mm deep, and (E) marrow products flowing into defect.

mesenchymal stem cells.67 The Chondrotissue technique involves performing microfracture followed by application of a scaffold composed of polyglycolic acid (PGA) and hyaluronic acid (HA) immersed with PRP. Different from the aforementioned enhanced microfracture techniques/products, as of the time of publication of this text, BioCartilage (Fig. 97.3) is available for routine use in the United States. The BioCartilage technique involves performing microfracture followed by the application of 1 mL of

dehydrated, micronized allograft articular cartilage extracellular matrix combined with 1 mL of autologous PRP.48,49 Each of these enhanced microfracture techniques are advantageous in that they are performed in the same general way as traditional microfracture, utilizing a single-stage, minimally invasive approach, and offer the theoretical benefit of improving the stability and biology of the defect repair site. These techniques can be performed either arthroscopically or through a mini-open

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Fig. 97.3  MRI images pre- and post-BioCartilage procedure to the patella (4 months postoperative).

arthrotomy, depending on the ability to fully visualize and treat the lesion.

Restorative For larger lesions, for lesions involving both the subchondral bone in addition to the cartilage, as well as for revision procedures, cartilage restoration surgery can be performed. A variety of restorative procedures are available, including autologous chondrocyte implantation (ACI), matrix-associated ACI (MACI), minced cartilage techniques, stem cell-scaffold techniques, osteochondral autograft transfer (OATS), surface allograft transplantation with “off-the-shelf ” allograft products, and osteochondral allograft transplantation (OCA). These techniques are considered restorative, as they aim to treat the cartilage defect by restoring hyaline-type articular cartilage to entire defect site, either with or without subchondral bone. While many of the restorative techniques can be performed in a single-stage and through arthroscopic techniques, some require two separate procedures in a staged fashion, and some cannot be performed arthroscopically and require a small arthrotomy. The advantages of these procedures include their ability to treat large lesions as well as lesions that have failed prior attempts at cartilage repair, the presence of hyaline-type cartilage (as opposed fibrocartilage), and their ability to treat the subchondral bone in addition to the cartilage (for the osteochondral grafting procedures; Fig. 97.4). Disadvantages include the potential high cost associated with allograft tissue, the relatively long recovery period needed for graft incorporation, the potential safety concerns with allografts (for allograft procedures), and the need for two procedures instead of a single surgery in some cases (for ACI and MACI procedures). As ACI, MACI, minced techniques, OATS, and OCA were covered in the previous chapter, the following section of this chapter will focus on emerging articular cartilage techniques, including stem cell-scaffold techniques, novel minced techniques, and off-the-shelf surface allograft transplantation.

Mesenchymal Stem Cells With Three-Dimensional Matrices Recently several unique products combining MSCs with threedimensional scaffolds have been introduced in an effort to provide an alternative option to ACI for the management of focal chondral defects that, unlike ACI, can be performed in a single operation. Similar to ACI, the aim of these techniques is to treat the defect by restoring the surface with durable hyaline-type cartilage. Described products in this category include Hyalofast (Anika Therapeutics, Bedford, MA), which utilizes autologous MSCs, and Cartistem (Medipost Co., Ltd., Korea), which utilizes allogeneic MSCs. The thought process behind these techniques is that the scaffold with create an environment that is biologically favorable for MSC differentiation into hyaline-type cartilage. Hyalofast, which is not currently available in the United States, is performed in a single stage by shaping/sizing the hyaluronan scaffold (HYAFF11 scaffold) to the defect shape/size, soaking the scaffold in the patient’s BMAC, and then securing the scaffold to the defect with 6-0 PDS suture and/or fibrin glue.68 BMAC is most often harvested from the patient’s iliac crest, and contains adult MSCs, platelets, cytokines, bone morphogenic protein (BMP) 2 and 7, and a variety of growth factors, including PDGF and TGFβ. The cells, proteins, and growth factors are thought to establish a favorable biologic environment for cartilage restoration due to their anabolic and anti-inflammatory properties. While clinical data is limited, Gobbi and colleagues have found that at 5 years, patients undergoing treatment with Hyalofast compared with microfracture had better rates of returning to preinjury activity levels, despite microfracture patients having better return rates at 2 years following treatment.68 Similar to Hyalofast, Cartistem is also performed in a single stage and combines MSCs with a three-dimensional scaffold. In contrast, Cartistem utilizes allogeneic stem cells, specifically culture-expanded human umbilical cord blood derived

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B A Fig. 97.4  Intraoperative example of (A) a full-thickness focal chondral defect of the medial femoral condyle (right knee) undergoing (B) osteochondral allograft transplantation.

mesenchymal stem cells (hUBC-MSCs), which avoids the donorsite morbidity associated with BMAC harvest. In this technique, the hUBC-MSCs are combined with a sodium hyaluronate scaffold and inserted implanted into the defect site. Preliminary outcomes from a clinical trial out of Korea including seven patients undergoing Cartistem are encouraging, though certainly further research is warranted.69 Several other stem cell-matrix combinations for the treatment of focal chondral defects have recently been described, and are currently in the initial phases of clinical testing. Specifically, the implantation of adipose derived stem cells (ADSCs) combined with scaffolds and bioactive factors have been reported by several groups.

Minced Cartilage Techniques While the DeNovo Natural Tissue (DeNovo NT, Zimmer Biomet, Warsaw, IN) cartilage restoration technique was discussed in the previous chapter, at least two other emerging minced cartilage techniques have been reported, including Cartilage Autograft Implantation System (CAIS) and CartiONE. In brief, minced (or particulated) cartilage restoration techniques involve the placement of either autologous or allogeneic hyaline cartilage into the cartilage defect, combined with a scaffold delivery system, and secured with fibrin glue. The cartilage is minced into 1 to 2 mm3 fragments, which is theorized to allow chondrocytes to escape the extracellular matrix and produce hyaline-type cartilage and, ultimately, integrate with the patient’s normal/healthy surrounding cartilage.43-47 DeNovo NT (see previous chapter for details; Fig. 97.5) is similar to BioCartilage, as both products utilize minced juvenile allograft cartilage, but is different in that the technique does not involve violation of the subchondral bone (no associated microfracture). Cartilage Autograft Implantation System (CAIS; DePuy Mitek, Raynham, MA) is another single-stage minced cartilage technique, but unlike DeNovo NT, CAIS utilizes autologous stem

cells harvested from the patient’s intercondylar notch or trochlear border. Following harvest, the cells are minced into 1 to 2 mm3 fragments, combined with a scaffold of polycaprolactone (35%) and polyglycolic acid (65%) with PDO mesh, and fixed to the defect using biodegradable anchors. While preliminary outcomes following the use of CAIS were promising, due to expense and poor patient enrollment, trials involving CAIS in the United States were discontinued. CartiONE (Orteq Ltd., London, United Kingdom) is another restorative technique involving minced cartilage that can be performed as a single operation. In this technique, autologous cartilage is harvested from the periphery of the patient’s trochlea (nonarticulating portion) or intercondylar notch, minced, treated with a patented cell-isolation technology, combined with BMAC, added to a scaffold, and implanted into the defect site. Early clinical outcomes, including histologic outcomes, imaging outcomes, and clinical outcomes, from the INSTRUCT trial utilizing this product have been promising.

Off-the-Shelf Surface Allograft Transplantation The utilization of osteochondral autografts and allografts was discussed in detail in the previous chapter. Among many reasons, both osteochondral autografts and allografts are advantageous, as they are composed of hyaline cartilage with associated bone and are thus are ideal for restoration of articular cartilage defects (especially those with symptomatic bone marrow edema), can be used to treat large defects, and can be used as a revision treatment solution for defects that have failed prior treatment. The main disadvantages of osteochondral autografts include their associated donor-site morbidity and their limited ability to treat large lesions. The main disadvantages of osteochondral allografts include their cost, potentially limited availability (especially outside the United States), and concerns regarding disease transmission. In an effort to provide an osteochondral solution that maintains the benefits but eliminates the disadvantages,

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B

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D

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Fig. 97.5  Intraoperative example of a full-thickness focal chondral defect of the patella undergoing DeNovo NT transplantation including (A) defect, (B) preparation of defect with stable vertical walls, (C) transplantation of cells, and (D) covering of defect with fibrin glue.

several off-the-shelf surface allograft products have been developed. Surface allografts available in the United States include Chondrofix (Zimmer Biomet, Warsaw, IN) Cartiform (Arthrex Inc., Naples, FL), and ProChondrix (AlloSource, Denver, CO). In 2012, Chondrofix was introduced as an off-the-shelf osteochondral allograft for single-stage treatment of full thickness articular cartilage lesions. This product was described as a preshaped, cylindrical, sterile, decellularized bone-cartilage construct with a shelf life of 24 months. The graft is precut to 10 mm in length, and comes in either 7, 9, 1, or 15 mm diameters. Preliminary data on 32 patients undergoing treatment with Chondrofix was reported by Farr et al. in 2016, and unfortunately failures were noted in 72% of the cohort (23 knees) at an average follow-up of 1.29 years (range, 0.11 to 2.8 years).41,42 The average defect size of the cohort was 2.9 ± 2.0 cm2, and a median of 2 allografts were implanted per knee (range, 1 to 5 grafts). Cartiform and ProChondrix are two more recently described off-the-shelf osteochondral allograft products available in the United States. Unlike Chondrofix, which does not contain any viable chondrocytes, both Cartiform and ProChondrix do contain viable chondrocytes. Cartiform (Fig. 97.6) is described as a cryopreserved, viable osteochondral allograft composed of full-thickness articular cartilage and a thin layer of subchondral bone, with a 24-month shelf-life (stored at –80°C), and

Fig. 97.6  Intraoperative example of a full-thickness focal chondral defect of the trochlea undergoing Cartiform cartilage restoration.

comes in four sizes (10 mm diameter, 20 mm diameter, 12 × 19 mm and 20 × 25 mm). The graft contains full-thickness pores/ perforations that allow the cryopreservation solution to bathe the entire graft and preserve cell viability during storage, and also allows for graft flexibility during implantation. ProChondrix is described as a cellular 3D fresh osteochondral allograft composed of viable chondrocytes, matrix, and growth factors, with a 35-day shelf life (stored at 4°C), and comes in 5 sizes

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(11, 13, 15, 17, and 20 mm diameter). The depth of the graft can be customized intraoperatively based on the depth of the osteochondral defect. As both of these off-the-shelf osteochondral allograft products are relatively new, clinical outcomes in patients undergoing treatment with these products are currently unavailable.

SUMMARY Focal chondral lesions of the knee, especially those involving the weight-bearing surfaces of the medial or lateral femoral condyles as well as those involving the patellofemoral joint, often result in pain, effusions, mechanical symptoms, and ultimately dysfunction and disability. For appropriately indicated patients, surgical intervention is helpful in reducing pain, improving function, and restoring normal joint mechanics. Emerging techniques including augmented microfracture, scaffold and matrix-associated constructs, minced cartilage transplantations, MACI, and off-the-shelf osteochondral allograft transplantations, have been described, and warrant additional research and comparison to more “conventional” techniques, including standard chondroplasty, traditional microfracture, ACI, OATS, and OCA. For a complete list of references, go to ExpertConsult.com.

Summary: Case series demonstrating a high failure rate following implantation of preshaped, cylindrical sterilized and decellularized osteochondral allografts.

Citation: Frank RM, et al. Do outcomes of osteochondral allograft transplantation differ based on age and sex? A comparative matched group analysis. Am J Sports Med. 2018;46(1):181–191.

Level of Evidence: III

Summary: Cohort study demonstrating that osteochondral allograft transplantation is a safe and reliable treatment option for osteochondral defects in patients aged ≥40 years. Male and female patients had similar outcomes.

Citation: Frank RM, et al. The utility of biologics, osteotomy, and cartilage restoration in the knee. J Am Acad Orthop Surg. 2018;26(1):e11–e25.

Level of Evidence: V

Summary: Review of the latest evidence over the use of biologics, osteotomies, and cartilage restoration.

SELECTED READINGS

Citation:

Citation:

Gille J, et al. Outcome of autologous matrix induced chondrogenesis (AMIC) in cartilage knee surgery: data of the AMIC Registry. Arch Orthop Trauma Surg. 2013;133(1):87–93.

Crawford DC, DeBerardino TM, Williams RJ 3rd. NeoCart, an autologous cartilage tissue implant, compared with microfracture for treatment of distal femoral cartilage lesions: an FDA phase-II prospective, randomized clinical trial after two years. J Bone Joint Surg Am. 2012;94(11):979–989.

Level of Evidence: I

Summary: Results from a Phase II RCT comparing the safety of autologous cartilage tissue implantation with NeoCart to traditional microfracture surgery.

Citation:

Level of Evidence: IV

Summary: Prognostic study demonstrating that AMIC is an effective and safe method of treating symptomatic chondral defects of the knee, but that a longer term is needed to determine if grafted area will maintain quality and integrity over time.

Citation: Moran CJ, et al. Restoration of articular cartilage. J Bone Joint Surg Am. 2014;96(4):336–344.

Farr J, et al. High failure rate of a decellularized osteochondral allograft for the treatment of cartilage lesions. Am J Sports Med. 2016;44(8):2015–2022.

Level of Evidence:

Level of Evidence:

Review of the latest evidence techniques for articular cartilage restoration.

IV

V

Summary:

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REFERENCES 1. Richter W. Mesenchymal stem cells and cartilage in situ regeneration. J Intern Med. 2009;266(4):390–405. 2. Chen FS, Frenkel SR, Di Cesare PE. Repair of articular cartilage defects: part I. Basic science of cartilage healing. Am J Orthop (Belle Mead NJ). 1999;28(1):31–33. 3. Curl WW, Krome J, Gordon ES, et al. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy. 1997;13(4):456–460. 4. Hjelle K, Solheim E, Strand T, et al. Articular cartilage defects in 1,000 knee arthroscopies. Arthroscopy. 2002;18(7):730–734. 5. Aroen A, Loken S, Heir S, et al. Articular cartilage lesions in 993 consecutive knee arthroscopies. Am J Sports Med. 2004;32(1): 211–215. 6. Gracitelli GC, Moraes VY, Franciozi CE, et al. Surgical interventions (microfracture, drilling, mosaicplasty, and allograft transplantation) for treating isolated cartilage defects of the knee in adults. Cochrane Database Syst Rev. 2016;(9):CD010675. 7. Anderson DE, Rose MB, Wille AJ, et al. Arthroscopic mechanical chondroplasty of the knee is beneficial for treatment of focal cartilage lesions in the absence of concurrent pathology. Orthop J Sports Med. 2017;5(5):2325967117707213. 8. Alford JW, Cole BJ. Cartilage restoration, part 1: basic science, historical perspective, patient evaluation, and treatment options. Am J Sports Med. 2005;33(2):295–306. 9. Wydra FB, York PJ, Vidal AF. Allografts: osteochondral, shell, and paste. Clin Sports Med. 2017;36(3):509–523. 10. York PJ, Wydra FB, Belton ME, et al. Joint preservation techniques in orthopaedic surgery. Sports Health. 2017;9(6): 545–554. 11. Camp CL, Stuart MJ, Krych AJ. Current concepts of articular cartilage restoration techniques in the knee. Sports Health. 2014;6(3):265–273. 12. Sherman SL, Garrity J, Bauer K, et al. Fresh osteochondral allograft transplantation for the knee: current concepts. J Am Acad Orthop Surg. 2014;22(2):121–133. 13. Sherman SL, Thyssen E, Nuelle CW. Osteochondral autologous transplantation. Clin Sports Med. 2017;36(3):489–500. 14. Redler LH, Caldwell JM, Schulz BM, et al. Management of articular cartilage defects of the knee. Phys Sportsmed. 2012;40(1):20–35. 15. Behery O, Siston RA, Harris JD, et al. Treatment of cartilage defects of the knee: expanding on the existing algorithm. Clin J Sport Med. 2014;24(1):21–30. 16. Frank RM, Lee S, Levy D, et al. Osteochondral allograft transplantation of the knee: analysis of failures at 5 years. Am J Sports Med. 2017;45(4):864–874. 17. Familiari F, Cinque ME, Chahla J, et al. Clinical outcomes and failure rates of osteochondral allograft transplantation in the knee: a systematic review. Am J Sports Med. 2017;363546517732531. 18. Degen RM, Coleman NW, Tetreault D, et al. Outcomes of patellofemoral osteochondral lesions treated with structural grafts in patients older than 40 years. Cartilage. 2017;8(3): 255–262. 19. Krych AJ, Harnly HW, Rodeo SA, et al. Activity levels are higher after osteochondral autograft transfer mosaicplasty than after microfracture for articular cartilage defects of the knee: a retrospective comparative study. J Bone Joint Surg Am. 2012;94(11):971–978. 20. Werner BC, Cosgrove CT, Gilmore CJ, et al. Accelerated return to sport after osteochondral autograft plug transfer. Orthop J Sports Med. 2017;5(4):2325967117702418.

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21. Solheim E, Hegna J, Inderhaug E. Long-term clinical follow-up of microfracture versus mosaicplasty in articular cartilage defects of medial femoral condyle. Knee. 2017. 22. Pareek A, Reardon PJ, Macalena JA, et al. Osteochondral autograft transfer versus microfracture in the knee: a metaanalysis of prospective comparative studies at midterm. Arthroscopy. 2016;32(10):2118–2130. 23. Pareek A, Reardon PJ, Maak TG, et al. Long-term outcomes after osteochondral autograft transfer: a systematic review at mean follow-up of 10.2 years. Arthroscopy. 2016;32(6):1174–1184. 24. Hinckel BB, Gomoll AH. Autologous chondrocytes and next-generation matrix-based autologous chondrocyte implantation. Clin Sports Med. 2017;36(3):525–548. 25. Gille J, Behrens P, Schulz AP, et al. Matrix-associated autologous chondrocyte implantation: a clinical follow-up at 15 years. Cartilage. 2016;7(4):309–315. 26. Wondrasch B, Risberg MA, Zak L, et al. Effect of accelerated weightbearing after matrix-associated autologous chondrocyte implantation on the femoral condyle: a prospective, randomized controlled study presenting MRI-based and clinical outcomes after 5 years. Am J Sports Med. 2015;43(1):146–153. 27. Ebert JR, Smith A, Fallon M, et al. Incidence, degree, and development of graft hypertrophy 24 months after matrixinduced autologous chondrocyte implantation: association with clinical outcomes. Am J Sports Med. 2015;43(9):2208–2215. 28. Niethammer TR, Pietschmann MF, Horng A, et al. Graft hypertrophy of matrix-based autologous chondrocyte implantation: a two-year follow-up study of NOVOCART 3D implantation in the knee. Knee Surg Sports Traumatol Arthrosc. 2014;22(6):1329–1336. 29. Edwards PK, Ebert JR, Janes GC, et al. Arthroscopic versus open matrix-induced autologous chondrocyte implantation: results and implications for rehabilitation. J Sport Rehabil. 2014;23(3): 203–215. 30. Ebert JR, Smith A, Fallon M, et al. Degree of preoperative subchondral bone edema is not associated with pain and graft outcomes after matrix-induced autologous chondrocyte implantation. Am J Sports Med. 2014;42(11):2689–2698. 31. Brix MO, Stelzeneder D, Chiari C, et al. Treatment of fullthickness chondral defects with Hyalograft C in the knee: long-term results. Am J Sports Med. 2014;42(6):1426–1432. 32. Ebert JR, Smith A, Edwards PK, et al. Factors predictive of outcome 5 years after matrix-induced autologous chondrocyte implantation in the tibiofemoral joint. Am J Sports Med. 2013;41(6):1245–1254. 33. Ventura A, Memeo A, Borgo E, et al. Repair of osteochondral lesions in the knee by chondrocyte implantation using the MACI(R) technique. Knee Surg Sports Traumatol Arthrosc. 2012;20(1):121–126. 34. Crawford DC, DeBerardino TM, Williams RJ 3rd. NeoCart, an autologous cartilage tissue implant, compared with microfracture for treatment of distal femoral cartilage lesions: an FDA phase-II prospective, randomized clinical trial after two years. J Bone Joint Surg Am. 2012;94(11):979–989. 35. Schneider U, Rackwitz L, Andereya S, et al. A prospective multicenter study on the outcome of type I collagen hydrogelbased autologous chondrocyte implantation (CaReS) for the repair of articular cartilage defects in the knee. Am J Sports Med. 2011;39(12):2558–2565. 36. Ochs BG, Muller-Horvat C, Albrecht D, et al. Remodeling of articular cartilage and subchondral bone after bone grafting and matrix-associated autologous chondrocyte implantation for

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46. 47. 48.

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osteochondritis dissecans of the knee. Am J Sports Med. 2011;39(4):764–773. Ebert JR, Robertson WB, Woodhouse J, et al. Clinical and magnetic resonance imaging-based outcomes to 5 years after matrix-induced autologous chondrocyte implantation to address articular cartilage defects in the knee. Am J Sports Med. 2011;39(4):753–763. Zeifang F, Oberle D, Nierhoff C, et al. Autologous chondrocyte implantation using the original periosteum-cover technique versus matrix-associated autologous chondrocyte implantation: a randomized clinical trial. Am J Sports Med. 2010;38(5):924–933. Trattnig S, Pinker K, Krestan C, et al. Matrix-based autologous chondrocyte implantation for cartilage repair with HyalograftC: two-year follow-up by magnetic resonance imaging. Eur J Radiol. 2006;57(1):9–15. Behrens P, Bitter T, Kurz B, et al. Matrix-associated autologous chondrocyte transplantation/implantation (MACT/MACI)–5year follow-up. Knee. 2006;13(3):194–202. Johnson CC, Johnson DJ, Garcia GH, et al. High short-term failure rate associated with decellularized osteochondral allograft for treatment of knee cartilage lesions. Arthroscopy. 2017. Farr J, Gracitelli GC, Shah N, et al. High failure rate of a decellularized osteochondral allograft for the treatment of cartilage lesions. Am J Sports Med. 2016;44(8):2015–2022. Riboh JC, Cole BJ, Farr J. Particulated articular cartilage for symptomatic chondral defects of the knee. Curr Rev Musculoskelet Med. 2015;8(4):429–435. Stevens HY, Shockley BE, Willett NJ, et al. Particulated juvenile articular cartilage implantation in the knee: a 3-year EPICmicroCT and histological examination. Cartilage. 2014;5(2): 74–77. Buckwalter JA, Bowman GN, Albright JP, et al. Clinical outcomes of patellar chondral lesions treated with juvenile particulated cartilage allografts. Iowa Orthop J. 2014;34:44–49. Farr J, Cole BJ, Sherman S, et al. Particulated articular cartilage: CAIS and DeNovo NT. J Knee Surg. 2012;25(1):23–29. Farr J, Yao JQ. Chondral defect repair with particulated juvenile cartilage allograft. Cartilage. 2011;2(4):346–353. Fortier LA, Chapman HS, Pownder SL, et al. BioCartilage improves cartilage repair compared with microfracture alone in an equine model of full-thickness cartilage loss. Am J Sports Med. 2016;44(9):2366–2374. Hirahara AM, Mueller KW Jr. BioCartilage: a new biomaterial to treat chondral lesions. Sports Med Arthrosc. 2015;23(3):143–148. Frank RM, Cole BJ. Complex cartilage cases in the athletic patient: advances in the malalignment, articular defects, and meniscal insufficiency. Phys Sports Med. 2013;41(4):41–52. McCormick F, Harris JD, Abrams GD, et al. Trends in the surgical treatment of articular cartilage lesions in the United States: an analysis of a large private-payer database over a period of 8 years. Arthroscopy. 2014;30(2):222–226. Frisbie DD, Trotter GW, Powers BE, et al. Arthroscopic subchondral bone plate microfracture technique augments healing of large chondral defects in the radial carpal bone and medial femoral condyle of horses. Vet Surg. 1999;28(4):242–255. Steadman JR, Briggs KK, Rodrigo JJ, et al. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy. 2003;19(5):477–484. Steadman JR, Rodkey WG, Briggs KK. Microfracture to treat full-thickness chondral defects: surgical technique, rehabilitation, and outcomes. J Knee Surg. 2002;15(3):170–176.

55. Steadman JR, Rodkey WG, Briggs KK. Microfracture: its history and experience of the developing surgeon. Cartilage. 2010;1(2):78–86. 56. Steadman JR, Rodkey WG, Briggs KK, et al. The microfracture technique in the management of complete cartilage defects in the knee joint. Orthopade. 1999;28(1):26–32. 57. Steadman JR, Rodkey WG, Rodrigo JJ. Microfracture: surgical technique and rehabilitation to treat chondral defects. Clin Orthop Relat Res. 2001;(391 suppl):S362–S369. 58. Bark S, Piontek T, Behrens P, et al. Enhanced microfracture techniques in cartilage knee surgery: fact or fiction? World J Orthop. 2014;5(4):444–449. 59. Strauss EJ, Barker JU, Kercher JS, et al. Augmentation strategies following the microfracture technique for repair of focal chondral defects. Cartilage. 2010;1(2):145–152. 60. Benthien JP, Behrens P. Autologous matrix-induced chondrogenesis (AMIC). A one-step procedure for retropatellar articular resurfacing. Acta Orthop Belg. 2010;76(2):260–263. 61. Benthien JP, Behrens P. Autologous matrix-induced chondrogenesis (AMIC): combining microfracturing and a collagen I/III matrix for articular cartilage resurfacing. Cartilage. 2010;1(1):65–68. 62. Benthien JP, Behrens P. The treatment of chondral and osteochondral defects of the knee with autologous matrixinduced chondrogenesis (AMIC): method description and recent developments. Knee Surg Sports Traumatol Arthrosc. 2011;19(8):1316–1319. 63. Gille J, Behrens P, Volpi P, et al. Outcome of autologous matrix induced chondrogenesis (AMIC) in cartilage knee surgery: data of the AMIC Registry. Arch Orthop Trauma Surg. 2013;133(1): 87–93. 64. Gille J, Schuseil E, Wimmer J, et al. Mid-term results of autologous matrix-induced chondrogenesis for treatment of focal cartilage defects in the knee. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1456–1464. 65. Shive MS, Stanish WD, McCormack R, et al. BST-CarGel treatment maintains cartilage repair superiority over microfracture at 5 years in a multicenter randomized controlled trial. Cartilage. 2015;6(2):62–72. 66. Stanish WD, McCormack R, Forriol F, et al. Novel scaffold-based BST-CarGel treatment results in superior cartilage repair compared with microfracture in a randomized controlled trial. J Bone Joint Surg Am. 2013;95(18):1640–1650. 67. Trattnig S, Ohel K, Mlynarik V, et al. Morphological and compositional monitoring of a new cell-free cartilage repair hydrogel technology–GelrinC by MR using semi-quantitative MOCART scoring and quantitative T2 index and new zonal T2 index calculation. Osteoarthritis Cartilage. 2015;23(12): 2224–2232. 68. Gobbi A, Scotti C, Karnatzikos G, et al. One-step surgery with multipotent stem cells and hyaluronan-based scaffold for the treatment of full-thickness chondral defects of the knee in patients older than 45 years. Knee Surg Sports Traumatol Arthrosc. 2017;25(8):2494–2501. 69. Park YB, Ha CW, Lee CH, et al. Cartilage regeneration in osteoarthritic patients by a composite of allogeneic umbilical cord blood-derived mesenchymal stem cells and hyaluronate hydrogel: results from a clinical trial for safety and proof-ofconcept with 7 years of extended follow-up. Stem Cells Transl Med. 2017;6(2):613–621.

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98  Anterior Cruciate Ligament Injuries Edward C. Cheung, David R. McAllister, Frank A. Petrigliano

HISTORY The anatomy and injury of the anterior cruciate ligament (ACL) has been well-documented in history for centuries, but it was not until the mid-1800s that reports of surgical treatment of ACL injuries began to appear in surgical literature.1 Although there are some reports of success with early repair, surgeons realized that a more robust reconstruction was necessary to provide adequate knee stability. Ernest William Hey Groves was one of the first to report on ACL reconstruction in the early 1900s. He used a fascia lata graft placed through femoral and tibial tunnels and sutured it to the periosteum.2 Over time, Hey Groves’ original idea of intra-articular ACL reconstruction has evolved with a number of different simultaneous advancements, including early proponents of extra-articular reinforcements like that described by MacIntosh, which used an iliotibial band around the anterolateral aspect of the knee.3 Additional attempts to use synthetic grafts such as GORE-TEX or polypropylene were used in the early stages of ACL reconstruction. Due to high failure rates, stretching and fragmentation, resultant knee effusions, pain, and instability, these were quickly replaced by tendon autografts and allografts.1,4 With the development of fiber optics and miniature television cameras in the 1970s arthroscopic assisted ACL surgery became more mainstream.5 Initially, femoral and tibial tunnels were drilled independently through a two-incision technique, and the grafts were fixed on the anterior tibia and lateral femur. However, in the early 1990s, a single-incision ACL reconstruction in which the femoral tunnel was drilled through a tibial tunnel became popular. In some instances, this approach resulted in a relatively vertical femoral tunnel. As arthroscopic instrumentation and imaging modalities like computed tomography (CT) and magnetic resonance imaging (MRI) continued to improve, more biomechanics research was performed, and a heightened understanding of ACL anatomy and its influence on knee kinematics and stability showed that a femoral tunnel placed in the center of the native femoral footprint might convey a biomechanical advantage.6–8

ANATOMY AND BIOMECHANICS The ACL originates on the tibial articular surface, just lateral and anterior to the medial intercondylar spine. Proximally, it courses posteriorly as well as laterally and inserts on the posteromedial

wall of the lateral femoral condyle. Two functional bundles are present, the anteromedial (AM) and the posterolateral (PL), which are named for their tibial insertion sites (Fig. 98.1).8,9 The ACL provides rotational stability and resists anterior tibial translation, varus stress, and valgus stress.10 The position of the AM and PL bundles varies with flexion and extension of the knee. In extension, the AM and PL bundles are parallel, but as the knee flexes, the bundles cross and the PL bundle moves anteriorly. The AM bundle is tight in flexion and the PL bundle is tight in extension.11 The tibial origin of the ACL is oval and is approximately 136 mm2 in size. The femoral attachment is circular and spans an average area of 113 mm2. ACL fibers do not pass anterior to the cruciate ridge (also referred to as the lateral intercondylar ridge), which runs proximal to distal on the lateral femoral condyle.12,13 Indirect comparison from various studies suggests that ACL strength decreases with age.14 Under normal walking conditions, the ACL experiences forces of approximately 400 N, whereas passive knee motion only produces 100 N. High-level activities such as cutting, accelerating, and decelerating are estimated to produce forces up to 1700 N, which approaches the average maximal tensile strength of the ligament, 2160 ± 157 N.15 Despite this narrow window, the ACL works in concert with other stabilizing structures in the knee to resist translational force and rotational torque, and usually requires a high load to rupture.16 Many other structures in the knee can be injured in conjunction with an ACL rupture, including the menisci, collateral ligaments, articular cartilage, and joint capsule.17–19 Though a complete discussion of anatomic structures that influence and/or are affected by ACL injury is beyond the scope of this chapter, the anterolateral ligament (ALL) and the proximal tibial slope (PTS) deserve mention as both have gained newfound interest. Though the specific anatomic description of the ALL location varies slightly by author, the consensus is that it courses from the lateral femoral condyle to an area near the anterolateral meniscus.20–22 Human cadaveric and biomechanic studies show that the ALL contributes to internal rotatory stability of the knee.23–29 With the resurgence of interest in the anterolateral region of the knee, modifications of early extra-articular ACL reconstructions are being performed in conjunction with modern intra-articular ACL reconstructions, with mixed early results.30–33 Further study is needed to clarify if and when these reconstructions are appropriate.

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CHAPTER 98  Anterior Cruciate Ligament Injuries

Abstract

Keywords

Objective: To provide a thorough discussion of the history, anatomy, diagnosis and management, rehabilitation, and authors’ preferred technique of anterior cruciate ligament (ACL) injury and reconstruction. Methods: Recent literature from a literature search is used to support the evidence provided in this summary of information. Results: ACL reconstruction and its rehabilitation is an everevolving topic in sports medicine. Technological advances have improved operative techniques and improved the postoperative management of these injuries.

anterior cruciate ligament ACL knee ligament

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A

B

C

Fig. 98.1  Functional bundles of anterior cruciate ligament (ACL) in a cadaveric specimen. (A) The anterior view with the knee in 90 degrees of flexion. 1, The anteromedial bundle of the ACL; 2, the posterolateral bundle of the ACL; 3, the tibial insertion of the ACL; 4, the anterior horn of the lateral meniscus; 5, the posterior horn of the lateral meniscus; 6, the anterior horn of the medial meniscus; 7, the femoral insertion of the posterior cruciate ligament; 8, the anterior meniscofemoral ligament (Humphrey ligament); and 9, the femoral trochlear groove. (B) The anterior view of the intercondylar notch with the ACL midsubstance resected. 1, The ACL tibial footprint; 2, the ACL femoral stump; 3, the anterior horn of the lateral meniscus; 4, the body of the lateral meniscus; 5, the posterior horn of the lateral meniscus; 6, the lateral tibial spine; 7, the anterior horn of the medial meniscus; 8, the posterior horn of the medial meniscus; 9, the medial tibial spine; 10, the anterolateral bundle of the posterior cruciate ligament; 11, the posteromedial bundle of the posterior cruciate ligament; and 12, the anterior meniscofemoral ligament (Humphrey ligament). (C) The sagittal view of the intercondylar notch and ACL. 1, The ACL midsubstance; 2, the anteromedial bundle of the ACL; 3, the posterolateral bundle of the ACL; 4, the body of the lateral meniscus; 5, the anterior horn of the medial meniscus; 6, the medial tibial spine; 7, the medial wall of the lateral femoral condyle; and 8, the medial femoral condyle. (Copyright Pau Golanó.)

The bony morphology of the proximal tibia can also influence ACL injury. When the knee is axially loaded with an increased PTS, sheer forces are directed anteriorly, which place increased stress on the ACL.34–36 With the ACL being the main restraint to anterior translation, the increased PTS is thought to be an anatomic risk factor for injury. The influence of the medial and the lateral tibial slope is currently being investigated, with some studies showing that the medial slope has a greater influence,37 some showing that the lateral slope has a greater influence,34,38–40 and some showing no association with slope and ACL injury.41 More research is needed to more clearly define the role of tibial bony anatomy and its influence on ACL injury and ACL reconstruction.

BASIC SCIENCE Microanatomy The ACL is composed of longitudinal collagen fibrils that range in diameter from 20 to 170 µm. The fibrils are composed primarily of type I collagen but also contain type III collagen.42 They are arranged to form a unit called the subfascicular unit, which is surrounded by a layer of connective tissue called the endotendineum. These units combine to form the fasciculus,

which has an outer layer called the epitendineum. The fasciculus is ensheathed by the paratenon, forming the largest ligamentous unit. The microscopic architecture changes to a more fibrocartilaginous appearance near the bony attachments on the tibia and femur.43,44 The blood supply to the ACL comes primarily from branches of the middle geniculate artery and secondarily from branches of the inferior medial and lateral geniculate arteries, the infrapatellar fat pad, and synovium. The proximal portion of the ACL has better vascularity because the middle geniculate artery gives rise to ligamentous branches proximally and courses distally along the dorsal aspect of the ACL. The largest ligamentous branch is the tibial intercondylar artery, which arises proximally and bifurcates distally at the tibial spine to supply the tibial condyles.45,46 Nerve fibers have been found in all regions of the ACL. These fibers primarily run parallel with the vasculature in a longitudinal manner, but also incorporate freely into the connective tissue. The proximity of the nerve fibers and vasculature suggests a role in vasomotor control. However, the diameter of the nerve fibers in the connective tissue suggests a role in pain or reflex activity.46 This role is supported by findings of altered proprioception in patients with capsuloligamentous injury and partial restoration of this function with ligamentous reconstruction.47

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CHAPTER 98  Anterior Cruciate Ligament Injuries

Anterior Cruciate Ligament Biology The ACL is an intra-articular structure encased by a thin soft tissue envelope formed by the synovial lining. Rupture of the ligament usually causes disruption of this synovial lining and hematoma formation throughout the joint space with very little local reaction. Extra-articular ligaments, such as the medial collateral ligament (MCL), are contained within a robust soft tissue envelope. Injury to these ligaments causes formation of local hematoma and fibrinogen mesh that allows for invasion of inflammatory cells, resulting in healing with granulation tissue and eventually organized fibrous tissue.48

Epidemiology ACL injuries comprise 40% to 50% of all ligamentous knee injuries, primarily as a result of sporting activity.25,49 Injury to the ACL is most common in young athletes and disproportionally high in female athletes during their adolescent years.50 Sports in which athletes are particularly prone to ACL injury are skiing, soccer, basketball, and football.51 Over 70% of ACL injuries occur in noncontact situations.52 Some studies have shown that the maximum strain on the ACL occurs with the knee near extension and a valgus force applied with internal tibial rotation and anterior tibial translation.53 Females have a higher risk of ACL injury, which many have suggested is the result of difference in ACL geometry, pelvic tilt, generalized joint laxity, hormonal influences, and differences in muscle reaction time.54–56 However, the exact reasons are currently unknown. The number of ACL reconstructions has increased over the years. Currently, it is estimated that 200,000 ACL reconstructions are performed annually in the United States with a 5% to 15% failure rate.57,58 Failure can occur early or late, with early failure occurring within 6 months of reconstruction and late failure occurring after 6 months. Failure can be due to recurrent trauma, nonanatomic placement of tibial or femoral tunnels, and lack of graft incorporation.59

CLINICAL HISTORY A detailed patient history, including the injury mechanism and symptoms, is the first step in diagnosing an ACL rupture. The initial presentation often includes a history of a noncontact, low-velocity, twisting injury with or without an audible pop or snap and immediate knee swelling.60 Though many patients may be unable to recall the exact mechanism of injury, some studies have demonstrated that as high as one out of every two patients with an acute hemarthrosis has an ACL injury.61,62 A large proportion of patients with an ACL rupture experience immediate pain, swelling, and a feeling of instability. Most are unable to return to sport. A severe knee effusion soon after injury is an indication of an intra-articular pathology. Early arthroscopic studies demonstrated that nearly 75% of patients with acute hemarthrosis of the knee after injury had some degree of disruption of the ACL.62,63 Rupture of the ligament disrupts the blood supply and causes this hemarthrosis. Though a high proportion of hemarthroses can be attributed to ACL injuries, it is important to consider

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other intra-articular pathology such as meniscal or osteochondral injuries, fractures, or posterior cruciate ligament (PCL) ruptures. Additionally, the lack of a large hemarthrosis should not rule out an ACL injury.

PHYSICAL EXAMINATION Physical examination is very important in diagnosing an ACL injury. Together with the patient history, the physical examination can often provide enough information for a definitive diagnosis. It is critically important to examine both the affected and unaffected knee to get a baseline measure for each patient. Examining the unaffected knee first can calm the patient, set expectations, and help the patient to relax, which will be important when testing for ligamentous stability of the injured knee. Examination of an acutely injured knee should start with inspection. An effusion can be an obvious clue to injury. The patient’s skin should be examined for cuts or abrasions or bruising. The affected knee will often be held in flexion which can relieve intra-articular pressure due to a hemarthrosis. If several days or weeks have passed since the injury occurred, the quadriceps may be atrophied compared with the contralateral leg.64 Following inspection, examiners should palpate the knee for warmth, a more subtle effusion, crepitus, and local tenderness. A large majority of acutely injured knees have tenderness to palpation either medially, laterally, or on both sides.63 Local swelling or tenderness over the lateral or medial aspects of the knee suggests injury to the medial or lateral collateral ligament (MCL or LCL). Focal joint-line tenderness could indicate meniscal or chondral injury. Osteochondral injury or the presence of loose bodies may present with crepitus on knee range of motion (ROM) testing although this is rare with most ACL injuries.64 Knee ROM is often restricted in patients with acute ACL injuries. Apprehension and guarding are common, and physical examination findings can be more revealing after aspiration or local intra-articular injection.64 Although it is not commonly performed, aspiration can also provide clues to the diagnosis because a hemarthrosis suggests ligamentous injury, whereas the presence of fat globules suggests a bony injury. Both active and passive ROM should be tested to determine if there is injury to the extensor mechanism or if there is a mechanical block from a meniscal tear, loose body, or ACL fragment that is obstructing motion.

Ligamentous Laxity There are various physical exam maneuvers that can help examiners diagnose ACL injuries. The Lachman test for anterior laxity testing of the knee is performed by translating the tibia anteriorly while stabilizing the femur at 20 to 30 degrees of knee flexion. The anterior drawer test is performed at 90 degrees of knee flexion but is of little diagnostic value. In a recent meta-analysis comparing physical examination maneuvers in the diagnosis of ACL injuries with and without anesthesia, examination under anesthesia had a higher sensitivity than examination without anesthesia. Without anesthesia, the anterior drawer had a sensitivity and specificity of 38% and 81% compared to a sensitivity and specificity of 81% and 81% for the Lachman test.65 The ACL

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not only provides anterior stability, but also provides rotational stability for the knee. The pivot shift test is performed using a combination of valgus stress with rotatory and axial loading during knee flexion. A positive test is marked by a palpable clunk produced by reduction of the subluxed lateral tibial plateau by the iliotibial band as the knee moves from full extension into flexion.66 The sensitivity and specificity of the pivot shift test in diagnosing an ACL tear without anesthesia is 28% and 81%, and increases to 73% and 98% with anesthesia.65 In all circumstances (with or without anesthesia, and in the acute or chronic setting), a 2006 study showed that the Lachman test is the most reliable test when considering combined sensitivity and specificity.67 Instrumented testing systems such as the KT-1000 and the KT-2000 can be used as an adjunct to manual maneuvers like the Lachman and anterior drawer tests, but are not necessary to diagnose ACL ruptures. They have sensitivities and specificities at maximal manual force of 93% and 93%.65 These instrumented systems are most commonly used for research purposes.

IMAGING Imaging studies should include standard anterior-posterior and lateral radiographs of the knee. These images can help exclude associated injuries such as loose bodies, tibial eminence avulsion fractures in younger patients, degenerative changes, and acute fractures of the proximal tibia or distal femur. Radiographic evidence of a lateral proximal tibia fracture, commonly known as a Segond fracture, is pathognomonic for an ACL injury. Recent literature suggests that the Segond fracture is an avulsion of the ALL.20,22,68 MRI is the imaging gold standard for diagnosing an ACL injury because it is both highly sensitive and specific in detecting ACL tears (Fig. 98.2).69 The majority of ACL tears occur in the mid-substance of the ligament and are visualized on MRI as increased signal intensity with discontinuity of the ligamentous

Fig. 98.2  A sagittal magnetic resonance imaging scan of the anterior cruciate ligament showing complete rupture.

fibers. Hemarthrosis is common. The presence of a bone bruise is observed on MRI in 84% of patients with an ACL rupture, with the highest incidence on the lateral tibial plateau and lateral femoral condyle, at 73% and 68%, respectively. Additionally, the LCL, which is oblique in orientation and typically not visualized in its entirety, may be seen from its origin to insertion on a single coronal image. MRI is also useful for evaluating meniscal injury and osteochondral defects. In patients with ACL rupture, injury is observed to the menisci in 51% of patients with injury to the medial meniscus at a rate of 13.9%, to the lateral meniscus in 24.9% of patients, and injury to both menisci observed in 13.1% of patients.70 MCL injury is observed in 23% of patients with an ACL rupture.71–73

DECISION-MAKING PRINCIPLES Operative Versus Nonoperative Treatment The desired activity level of the patient must factor into the decision about whether to pursue nonoperative management of an ACL rupture or ACL reconstruction. The most common complaint of patients with a deficient ACL is recurrent instability, “giving way,” and difficulty with cutting sports.74 No large prospective trials have been conducted to demonstrate the natural history of ACL deficiency and the risk for further injury and osteoarthritis. There have been smaller studies showing that patients treated without ligament reconstruction after ACL tear have a higher risk of meniscal tears, arthritis, and knee arthroplasty compared to normal controls without ACL injury.75 In patients with ACL injuries treated operatively and nonoperatively, there is a lower risk of secondary meniscal injuries after ACL reconstruction compared to those patients managed conservatively.76 Although ACL reconstruction may protect the meniscus, it does not completely guard against rerupture, nor does it prevent subsequent osteoarthritis.77

Age Age is an important factor when considering treatment options for patients with ACL injuries. As reported in a cohort study looking at more than 21,000 patients undergoing primary ACL reconstruction, the 5-year risk of revision was 9% in patients less than 21 years of age, 8.3% in those between 20 and 40, and 1.9% in those greater than 40 years of age.78 The higher rate of revision may be due to the higher activity levels of younger patients. As youth become more active, there is an increasing frequency of ACL injuries in the skeletally immature. In New York state, one study showed that there has been a threefold increase in ACL reconstruction from 1990 to 2009 in patients less than 20 years old.50 Historically, skeletally immature patients with ACL injuries were treated nonoperatively. However, a better understanding of the risks of nonoperative management, along with the development of new techniques, has supported a trend for earlier surgical treatment of pediatric patients.79 Overall, patients between 20 and 40 years of age do well with ACL reconstructions. Though some argue that nonoperative means should be attempted first,80 many have attempted to categorize patients with ACL injuries into the copers and the

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noncopers. Those who are unable to return to high-level sporting activities, or those with symptomatic instability are those who are categorized as noncopers. Those who are able to return to sport and activity are categorized as copers.81 The success of ACL reconstruction is age independent, with 91% of patients older than 40 years reporting excellent or good results at 2-year follow-up, compared with 89% for patients younger than 40 years.82 Nonoperative management with activity modification produces good to excellent results in 57% of patients older than 40 years.82 Older patients often have more social and professional obligations that may prevent them from proceeding with ACL reconstruction and successfully completing a rehabilitation program, which highlights the importance of stratifying patients by activity level to determine the indication for ACL reconstruction. The use of an allograft instead of an autograft in the older population decreases morbidity and has been shown to produce comparable results.83 Ultimately, physiologic age and activity level seem to be more important than chronologic age when deciding between operative and nonoperative management.

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instability. Options for conservative management include rehabilitation, focusing on hamstring (HS) strengthening, activity modification, and brace wear during activity. Proposed operative treatments include augmentation, partial (selective) ACL reconstruction, or traditional ACL reconstruction.94 Well-designed prospective clinical trials are needed to accurately compare treatment regimens for partial ACL injuries.

Associated Injuries

Female athletes are at a two- to eightfold greater risk for ACL injury compared with their male counterparts.84 Many studies have looked at high school and collegiate athletes in soccer, basketball, and volleyball. The majority of injuries occurred as a result of noncontact mechanisms, which led to investigation and speculation about gender differences that can account for this significant disparity.85,86 Possible etiologies have centered on hormonal and neuromuscular differences, environmental conditions, and differences in anatomy, such as alignment or joint laxity.87 Anatomic differences that have been evaluated include Q angle, the size and shape of the intercondylar notch, the size of the ACL, material properties of the ACL, foot pronation, body mass index, and generalized ligament laxity.88 None of these differences alone places females at a greater risk of ACL injury. A study of West Point cadets produced a logistic regression model that could predict risk for noncontact ACL injury in 75% of cases, based on anatomic characteristics such as a narrow femoral notch, a high body mass index, and generalized joint laxity.89 Some studies have shown that hormonal changes during the menstrual cycle affect the material and mechanical properties of the ACL, which could make it more vulnerable to injury during specific phases of the cycle.90 However, this effect has not been shown definitively and requires further investigation.91

Rupture of the ACL can be associated with injury to other structures in the knee, including the medial and lateral menisci, MCL and LCL, chondral surfaces, PL corner structures, and fracture of the distal femur and/or proximal tibia.95 Many years ago, the phrase “unhappy triad” was coined by O’Donoghue to refer to the constellation of ACL rupture, MCL injury, and tearing of the medial meniscus.17 Subsequent studies have shown that lateral meniscal tears are equally common with ACL rupture.73 A recent review demonstrates that increased time from injury to ACL reconstruction increases the risk of intra-articular pathology, which included the trochlea, lateral femoral condyle, medial tibial plateau, and meniscus across all age ranges included.96 Therefore surgical timing should be considered when deciding to pursue operative reconstruction to reduce associated injuries. All associated meniscus injuries should be evaluated individually to form an overall management plan. There is some evidence that stable lateral meniscus tears, or partial thickness lateral meniscus tears, may respond particularly well to nonoperative management.97–99 Injury to the medial meniscus should be addressed aggressively, and it has been shown that repair of stable peripheral tears decreases the risk of postoperative pain and the need for subsequent partial meniscectomy.62 MCL injuries are common in the setting of ACL rupture, occurring in approximately 23% of cases.73 A consensus of ACL reconstruction and nonsurgical management of grade I and II MCL injuries is accepted; however, there is controversy in the management of grade III MCL injuries in the setting of ACL injury.100 It was previously thought that high-grade MCL injuries may need to be treated operatively in the setting of ACL rupture. However, recent data have shown that nonoperative bracing of MCL injuries after ACL reconstruction results in equivalent clinical outcome as tested by anterior tibial displacement, function, participation in sporting activities, strength, and one-leg–hop testing.101 However, in some persons with severe combined ligamentous injuries, MCL repair may be indicated, and there is no consensus on the timing of surgical management or reconstruction of the MCL in relation to the ACL.102

Partial Anterior Cruciate Ligament Tears

Revision Anterior Cruciate Ligament

Diagnosis of a partial ACL tear can be challenging and requires close evaluation of the history, physical examination, and MRI findings. The gold standard for diagnosis is arthroscopy.92 Partial tears comprise 10% to 28% of all ACL tears, and if left untreated, 42% will proceed to complete rupture. In addition, a large majority of patients with partial tears are unable to return to their preinjury activity level.93 Decision-making regarding treatment of partial ACL tears should include evaluation of the patient’s desired activity level, the degree of laxity, and symptomatic

As the number of ACL reconstructions increases, so does the total number of failures. These failures can typically be categorized as biologic, technical, or traumatic. The majority of failures in the past were due to technical errors, such as improper graft placement, inadequate notchplasty, inadequate graft fixation, improper graft tensioning, use of a graft with inadequate tensile strength, or failure to correct other causes of instability in the knee.103 However, more recent data have shown that traumatic reinjury, which occurs in 32% of patients, is the primary mode

Gender

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of failure.104 The technical approach to revision ACL reconstruction has been refined during the past 10 to 20 years; however, the results of revision surgery are worse than those for primary reconstruction.105,106 The risk of chondral damage in the lateral compartment and patellofemoral space is increased with revision ACL reconstruction.107 Moreover, risk of chondral lesions at revision reconstruction increases in the presence of a previous partial meniscectomy.108 Patients must be counseled regarding the limitations of revision surgery and the potential for future failures.

TREATMENT OPTIONS Nonoperative Options In a 2016 Cochrane review analyzing current research comparing operative and nonoperative treatment of ACL injuries, the authors concluded that there was insufficient evidence to recommend ACL reconstruction based on patient-reported outcomes alone.109 Some authors in the past have advocated for conservative treatment in lower demand patients.110 Others have tried to determine if patients will be copers or noncopers to help guide treatment.74 Conservative management can lead to recurrent instability and meniscal injury in athletes.111,112 For this reason, ACL reconstruction is recommended in patients who are active, have symptomatic instability, have failed conservative management, or require the ability to cut or pivot during physical activity. Persons older than 40 years can do well with a conservative training program but should be advised that a return to their previous activity level is unlikely.113 Patients should not make a decision whether or not to pursue surgical management based on their age alone, because studies have shown equivalent outcomes in patients younger and older than 40 years.114,115 In a randomized controlled trial of young, active adults, early reconstruction versus rehabilitation with the option of delayed reconstruction was evaluated. Patients undergoing delayed reconstruction had outcomes similar to those receiving early reconstruction, and the majority of patients assigned to the rehabilitation group elected to continue with nonoperative management.116

Operative Options Timing The timing of when to reconstruct ACL injuries has been debated in the past, with many studies recommending delayed reconstruction as some patients are able to cope with their injuries with rehabilitation.74 Additionally, some have argued that there is a risk of arthrofibrosis with early reconstruction within the first month.117,118 If postoperative stiffness occurs, loss of terminal extension is the primary difficulty encountered, and patient satisfaction is greatly influenced by stiffness and restricted ROM.119 Patients who have an effusion, swelling, inflammation, and stiffness beyond 4 weeks after the injury was sustained, and who undergo ACL reconstruction, have an equal likelihood of experiencing arthrofibrosis, suggesting that it is the amount of effusion, stiffness, and inflammation present at the time of surgery that results in an increased risk of the development of arthrofibrosis.120 The risk of arthrofibrosis with early treatment is concerning, with one study suggesting that operative treatment should wait

for 2 to 6 weeks when motion returns.121 Preoperative loss of motion has a significant correlation with postoperative loss of motion. Sixty-seven percent of patients who have restricted ROM after surgery had limited ROM at the time of reconstruction.117 Other studies have argued for early reconstruction. They cite cost savings and improved quality adjusted life years (QALYs) with early reconstruction within 10 weeks of injury, compared to rehabilitation and optional delayed reconstruction.122 Additionally, a meta-analysis of the current literature found no difference in knee stiffness when reconstruction was performed between 1 and 20 weeks.123 We believe that the best approach is to allow time for the swelling to resolve and wait for the patient to regain good preoperative ROM prior to surgery. The amount of time for this to occur varies considerably from patient to patient.

Graft Selection When choosing the appropriate graft for ACL reconstruction, it is important that the graft exhibits material properties similar to the native ACL, allows for secure fixation, incorporates into the bone tunnels, and limits donor-site morbidity.124,125 All autografts including bone patellar tendon bone (BPTB), quadruple HS, and quadriceps tendon (QT) have greater tensile strength and stiffness compared with the native ACL.126,127 This also holds true for BPTB allografts. Synthetic devices are no longer used in the United States because of an unacceptably high rate of complications, including failure and persistent effusion.128 HS and BPTB autografts are popular, but the choice of graft should be discussed with the patient. It has been shown that though there is no clear consensus on the “best” graft, there are advantages and disadvantages of each, and ultimately, patients rely heavily on their surgeons to guide their decision on a graft choice.129 The first step in decision-making is choosing between an autograft and an allograft. An autograft incorporates into bone earlier, matures more rapidly, and avoids the risk of a host immune reaction, as well as disease transmission. Conversely, the use of an allograft is associated with less morbidity and requires a shorter surgical time.130,131 A meta-analysis of BPTB autografts versus allografts showed that patients treated with an autograft had a lower incidence of graft rupture and performed better on hop testing. However, return to preinjury activity level and a decrease in anterior knee pain were significantly in favor of allografts.132 In the same study, there was a three-fold increase in failure of BPTB allografts compared to autografts. Patients who underwent allograft reconstruction more commonly reported a final International Knee Documentation Committee (IKDC) score of A (normal knee). However, if a good result was defined as an IKDC score of A or B, no difference existed between the groups.133 Recent evidence suggests a higher failure rate of ACL allografts in young, active patients.134 A retrospective cohort study found that patients 25 years and younger undergoing ACL reconstruction had a 29.2% failure rate with allograft tissue compared with an 11.8% failure rate with BPTB autografts.135 Patients in a large, young, active cohort, comprised of members of the United States Military Academy, were more likely to experience clinical failure if they underwent ACL reconstruction with allograft.136

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Sterilization and preservation techniques can alter allograft tissue structure. Allografts sterilized with radiation or ethylene oxide are significantly weakened. The current technique of cryopreservation maintain the biomechanical properties of tendon allografts.137,138 Disease transmission from tendon allografts has been reported, but the incidence is infrequent, occurring on average in less than one patient per year. Stringent guidelines have almost eliminated the risk of hepatitis C or human immunodeficiency virus (HIV), but there is still a theoretical risk of transmission. These risks fall between 1 in 173,000 and 1 in 1 million for HIV and approximately 1 in 421,000 for hepatitis C.139 A few reports of bacterial infection from donor grafts have been reported in the past 10 years.140 A large retrospective cohort examining greater than 1400 patients demonstrated no difference in infection between BPTB allograft or autograft with an infection risk of 0.5% and 0.6%. For HS autografts, there was an infection risk of 2.5%, which was higher than HS allograft.141 BPTB and HS tissues are most commonly used for ACL reconstruction. There are advantages and disadvantages to each graft choice. Numerous studies have compared BPTB and HS autografts and have found that BPTB autograft has a greater improvement of instability symptoms than HS autograft, without differences in clinical knee scores,142–145 or rate of failure.143,145–147 The use of the patellar tendon is not without potential complication. Compared to the HS group, greater number of patients in the BPTB group reported anterior knee pain (17.4% vs. 11.5%) and required manipulation under anesthesia for lysis of adhesions (6.3% vs. 3.3%).148 Additionally, the risk of patellar tendon rupture, patellar fracture, and quadriceps weakness is increased with a BPTB autograft. The morbidity with HS autograft includes pain from hardware prominence or HS weakness. There is a higher rate of hardware removal (5.5% vs. 3.1%) for HS autografts versus BPTB, and though there is increased HS weakness associated with HS autograft, this weakness generally resolves within 1 year.148,149 A systematic review of current literature found that no single graft source is clearly superior to others.150 There may be early postoperative anterior knee pain with BPTB autograft, and early ROM limitations,151 but at long-term follow-up, there do not appear to be differences in patient ROM or osteoarthritis compared to HS autografts. Those patients with BPTB were more likely to be participating in sport on a weekly basis compared to HS autograft patients.152 QT has been proposed as another source of autograft tissue. Recently, there has been some resurgence in interest in QT grafts. In a survey of orthopaedic surgeons, only 1% of orthopaedic surgeons utilize the QT for ACL reconstruction.153 Biomechanically, QT autograft has been shown to be equivalent to quadrupled HS tendon.154 When compared to BPTB, early results show equal postoperative laxity with a KT-1000, less anterior knee pain, and less loss of sensation. At 1 to 2 years follow-up, there were no differences in IKDC scores.155 A systematic review of the literature on QT autograft versus other graft options and showed similar outcomes in terms of patient satisfaction, Lachman, pivot shift, instrumented laxity, and IKDC scores, with less donor site morbidity with QT autograft.156 We prefer using autografts rather than allografts in most patients having an index procedure because of the lower failure

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rate with autografts and the slight risk of disease transmission with allografts. Our preferred choice for an autograft in patients who place a high demand on their knees is BPTB because of earlier incorporation of the bone plugs into the tibial and femoral tunnels and excellent clinical results. We reserve the use of allografts for patients who place a lower demand on their knees, in the revision setting, or in cases of specific patient preference.

Graft Harvest Harvesting of each type of tendon provides unique technical challenges. Patellar tendon autografts require harvesting bone from the patella and tibial tubercle, which can increase the risk of fracture and damage the articular cartilage of the patella.124 Many surgeons prefer repairing the paratenon to improve glide and prevent scarring to the overlying tissue.157 HS harvest requires elevating the sartorius to access the semitendinosus and gracilis and can put the superficial branch of the saphenous nerve at risk. Amputating the tendon prematurely during the harvest is also a risk. The QT is another autograft option.124 If bone QT is taken, there is a risk of patella fracture as well as possible quadriceps rupture. Graft Tension and Fixation Graft tension is influenced by the amount of force placed on the graft, as well as the amount of knee flexion and rotation. The graft needs enough tension to stabilize the knee, but too much tension can stretch the graft and lead to failure of the graft itself or failure of fixation. It has also been suggested that grafts should be preconditioned prior to implantation to prevent creep. There has been cadaveric research examining the effect of multiple pretensioning protocols, but none have shown superiority, with pretensioning ranging from 80 to 500 N.158 Previously, cadaveric studies have advocated for pretensioning between 40 and 60 N.159,160 It has been shown that physicians are unable to reproduce the same graft tension utilizing a one-handed pull, and that intra-articular graft tension is different than extraarticular graft tension.161,162 There is disagreement as to whether pretensioning the graft has an effect on knee laxity after ACL reconstruction.163,164 Some authors recommend providing tension with the knee in full extension, whereas other authors argue that it is best to provide tension with the knee in 20 to 30 degrees of flexion.165 Evaluation of outcome is complicated because most surgeons provide tension manually and in various knee positions, so comparison between studies is difficult. Graft-tensioning boots are used by some surgeons because they eliminate the need for manual provision of tension and allow the surgeon to use both hands for tibial fixation. Further trials are required to provide more comprehensive data regarding provision of graft tension. Graft fixation should be strong enough to withstand closedchain exercises for at least 12 weeks until the bone or tendon is able to incorporate into the bone tunnels. Closed-chain exercises produce on average 200 N of force but can produce up to 500 N of force.166 Poor fixation can cause the graft to slip or the fixation to fail altogether.166 Interference screw fixation of patellar bone blocks has the highest stiffness and fixation strength, ranging from 423 N to 558 N. Screw placement parallel to the bone block

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is optimal for maximum pull-out strength, whereas divergence greater than 30 degrees has increased risk of failure from pullout.167 Screw diameter and length also influence fixation strength.168,169 The use of tibial dilators has no effect on fixation strength, nor does the use of bioabsorbable instead of metallic screws.170,171 Many graft fixation devices are commercially available. Softtissue grafts can be secured with use of interference screws, suture posts, screw and washer constructs, and staples on the tibial side. Similar fixation can be used on the femoral side in addition to cross-pins and buttons.124 Cross-pins, screw and washer constructs, and buttons all provide indirect fixation, meaning the graft is suspended within the bony tunnel. All others provide direct fixation, which compresses the graft against the side of the bone tunnel. It should be noted that the clinical implications of most biomechanical fixation pull-out studies are limited because they were performed on porcine and bovine specimens at time zero.

Graft Healing A successful ACL reconstruction relies on incorporation of the graft into the surrounding bone, as well as ligamentization and revascularization of the graft. Bone-to-bone healing is stronger and faster than soft tissue healing to bone. BPTB allografts and autografts heal in a process similar to fracture healing.124 With soft-tissue grafts, the tendon takes 12 weeks to incorporate into the surrounding bone through remodeling of a cellular and fibrous layer formed at the tendon-bone interface. At 12 weeks, collagen fibers form an attachment to bone that resembles Sharpey fibers.172 At 12 months after ACL reconstruction, all histologic markers of ligamentization and revascularization, including fiber pattern, cellularity, and degree of metaplasia, resemble those of a native ACL. Vascularity and fiber pattern demonstrate no maturation after 6 months, suggesting that tendon autografts may be mature enough at 6 months to proceed with more aggressive rehabilitation and possible return to sport.173 Patellar tendon autografts incorporate faster than allografts and have stronger mechanical properties at 6 months. Allografts have a prolonged inflammatory response, decreased strength, and a slower rate of incorporation and tissue remodeling at the 6-month time point.130

Extra-Articular Augmentation There have long been discussions regarding contributions to extra-articular structure for secondary rotatory stability of the knee. The iliotibial band has historically been proposed, and Segond in 1897 discussed a “pearly fibrous resistant band” that was under tension in severe internal rotation.174 Claes suggested that the classic avulsion of the proximal lateral tibial plateau is actually an avulsion of the bony attachment of the ALL in 2014.68 Since then, there has been a recent resurgence of interest in the anterolateral capsule of the knee or ALL providing secondary external rotatory stability in the knee. Though there have been various anatomic descriptions in the literature, an expert consensus group has decided that (1) the ALL is a distinct ligament on the anterolateral side of the knee, (2) that the femoral attachment is posterior and proximal to the lateral epicondyle, (3) that the tibial attachment lies between Gerdy’s tubercle and the fibular

head, and (4) that the ALL has a constant attachment to the lateral meniscus.25 Biomechanical and clinical studies have shown that the anterolateral structures of the knee provide significant secondary rotatory stability and when ruptured lead to a higher pivot shift grade.26,27,175 Various methods of ALL reconstruction have been described.30,176,177 Some authors argue for concomitant ALL and ACL reconstruction in selective patients. Though there is an increased interest in the ALL and its role in rotatory stability of the knee in the setting of ACL injury, more definitive evidence is needed to determine how to select patients that could benefit most from combined ALL and ACL reconstruction.

Role of Tibial Slope The role of tibial slope on the risk of ACL injury has gained increased popularity in the literature.36,178,179 Though there is some debate in biomechanical studies about the effect of increased tibial slope on anterior tibial translation, it appears that increased tibial slope leads to increased anterior tibial translation, which places more strain on the ACL.34,36 Clinical studies suggest that increased posterior tibial slope is a risk factor for ACL rupture and rerupture after reconstruction.39,180,181 There has been some suggestion regarding proximal tibial osteotomy in combination with ACL reconstruction in the setting of a previously failed ACL reconstruction,182,183 but further research is needed to better examine the efficacy of these procedures and how to best select patients.

Revision Options Determining the cause of failure is the key to successful revision ACL reconstruction. Physicians and patients should discuss the expected outcomes and the anticipated postoperative activity levels. Planning for a revision ACL reconstruction should involve all the steps of a primary reconstruction, including evaluation for associated injuries. In addition, thought should be given to correcting any technical error from the primary surgery and graft selection for revision. The same graft options in primary ACL reconstruction exist for revision surgery, although reharvesting previously harvested graft tissue is not advised. In one recent study, it was reported that only 54% of patients returned to their preinjury activity level after revision surgery.184 Patellar tendon autografts and allografts used for revision ACL reconstruction have produced equivalent clinical results and ligamentous stability on arthrometer testing.185 Overall, revision ACL reconstruction should be viewed largely as a salvage procedure, and patients should be aware that they may never return to their preinjury function and activity level.

POSTOPERATIVE MANAGEMENT Rehabilitation Advancements in surgical technique and graft fixation have enabled patients to participate in early postoperative rehabilitation, focusing on ROM and progressing to patellar mobilization and strengthening. Patients can bear weight on the affected limb immediately. Early weight bearing and rehabilitation do not compromise ligamentous stability and result in a lower incidence of anterior knee pain compared with non–weight bearing.188,189

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Authors’ Preferred Technique Primary Anterior Cruciate Ligament Reconstruction A single-bundle ACL reconstruction uses one large graft that is fixed in place at the insertion site of the ACL on the tibia and femur (the so-called footprints of the ACL).

the tibial bone plug. Heavy nonabsorbable suture is loaded onto a Keith needle and passed through each hole. The bone-tendon junction is marked with a sterile marker to allow for visualization during graft passage. The tendinous portion of the graft is measured with a sterile ruler.

Positioning and Setup The patient is positioned supine on the operating table. After administration of an appropriate anesthetic, both the operative and uninvolved legs are examined, including ROM and anterior drawer, Lachman, and pivot-shift tests. Special attention is given to varus, valgus, and posterolateral instability because those structures are not assessed arthroscopically. A post is placed proximally and laterally against the thigh to allow for valgus stress on the knee and visualization of the medial compartment.

Portal Placement and Diagnostic Arthroscopy The AM, anterolateral, and superolateral arthroscopic portals are established. The suprapatellar pouch, patellofemoral joint, medial and lateral gutters, medial and lateral compartments, and femoral notch (Fig. 98.6) are evaluated for concomitant intra-articular pathology. Meniscal injuries in the poorly vascularized white zone are débrided. Meniscal tears in the red-red or red-white zones are repaired whenever possible using an inside-out or all-inside technique.

Graft Harvest If examination of the anesthetized patient confirms the diagnosis of an ACL tear, we proceed directly to harvesting of the graft. We most commonly use a BPTB autograft. The incision is marked 1 cm medial to the inferior pole of the patella, extending longitudinally 1 cm medial to the tibial tubercle (Fig. 98.3). The skin is incised and sharp dissection is carried down through the skin and subcutaneous tissue to the level of the patellar tendon paratenon. The paratenon is incised at the midline and separated from the underlying tendon with use of a scalpel. The knee is slightly flexed and a scalpel is used to harvest the central portion (usually 9 to 10 mm) of the patellar tendon. An oscillating saw is used to make the bone cut on the tibial side. Our goal is to make the tibial bone plug 20 to 25 mm in length and trapezoidal in shape, which is achieved by making a cut perpendicular to the surface of the bone medially and a lateral cut that is angled 20 degrees toward the medial cut. The distal cut is made last, and the bone plug is extracted by hand with use of a 0.5-inch curved osteotome (Fig. 98.4). The knee is then placed into extension with the inferior two thirds of the patella exposed. The patellar bone cut should be 20 to 25 mm in length and triangular in shape, which is achieved by making medial and lateral bone cuts angled 45 degrees from the bone surface with an oscillating saw. The cuts should be made to a depth of 10 to 12 mm and should meet, allowing for easy extraction. Graft Preparation The bone plugs are shaped to fit into a 10-mm tunnel, and any excess bone is reduced to morsels for bone grafting of the patellar defect (Fig. 98.5). Because loss of fixation is more likely in the tibial tunnel, the patellar bone plug (which has a denser architecture) is placed into the tibial tunnel to maximize purchase with the interference screw. Two perpendicular 2-mm drill holes are made at the distal one third of the patellar bone plug, and two drill holes are placed in

Fig. 98.3  Superolateral, anteromedial, and anterolateral portal sites and the patellar tendon graft incision.

Fig. 98.4  Harvesting of the patellar tendon.

Fig. 98.5  Sizing of the patellar tendon autograft.

Fig. 98.6  The arthroscopic view of a torn anterior cruciate ligament. Continued

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Authors’ Preferred Technique—cont’d Tunnel Placement The precise positions for both femoral and tibial tunnel placement remain a matter of debate. The definition of an “anatomic reconstruction” has not been consistently described, and accordingly, we avoid this nomenclature. However, the available literature suggests that (1) the graft should be placed in an oblique position to resist rotational laxity and (2) the femoral and tibial tunnels should be placed within the native footprint of the ACL to achieve this goal.186 We typically use a motorized shaver to débride the torn ACL down to the footprint on both the femur and tibia. A small portion of the footprint is left intact to permit identification of the native ACL origin and insertion. Enough tissue should be débrided from the lateral and superior aspects of the notch to allow for visualization of the over-the-top position (Fig. 98.7). A motorized burr is used to perform a small notchplasty as needed to prevent impingement of the graft and to visualize the periosteum on the posterior aspect of the lateral condyle. The center of the femoral footprint is then marked with an awl or curette. This position is typically 6 to 7 mm anterior to the back wall and midway between the lateral edge of the PCL and the articular cartilage of the lateral femoral condyle. The angle on the tibial drill guide is set to N+7, in which N is the length (mm) of the tendinous portion of the graft.187 The guide arm is oriented so the path of the guide pin points from the ACL footprint on the tibia to the footprint on the lateral condyle of the femur. The drill should penetrate the center of the tibial footprint, which is typically located in line with the posterior aspect of the anterior horn of the lateral meniscus (Fig. 98.8). The length of the tunnel is measured from the tibial drill guide and should be at least 2 mm longer than the

Fig. 98.7  An anteromedial guidewire placed in the center of the femoral anterior cruciate ligament footprint.

Fig. 98.8  The tibial footprint of the anterior cruciate ligament (ACL). The insertion of the ACL remains as a guide for positioning of the tibial tunnel.

soft tissue portion of the tendon graft based on the N+2 rule if using a BPTB graft.115 If the proposed tunnel length is too short, it can be lengthened by increasing the angle on the guide. After the proper tibial tunnel length is confirmed, the guidewire is advanced and the tibial tunnel is created with use of a cannulated drill. A large curette is used to control the guide pin and protect the articular cartilage during drilling. The reamings are collected and used later for bone grafting of the patellar defect. A rasp is used to smooth out the surface of the tibial tunnel, and a shaver is used to remove soft tissue around the tibial tunnel entrance. A Beath pin is placed through the tibial tunnel and directed toward the previously marked spot at the center of the femoral footprint. The pin is advanced through the femur and out the anterolateral thigh. This maneuver is referred to as the transtibial technique because the femoral tunnel is established through the tibial tunnel. A cannulated reamer is advanced to a depth of 10 mm and the posterior wall is visualized to confirm adequate positioning and bone tunnel integrity (Fig. 98.9). If the tunnel position is adequate, the tunnel is drilled to a depth of 30 mm. In some cases, it is not possible to reach the appropriate position in the femoral notch via a transtibial approach. In these cases, the femoral tunnel can be drilled through the AM portal with a straight reamer or flexible reamer system. Commercially available flexible reamers permit reaming through the AM portal with knee flexion of 100 to 110 degrees. When using a flexible reamer system, a flexible guidewire is introduced through the AM portal with a cannulated guide to position the guidewire in a superior and lateral position prior to advancing the wire into the femoral footprint and out the anterolateral thigh. A flexible 10-mm reamer is placed over the guidewire under direct visualization to avoid damaging the medial femoral condyle. Another approach to achieving the appropriate position of the femoral tunnel is to use a straight reamer introduced through an AM portal. In these cases, it is important to hyperflex the knee during femoral tunnel reaming to avoid creating a short tunnel or violating the back wall of the femoral tunnel. Finally, an outside-in or two-incision technique can be used to ream the femoral tunnel. In these instances, a femoral aiming guide is placed through a second incision over the anterolateral femur and reamed from outside-in. Graft Placement and Fixation If the femoral tunnel was made transtibially, the eyelet of the pin is loaded with the suture from the graft and the graft is gently pulled into the femoral and tibial tunnels. If the femoral tunnel was created via AM portal reaming, a suture is placed through the eyelet of the guide pin and the pin is passed through the femoral tunnel. A probe is used to retrieve the suture loop through the tibial tunnel. Suture on the tibial tubercle bone plug (intended for the femoral tunnel) is placed through the loop of suture and the graft is passed through the tunnels. When an AM reaming portal is used, the femoral bone plug is often shortened

Fig. 98.9  The intact back wall after flexible anteromedial reaming.

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Authors’ Preferred Technique—cont’d to 20 mm to facilitate passage of the graft through the acute angle between the tibial and femoral tunnels. The bone plug is then oriented in the femoral tunnel with the cancellous side facing anteriorly. The bone plug is left slightly proud on the articular surface to allow for placement of the interference screw guidewire. A guidewire is introduced through the AM portal and placed anteriorly between the graft and tunnel (Fig. 98.10). The graft is advanced so it is flush with the surrounding bone and a 7 × 20-mm or 25-mm cannulated metal interference screw is inserted over the guidewire (Fig. 98.11). The interference screw should be flush with the bone block, and care should be taken to avoid damaging the tendon with the threads of the screw. The knee should be ranged under visualization to evaluate for impingement of the graft on the femoral notch.

Fig. 98.10  Tibial bone block docking in the femoral tunnel. A guidewire is placed for later interference screw fixation.

A survey conducted by the American Orthopaedic Society for Sports Medicine reported that 63% of surgeons who perform ACL reconstructions use functional bracing postoperatively.190 The advantage of bracing is that it can improve patient confidence, reduce tibiofemoral motion by normalizing translational, rotatory, and valgus loads across the knee.191 The potential disadvantages are that it can cause altered gait if worn inappropriately, there is an increased risk for muscle atrophy, and braces have increased cost.192–194 A 2007 systematic review of level 1 randomized controlled trials found no evidence that braces provided added benefit to postoperative recovery.195 A 2017 systematic review of the literature looking at level I and II trials as well as a retrospective comparative study demonstrated mixed results. Some studies demonstrated improved knee kinematics and gait with bracing, with decreased quadriceps activation and ROM, while others showed no differences between those with and without braces.196 There is no definitive evidence if functional bracing is beneficial in the immediate postoperative period. The goal during rehabilitation in the early postoperative period is to preserve full extension and work on gaining 10 degrees of flexion every day. Several systematic reviews have demonstrated moderate evidence that there is no added benefit to a continuous passive motion (CPM) machine.197,198 Though a CPM machine can be used to supplement early active and passive ROM, although we do not routinely use this machine.

The knee is cycled 10 times with approximately 10 lb of tension with use of the sutures in the distal bone plug to create tension. The graft should tighten (shorten) over the terminal 30 degrees of each cycle. Tibial fixation is performed with the knee in 0 to 30 degrees of flexion. Grafts fixed closer to extension will avoid excessive tension on the graft in extension. A guidewire is placed between the bone plug and tunnel wall. Manual tension should be maintained while a 9 × 20-mm or 25-mm tibial interference screw is placed over the guidewire. We do not apply a posterior drawer force on the proximal tibia during fixation. The Lachman test is performed to ensure adequate fixation and elimination of anterior laxity.

Fig. 98.11  Femoral interference screw placement.

Muscle Training (Open and Closed Kinetic Chain) Quadriceps strength correlates with functional stability and correlates with self-reported function of the knee postoperatively and has been the focus of many postoperative training programs.199,200 However, biomechanical studies of quadriceps and HS contraction showed that HS contraction decreases strain on the ACL through a posterior force on the proximal tibia during knee flexion.201 Analysis of forces during knee flexion showed that force of contraction between the quadriceps and HS is balanced at a flexion angle of 22 degrees. At flexion angles greater than 22 degrees, the quadriceps, HS, and gastrocnemius muscle groups work together to unload the ACL.202 Debate in postoperative rehabilitation protocols has focused on open versus closed kinetic chain exercises. In the early postoperative period, closed-chain exercises are thought to be safer than open-chain exercises. Closed kinetic chain exercises are performed with the foot fixed in place in constant contact with the ground. Examples of closed kinetic chain exercises are squats and the leg press, which require activation of multiple muscle groups for stabilization and also distribute ground reaction force to all lower limb joints (Fig. 98.12A). During open kinetic chain exercises, such as leg extension, the limb is free to move and the joint reactive force is focused on the knee (Fig. 98.12B). In a study by Kvist and Gillquist, it was found that tibial translation

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A

B Fig. 98.12  Closed-chain (A) and open-chain (B) kinetic exercises after anterior cruciate ligament reconstruction.

is less in closed-chain exercises (between 10 and 40 degrees of knee flexion) but is greater at knee flexion greater than 70 degrees. These investigators also found that squats with the center of gravity behind the feet result in the least amount of tibial translation.203 A prospective randomized trial of patients participating in open versus closed kinetic chain exercises after ACL reconstruction showed superior results with closed-chain exercises. Early results show that open-chain exercises lead to a 9% increase in laxity compared to closed-chain exercises.204 Another prospective randomized controlled trial showed that compared to an open-chain group, patients performing closed-chain exercises postoperatively had greater knee stability, less patellofemoral pain, and greater overall satisfaction and return to activity. Ninetyfive percent of patients in both groups regained full ROM.205 Other reviews of current literature suggest that a combination of open and closed kinetic chain exercises should be considered, especially in patients who require strengthening of the quadriceps muscle. Some show no difference in laxity, pain, and function after open- and close-chained rehabilitation.206 Proponents of integrating open-chain exercises argue that the exercises can be modified to minimize strain on the ACL and decrease stress on the patellofemoral joint.201 Functional outcomes are similar in patients participating in open versus closed kinetic chain exercises in the first 2 to 6 weeks after surgery.207 However, patients who participate in open kinetic chain exercises plus closed kinetic chain exercises starting 6 weeks after surgery increase their quadriceps torque and return to sports 2 months earlier compared with patients who performed closed-chain exercises alone.208 The literature supports a combination of closed- and open-chain rehabilitation, but the timing of each exercise during the postoperative period is not yet defined.

gait pattern and stronger quadriceps muscle activity.209 A review of eight randomized controlled trials found that neuromuscular electrical stimulation may be more effective than exercise alone in restoring quadriceps strength after ACL reconstruction. The effect on functional performance was inconclusive, and overall analysis was complicated by inconsistencies in electrical stimulation protocols.210 Muscle strength depends on neural signaling, motor unit activation, and muscle contraction. Although electrical stimulation addresses muscle contraction, it does not require initiation of the movement or a sustained effort by the patient to maintain muscle contraction. Electromyographic biofeedback has been used to help patients monitor the quality of muscle contraction during a voluntary contraction. This modality is more effective than electrical stimulation in restoring peak torque in the quadriceps extensor mechanism after ACL reconstruction.211 The importance of proprioception has been described by several studies that have examined the neural anatomy of the ACL and how disruption of the sensory system can lead to decreased functional stability. Johansson and colleagues212 showed that the ACL has a sensory system and mechanoreceptors that detect stretching at moderate loads, which signals to modify muscular stiffness around the knee. Knee proprioception is impaired for 6 to 12 months after ACL reconstruction, and improved proprioception correlates well with improved functional outcome and patient satisfaction after surgery.213,214 These findings suggest that restoring mechanical stability alone is insufficient for optimizing functional outcome. Because proprioception does not return for up to 1 year after reconstruction, patients should incorporate proprioception training exercises throughout the rehabilitation process.

Electrical Stimulation, Biofeedback, and Proprioception

Functional Training

The use of electrical stimulation in the rehabilitation protocol is controversial because it has not produced consistent results. However, all studies have shown that it is safe, and when combined with volitional exercises, it can result in a more normal

Rehabilitation programs have advanced to incorporate proprioception and neuromuscular control. Focus is placed on ankle, knee, and hip ROM, functional exercises to re-establish confidence, working on form, posture and dynamic joint stability, resistance, sensorimotor training, and neuromuscular training.215

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In addition to restoring basic proprioception, it is important to emphasize neuromuscular control when the dynamic stabilizers are fatigued, especially in athletes, who require endurance and muscle stabilization at the end of exercise. Sensorimotor training places patients on uneven surfaces in a controlled manner to help regain muscle reaction and provide more stability. Lowresistance exercises such as stair climbing, cycling, use of an elliptical machine, and slide boards are safe repetitive activities that can be used at the end of a training session to encourage dynamic stabilization.216

Techniques to Limit Pain and Swelling Cryotherapy has been used to lower the temperature of the knee joint and surrounding tissue, which can provide pain relief and shorten the recovery period after ACL reconstruction. Improved pain relief allows for more aggressive early rehabilitation, which is thought to result in better long-term results.217 However, a meta-analysis of all studies on cryotherapy showed that it is effective for pain control but does not influence long-term outcome.218 Martimbianco compared outcomes for cryotherapy versus ice pack, no treatment, or placebo and demonstrated that cryotherapy is better at controlling pain postoperatively than placebo in the immediate postoperative period.219

Rehabilitation Protocol Our patients who undergo primary and revision ACL reconstruction are allowed to bear weight on the surgical extremity with crutches after surgery with a hinged knee brace locked in extension. Physical therapy begins immediately, with an initial emphasis on ROM and progressive patellar mobilization and strengthening. Use of the brace is discontinued 1 to 2 weeks after surgery. Stationary cycling begins when the patient is out of the brace. Associated meniscal injuries that were repaired at the time of ACL reconstruction do not change the rehabilitation program. Studies have shown that no difference exists in the failure rate of meniscal repair in patients who underwent ACL reconstruction and immediate postoperative rehabilitation compared with the published rate for meniscal repair alone.220

Return to Play No standard or objective criteria are currently available to determine when a patient is ready to return to competitive sport or unrestricted activity after ACL reconstruction. In a systematic review looking at return to play (RTP) criteria, Harris et al. demonstrated that 40% to 65% of articles included did not have specific criteria for RTP.221 In a meta-analysis, Ardern et al. demonstrated that 81% to 82%, 63% to 65% and 44% to 55% of patients following ACL reconstruction returned to any sport, previous level of competition and competitive sports, respectively.222 Historically, a major consideration to deciding when to return to sport was the amount of time since ACL reconstruction. There has been a movement towards more specific criteria and functional testing to determine RTP criteria. Some suggestions have included quadriceps size, patient-reported outcome measures, single-leg stance and hop tests, and sport specific tests.223 To date, there is no consensus on a standard RTP criteria.

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With our patients, if ROM, strength, and balance have returned, we allow patients to begin running in a straight line at 3 months after surgery and return to full sport without restrictions 8 to 9 months after surgery.

RESULTS Good overall results have been achieved with ACL reconstruction using BPTB and HS grafts. Patient satisfaction rates are greater than 90%, and 95% of patients report normal to near-normal knee function at long-term follow-up.224

Graft Type Current level I evidence from randomized controlled trials shows no overall difference in outcome between BPTB and quadrupled HS grafts in postoperative laxity, clinical outcome, return to sport, one-leg–hop test, ROM, anterior knee sensory deficit, patellofemoral crepitus, osteoarthritis, or thigh muscle circumference.149 A systematic review of patients after ACL reconstruction found greater anterior knee pain and kneeling pain in the BPTB group but equivalent patient-recorded outcomes and clinical assessments in both groups.149,225

Single Versus Double Bundle It is currently unclear if the native ACL bundles function independently of one another. Double-bundle reconstruction has been advocated by some authors because it more closely mimics the normal anatomy of the ACL. However, clinical studies of conventional anatomic single-bundle and anatomic double-bundle ACL reconstruction have shown mixed results. Some studies have shown increased rotatory laxity on pivot-shift examination after single-bundle reconstruction but no difference in clinical outcome, return to sports, or functionality between the singlebundle and double-bundle groups.149 Other studies have shown no difference in anterior laxity or rotatory stability in patients treated with double-bundle versus single-bundle reconstruction.226,227 Most studies have failed to show a difference in clinical outcome as measured by Lysholm scores, IKDC scores, or other outcome measures.228,229 Therefore further randomized studies are required to show superiority of the double-bundle repair.

Complications The most severe complications of ACL reconstruction are infection and graft failure. Fortunately, infection is rare occurring between 0.3% and 1.7% of the time.230 The graft failure rate is around 5% and is generally due to improper tunnel placement, repeat traumatic rupture, or failure to diagnose concurrent injuries to other structures in the knee.231 Loss of ROM is the most common complication and can be minimized by regaining full ROM prior to surgery and being diligent with postoperative rehabilitation under supervision.232 Patellar fracture and patellar tendon rupture can occur with BPTB autograft reconstruction but are rare occurrences. Between 30% and 50% of patients report anterior knee pain with BPTB reconstruction.233 However, the pain improves with time and usually does not prevent highlevel athletic activity.222 Injury to the saphenous nerve is a concern with harvesting of the HS and can result in decreased sensation

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but is rarely a concern in the long term.234 Osteoarthritis develops in many patients who rupture their ACL, but evidence is lacking to show that ACL reconstruction protects patients from the development of osteoarthritis. Tunnel widening is a known radiographic complication of ACL reconstruction. Two separate studies of patients who underwent ACL reconstruction with HS versus BPTB showed a significant increase in tibial and femoral tunnel diameters in the HS group, although the two groups had similar clinical outcomes.235

methods, rehabilitation advancements, outcomes of operative and nonoperative treatments, and complications related to surgical reconstruction.

Citation: Beynnon BD, Johnson RJ, Abate JA, et al. Treatment of anterior cruciate ligament injuries, part 1. Am J Sports Med. 2005;33(10): 1579–1602.

Level of Evidence: III, retrospective cohort

Summary:

FUTURE CONSIDERATIONS Soft-tissue grafts have a slower rate of healing and incorporate into the bone tunnel later than bone grafts (BPTB). Many techniques for accelerating the healing process have been explored, including the use of growth factors, mesenchymal stem cells (MSCs), and periosteum augmentation. Platelet-derived growth factor and transforming growth factor β-1 have shown some promise in increasing the density of collagen fibrils.236,237 Bone morphogenic protein-2 has been used to accelerate bone growth around the graft.238 Periosteum has been used to enhance soft tissue and bone-graft incorporation into the surrounding bone tunnel. A prospective clinical trial using HS autograft enveloped with autologous periosteum found decreased femoral tunnel widening after reconstruction.239 With the popularity of platelet rich protein (PRP), there is increased interest to see if it could have a role in ACL healing and graft incorporation. A recent systematic review demonstrated that there is still a paucity of clinical trials looking at the effect of PRP on clinical outcomes, bone-graft integration, and prevention of bone tunnel enlargement.240 Attempts have also been made to create ligaments in vitro through tissue engineering. However, further efforts are required to make this process a reality. A study by Vavken and colleagues demonstrated comparable biomechanical results with bioenhanced ACL repair using a collagen-platelet composite compared with ACL reconstruction in a large animal model.241 However, this technique is still under investigation and has not been introduced into clinical practice. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS

The authors of this article provide a review of the current knowledge regarding anterior cruciate ligament (ACL) injuries, focusing on biomechanics of the ACL, prevalence of injury and risk factors, natural history of ACL-deficient knees, associated injuries, indications for treatment, and management.

Citation: Beynnon BD, Johnson RJ, Abate JA, et al. Treatment of anterior cruciate ligament injuries, part 2. Am J Sports Med. 2005;33(11): 1751–1767.

Level of Evidence: III, retrospective cohort

Summary: The authors of this article provide a review of the technical aspects of anterior cruciate ligament reconstruction, bone tunnel widening, graft healing, rehabilitation, and the effect of age, sex, and activity level on outcome.

Citation: Maletis GB, Chen J, Inacio MC, et al. Increased risk of revision after anterior cruciate ligament reconstruction with bone-patellar tendon-bone allografts compared with autografts. Am J Sports Med. 2017;363546517690386.

Level of Evidence: III, retrospective cohort

Summary: The authors of this article examine a large anterior cruciate ligament (ACL) registry and identify risk of revision surgery after an ACL reconstruction with bone patellar tendon bone (BPTB) autografts versus BPTB allografts. They find that BPTB allografts have a 4.5 times higher risk of revision compared to BPTB autograft.

Citation:

Citation: Anderson MJ, Browning WM 3rd, Urband CE, et al. A systematic summary of systematic reviews on the topic of the anterior cruciate ligament. Orthop J Sports Med. 2016;4(3): 2325967116634074.

Level of Evidence:

Bottoni CR, Smith EL, Shaha J, et al. Autograft versus allograft anterior cruciate ligament reconstruction: a prospective, randomized clinical study with a minimum 10-year follow-up. Am J Sports Med. 2015;43(10):2501–2509.

Level of Evidence: I, randomized controlled trial

Summary:

IV, systematic review

Summary: A comprehensive review of the anterior cruciate ligament (ACL) literature. The authors discuss ACL anatomy, epidemiology of ACL injuries, prevention strategies, associated injuries, the diagnosis of ACL injuries, operative versus nonoperative treatment, graft choice, surgical techniques including fixation

Ninety-nine active military patients were randomized to hamstring autograft versus tibialis posterior allograft anterior cruciate ligament (ACL) reconstruction and followed for 10 years. There were 4 autograft and 13 allograft failures. The authors conclude that at a minimum of 10 years following ACL reconstruction, 80% of all grafts were intact with good stability, but allografts failed at a rate 3 times higher than autografts.

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110. Buss DD, Min R, Skyhar M, et al. Nonoperative treatment of acute anterior cruciate ligament injuries in a selected group of patients. Am J Sports Med. 1995;23(2):160–165. 111. Nebelung W, Wuschech H. Thirty-five years of follow-up of anterior cruciate ligament—deficient knees in high-level athletes. Arthroscopy. 2005;21(6):696–702. 112. Kennedy J, Jackson MP, O’Kelly P, et al. Timing of reconstruction of the anterior cruciate ligament in athletes and the incidence of secondary pathology within the knee. J Bone Joint Surg Br. 2010;92(3):362–366. 113. Ciccotti MG, Lombardo SJ, Nonweiler B, et al. Non-operative treatment of ruptures of the anterior cruciate ligament in middle-aged patients. Results after long-term follow-up. J Bone Joint Surg Am. 1994;76(9):1315–1321. 114. Barrett G. Anterior cruciate ligament reconstruction in patients older than 40 years: allograft versus autograft patellar tendon. Am J Sports Med. 2005;33(10):1505–1512. 115. Mall NA, Frank RM, Saltzman BM, et al. Results after anterior cruciate ligament reconstruction in patients older than 40 years: how do they compare with younger patients? A systematic review and comparison with younger populations. Sports Health. 2016;8(2):177–181. 116. Frobell RB, Roos EM, Roos HP, et al. A randomized trial of treatment for acute anterior cruciate ligament tears. N Engl J Med. 2010;363(4):331–342. 117. Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction? Reasons and outcome. Arch Orthop Trauma Surg. 2004;124(8):518–522. 118. Almekinders LC, Moore T, Freedman D, et al. Post-operative problems following anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 1995;3(2):78–82. 119. Kocher MS, Steadman JR, Briggs K, et al. Determinants of patient satisfaction with outcome after anterior cruciate ligament reconstruction. J Bone Joint Surg Am. 2002;84(9):1560–1572. 120. Noyes FR, Mangine RE, Barber SD. The early treatment of motion complications after reconstruction of the anterior cruciate ligament. Clin Orthop Relat Res. 1992;277:217–228. 121. Frank CB, Jackson DW. Current concepts review–the science of reconstruction of the anterior cruciate ligament. J Bone Joint Surg Am. 1997;79(10):1556–1576. 122. Mather RC 3rd, Hettrich CM, Dunn WR, et al. Costeffectiveness analysis of early reconstruction versus rehabilitation and delayed reconstruction for anterior cruciate ligament tears. Am J Sports Med. 2014;42(7):1583–1591. 123. Kwok CS, Harrison T, Servant C. The optimal timing for anterior cruciate ligament reconstruction with respect to the risk of postoperative stiffness. Arthroscopy. 2013;29(3): 556–565. 124. West RV, Harner CD. Graft selection in anterior cruciate ligament reconstruction. J Am Acad Orthop Surg. 2005;13(3): 197–207. 125. Mehran N, Moutzouros VB, Bedi A. A review of current graft options for anterior cruciate ligament reconstruction. JBJS Rev. 2015;3(11). 126. Pailhe R, Cavaignac E, Murgier J, et al. Biomechanical study of ACL reconstruction grafts. J Orthop Res. 2015;33(8):1188–1196. 127. Hamner DL, Brown CH Jr, Steiner ME, et al. Hamstring tendon grafts for reconstruction of the anterior cruciate ligament: biomechanical evaluation of the use of multiple strands and tensioning techniques. J Bone Joint Surg Am. 1999;81(4):549–557.

128. McPherson GK, Mendenhall HV, Gibbons DF, et al. Experimental mechanical and histologic evaluation of the Kennedy ligament augmentation device. Clin Orthop Relat Res. 1985;(196):186–195. 129. Salminen M, Kraeutler MJ, Freedman KB, et al. Choosing a graft for anterior cruciate ligament reconstruction: surgeon influence reigns supreme. Am J Orthop. 2016;45(4): E192–E197. 130. Jackson DW, Grood ES, Goldstein JD, et al. A comparison of patellar tendon autograft and allograft used for anterior cruciate ligament reconstruction in the goat model. Am J Sports Med. 1993;21(2):176–185. 131. Sachs RA, Daniel DM, Stone ML, et al. Patellofemoral problems after anterior cruciate ligament reconstruction. Am J Sports Med. 1989;17(6):760–765. 132. Kraeutler MJ, Bravman JT, McCarty EC. Bone-patellar tendon-bone autograft versus allograft in outcomes of anterior cruciate ligament reconstruction: a meta-analysis of 5182 patients. Am J Sports Med. 2013;41(10):2439–2448. 133. Foster TE, Wolfe BL, Ryan S, et al. Does the graft source really matter in the outcome of patients undergoing anterior cruciate ligament reconstruction? An evaluation of autograft versus allograft reconstruction results: a systematic review. Am J Sports Med. 2010;38(1):189–199. 134. Kane PW, Wascher J, Dodson CC, et al. Anterior cruciate ligament reconstruction with bone-patellar tendon-bone autograft versus allograft in skeletally mature patients aged 25 years or younger. Knee Surg Sports Traumatol Arthrosc. 2016;24(11):3627–3633. 135. Barrett AM, Craft JA, Replogle WH, et al. Anterior cruciate ligament graft failure: a comparison of graft type based on age and Tegner activity level. Am J Sports Med. 2011;39(10): 2194–2198. 136. Pallis M, Svoboda SJ, Cameron KL, et al. Survival comparison of allograft and autograft anterior cruciate ligament reconstruction at the United States Military Academy. Am J Sports Med. 2012;40(6):1242–1246. 137. Smith CW, Young IS, Kearney JN. Mechanical properties of tendons: changes with sterilization and preservation. J Biomech Eng. 1996;118(1):56. 138. Jackson DW, Windler GE, Simon TM. Intraarticular reaction associated with the use of freeze-dried, ethylene oxide-sterilized bone-patella tendon-bone allografts in the reconstruction of the anterior cruciate ligament. Am J Sports Med. 1990;18(1): 1–11. 139. McAllister DR, Joyce MJ, Mann BJ, et al. Allograft update: the current status of tissue regulation, procurement, processing, and sterilization. Am J Sports Med. 2007;35(12):2148–2158. 140. From the Centers for Disease Control and Prevention. Update: allograft-associated bacterial infections–United States, 2002. JAMA. 2002;287(13):1642–1644. 141. Murphy MV, Du DT, Hua W, et al. Risk factors for surgical site infections following anterior cruciate ligament reconstruction. Infect Control Hosp Epidemiol. 2016;37(7):827–833. 142. Biau DJ, Tournoux C, Katsahian S, et al. ACL reconstruction: a meta-analysis of functional scores. Clin Orthop Relat Res. 2007;458:180–187. 143. Forster MC, Forster IW. Patellar tendon or four-strand hamstring? A systematic review of autografts for anterior cruciate ligament reconstruction. Knee. 2005;12(3):225–230. 144. Herrington L, Wrapson C, Matthews M, et al. Anterior cruciate ligament reconstruction, hamstring versus bone-patella

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ACL reconstruction. Clin Biomech (Bristol, Avon). 2005;20(6):636–644. O’Neill BJ, Byrne FJ, Hirpara KM, et al. Anterior cruciate ligament graft tensioning. Is the maximal sustained onehanded pull technique reproducible? BMC Res Notes. 2011;4:244. Nishizawa Y, Hoshino Y, Nagamune K, et al. Comparison between intra- and extra-articular tension of the graft during fixation in anterior cruciate ligament reconstruction. Arthroscopy. 2017. Boguszewski DV, Joshi NB, Wang D, et al. Effect of different preconditioning protocols on anterior knee laxity after ACL reconstruction with four commonly used grafts. J Bone Joint Surg Am. 2015;97(13):1059–1066. Lockwood WC, Marchetti DC, Dahl KD, et al. High-load preconditioning of human soft tissue hamstring grafts: an in vitro biomechanical analysis. Knee Surg Sports Traumatol Arthrosc. 2017;25(1):138–143. Heis FT, Paulos LE. Tensioning of the anterior cruciate ligament graft. Orthop Clin North Am. 2002;33(4):697–700. Frank CB, Jackson DW. The science of reconstruction of the anterior cruciate ligament. J Bone Joint Surg Am. 1997;79(10): 1556–1576. Lemos MJ, Jackson DW, Lee TQ, et al. Assessment of initial fixation of endoscopic interference femoral screws with divergent and parallel placement. Arthroscopy. 1995;11(1): 37–41. Butler JC, Branch TP, Hutton WC. Optimal graft fixation—The effect of gap size and screw size on bone plug fixation in ACL reconstruction. Arthroscopy. 1994;10(5):524–529. Selby JB, Johnson DL, Hester P, et al. Effect of screw length on bioabsorbable interference screw fixation in a tibial bone tunnel. Am J Sports Med. 2001;29(5):614–619. Kousa P, Jarvinen TL, Vihavainen M, et al. The fixation strength of six hamstring tendon graft fixation devices in anterior cruciate ligament reconstruction. Part II: tibial site. Am J Sports Med. 2003;31(2):182–188. Nurmi JT, Jarvinen TL, Kannus P, et al. Compaction versus extraction drilling for fixation of the hamstring tendon graft in anterior cruciate ligament reconstruction. Am J Sports Med. 2002;30(2):167–173. Rodeo SA, Arnoczky SP, Torzilli PA, et al. Tendon-healing in a bone tunnel. A biomechanical and histological study in the dog. J Bone Joint Surg Am. 1993;75(12):1795–1803. Falconiero RP, DiStefano VJ, Cook TM. Revascularization and ligamentization of autogenous anterior cruciate ligament grafts in humans. Arthroscopy. 1998;14(2):197–205. Segond P. Recherches cliniques et experimentales sur les epanchements sanguins du genou par entorse. Progres Medical. 7:297–299, 319–321, 340–341. Song GY, Zhang H, Wu G, et al. Patients with high-grade pivot-shift phenomenon are associated with higher prevalence of anterolateral ligament injury after acute anterior cruciate ligament injuries. Knee Surg Sports Traumatol Arthrosc. 2017. Chahla J, Menge TJ, Mitchell JJ, et al. Anterolateral ligament reconstruction technique: an anatomic-based approach. Arthrosc Tech. 2016;5(3):e453–e457. Sonnery-Cottet B, Barbosa NC, Tuteja S, et al. Minimally invasive anterolateral ligament reconstruction in the setting of anterior cruciate ligament injury. Arthrosc Tech. 2016;5(1): e211–e215.

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178. Hendrix ST, Barrett AM, Chrea B, et al. Relationship between posterior-inferior tibial slope and bilateral noncontact ACL injury. Orthopedics. 2017;40(1):e136–e140. 179. Wang YL, Yang T, Zeng C, et al. Association between tibial plateau slopes and anterior cruciate ligament injury: a meta-analysis. Arthroscopy. 2017. 180. Hohmann E, Bryant A, Reaburn P, et al. Does posterior tibial slope influence knee functionality in the anterior cruciate ligament-deficient and anterior cruciate ligament-reconstructed knee? Arthroscopy. 2010;26(11):1496–1502. 181. Feucht MJ, Mauro CS, Brucker PU, et al. The role of the tibial slope in sustaining and treating anterior cruciate ligament injuries. Knee Surg Sports Traumatol Arthrosc. 2013;21(1): 134–145. 182. Dejour D, Saffarini M, Demey G, et al. Tibial slope correction combined with second revision ACL produces good knee stability and prevents graft rupture. Knee Surg Sports Traumatol Arthrosc. 2015;23(10):2846–2852. 183. Sonnery-Cottet B, Mogos S, Thaunat M, et al. Proximal tibial anterior closing wedge osteotomy in repeat revision of anterior cruciate ligament reconstruction. Am J Sports Med. 2014;42(8): 1873–1880. 184. Uribe JW, Hechtman KS, Zvijac JE, et al. Revision anterior cruciate ligament surgery: experience from Miami. Clin Orthop Relat Res. 1996;325:91–99. 185. Noyes FR, Barber-Westin SD. Revision anterior cruciate ligament surgery: experience from Cincinnati. Clin Orthop Relat Res. 1996;325:116–129. 186. Pearle AD, McAllister D, Howell SM. Rationale for strategic graft placement in anterior cruciate ligament reconstruction: I.D.E.A.L. femoral tunnel position. Am J Orthop. 2015;44(6): 253–258. 187. Miller MMD, Hinkin LCDT. The “N + 7 Rule” for tibial tunnel placement in endoscopic anterior cruciate ligament reconstruction. Arthroscopy. 1996;12(1):124–126. 188. Shelbourne KD, Nitz P. Accelerated rehabilitation after anterior cruciate ligament reconstruction. Am J Sports Med. 1990;18(3): 292–299. 189. Tyler TF, McHugh MP, Gleim GW, et al. The effect of immediate weightbearing after anterior cruciate ligament reconstruction. Clin Orthop Relat Res. 1998;357:141–148. 190. Delay BS, Smolinski RJ, Wind WM, et al. Current practices and opinions in ACL reconstruction and rehabilitation: results of a survey of the American Orthopaedic Society for Sports Medicine. Am J Knee Surg. 2001;14(2):85–91. 191. Beynnon BD, Fleming BC, Churchill DL, et al. The effect of anterior cruciate ligament deficiency and functional bracing on translation of the tibia relative to the femur during nonweightbearing and weightbearing. Am J Sports Med. 2003;31(1):99–105. 192. Deppen RJ, Landfried MJ. Efficacy of prophylactic knee bracing in high school football players. J Orthop Sports Phys Ther. 1994;20(5):243–246. 193. Risberg MA, Holm I, Steen H, et al. The effect of knee bracing after anterior cruciate ligament reconstruction. A prospective, randomized study with two years’ follow-up. Am J Sports Med. 1999;27(1):76–83. 194. Smith SD, Laprade RF, Jansson KS, et al. Functional bracing of ACL injuries: current state and future directions. Knee Surg Sports Traumatol Arthrosc. 2014;22(5):1131–1141. 195. Wright RW, Fetzer GB. Bracing after ACL reconstruction: a systematic review. Clin Orthop Relat Res. 2007;455:162–168.

196. Lowe WR, Warth RJ, Davis EP, et al. Functional bracing after anterior cruciate ligament reconstruction: a systematic review. J Am Acad Orthop Surg. 2017;25(3):239–249. 197. Kruse LM, Gray B, Wright RW. Rehabilitation after anterior cruciate ligament reconstruction: a systematic review. J Bone Joint Surg Am. 2012;94(19):1737–1748. 198. Lobb R, Tumilty S, Claydon LS. A review of systematic reviews on anterior cruciate ligament reconstruction rehabilitation. Phys Ther Sport. 2012;13(4):270–278. 199. Blackburn JT, Pietrosimone B, Harkey MS, et al. Quadriceps function and gait kinetics after anterior cruciate ligament reconstruction. Med Sci Sports Exerc. 2016;48(9):1664–1670. 200. Pietrosimone B, Lepley AS, Harkey MS, et al. Quadriceps Strength predicts self-reported function post-ACL reconstruction. Med Sci Sports Exerc. 2016;48(9):1671–1677. 201. Biscarini A, Benvenuti P, Botti FM, et al. Voluntary enhanced cocontraction of hamstring muscles during open kinetic chain leg extension exercise: its potential unloading effect on the anterior cruciate ligament. Am J Sports Med. 2014;42(9): 2103–2112. 202. O’Connor JJ. Can muscle co-contraction protect knee ligaments after injury or repair? J Bone Joint Surg Br. 1993;75(1):41–48. 203. Kvist J, Gillquist J. Sagittal plane knee translation and electromyographic activity during closed and open kinetic chain exercises in anterior cruciate ligament-deficient patients and control subjects. Am J Sports Med. 2001;29(1):72–82. 204. Morrissey MC, Hudson ZL, Drechsler WI, et al. Effects of open versus closed kinetic chain training on knee laxity in the early period after anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2000;8(6):343–348. 205. Bynum EB, Barrack RL, Alexander AH. Open versus closed chain kinetic exercises after anterior cruciate ligament reconstruction: a prospective randomized study. Am J Sports Med. 1995;23(4):401–406. 206. Glass R, Waddell J, Hoogenboom B. The effects of open versus closed kinetic chain exercises on patients with ACL deficient or reconstructed knees: a systematic review. N Am J Sports Phys Ther. 2010;5(2):74–84. 207. Hooper DM, Morrissey MC, Drechsler W, et al. Open and closed kinetic chain exercises in the early period after anterior cruciate ligament reconstruction. Improvements in level walking, stair ascent, and stair descent. Am J Sports Med. 2001;29(2):167–174. 208. Mikkelsen C, Werner S, Eriksson E. Closed kinetic chain alone compared to combined open and closed kinetic chain exercises for quadriceps strengthening after anterior cruciate ligament reconstruction with respect to return to sports: a prospective matched follow-up study. Knee Surg Sports Traumatol Arthrosc. 2000;8(6):337–342. 209. Snyder-Mackler L, Ladin Z, Schepsis AA, et al. Electrical stimulation of the thigh muscles after reconstruction of the anterior cruciate ligament. Clin J Sport Med. 1992;2(3):227. 210. Kim K-M, Croy T, Hertel J, et al. Effects of neuromuscular electrical stimulation after anterior cruciate ligament reconstruction on quadriceps strength, function, and patientoriented outcomes: a systematic review. J Orthop Sports Phys Ther. 2010;40(7):383–391. 211. Draper V, Ballard L. Electrical stimulation versus electromyographic biofeedback in the recovery of quadriceps femoris muscle function following anterior cruciate ligament surgery. Phys Ther. 1991;71(6):455–461.

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CHAPTER 98  Anterior Cruciate Ligament Injuries 212. Johansson H, Sjolander P, Sojka P. A sensory role for the cruciate ligaments. Clin Orthop Relat Res. 1991;268:161–178. 213. Co FH, Skinner HB, Cannon WD. Effect of reconstruction of the anterior cruciate ligament on proprioception of the knee and the heel strike transient. J Orthop Res. 1993;11(5):696–704. 214. Barrett DS. Proprioception and function after anterior cruciate reconstruction. J Bone Joint Surg Br. 1991;73(5):833–837. 215. Nyland J, Brand E, Fisher B. Update on rehabilitation following ACL reconstruction. Open Access J Sports Med. 2010;1:151–166. 216. Grant JA. Updating recommendations for rehabilitation after ACL reconstruction: a review. Clin J Sport Med. 2013;23(6): 501–502. 217. Ohkoshi Y, Ohkoshi M, Nagasaki S, et al. The effect of cryotherapy on intraarticular temperature and postoperative care after anterior cruciate ligament reconstruction. Am J Sports Med. 1999;27(3):357–362. 218. Raynor M, Pietrobon R, Guller U, et al. Cryotherapy after ACL reconstruction–a meta-analysis. J Knee Surg. 2005;18(02): 123–129. 219. Martimbianco AL, Gomes da Silva BN, de Carvalho AP, et al. Effectiveness and safety of cryotherapy after arthroscopic anterior cruciate ligament reconstruction. A systematic review of the literature. Phys Ther Sport. 2014;15(4):261–268. 220. Westermann RW, Wright RW, Spindler KP, et al. Meniscal repair with concurrent anterior cruciate ligament reconstruction: operative success and patient outcomes at 6-year follow-up. Am J Sports Med. 2014;42(9):2184–2192. 221. Harris JD, Abrams GD, Bach BR, et al. Return to sport after ACL reconstruction. Orthopedics. 2014;37(2):e103–e108. 222. Ardern CL, Taylor NF, Feller JA, et al. Fifty-five per cent return to competitive sport following anterior cruciate ligament reconstruction surgery: an updated systematic review and meta-analysis including aspects of physical functioning and contextual factors. Br J Sports Med. 2014;48(21):1543–1552. 223. Dingenen B, Gokeler A. Optimization of the return-to-sport paradigm after anterior cruciate ligament reconstruction: a critical step back to move forward. Sports Med. 2017. 224. Leys T, Salmon L, Waller A, et al. Clinical results and risk factors for reinjury 15 years after anterior cruciate ligament reconstruction: a prospective study of hamstring and patellar tendon grafts. Am J Sports Med. 2011;40(3):595–605. 225. Magnussen RA, Carey JL, Spindler KP. Does autograft choice determine intermediate-term outcome of ACL reconstruction? Knee Surg Sports Traumatol Arthrosc. 2011;19(3):462–472. 226. Gobbi A, Mahajan V, Karnatzikos G, et al. Single- versus double-bundle ACL reconstruction: is there any difference in stability and function at 3-year followup? Clin Orthop Relat Res. 2011;470(3):824–834. 227. Meredick RB, Vance KJ, Appleby D, et al. Winner of the 2007 systematic review competition: outcome of single-bundle versus double-bundle reconstruction of the anterior cruciate ligament. Am J Sports Med. 2008;36(7):1414–1421.

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228. Adravanti P, Dini F, de Girolamo L, et al. Single-bundle versus double-bundle anterior cruciate ligament reconstruction: a prospective randomized controlled trial with 6-year follow-up. J Knee Surg. 2017. 229. Torkaman A, Yazdi H, Hosseini MG. The results of single bundle versus double bundle ACL reconstruction surgery, a retrospective study and review of literature. Med Arch. 2016;70(5):351–353. 230. Mouzopoulos G, Fotopoulos VC, Tzurbakis M. Septic knee arthritis following ACL reconstruction: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2009;17(9):1033–1042. 231. Ponce BA, Cain EL Jr, Pflugner R, et al. Risk factors for revision anterior cruciate ligament reconstruction. J Knee Surg. 2016;29(4):329–336. 232. Mikkelsen C, Cerulli G, Lorenzini M, et al. Can a postoperative brace in slight hyperextension prevent extension deficit after anterior cruciate ligament reconstruction? Knee Surg Sports Traumatol Arthrosc. 2003;11(5):318–321. 233. Culvenor AG, Oiestad BE, Holm I, et al. Anterior knee pain following anterior cruciate ligament reconstruction does not increase the risk of patellofemoral osteoarthritis at 15- and 20-year follow-ups. Osteoarthritis Cartilage. 2017;25(1):30–33. 234. Liden M, Ejerhed L, Sernert N, et al. Patellar tendon or semitendinosus tendon autografts for anterior cruciate ligament reconstruction: a prospective, randomized study with a 7-year follow-up. Am J Sports Med. 2007;35(5):740–748. 235. Beynnon BD. Treatment of anterior cruciate ligament injuries, part 2. Am J Sports Med. 2005;33(11):1751–1767. 236. Hao ZC, Wang SZ, Zhang XJ, et al. Stem cell therapy: a promising biological strategy for tendon-bone healing after anterior cruciate ligament reconstruction. Cell Prolif. 2016;49(2):154–162. 237. Hirzinger C, Tauber M, Korntner S, et al. ACL injuries and stem cell therapy. Arch Orthop Trauma Surg. 2014;134(11): 1573–1578. 238. Dong Y, Zhang Q, Li Y, et al. Enhancement of tendon-bone healing for anterior cruciate ligament (ACL) reconstruction using bone marrow-derived mesenchymal stem cells infected with BMP-2. Int J Mol Sci. 2012;13(10):13605–13620. 239. Robert H, Es-Sayeh J. The role of periosteal flap in the prevention of femoral widening in anterior cruciate ligament reconstruction using hamstring tendons. Knee Surg Sports Traumatol Arthrosc. 2004;12(1):30–35. 240. Di Matteo B, Loibl M, Andriolo L, et al. Biologic agents for anterior cruciate ligament healing: a systematic review. World J Orthop. 2016;7(9):592–603. 241. Vavken P, Fleming BC, Mastrangelo AN, et al. Biomechanical outcomes after bioenhanced anterior cruciate ligament repair and anterior cruciate ligament reconstruction are equal in a porcine model. Arthroscopy. 2012;28(5):672–680.

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99  Revision Anterior Cruciate Ligament Injuries Joseph D. Lamplot, Liljiana Bogunovic, Rick W. Wright

As the number of primary anterior cruciate ligament (ACL) reconstructions performed annually continues to increase, the number of revision procedures is also projected to increase.1,2 A larger number of patients returning to high-demand sports and activities following primary reconstruction has resulted in an increased number of revision and repeat revision reconstructions.3,4 Failure of primary ACL reconstruction, defined by recurrent laxity or graft failure, has been reported in 2.9% to 44% of patients, with higher failure rates in younger patients and following allograft reconstruction.5-15 It is estimated that between 1.7% and 7.7% of patients who underwent primary ACL reconstruction will undergo revision reconstruction.1,16-20 As approximately 175,000 to 200,000 primary reconstruction procedures are performed in the United States annually, it is estimated that approximately 3000 to 13,000 patients will undergo revision ACL reconstruction each year. This group is typically composed of a young, active population that desires a return to their previous activities.21,22 Revision ACL reconstruction is a challenging procedure with technical issues that can include retained hardware, incorrect bone tunnel placement and dilation, and limited graft choices.3,23-26 This procedure requires proficiency with multiple techniques and flexibility when encountering unexpected obstacles to a successful revision reconstruction. Furthermore, patients undergoing revision ACL reconstruction have a lower rate of return to sport, an increased incidence of meniscal and chondral injuries, and inferior clinical outcomes compared with primary reconstruction.8,9,11,21,27-29 Although excellent results can be achieved following a well-executed revision ACL reconstruction, patients must be counseled regarding expectations following this procedure.

Epidemiology Recurrent instability is defined as failure of the reconstructed ligament to provide adequate anterior and rotatory stability to the knee. Recurrent instability or graft failure necessitating revision most commonly affects patients in the third decade of life.8,22,30,31 Risk factors for graft failure include male gender, return to sports involving pivoting or jumping, contact sports, allograft, and age younger than 25 years.14,21,29,32-35 Although patients in their 20s comprise the highest absolute number of revision ACL reconstructions, those aged 10 to 19 have the highest incidence of graft failure, and each 10-year decrease in age has been shown to increase the odds of graft failure by 2.3-fold.14 This is likely attributable to a higher activity level among younger patients

with ACL injuries, as well as a higher likelihood of premature return to activities prior to adequate rehabilitation.35 Although females have a higher rate of tearing an intact contralateral ACL, males are more likely to tear the reconstructed graft within the first 2 years following ACL reconstruction21; 55% to 70% of revision reconstructions are performed in male patients.11,21,22,33,36-39 Although the reasons for higher rates of revision reconstructions among males have not been elucidated, males may have an increased propensity to return to high-risk activities that put the graft at risk. Approximately 90% of revision reconstructions are first-time revision procedures.22 Seventy percent of patients report a noncontact injury resulting in rerupture, with 40% occurring during cutting and 30% during jumping activities. Three-quarters of patients report an injury while playing sports, with most occurring during soccer and basketball. The mean time from prior reconstruction to revision is greater than 2 years in approximately 66% of patients, 1 to 2 years in 20% of patients, and less than 1 year in 15% of patients.22 Of all patients undergoing revision ACL reconstruction, autograft was found to be used in the prior reconstruction in approximately 70% of cases and allograft in 30% of cases.22

HISTORY ACL graft failure should be considered in the setting of objective sagittal (anteroposterior [AP]) or rotatory knee laxity, subjective knee instability, knee pain following prior ACL reconstruction, extensor mechanism dysfunction, and infection.29 Knee pain should be distinguished from instability.28 A complete history should be obtained, including mechanism of injury, quality of symptoms (swelling, giving way, locking, catching, crepitus, gait changes), symptom duration, previous injuries and surgical interventions including ligamentous, meniscal, and articular cartilage injuries, graft type and source, and graft fixation.28,29 If the patient describing recurrent instability is unable to recall a causative traumatic episode, this may suggest technical or biologic reasons for graft failure. The patient should be asked to describe the postoperative course following the previous reconstruction, detailing the time course to rehabilitation milestones and return to activity/sport. Failure to return to the same level of activity postoperatively may suggest a technical error or inadequate rehabilitation.29 Inadequate postoperative rehabilitation resulting in poor proprioception, deconditioning, stiffness, and

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Abstract

Keywords

Revision anterior cruciate ligament (ACL) reconstruction is a challenging procedure with technical issues requiring proficiency with multiple techniques and flexibility when encountering unexpected obstacles to a successful revision reconstruction. Patients undergoing revision ACL reconstruction have a lower rate of return to sport, an increased incidence of meniscal and chondral injuries, and inferior clinical outcomes compared with primary reconstruction. As such, these patients must be counseled regarding expectations following this procedure. In addition to a complete history and physical examination, preoperative evaluation should include imaging to assess tunnel positioning. Tunnel malpositioning is the most technical error during both primary and revision ACL reconstruction and must be addressed at the time of revision reconstruction. Untreated ligamentous injury and malalignment must also be addressed before or during revision reconstruction to help prevent graft failure. Similar to primary reconstruction, allograft has been shown to have higher failure rate than autograft in the revision setting. Several factors must be considered in the setting of revision ACL reconstruction, including graft selection, tunnel locations, tunnel sizes and need for bone grafting, previous fixation type and need for removal, method of revision fixation, and postoperative protocol. The revision reconstruction often must be adapted to the technique previously used. We describe our preferred technique, using a rear-entry two-incision approach to facilitate femoral tunnel drilling independent of the tibial tunnel position. While the principles of postoperative management are similar to primary reconstruction, rehabilitation and return to sport is generally slower than primary reconstruction.

revision ACL revision ACL reconstruction ACL failure revision ACL graft choice revision ACL technique ACL outcomes

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pain may be unimproved after a revision reconstruction.28,29,40,41 Such patients benefit from preoperative rehabilitation. Previous operative notes, clinic notes, therapy notes, imaging studies, and intraoperative arthroscopic images should be reviewed. Associated intra-articular injuries, including meniscal and chondral injuries, diagnosed at the time of the previous reconstruction must be considered in the setting of patient dissatisfaction following a previous reconstruction.42

In addition to these ACL-specific examination tests, a complete knee exam should be performed including examination of the posterior cruciate ligament (PCL), medial collateral ligament (MCL) and lateral collateral ligament (LCL), posterolateral corner, and menisci. As described later in greater detail, associated injury to other ligamentous and soft tissue structures may contribute to instability following ACL reconstruction.58

IMAGING

PHYSICAL EXAM Physical exam begins with assessment of lower extremity alignment, gait, muscle tone, specifically evaluating the bulk of the vastus medialis obliquus (VMO), and the location of previous incisions.29 Range of motion (ROM) should be measured, assessing for a flexion contracture or extensor lag, and prone heel height examination may identify a subtle flexion contracture not appreciated while supine.29 The ACL should be evaluated with the Lachman test to determine anterior laxity, and a pivot shift exam should be attempted to determine rotatory instability, with both exams compared with the uninjured contralateral leg.40,43 However, approximately 32% of autograft-reconstructed knees may have positive findings on a Lachman test and 22% positive findings on the pivot-shift test, suggesting that postoperative laxity may exist in a large number of patients after reconstruction despite satisfactory subjective outcomes.28 Conversely, despite normal findings on Lachman and pivot shift examination, some patients may describe the subjective perception of knee instability, with an inability to trust their knee during pivoting and twisting activities. In equivocal cases, the KT-1000/2000 arthrometer (MEDmetric, San Diego, CA) may be used to provide a more objective measurement of AP laxity.28,29,44 A greater than 3-mm side-to-side difference correlates with failure of the native ACL, and multiple studies have used this criterion to quantify failure of a reconstructed ACL.45-51 Other studies have defined graft failure as a greater than 5 mm side-to-side difference.24,52-57

A complete weight-bearing series of knee radiographs, including AP in extension, flexion posteroanterior (PA) (Rosenberg), lateral, and axial (sunrise or merchant) views should be obtained in the setting of pain or instability following ACL reconstruction (Fig. 99.1). If there is concern for coronal malalignment or instability, full-length standing AP radiographs should also be obtained. Radiographs should be used to assess tunnel location, tunnel expansion and associated bone loss, osteoarthritis (OA) progression, coronal or sagittal malalignment, and the presence of hardware or implants that may affect revision surgical planning. A full extension lateral with the ankle supported to allow hyperextension can assess tibial tunnel position in relation to Blumensaat line.

Radiographic Tunnel Positioning A malpositioned femoral tunnel is typically either too anterior and/or too vertical, and a malpositioned tibial tunnel is typically too anterior. On a lateral radiograph, the tibial plateau and Blumensaat line may be divided from anterior to posterior into four equal quadrants.59 The tibial tunnel should enter the joint in the posterior third of the second quadrant, and the femoral tunnel should enter in the most posterior quadrant.59,60 Taking 0% as the anterior and 100% as the posterior extent of Blumensaat line, a femoral tunnel more than 40% anteriorly along Blumensaat line is considered excessively anterior.60 Femoral tunnels located at least 60% posteriorly along Blumensaat line and tibial tunnels at least 20% posteriorly along the tibial plateau have

B A Fig. 99.1  Preoperative radiographs. (A) Standing anteroposterior radiographs demonstrate varus malalignment of the left knee in setting of prior anterior cruciate ligament (ACL) reconstruction. Full-length standing anteroposterior radiographs may be obtained in this setting to plan for concomitant high tibial osteotomy (HTO), which may be performed prior to or during revision ACL reconstruction. (B) Full extension lateral radiograph with ankle supported to allow hyperextension may be used to assess tibial tunnel position in relation to Blumensaat line. Notice knee hyperextension in setting of prior failed ACL reconstruction.

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demonstrated improved clinical outcomes,61 whereas those with more anterior femoral or tibial tunnels are associated with increased failure rates and inferior clinical outcomes.62 Outcomes following revision for excessively anterior femoral tunnel malpositioning primary are improved compared to revision for another cause.63 Femoral tunnel malpositioning in the coronal plane can also contribute to graft failure. On an AP or PA radiograph, fixation

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along the anterior rather than lateral cortex may indicate a “vertical” femoral tunnel (Fig. 99.2).64 A double-blinded study assessing the results of high and low femoral wall position showed improved International Knee Documentation Committee (IKDC) scores for the low position group.65 The tibial tunnel should penetrate the articular surface at the midpoint of the plateau on an AP or PA radiograph. A cadaveric study using landmarks to determine anatomic tunnel location demonstrated the sagittal tibial

A

B Fig. 99.2  Examples of incorrect tunnel placement. (A) Excessively anterior femoral and tibial tunnels. Taking 0% as the anterior and 100% as the posterior extent of Blumensaat line, a femoral tunnel more than 40% anteriorly along Blumensaat line is considered excessively anterior. The tibial tunnel should enter the joint in the posterior third of the second quadrant of the tibial plateau, and the femoral tunnel should enter in the most posterior quadrant of Blumensaat line. (B) Vertical femoral tunnel placement, best visualized on anteroposterior or posteroanterior (PA) radiograph. On a PA radiograph, fixation along the anterior rather than lateral cortex may indicate a “vertical” femoral tunnel. Lateral view also demonstrates anterior femoral and tibial tunnel placement.

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tunnel angle to be 75 degrees and the coronal angle to be 65.7 degrees.66 A tibial tunnel angle greater than 75 degrees in the coronal plane may result in a loss of flexion and increased sagittal (AP) laxity.74,75

be compromised by artifact if metallic implants were used for fixation during the prior reconstruction.77

Graft Impingement

Causes of Failure of Anterior Cruciate Ligament Reconstruction

A hyperextension lateral radiograph is the best method to assess for anterior graft impingement,67 which is associated with increased rates of effusion, lack of extension, and increased failure rates.68-71 The Multicenter ACL Revision Study (MARS) group demonstrated that approximately 51% of patients undergoing revision reconstruction had no graft impingement, 47% had some degree of impingement, and 2% had complete impingement with the tibial tunnel completely anterior to Blumensaat line.60 A study defined the distance posterior to the anterior edge of the tibia that minimizes the risk of anterior graft impingement,72 and if the center of the tibial tunnel at the articular surface was at least 22 to 28 mm posterior to the anterior edge of the tibia, then no graft impingement resulted.73 Another study demonstrated that if the tibial tunnel is positioned in the posteromedial portion of the native ACL footprint, then graft impingement does not occur.67

Advanced Imaging Computed tomography (CT) may be obtained to provide a more detailed assessment of existing tunnel location, tunnel dilation, and bone quality (Fig. 99.3). Excessively posterior femoral tunnel placement may result in posterior wall blowout, limiting fixation options at the time of revision surgery to those relying on lateral cortical fixation or necessitating bone grafting followed by staged ACL reconstruction.76,77 The authors routinely obtain magnetic resonance imaging (MRI) preoperatively to assess for concomitant meniscal, chondral, and ligamentous injury, and it can also be useful to assess graft integrity and tunnel dilation. The authors routinely obtain MRI preoperatively. However, its utility may

A

DECISION-MAKING PRINCIPLES

Instability following ACL reconstruction may be categorized into early (less than 6 months postoperative) or late (greater than 6 months postoperative) instability. Early laxity generally results from technical errors, failure of graft incorporation, loss of graft fixation, premature return to activity/sport, overly aggressive rehabilitation, or a combination of these factors.11,28,78-80 Late instability generally results from traumatic rerupture and less often from technical errors.32 A less common cause of late instability is failure to address concomitant ligamentous pathology at the time of primary reconstruction.77,81 With appropriate surgical technique and rehabilitation, primary ACL grafts are at no greater risk of rupture compared with the contralateral uninjured ACL.14,32,82 Patients undergoing revision reconstructions report trauma resulting in recurrent instability in approximately 55% to 70% of cases, most often from a noncontact injury during sports.22 However, at the time of revision, the MARS surgeons have deemed the cause of failure to be traumatic in only one-third of cases, technical error in approximately one-quarter of cases, biologic failure (lack of graft incorporation) in 7% of cases, and multifactorial in 31%.22 Up to 53% of patients undergoing revision reconstruction have some degree of technical error contributing to graft failure,29,83 and among these patients, 80% have femoral tunnel malposition. Injury resulting in rupture of a well-positioned and well-fixed graft is nearly as frequent as failure due to incorrect femoral tunnel placement.22,33,55,63,84 Interestingly, two decades ago, failure due to malpositioned tunnels was two to three times more likely than traumatic rerupture of

B

Fig. 99.3  Preoperative computed tomography scan may be obtained to assess tunnel location, size and bone quality. (A) Selected sagittal cut of lateral femoral condyle demonstrates two femoral tunnels occupying large portion of proximal lateral intercondylar notch. (B) Selected axial cut redemonstrates femoral tunnels. In this case a two-stage revision was performed in which these femoral tunnels were bone grafted prior to revision reconstruction. The large size and location of the existing femoral tunnels prevented the placement of a new, properly placed revision femoral tunnel.

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a well-positioned, well-healed graft. These differences may be attributable to higher-demand patients expecting a return to their previous activity level, overaggressive rehabilitation protocols that may prevent adequate graft healing, and improved surgical techniques resulting in more consistently accurate tunnel placement during primary reconstruction.63,85,86

Tunnel Malpositioning Tunnel malpositioning is the most common technical error during primary and revision ACL reconstruction and can result in excessive graft forces and strain resulting in inadequate graft incorporation, graft loosening, and atraumatic graft failure.21,63,84,87,88 Occurring three times more frequently than tibial tunnel malpositioning, excessively anterior placement of the femoral tunnel is the most frequent technical error.29,84 This is, in part, due to difficulties in visualizing the native femoral footprint89,90 and results in a short graft with excessive graft tension in flexion and an initial loss of knee flexion.63,84 During rehabilitation and return to sport, recurrent stretching of the graft leads to laxity and eventual failure.29,63,84,91 Conversely, excessively posterior femoral tunnel placement results in excessive graft tension in extension with laxity in flexion.84 A vertical femoral tunnel may provide sagittal (AP) stability but will result in rotational instability.92 An excessively anterior tibial tunnel results in graft impingement against the intercondylar notch with loss of terminal extension.69,70,93-95 Excessively posterior tunnel placement results in graft impingement against the PCL and a vertical graft. This initially results in a loss of terminal flexion, with eventual graft laxity if full flexion is achieved.84,96 Errant placement of a tibial tunnel too far medially or laterally can also result in graft impingement on the intercondylar notch, potentially causing articular cartilage injury.97

Untreated Ligamentous Laxity Of patients undergoing revision ACL reconstruction, 3% to 31% of patients may have had unrecognized collateral ligament instability or malalignment contributing to graft failure.6,24,29,33, 49,51-54,56,57,61,91,98-100 Untreated varus malalignment can result in varus thrust and graft attenuation.81 Similarly, untreated posterolateral or posteromedial corner injuries may result in excessive forces within the graft and early failure; these injuries should be addressed before or during revision ACL reconstruction.25,81,100 In the setting of combined ACL and PCL injury, reconstruction of the ACL prior to addressing PCL insufficiency will predictably lead to ACL failure.58 As the medial meniscus is a secondary constraint to anterior tibial translation, the graft within a medial meniscus-deficient knee experiences increased forces that contribute to early failure.63,77 Meniscal transplant should be considered in these patients.11,21

Primary Reconstruction Graft Choice Numerous studies and meta-analyses of primary hamstring and patellar tendon autograft ACL reconstructions have demonstrated average failure rates of 3.6%, with no difference in failure rates between these autografts.10,34,137-142 However, allograft reconstructions have a three- to five-times higher likelihood of graft failure compared with autograft.48,101-103 This may be attributable, in

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part, to patients having relatively less postoperative pain and a more rapid postoperative rehabilitation following allograft reconstruction, thereby returning to a higher activity level prior to adequate graft healing.34,104 Allograft processing may also increase the risk of graft failure, as irradiated grafts have demonstrated a significantly higher failure rate compared with nonirradiated grafts.103,105

Concomitant Intra-Articular Pathology Knees undergoing revision ACL reconstruction have a higher incidence of chondral injuries and meniscal tears compared to primary reconstruction.24,28,52,106,107 In one study, 90% of knees undergoing revision reconstruction had a meniscus or chondral injury and greater than 50% demonstrated both.22 Similarly, MARS group reported modified Outerbridge grade 2 or higher lesions in 73% of patients undergoing revision, with concurrent meniscal and cartilage damage in 57%.22

Meniscus Injury Although is it known that the medial meniscus plays a critical role in limiting anterior tibial translation in an ACL-deficient knee, it remains unknown if there is a critical amount of medial meniscus that, if removed, predisposes the reconstruction to failure.21,108 Previous partial meniscectomy, but not meniscal repair, is associated with a higher incidence of articular cartilage lesions at the time of revision.21,106 The MARS group demonstrated an overall 74% incidence of meniscal injury at the time of revision reconstruction,22 similar to that at the time of primary reconstruction.109-111 The prevalence of medial meniscus tears at the time of revision is 40% to 46%, higher than at the time of primary reconstruction.8,22,112 Conversely, there is actually a decreased incidence of new, untreated lateral meniscal tears at revision compared with primary reconstruction.11 Thus patients undergoing revision due to recurrent instability appear to be continuing to put the medial meniscus at risk for further injury.

Articular Cartilage Injury Inferior patient-reported outcome scores have been reported following revision ACL reconstruction compared with primary reconstruction, and this is associated with an increased incidence and severity of chondral lesions at the time of revision.6,53 Although it is unlikely that these lesions affect stability in the reconstructed knee, increased chondrosis at the time of revision may have detrimental effects on clinical outcomes despite appropriate surgical technique, graft healing, and adequate clinical laxity.29 Even when controlling for meniscus status (prior meniscectomy versus no prior meniscectomy), there is an increased risk of lateral and patellofemoral compartment chondrosis at the time of revision compared with primary reconstruction.11 There is a strong association between ACL deficiency and acceleration of degenerative changes,23,113,114 and the status of the articular cartilage at the time of revision reconstruction may be one of the most important predictors of a successful clinical outcome.33 Patients undergoing delayed revision reconstruction (greater than 6 months following onset of symptomatic instability) have a markedly higher incidence of articular cartilage

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degeneration compared with earlier revisions (53% vs. 24%), and the prevalence of advanced degenerative changes is also significantly higher in the delayed group.23 Early restoration of stability may lead to reduced secondary articular cartilage damage and a return to previous activity levels,7,23,115 and it has been suggested that revision reconstruction should be performed within 6 months of graft failure to minimize the risk of degenerative changes and arthritis progression.23,53,116

TREATMENT OPTIONS Several factors must be considered in the setting of revision ACL reconstruction, including graft selection, incision locations, tunnel locations, tunnel sizes and need for bone grafting, previous fixation type and need for removal, method of revision fixation, and postoperative protocol. The revision reconstruction often must be adapted to the technique previously used.91 The revising surgeon must be proficient with a variety of techniques to address such issues as retained implants, malpositioned tunnels, bone loss, and expanded tunnels. Additional knee pathology, including meniscus or ligamentous injury, may be addressed at the time of revision ACL reconstruction or staged, with the revision ACL reconstruction often the final procedure. Although most revisions are performed as single-stage procedures, specific situations in which two-stage procedures should be considered are patients with incomplete ROM requiring lysis of adhesions, malalignment requiring corrective osteotomy, significant tunnel widening necessitating bone graft, and infection.91

A

Evaluation of Tunnels Prior tunnel placement may be categorized in one of three ways: (1) accurate and not requiring redirection, (2) completely inaccurate in a location that will not interfere with new tunnel creation, or (3) overlapping, such that the prior tunnel and a properly placed tunnel will partially overlap.76 Partially overlapping tunnels are generally the most challenging of these three because they require the surgeon to adjust his or her technique due to enlarged tunnels. The scope should be inserted into each tunnel to assess tunnel size and the quality of the surrounding bone to determine the need for grafting and the best method of fixation.91 The tibial tunnel can be viewed by placing the scope directly into the tunnel through the previously made tibial skin incision. The femoral tunnel can be visualized by placing the scope through the previous anteromedial portal.

Prior Fixation Bioabsorbable implants are generally difficult to remove and may be left in place and overreamed after guide pin placement. However, metal interference screws must be removed if interfering with the planned tunnel location. In the rare case that properly placed tunnels can be made independent of prior tunnels and metallic implants, the implants may be left in place (Fig. 99.4). If metallic hardware is removed, the size and location of the resulting defect must be considered. The defect may necessitate grafting, either as part of a single-stage of two-stage revision, or the use of larger bone blocks with a patellar tendon autograft or various bone block allograft options.

B Fig. 99.4  Correction of femoral tunnel malpositioning. (A) Preoperative radiographs with fixation from prior failed anterior cruciate ligament (ACL) reconstruction demonstrate excessively posterior tibial tunnel and vertical femoral tunnel. (B) Postoperative radiographs following revision ACL reconstruction with new tibial tunnel anterior to Blumensaat line and less vertical femoral tunnel at approximately 1030 position.

Tunnel Grafting Bone grafting of existing tunnels should be strongly considered when expanded tunnels measure more than 15 mm, because ACL graft options are limited and fixation may be compromised in tunnels this large.76 Bone grafting may be performed at the time of revision ACL reconstruction or as a staged procedure, with staged reconstructions generally performed for larger defects (Fig. 99.5). Of all patients undergoing revision ACL reconstruction, approximately 9% undergo tibial tunnel grafting and 8% undergo femoral tunnel grafting as a staged procedure prior to revision reconstruction.22 Conversely, concomitant revision reconstruction and bone is performed in only 3% of patients.22 In the setting of a two-stage procedure, serial radiographs should be obtained to confirm complete graft incorporation prior to the second-stage procedure, which generally follows grafting by approximately 6 months.76 Prior to grafting, a thorough débridement of any prior graft and fixation material must be performed to facilitate new graft

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plugs harvested from the iliac crest or medial tibial metaphysis,118,119 allograft dowel plug grafting (which may allow for larger diameter plugs), and calcium phosphate putties have been described as well, but no long-term results of biologic incorporation in the setting of revision ACL reconstruction are available at this time.120 Expanded tibial tunnels may be filled with graft placed in an inferior to superior direction directly through the tibial skin incision using a small tamp. When grafting the femoral side, dry arthroscopy may be useful to prevent washing out graft. During femoral tunnel grafting, a small arthroscopic cannula or skid can be placed through an accessory medial portal made in line with the previous femoral tunnel. Allograft dowels may be sized to fit the dilated tunnel size and impacted into place.121 A

Tunnel Preparation Revision ACL reconstruction is typically performed using a single-bundle technique with tunnels placed in the center of the anatomic footprints.76 In the setting of overlapping tunnels, in which the previous and newly planned tunnels will overlap, the new femoral or tibial tunnels may be created using the concept of divergent tunnels.87 Although the previous and new tunnels may converge as they approach the intracondylar notch, the tunnels should separate as they progress further away from the joint, and the new tunnel should sufficiently diverge from the previous tunnel to provide a cylinder of native bone for adequate graft fixation.76 In the setting of tunnel overlap, an expanded tunnel may also be created by progressively reaming until a uniform cylinder results. Following this, depending on defect size, a custom autograft or allograft plug may be sized to fill the entire defect.83,122

B

Femoral Tunnel

C Fig. 99.5  Tunnel expansion in revision anterior cruciate ligament (ACL) reconstruction. (A) Preoperative radiographs prior to revision ACL reconstruction demonstrate fixation from prior failed ACL reconstruction. Tunnels are in a position that would overlap with planned revision ACL tunnels. (B) Computed tomography obtained prior to revision ACL reconstruction demonstrates expansion of tibial tunnel, with tunnel diameter measuring approximately 17 mm. Tunnel expansion would preclude a single stage procedure. (C) Revision ACL reconstruction was performed in staged manner, with allograft dowel plugs used to fill previous tunnels 6 months prior to revision ACL reconstruction.

healing to native bone. Autograft may be harvested from Gerdy tubercle, distal femur, or in the setting of larger defects, the iliac crest. Cancellous allograft can be used alone or in combination with autograft. Alternative autograft sources, including single or multiple press-fit osteochondral autograft transplantation (OAT)

Transtibial drilling of the femoral tunnel limits the position from which the femoral footprint can be accessed. Other options that can be used to access the femoral footprint in an anatomic trajectory include outside-in femoral tunnel creation using a rearentry technique or using an accessory anteromedial portal, both of which allow creation of an independent femoral tunnel. Notchplasty in the revision setting may result in inferior patientreported outcomes and should not routinely be performed unless deemed necessary at the time of surgery.123 For the outside-in rear-entry technique, an incision is made over the lateral aspect of the distal femur, splitting the iliotibial band to allow introduction of a drilling guide (Fig. 99.6). Care should be taken to avoid prior tunnels by using a more horizontal trajectory. Allowing for creation of a completely new femoral tunnel, this technique can provide an excellent way to obtain a new fixation point in the revision setting. Alternatively, an accessory anteromedial portal can be made using arthroscopic visualization with a spinal needle, as varying inferior and medial portal positioning provides a variety of angles to approach the femoral footprint. The knee should be hyperflexed to optimize the length and anterior direction of the newly created tunnel, thereby helping to prevent posterior condyle blowout and peroneal nerve injury.124 A guide pin may then be placed through this newly created accessory medial portal, directed into the femoral footprint, and driven

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A

B

C

D

Fig. 99.6  Outside-in rear-entry femoral tunnel preparation. (A) Lateral thigh incision for outside-in rear-entry technique. (B) Guides for rear-entry femoral approach. (C) Rear entry guide pulled through anterolateral portal into notch with curved hook. (D) This technique allows the ability to place guide and drill tunnel at desired location within the intercondylar notch—here femoral tunnel is placed low in notch.

through the lateral cortex of the femur. The guide pin should exit above the level of the superior pole of the patella and anterior to the midline of the femur. With the knee remaining hyperflexed and the surgeon taking care to avoid iatrogenic articular cartilage damage, the guide pin should be overreamed to complete creation of the new femoral tunnel. Use of a unipolar or low-profile reamer may decrease the risk of iatrogenic articular cartilage damage. Following creation of the femoral tunnel, a motorized shaver may be used to remove debris.

Tibial Tunnel Tibial tunnel management is generally less challenging than on the femoral side because the tibial tunnel is directly accessible through a prior open incision. A variable-angle drilling guide should be directed to enter the tibial articular surface in an anatomic and, if possible, a distinct location from the prior tunnel in order to facilitate adequate fixation. The angle of the new tunnel may be adjusted to create a longer tunnel, if necessary. An excessively posterior tibial tunnel presents a challenge in that the new, more anterior tunnel may overlap with the previous tunnel. Analogous to a blocking screw, a bioabsorbable screw or allograft bone dowel may be placed posteriorly to fill the previous tunnel and facilitate new graft placement in a more anterior position.

Graft Fixation Prior to graft insertion and fixation, the new tunnel diameters, bone quality, and graft size must be carefully evaluated to ensure

an environment that is adequate for graft fixation and healing. If tunnel expansion is anticipated or occurs following tunnel creation, soft tissue grafts should be used with caution. If 2 to 3 mm of graft-tunnel mismatch occurs, a stacked-screw technique may be used.76 Alternatively, a bone-patellar tendon-bone (BPTB) autograft with appropriately sized blocks to fill the mismatch may be used. In the setting of larger graft-tunnel mismatch, allograft with affixed bone block (Achilles tendon, BPTB) with appropriately large bone plugs should be prepared taking into account the mismatch. Synthetic dowels and allograft bone plugs have also been used to provide supplemental interference fixation within tunnels.83,122 In the setting of a loss of tunnel integrity, such as femoral tunnel blowout, or if the bone quality is poor, alternative methods of fixation besides inference screws should be considered. Laterally based bioabsorbable cross-fixation pins and arthroscopic buttons can provide improved fixation on the intact lateral cortex in this setting. Stay sutures may also be inserted through the graft and fixed to a femoral post, with a supplemental post placed on the lateral femur or anterior tibia. Recently, the MARS group has demonstrated improved results with metal screw fixation, and, although the reasons for these results are not yet understood, this should be taken under consideration.123

Double-Bundle Reconstruction in Revision Setting Although double-bundle reconstruction has gained popularity in the past decade,125-127 there are no absolute indications for this technique in the setting of primary or revision ACL

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reconstruction.76,128,129 A failed double-bundle primary reconstruction may present specific challenges because prior tunnel placement with two separate tunnels and soft tissue grafts often interferes with planned tunnels at the time of revision. Although it has been described as feasible, there is currently no evidence that double-bundle reconstruction provides improved stability or clinical outcomes compared to single-bundle reconstruction in the revision setting.130,131 In addition, conversion from a singleto a double-bundle reconstruction may require staged procedures, with initial bone grafting followed by revision reconstruction, which may unnecessarily delay revision reconstruction, increasing the likelihood of progressive chondrosis.23 In the setting of a vertical graft with an excessively posterior tibial tunnel that provides adequate sagittal plane stability but inadequate rotatory stability, an augmentation procedure may be considered in which the previous vertical graft is left intact.131 A second graft may be placed anterior to the excessively posterior tibial tunnel into a femoral tunnel site located within femoral footprint of the posterolateral bundle. No long-term outcomes following this procedure have been reported, and due to a lack of available data at this time, we cannot recommend the use of any double-bundle reconstruction technique in the revision setting.

Graft Choice Multiple factors impact the choice of graft in revision ACL reconstruction, including age, sex, previous graft choice, ACL revision number, concurrent ligamentous repair, surgeon preference, and the surgeon’s opinion of the prior failure.132 Although graft choice may impact outcomes in the revision setting, the ability to choose a graft may be limited by a number of other factors.

Factors Affecting Graft Choice Graft choices for revision reconstruction include semitendinosus and gracilis (hamstring autograft), BPTB, quadriceps tendon, and various allograft choices.91,138 If autograft is chosen, it should be harvested only after determining that all of the technical steps of the revision reconstruction can be successfully performed.91 In 2010 the MARS group investigated graft choice at the time of revision ACL reconstruction and found that autograft was used in 45% of cases and allograft in 54%; 64% of autografts 55% of allograft were BPTB. Hamstrings graft made up 29% of autografts and only 5% of allografts.22 More recently, the MARS group reported that autograft was used in 48% of revision reconstructions and allograft in 49%, with 3% using a combination of both.132 Surgeon preference was found to be the most important factor in determining revision graft choice. Other factors affecting graft choice were prior graft type and patient age. If an autograft was used previously, an allograft was 3.6 times more likely to be chosen for the revision. It is well established that there is a higher rate of allograft failure in young, active athletes following primary reconstruction,34 and recent data suggest higher rates of reoperation following prior reconstruction with allograft.133 The surgeon’s opinion of the failure has also been shown to impact graft choice at the time of revision, and a belief that an allograft failed for biologic reasons leads to a higher likelihood of using autograft.

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Comparison Among Graft Choices The use of autograft hamstring, BPTB, and combinations of hamstring, BPTB, and quadriceps tendon autograft has yielded results similar to those reported after primary reconstruction in terms of objective laxity.51,53,55,56,91,116 The MARS group reported improved patient-reported outcome scores and sports function following autograft revision reconstruction compared with allograft.134 Furthermore, autograft resulted in a decreased risk of graft failure at 2-year follow-up, and these patients were 2.78 times less likely to undergo subsequent revision reconstruction compared with allograft. No studies have demonstrated differences in terms of graft failure or patient-reported outcomes comparing soft tissue and BPTB autografts. Key factors predisposing to allograft failure appear to be patient age, activity level, and the method of graft processing.34,135 Irradiation of allograft likely adversely affects graft laxity, predisposing to reconstructions failure.49,136 In the setting of graft failure without evidence of technical error from the original procedure, the contralateral or ipsilateral patellar tendon may be the preferred graft source. The contralateral hamstring tendon may be considered as a graft choice if the primary procedure was performed with ipsilateral hamstring autograft.29 Allograft should be given considering when tunnel expansion precludes the use of autograft alone.

Two-Stage Revision Anterior Cruciate Ligament Reconstruction Two-stage revision reconstruction is often performed to avoid overlap between tunnels used at the time of revision ACL reconstruction and those made during the previous reconstruction.24 Because increased time to revision correlates with a higher incidence of meniscal and chondral lesions,23,53 the revising surgeon must be judicious when deciding whether a two-stage procedure is necessary or a single-stage procedure will suffice. A two-stage procedure generally requires a 6-month window between procedures in which the patient may continue to have instability.24 When possible, preference should be given to a single-stage procedure as long as appropriate tunnel placement and graft fixation can be achieved. A two-stage revision should be reserved for cases in which tunnel expansion precludes a single-stage procedure.

POSTOPERATIVE MANAGEMENT Principles of Rehabilitation The principles of postoperative management following revision ACL reconstruction are similar to primary reconstruction.143 However, although specific protocols describing the goals and timing for rehabilitation following primary reconstruction are well described,143-145 there are limited data on rehabilitation following revision surgery. Rehabilitation and eventual return to sport are generally slower than primary reconstruction,146 especially in the setting of allograft reconstruction in which graft incorporation may take longer.147,146 Overaggressive rehabilitation may result in early graft failure or late-onset laxity.29 As previously mentioned, revision patients are more likely to have concomitant intra-articular pathology addressed at the time of

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Authors’ Preferred Technique General Principles As previously mentioned, surgical options may be limited in the revision setting by what was done during the previous reconstruction, as well as based on the etiology of graft failure. Prior graft selection may limit choices in the revision setting. The location and size of previous tunnels may dictate whether graft is necessary and whether the procedure may be successfully completed in one or two stages. The authors use a single-stage procedure unless tunnel dilation exceeds 15 mm, in which case the tunnels are grafted and the revision reconstruction performed in a staged fashion, typically approximately 6 months following tunnel grafting and complete graft incorporation. The second stage procedure is then performed similar to a primary ACL reconstruction but generally rehabilitated more slowly, as described later. When possible, the authors use autograft, even if the contralateral extremity needs to be used. The authors use a rear-entry two-incision technique unless the locations of prior incisions prohibit this. A rear-entry two-incision approach allows femoral tunnel drilling to be performed independent of the tibial tunnel position, thereby allowing more flexibility in the revision setting. What remains most critical is creating tunnels in a fashion that the surgeon is comfortable with while allowing for adequate fixation. We describe our preferred technique for single-stage, single-bundle revision ACL reconstruction.

Tunnel Preparation An incision over the planned tibial tunnel site is made, usually using or extending the prior incision used for tibial tunnel preparation. The exit point of the planned tibial tunnel should lie at the anatomic insertion of the native ACL. If the exit point of the existing tibial tunnel is appropriate, then the newly planned tunnel may be designed to converge with the existing tunnel at the articular surface. If this approach is used, care must be taken to ensure that the two tunnels diverge as they move away from the joint to prevent excessive tunnel dilation. Alternatively, if the previously drilled tunnel is in an appropriate location without excessive tunnel dilation, any hardware interfering with fixation may be removed and the same tunnel used. Next, the femoral tunnel is prepared. The native femoral insertion should be identified and any graft stump débrided from this location. An accessory anteromedial tunnel is created or extended using a prior incision. Care must be taken not to violate the posterior condylar wall if the newly planned tunnel lies posterior to the previously drilled tunnel. If the previously drilled tunnel enters the joint appropriately at the native insertion, then converging tunnels may be used, as described previously for the tibia. Alternatively, if the previous drilled tunnel is in an appropriate, anatomic position, it may be used in a similar fashion as described for the tibia.

Diagnostic Arthroscopy Standard diagnostic arthroscopy is performed, generally using prior portal incisions. Any additional intra-articular pathology may be treated prior to beginning revision ACL reconstruction. The remnant ACL is débrided and prior tunnel locations identified and assessed. The location of planned tunnels should be compared with the existing tunnels. Hardware is removed if it will affect the revision.

Graft Insertion Following tunnel preparation, the graft is passed from the distal aspect of the tibial tunnel and pulled through the femoral tunnel similar to a primary reconstruction. The authors generally use interference screw fixation in both the primary and revision setting.

surgery, which can also slow rehabilitation depending on which specific structures are injured or repaired.84,148,149

Rehabilitation Protocol Phase 1: Acute Postoperative Phase (0 to 4 Weeks) The patient is allowed weight bearing as tolerated beginning immediately postoperative as long as there are no contraindications due to other intra-articular injuries. Similar to previous findings in primary ACL reconstructions, recent data demonstrated no improvement from a rehabilitative brace or knee immobilizer (Wright et al., 2017, unpublished data). Crutches are provided for assistance. Patients begin quadriceps activation with active knee ROM and gentle assist on postoperative day 1, with a goal of at least 90 degrees of knee flexion and full extension. Elevation, compression, and icing should be used to minimize effusion.150 Specific exercises in the acute postoperative phase include quadriceps sets, straight-leg raises, and hamstring activation (heel slides, standing knee flexion). Gait training may begin during the later stages of this first phase.149 Closed kinetic chain (CKC) exercises, including heel raises and mini-squats, may also commence late in the first stage. Phase 2: Subacute Postoperative Phase (2 to 8 Weeks) As the knee joint effusion and pain levels decrease over the first postoperative month, the ability to weight bear without assist and achieve greater motion will also improve. Exercises to improve motion including supine wall slides, active-assisted

heel slides, and prone/standing hamstring curls.149 Aggressive passive knee flexion should be avoided. Patients who have advanced through the first phase may progress to limited open kinetic chain (OKC) exercise (limited isometric knee extension from 45 to 90 degrees), additional CKC exercises through a greater ROM (terminal extension with TheraBand, split squat, hip dominant squat, leg press, step-ups), core strengthening, more advanced gait training, balance exercises, and low-level cardiovascular conditioning including stationary bike.149,151-154 Aquatic therapy may also be implemented.

Phase 3: Neuromuscular Conditioning (6 Weeks to 8 Months) Knee ROM should be full extension to greater than 120 degrees of flexion and a normal gait achieved by approximately 12-weeks postoperative. Strengthening and cardiovascular exercises may be intensified. Until approximately 3 months postoperative, CKC exercises predominate, including body-weight squatting, lunges, and leg press. At 3 months postoperative, patients should not yet be progressed to agility training, instead focusing on an increased intensity of both OKC and CKC exercises, along with progression of core exercises. At approximately 5 to 6 months postoperative, complex movement training reflecting the patient’s demands should be implemented. To begin these exercises, which often impart rotational forces about the knee, the patient must have sufficiently progressed in terms of strength and ROM. Cardiovascular training

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may include progression to jogging and careful incorporation of form running drills, with change of direction drills introduced late in the phase as indicated by patient progression.149

Phase 4: Return to Activity (8 Months to 1 Year) Critical assessment of patient-specific demands in the context of rehabilitation milestones must take place prior to return to full activity. Requisite neuromuscular control and endurance must be achieved to safely meet their sport/activity-specific demands. Functional testing may be performed, including singlehop tests, vertical leap, agility tests, and functional performance testing.149,155 Reaction drills may be also implemented.156 Once all deficiencies have been addressed and the patient is psychologically prepared for return to preinjury level of activity, they may be cleared for full a return.157,158 Recent data suggest that the use of an ACL derotation brace at the time of return to sport may improve patient-reported outcome scores among patients undergoing revision reconstruction and thus should be considered (Wright et al., unpublished data 2016).

RESULTS Results following revision ACL have been repeatedly demonstrated as inferior to those after primary reconstruction. Although objective rotatory and sagittal laxity can be restored to similar levels as those seen after primary reconstruction, failure rates following revision are three to four times higher than after primary reconstruction.9 Clinical outcomes scores are also significantly worse compared with primary reconstruction, with lower Cincinnati, Lysholm, Tegner, Marx activity, IKDC, and multiple Knee injury and Osteoarthritis Outcomes Score (KOOS) subscale scores.9,28,76,159 However, these measures are all significantly improved compared with before revision reconstruction.3,6,29,87 Approximately 40% of patients undergoing revision ACL reconstruction do not return to the same level of sport or competition.6,33,54,57,91,98,116,160 An increased incidence of meniscal and chondral injuries plays significant role in the inferior outcomes compared with primary reconstruction.6,53 Multiple studies have demonstrated inferior outcomes in patients undergoing revision reconstruction when chondral lesions or meniscal tears are present at the time of revision.6,53 One study found lower subjective and objective IKDC scores in patients who had undergone prior meniscectomy or were found to have significant cartilage damage at the time of revision ACL reconstruction.6

Multiple Revisions Repeat revision ACL reconstruction restores AP and rotational graft stability while improving the functional outcomes in patients who have failed prior revision reconstruction. However, most patients do not return to the same level of activity following repeat revision.3,21,117 Although the most common cause of firsttime recurrent laxity is a traumatic noncontact injury, multiplerevision patients tend to have recurrent instability without a traumatic injury.21 This suggests that there may be fundamental differences in how ACL grafts fail in the multiple-revision setting. There is also an increased rate of chondral injuries both within the medial and patellofemoral compartments, suggesting that

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medial compartment degeneration may be an important factor in recurrent graft injury.21 There have been limited reports of multiple revisions, with failure rates ranging from 0% to 13%.3,117 Repeat revision for recurrent instability without an identifiable traumatic event, the presence of International Cartilage Repair Society (ICRS) grade 3 or 4 chondrosis, and obesity have been associated with inferior outcomes following multiple revision reconstruction.3,117 In one study, technical error (most often tunnel malposition) was more common in the multiple-revision group than the first-time revision group. Furthermore, staged bone grafting is performed 22% of the time in the multiple-revision knee, double the rate of first-time revision, suggesting that the remaining host tibial and femoral bone is limited after two or more ACL reconstructions. These data also suggest that femoral tunnel malpositioning should be corrected at the time of first revision to lower the risk of recurrent failure.

COMPLICATIONS Revision ACL reconstruction has a higher complication rate than primary reconstruction, but overall numbers are still relatively low.7,21,29,61,161 The types of complications following revision reconstruction are similar to those following primary surgery, including infection, stiffness, and venous thromboembolism. Deep surgical site infections occur in 0.5% to 0.8% of patients undergoing revision reconstruction and venous thromboembolism in less than 0.5%.21,162

FUTURE CONSIDERATIONS Revision remains a challenging clinical scenario that requires the widest skill set of any sports procedure including hardware removal, bone grafting, and meniscal and chondral work, along with consideration of alignment and graft choices. The challenge remains to return patients to their previous activity and prevent future injury. Continued evaluation by large prospective cohorts will hopefully continue to elucidate subtle issues contributing to failure and worse outcomes. The MARS group embarked upon a 10-year follow-up with onsite evaluation that may show new findings not found with questionnaire-based follow-up. For a complete list of references, go to ExpertConsult.com.

SELECTED READING Citation: Wright RW, Gill CS, Chen L, et al. Outcome of revision anterior cruciate ligament reconstruction: a systematic review. J Bone Joint Surg Am. 2012;94(6):531–536.

Level of Evidence: IV, systematic review of level I-IV studies

Summary: This systematic review evaluates 21 eligible studies reporting outcomes of revision ACL reconstruction at minimum 2-year follow-up. The authors report that ACL reconstruction results in a worse outcome compared with primary ACL reconstruction and a dramatically elevated failure rate, 3-4 times higher than primary ACL reconstruction.

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Citation:

Citation:

Group MARS, Wright RW, Huston LJ, et al. Descriptive epidemiology of the Multicenter ACL Revision Study (MARS) cohort. Am J Sports Med. 2010;38(10):1979–1986.

Borchers JR, Kaeding CC, Pedroza AD, et al. Intra-articular findings in primary and revision anterior cruciate ligament reconstruction surgery: a comparison of the MOON and MARS study groups. Am J Sports Med. 2011;39(9):1889–1893.

Level of Evidence:

Level of Evidence:

II, cross-sectional study

II, prospective cohort study

Summary: This study describes the formation of the prospective MARS cohort and reports patient demographic and clinical features of this group of patients. This comprises the largest revision ACL reconstruction cohort in the literature.

Citation: MARS Group. Effect of graft choice on the outcome of revision anterior cruciate ligament reconstruction in the Multicenter ACL Revision Study (MARS) cohort. Am J Sports Med. 2014;42(10): 2301–2310.

Summary: This study compares meniscal and articular cartilage injuries found at the time of primary and revision ACL reconstruction using two of the largest available prospectively collected patient cohorts. The authors report a significantly higher incidence of lateral and patellofemoral compartment chondrosis in the revision setting, with a higher incidence of articular cartilage damage following prior meniscectomy.

Level of Evidence: II, prospective cohort study

Summary: This multicenter prospective study of 1205 patients demonstrates improved sports function and patient-reported outcomes decreased risk of graft rerupture after use of autograft compared with allograft in revision ACL reconstruction.

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REFERENCES 1. Leroux T, Wasserstein D, Dwyer T, et al. The epidemiology of revision anterior cruciate ligament reconstruction in Ontario, Canada. Am J Sports Med. 2014;42(11):2666–2672. 2. Lyman S, Koulouvaris P, Sherman S, et al. Epidemiology of anterior cruciate ligament reconstruction: trends, readmissions, and subsequent knee surgery. J Bone Joint Surg. 2009;91(10): 2321–2328. 3. Griffith TB, Allen BJ, Levy BA, et al. Outcomes of repeat revision anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(6):1296–1301. 4. Fithian DC, Paxton LW, Goltz DH. Fate of the anterior cruciate ligament-injured knee. Orthop Clin North Am. 2002;33(4):621– 636, v. 5. Carlisle JC, Parker RD, Matava MJ. Technical considerations in revision anterior cruciate ligament surgery. J Knee Surg. 2007;20(4):312–322. 6. Grossman MG, ElAttrache NS, Shields CL, et al. Revision anterior cruciate ligament reconstruction: three- to nine-year follow-up. Arthroscopy. 2005;21(4):418–423. 7. Noyes FR, Barber-Westin SD. A comparison of results in acute and chronic anterior cruciate ligament ruptures of arthroscopically assisted autogenous patellar tendon reconstruction. Am J Sports Med. 1997;25(4):460–471. 8. Wright RW, Dunn WR, Amendola A, et al. Anterior cruciate ligament revision reconstruction: two-year results from the MOON cohort. J Knee Surg. 2007;20(4):308–311. [Epub November 13, 2007]. 9. Wright RW, Gill CS, Chen L, et al. Outcome of revision anterior cruciate ligament reconstruction: a systematic review. J Bone Joint Surg. 2012;94(6):531–536. 10. Spindler KP, Kuhn JE, Freedman KB, et al. Anterior cruciate ligament reconstruction autograft choice: bone-tendon-bone versus hamstring: does it really matter? A systematic review. Am J Sports Med. 2004;32(8):1986–1995. 11. Borchers JR, Kaeding CC, Pedroza AD, et al. Intra-articular findings in primary and revision anterior cruciate ligament reconstruction surgery: a comparison of the MOON and MARS study groups. Am J Sports Med. 2011;39(9):1889–1893. 12. Ferretti A, Conteduca F, De Carli A, et al. Osteoarthritis of the knee after ACL reconstruction. Int Orthop. 1991;15(4):367–371. 13. Oiestad BE, Engebretsen L, Storheim K, et al. Knee osteoarthritis after anterior cruciate ligament injury: a systematic review. Am J Sports Med. 2009;37(7):1434–1443. 14. Wright RW, Dunn WR, Amendola A, et al. Risk of tearing the intact anterior cruciate ligament in the contralateral knee and rupturing the anterior cruciate ligament graft during the first 2 years after anterior cruciate ligament reconstruction: a prospective MOON cohort study. Am J Sports Med. 2007;35(7):1131–1134. 15. Pallis M, Svoboda SJ, Cameron KL, et al. Survival comparison of allograft and autograft anterior cruciate ligament reconstruction at the United States Military Academy. Am J Sports Med. 2012;40(6):1242–1246. 16. Ahlden M, Samuelsson K, Sernert N, et al. The Swedish National Anterior Cruciate Ligament register: a report on baseline variables and outcomes of surgery for almost 18,000 patients. Am J Sports Med. 2012;40(10):2230–2235. 17. Hettrich CM, Dunn WR, Reinke EK, et al. The rate of subsequent surgery and predictors after anterior cruciate ligament reconstruction: two- and 6-year follow-up results

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from a multicenter cohort. Am J Sports Med. 2013;41(7):1534–1540. Lind M, Menhert F, Pedersen AB. Incidence and outcome after revision anterior cruciate ligament reconstruction: results from the Danish registry for knee ligament reconstructions. Am J Sports Med. 2012;40(7):1551–1557. Maletis GB, Inacio MC, Funahashi TT. Analysis of 16,192 anterior cruciate ligament reconstructions from a communitybased registry. Am J Sports Med. 2013;41(9):2090–2098. Wasserstein D, Khoshbin A, Dwyer T, et al. Risk factors for recurrent anterior cruciate ligament reconstruction: a population study in Ontario, Canada, with 5-year follow-up. Am J Sports Med. 2013;41(9):2099–2107. Chen JL, Allen CR, Stephens TE, et al. Differences in mechanisms of failure, intraoperative findings, and surgical characteristics between single- and multiple-revision ACL reconstructions: a MARS cohort study. Am J Sports Med. 2013;41(7):1571–1578. Group M, Wright RW, Huston LJ, et al. Descriptive epidemiology of the Multicenter ACL Revision Study (MARS) cohort. Am J Sports Med. 2010;38(10):1979–1986. Ohly NE, Murray IR, Keating JF. Revision anterior cruciate ligament reconstruction: timing of surgery and the incidence of meniscal tears and degenerative change. J Bone Joint Surg Br. 2007;89(8):1051–1054. Thomas NP, Kankate R, Wandless F, et al. Revision anterior cruciate ligament reconstruction using a 2-stage technique with bone grafting of the tibial tunnel. Am J Sports Med. 2005;33(11):1701–1709. Getelman MH, Friedman MJ. Revision anterior cruciate ligament reconstruction surgery. J Am Acad Orthop Surg. 1999;7(3):189–198. Harilainen A, Sandelin J. Revision anterior cruciate ligament surgery. A review of the literature and results of our own revisions. Scand J Med Sci Sports. 2001;11(3):163–169. Taggart TF, Kumar A, Bickerstaff DR. Revision anterior cruciate ligament reconstruction: a midterm patient assessment. Knee. 2004;11(1):29–36. George MS, Dunn WR, Spindler KP. Current concepts review: revision anterior cruciate ligament reconstruction. Am J Sports Med. 2006;34(12):2026–2037. Kamath GV, Redfern JC, Greis PE, et al. Revision anterior cruciate ligament reconstruction. Am J Sports Med. 2011;39(1): 199–217. [Epub August 17, 2010]. Magnussen RA, Trojani C, Granan LP, et al. Patient demographics and surgical characteristics in ACL revision: a comparison of French, Norwegian, and North American cohorts. Knee Surg Sports Traumatol Arthrosc. 2015;23(8): 2339–2348. Trojani C, Beaufils P, Burdin G, et al. Revision ACL reconstruction: influence of a lateral tenodesis. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1565–1570. Shelbourne KD, Gray T, Haro M. Incidence of subsequent injury to either knee within 5 years after anterior cruciate ligament reconstruction with patellar tendon autograft. Am J Sports Med. 2009;37(2):246–251. Salmon LJ, Pinczewski LA, Russell VJ, et al. Revision anterior cruciate ligament reconstruction with hamstring tendon autograft: 5- to 9-year follow-up. Am J Sports Med. 2006; 34(10):1604–1614. Kaeding CC, Aros B, Pedroza A, et al. Allograft versus autograft anterior cruciate ligament reconstruction: predictors of failure

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35.

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43. 44.

45.

46.

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48.

49.

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51.

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from a MOON prospective longitudinal cohort. Sports Health. 2011;3(1):73–81. Marx RG, Stump TJ, Jones EC, et al. Development and evaluation of an activity rating scale for disorders of the knee. Am J Sports Med. 2001;29(2):213–218. Marx RG, Connor J, Lyman S, et al. Multirater agreement of arthroscopic grading of knee articular cartilage. Am J Sports Med. 2005;33(11):1654–1657. [Epub August 12, 2005]. Wright RW, Huston LJ, Spindler KP, et al. Descriptive epidemiology of the Multicenter ACL Revision Study (MARS) cohort. Am J Sports Med. 2010;38(10):1979–1986. [Epub October 5, 2010]. Shelbourne KD, Thomas J. Contralateral patellar tendon and the Shelbourne experience: part 1. Revision anterior cruciate ligament reconstruction and rehabilitation. Sports Med Arthrosc. 2005;13(1):25–31. In Y, Kwak DS, Moon CW, et al. Biomechanical comparison of three techniques for fixation of tibial avulsion fractures of the anterior cruciate ligament. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1470–1478. Kocher MS, Steadman JR, Briggs K, et al. Determinants of patient satisfaction with outcome after anterior cruciate ligament reconstruction. J Bone Joint Surg. 2002;84-A(9): 1560–1572. Kocher MS, Steadman JR, Briggs KK, et al. Reliability, validity, and responsiveness of the Lysholm knee scale for various chondral disorders of the knee. J Bone Joint Surg. 2004;86-A(6):1139–1145. Kowalchuk DA, Harner CD, Fu FH, et al. Prediction of patient-reported outcome after single-bundle anterior cruciate ligament reconstruction. Arthroscopy. 2009;25(5):457–463. Lucie RS, Wiedel JD, Messner DG. The acute pivot shift: clinical correlation. Am J Sports Med. 1984;12(3):189–191. Eastlack ME, Axe MJ, Snyder-Mackler L. Laxity, instability, and functional outcome after ACL injury: copers versus noncopers. Med Sci Sports Exerc. 1999;31(2):210–215. Anderson AF, Snyder RB, Lipscomb AB Jr. Anterior cruciate ligament reconstruction. A prospective randomized study of three surgical methods. Am J Sports Med. 2001;29(3):272–279. Beynnon BD, Johnson RJ, Fleming BC, et al. Anterior cruciate ligament replacement: comparison of bone-patellar tendonbone grafts with two-strand hamstring grafts. A prospective, randomized study. J Bone Joint Surg. 2002;84-A(9):1503–1513. Brandsson S, Faxen E, Eriksson BI, et al. Reconstruction of the anterior cruciate ligament: comparison of outside-in and all-inside techniques. Br J Sports Med. 1999;33(1):42–45. Foster TE, Wolfe BL, Ryan S, et al. Does the graft source really matter in the outcome of patients undergoing anterior cruciate ligament reconstruction? An evaluation of autograft versus allograft reconstruction results: a systematic review. Am J Sports Med. 2010;38(1):189–199. [Epub January 7, 2010]. Fox JA, Pierce M, Bojchuk J, et al. Revision anterior cruciate ligament reconstruction with nonirradiated fresh-frozen patellar tendon allograft. Arthroscopy. 2004;20(8):787–794. O’Neill DB. Arthroscopically assisted reconstruction of the anterior cruciate ligament. A follow-up report. J Bone Joint Surg. 2001;83-A(9):1329–1332. Weiler A, Schmeling A, Stohr I, et al. Primary versus singlestage revision anterior cruciate ligament reconstruction using autologous hamstring tendon grafts: a prospective matchedgroup analysis. Am J Sports Med. 2007;35(10):1643–1652. [Epub June 19, 2007].

52. Ahn JH, Lee YS, Ha HC. Comparison of revision surgery with primary anterior cruciate ligament reconstruction and outcome of revision surgery between different graft materials. Am J Sports Med. 2008;36(10):1889–1895. 53. Diamantopoulos AP, Lorbach O, Paessler HH. Anterior cruciate ligament revision reconstruction: results in 107 patients. Am J Sports Med. 2008;36(5):851–860. 54. Garofalo R, Djahangiri A, Siegrist O. Revision anterior cruciate ligament reconstruction with quadriceps tendon-patellar bone autograft. Arthroscopy. 2006;22(2):205–214. 55. Ferretti A, Conteduca F, Monaco E, et al. Revision anterior cruciate ligament reconstruction with doubled semitendinosus and gracilis tendons and lateral extra-articular reconstruction. J Bone Joint Surg. 2006;88(11):2373–2379. 56. Noyes FR, Barber-Westin SD. Revision anterior cruciate ligament reconstruction using a 2-stage technique with bone grafting of the tibial tunnel. Am J Sports Med. 2006;34(4):678– 679, author reply 679–680. 57. Noyes FR, Barber-Westin SD. Revision anterior cruciate surgery with use of bone-patellar tendon-bone autogenous grafts. J Bone Joint Surg. 2001;83-A(8):1131–1143. 58. Samitier G, Marcano AI, Alentorn-Geli E, et al. Failure of anterior cruciate ligament reconstruction. Arch Bone Jt Surg. 2015;3(4):220–240. 59. Hoser C, Tecklenburg K, Kuenzel KH, et al. Postoperative evaluation of femoral tunnel position in ACL reconstruction: plain radiography versus computed tomography. Knee Surg Sports Traumatol Arthrosc. 2005;13(4):256–262. 60. Group M. Radiographic findings in revision anterior cruciate ligament reconstructions from the MARS cohort. J Knee Surg. 2013;26(4):239–248. 61. Battaglia MJ 2nd, Cordasco FA, Hannafin JA, et al. Results of revision anterior cruciate ligament surgery. Am J Sports Med. 2007;35(12):2057–2066. 62. Sommer C, Friederich NF, Muller W. Improperly placed anterior cruciate ligament grafts: correlation between radiological parameters and clinical results. Knee Surg Sports Traumatol Arthrosc. 2000;8(4):207–213. 63. Trojani C, Sbihi A, Djian P, et al. Causes for failure of ACL reconstruction and influence of meniscectomies after revision. Knee Surg Sports Traumatol Arthrosc. 2011;19(2):196–201. 64. Lee MC, Seong SC, Lee S, et al. Vertical femoral tunnel placement results in rotational knee laxity after anterior cruciate ligament reconstruction. Arthroscopy. 2007;23(7):771–778. 65. Jepsen CF, Lundberg-Jensen AK, Faunoe P. Does the position of the femoral tunnel affect the laxity or clinical outcome of the anterior cruciate ligament-reconstructed knee? A clinical, prospective, randomized, double-blind study. Arthroscopy. 2007;23(12):1326–1333. 66. Raffo CS, Pizzarello P, Richmond JC, et al. A reproducible landmark for the tibial tunnel origin in anterior cruciate ligament reconstruction: avoiding a vertical graft in the coronal plane. Arthroscopy. 2008;24(7):843–845. 67. Miller MD, Olszewski AD. Posterior tibial tunnel placement to avoid anterior cruciate ligament graft impingement by the intercondylar roof. An in vitro and in vivo study. Am J Sports Med. 1997;25(6):818–822. 68. Khalfayan EE, Sharkey PF, Alexander AH, et al. The relationship between tunnel placement and clinical results after anterior cruciate ligament reconstruction. Am J Sports Med. 1996;24(3):335–341.

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CHAPTER 99  Revision Anterior Cruciate Ligament Injuries 69. Howell SM, Berns GS, Farley TE. Unimpinged and impinged anterior cruciate ligament grafts: MR signal intensity measurements. Radiology. 1991;179(3):639–643. 70. Howell SM, Taylor MA. Failure of reconstruction of the anterior cruciate ligament due to impingement by the intercondylar roof. J Bone Joint Surg. 1993;75(7):1044–1055. 71. Watanabe BM, Howell SM. Arthroscopic findings associated with roof impingement of an anterior cruciate ligament graft. Am J Sports Med. 1995;23(5):616–625. 72. Howell SM, Barad SJ. Knee extension and its relationship to the slope of the intercondylar roof. Implications for positioning the tibial tunnel in anterior cruciate ligament reconstructions. Am J Sports Med. 1995;23(3):288–294. 73. Howell SM, Clark JA. Tibial tunnel placement in anterior cruciate ligament reconstructions and graft impingement. Clin Orthop Relat Res. 1992;283:187–195. 74. Howell SM, Gittins ME, Gottlieb JE, et al. The relationship between the angle of the tibial tunnel in the coronal plane and loss of flexion and anterior laxity after anterior cruciate ligament reconstruction. Am J Sports Med. 2001;29(5):567–574. 75. Morgan CD, Kalman VR, Grawl DM. Definitive landmarks for reproducible tibial tunnel placement in anterior cruciate ligament reconstruction. Arthroscopy. 1995;11(3):275–288. 76. Kamath GV, Redfern JC, Burks RT. Femoral radiographic landmarks for lateral collateral ligament reconstruction and repair: a new method of reference. Am J Sports Med. 2010;38(3):570–574. [Epub December 8, 2009]. 77. Harner CD, Giffin JR, Dunteman RC, et al. Evaluation and treatment of recurrent instability after anterior cruciate ligament reconstruction. Instr Course Lect. 2001;50:463–474. 78. Eitzen I, Holm I, Risberg MA. Preoperative quadriceps strength is a significant predictor of knee function two years after anterior cruciate ligament reconstruction. Br J Sports Med. 2009;43(5):371–376. 79. Johnson DL, Swenson TM, Irrgang JJ, et al. Revision anterior cruciate ligament surgery: experience from Pittsburgh. Clin Orthop Relat Res. 1996;325:100–109. 80. Uribe JW, Hechtman KS, Zvijac JE, et al. Revision anterior cruciate ligament surgery: experience from Miami. Clin Orthop Relat Res. 1996;325:91–99. 81. Noyes FR, Barber SD, Simon R. High tibial osteotomy and ligament reconstruction in varus angulated, anterior cruciate ligament-deficient knees. A two- to seven-year follow-up study. Am J Sports Med. 1993;21(1):2–12. 82. Salmon L, Russell V, Musgrove T, et al. Incidence and risk factors for graft rupture and contralateral rupture after anterior cruciate ligament reconstruction. Arthroscopy. 2005;21(8): 948–957. 83. Barrett GR, Brown TD. Femoral tunnel defect filled with a synthetic dowel graft for a single-staged revision anterior cruciate ligament reconstruction. Arthroscopy. 2007;23(7):796, e1–e4. 84. Carson EW, Anisko EM, Restrepo C, et al. Revision anterior cruciate ligament reconstruction: etiology of failures and clinical results. J Knee Surg. 2004;17(3):127–132. 85. Amiel D, Kleiner JB, Roux RD, et al. The phenomenon of “ligamentization”: anterior cruciate ligament reconstruction with autogenous patellar tendon. J Orthop Res. 1986;4(2): 162–172. 86. Pinczewski LA, Clingeleffer AJ, Otto DD, et al. Integration of hamstring tendon graft with bone in reconstruction of the anterior cruciate ligament. Arthroscopy. 1997;13(5):641–643.

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87. Bach BR Jr. Revision anterior cruciate ligament surgery. Arthroscopy. 2003;19(suppl 1):14–29. 88. Colosimo AJ, Heidt RS Jr, Traub JA, et al. Revision anterior cruciate ligament reconstruction with a reharvested ipsilateral patellar tendon. Am J Sports Med. 2001;29(6):746–750. 89. Greis PE, Johnson DL, Fu FH. Revision anterior cruciate ligament surgery: causes of graft failure and technical considerations of revision surgery. Clin Sports Med. 1993;12(4):839–852. 90. Jaureguito JW, Paulos LE. Why grafts fail. Clin Orthop Relat Res. 1996;325:25–41. 91. Denti M, Lo Vetere D, Bait C, et al. Revision anterior cruciate ligament reconstruction: causes of failure, surgical technique, and clinical results. Am J Sports Med. 2008;36(10):1896–1902. [Epub June 24, 2008]. 92. Woo SL, Kanamori A, Zeminski J, et al. The effectiveness of reconstruction of the anterior cruciate ligament with hamstrings and patellar tendon. A cadaveric study comparing anterior tibial and rotational loads. J Bone Joint Surg. 2002;84-A(6):907–914. 93. Aglietti P, Buzzi R, D’Andria S, et al. Long-term study of anterior cruciate ligament reconstruction for chronic instability using the central one-third patellar tendon and a lateral extraarticular tenodesis. Am J Sports Med. 1992;20(1):38–45. 94. Aglietti P, Buzzi R, D’Andria S, et al. Arthroscopic anterior cruciate ligament reconstruction with patellar tendon. Arthroscopy. 1992;8(4):510–516. 95. Romano VM, Graf BK, Keene JS, et al. Anterior cruciate ligament reconstruction. The effect of tibial tunnel placement on range of motion. Am J Sports Med. 1993;21(3):415–418. 96. Jackson DW, Gasser SI. Tibial tunnel placement in ACL reconstruction. Arthroscopy. 1994;10(2):124–131. 97. Muneta T, Yamamoto H, Ishibashi T, et al. The effects of tibial tunnel placement and roofplasty on reconstructed anterior cruciate ligament knees. Arthroscopy. 1995;11(1):57–62. 98. O’Neill DB. Revision arthroscopically assisted anterior cruciate ligament reconstruction with previously unharvested ipsilateral autografts. Am J Sports Med. 2004;32(8):1833–1841. 99. Ferretti A, Conteduca F, Monaco E, et al. Revision ACL reconstruction using doubled semitendinosus and gracilis tendons: a follow-up study. J Orthop Traumatol. 2004;5(3): 142–146. 100. Gersoff WK, Clancy WG Jr. Diagnosis of acute and chronic anterior cruciate ligament tears. Clin Sports Med. 1988;7(4): 727–738. 101. Singhal MC, Gardiner JR, Johnson DL. Failure of primary anterior cruciate ligament surgery using anterior tibialis allograft. Arthroscopy. 2007;23(5):469–475. 102. Prodromos C, Joyce B, Shi K. A meta-analysis of stability of autografts compared to allografts after anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):851–856. 103. Krych AJ, Jackson JD, Hoskin TL, et al. A meta-analysis of patellar tendon autograft versus patellar tendon allograft in anterior cruciate ligament reconstruction. Arthroscopy. 2008;24(3):292–298. [Epub March 1, 2008]. 104. Poehling GG, Curl WW, Lee CA, et al. Analysis of outcomes of anterior cruciate ligament repair with 5-year follow-up: allograft versus autograft. Arthroscopy. 2005;21(7):774–785. 105. Rappe M, Horodyski M, Meister K, et al. Nonirradiated versus irradiated Achilles allograft: in vivo failure comparison. Am J Sports Med. 2007;35(10):1653–1658.

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SECTION 7  Knee

106. Brophy RH, Wright RW, David TS, et al. Association between previous meniscal surgery and the incidence of chondral lesions at revision anterior cruciate ligament reconstruction. Am J Sports Med. 2012;40(4):808–814. 107. Drogset JO, Grontvedt T. Anterior cruciate ligament reconstruction with and without a ligament augmentation device: results at 8-year follow-up. Am J Sports Med. 2002;30(6):851–856. 108. Allen CR, Wong EK, Livesay GA, et al. Importance of the medial meniscus in the anterior cruciate ligament-deficient knee. J Orthop Res. 2000;18(1):109–115. 109. Keene GC, Bickerstaff D, Rae PJ, et al. The natural history of meniscal tears in anterior cruciate ligament insufficiency. Am J Sports Med. 1993;21(5):672–679. 110. Indelicato PA, Bittar ES. A perspective of lesions associated with ACL insufficiency of the knee. A review of 100 cases. Clin Orthop Relat Res. 1985;198:77–80. 111. Cipolla M, Scala A, Gianni E, et al. Different patterns of meniscal tears in acute anterior cruciate ligament (ACL) ruptures and in chronic ACL-deficient knees. Classification, staging and timing of treatment. Knee Surg Sports Traumatol Arthrosc. 1995;3(3):130–134. 112. Widener DB, Wilson DJ, Galvin JW, et al. The prevalence of meniscal tears in young athletes undergoing revision anterior cruciate ligament reconstruction. Arthroscopy. 2014; December 15. 113. Segawa H, Omori G, Koga Y. Long-term results of nonoperative treatment of anterior cruciate ligament injury. Knee. 2001;8(1):5–11. 114. Gillquist J, Messner K. Anterior cruciate ligament reconstruction and the long-term incidence of gonarthrosis. Sports Med. 1999;27(3):143–156. 115. Noyes FR, Barber-Westin SD. Revision anterior cruciate ligament reconstruction: report of 11-year experience and results in 114 consecutive patients. Instr Course Lect. 2001;50:451–461. 116. Noyes FR, Barber-Westin SD. Anterior cruciate ligament revision reconstruction: results using a quadriceps tendonpatellar bone autograft. Am J Sports Med. 2006;34(4):553–564. 117. Wegrzyn J, Chouteau J, Philippot R, et al. Repeat revision of anterior cruciate ligament reconstruction: a retrospective review of management and outcome of 10 patients with an average 3-year follow-up. Am J Sports Med. 2009;37(4): 776–785. 118. Franceschi F, Papalia R, Di Martino A, et al. A new harvest site for bone graft in anterior cruciate ligament revision surgery. Arthroscopy. 2007;23(5):558, e1–e4. 119. Said HG, Baloch K, Green M. A new technique for femoral and tibial tunnel bone grafting using the OATS harvesters in revision anterior cruciate ligament reconstruction. Arthroscopy. 2006;22(7):796, e1–e3. 120. Vaughn ZD, Schmidt J, Lindsey DP, et al. Biomechanical evaluation of a 1-stage revision anterior cruciate ligament reconstruction technique using a structural bone void filler for femoral fixation. Arthroscopy. 2009;25(9):1011–1018. 121. Werner BC, Gilmore CJ, Hamann JC, et al. Revision anterior cruciate ligament reconstruction: results of a single-stage approach using allograft dowel bone grafting for femoral defects. J Am Acad Orthop Surg. 2016;24(8):581–587. 122. Sgaglione NA, Douglas JA. Allograft bone augmentation in anterior cruciate ligament reconstruction. Arthroscopy. 2004;20(suppl 2):171–177.

123. The MARS Group, Allen CR, Anderson AF, et al. Surgical predictors of clinical outcomes after revision anterior cruciate ligament reconstruction. Am J Sports Med. 2017;45(11):2586–2594. 124. Harner CD, Honkamp NJ, Ranawat AS. Anteromedial portal technique for creating the anterior cruciate ligament femoral tunnel. Arthroscopy. 2008;24(1):113–115. 125. Yamamoto Y, Hsu WH, Woo SL, et al. Knee stability and graft function after anterior cruciate ligament reconstruction: a comparison of a lateral and an anatomical femoral tunnel placement. Am J Sports Med. 2004;32(8):1825–1832. 126. Yagi M, Wong EK, Kanamori A, et al. Biomechanical analysis of an anatomic anterior cruciate ligament reconstruction. Am J Sports Med. 2002;30(5):660–666. 127. Shen W, Forsythe B, Ingham SM, et al. Application of the anatomic double-bundle reconstruction concept to revision and augmentation anterior cruciate ligament surgeries. J Bone Joint Surg. 2008;90(suppl 4):20–34. 128. Ho JY, Gardiner A, Shah V, et al. Equal kinematics between central anatomic single-bundle and double-bundle anterior cruciate ligament reconstructions. Arthroscopy. 2009;25(5): 464–472. 129. Markolf KL, Hame S, Hunter DM, et al. Effects of femoral tunnel placement on knee laxity and forces in an anterior cruciate ligament graft. J Orthop Res. 2002;20(5):1016–1024. 130. Kaz R, Starman JS, Fu FH. Anatomic double-bundle anterior cruciate ligament reconstruction revision surgery. Arthroscopy. 2007;23(11):1250, e1–e3. 131. Brophy RH, Selby RM, Altchek DW. Anterior cruciate ligament revision: double-bundle augmentation of primary vertical graft. Arthroscopy. 2006;22(6):683, e1–e5. 132. Group M. Factors influencing graft choice in revision anterior cruciate ligament reconstruction in the MARS group. J Knee Surg. 2016;29(6):458–463. 133. Group M, Ding DY, Zhang AL, et al. Subsequent surgery after revision anterior cruciate ligament reconstruction: rates and risk factors from a multicenter cohort. Am J Sports Med. 2017;d oi:10.1177/0363546517707207. May 1. 134. Group M, Group M. Effect of graft choice on the outcome of revision anterior cruciate ligament reconstruction in the Multicenter ACL Revision Study (MARS) cohort. Am J Sports Med. 2014;42(10):2301–2310. 135. Carey JL, Dunn WR, Dahm DL, et al. A systematic review of anterior cruciate ligament reconstruction with autograft compared with allograft. J Bone Joint Surg. 2009;91(9):2242– 2250. [Epub September 3, 2009]. 136. Noyes FR, Barber-Westin SD, Roberts CS. Use of allografts after failed treatment of rupture of the anterior cruciate ligament. J Bone Joint Surg. 1994;76(7):1019–1031. 137. Maletis GB, Cameron SL, Tengan JJ, et al. A prospective randomized study of anterior cruciate ligament reconstruction: a comparison of patellar tendon and quadruple-strand semitendinosus/gracilis tendons fixed with bioabsorbable interference screws. Am J Sports Med. 2007;35(3):384– 394. 138. Pinczewski LA, Lyman J, Salmon LJ, et al. A 10-year comparison of anterior cruciate ligament reconstructions with hamstring tendon and patellar tendon autograft: a controlled, prospective trial. Am J Sports Med. 2007;35(4):564–574. 139. Sajovic M, Vengust V, Komadina R, et al. A prospective, randomized comparison of semitendinosus and gracilis tendon versus patellar tendon autografts for anterior cruciate ligament

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152. Mikkelsen C, Werner S, Eriksson E. Closed kinetic chain alone compared to combined open and closed kinetic chain exercises for quadriceps strengthening after anterior cruciate ligament reconstruction with respect to return to sports: a prospective matched follow-up study. Knee Surg Sports Traumatol Arthrosc. 2000;8(6):337–342. 153. Sherry MA, Best TM. A comparison of 2 rehabilitation programs in the treatment of acute hamstring strains. J Orthop Sports Phys Ther. 2004;34(3):116–125. 154. Zazulak BT, Hewett TE, Reeves NP, et al. Deficits in neuromuscular control of the trunk predict knee injury risk: a prospective biomechanical-epidemiologic study. Am J Sports Med. 2007;35(7):1123–1130. 155. Borotikar BS, Newcomer R, Koppes R, et al. Combined effects of fatigue and decision making on female lower limb landing postures: central and peripheral contributions to ACL injury risk. Clin Biomech (Bristol, Avon). 2008;23(1):81–92. 156. Sell TC, Ferris CM, Abt JP, et al. The effect of direction and reaction on the neuromuscular and biomechanical characteristics of the knee during tasks that simulate the noncontact anterior cruciate ligament injury mechanism. Am J Sports Med. 2006;34(1):43–54. 157. Chmielewski TL, Jones D, Day T, et al. The association of pain and fear of movement/reinjury with function during anterior cruciate ligament reconstruction rehabilitation. J Orthop Sports Phys Ther. 2008;38(12):746–753. 158. Kvist J, Ek A, Sporrstedt K, et al. Fear of re-injury: a hindrance for returning to sports after anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2005;13(5):393–397. 159. Wright R, Spindler K, Huston L, et al. Revision ACL reconstruction outcomes: MOON cohort. J Knee Surg. 2011;24(4):289–294. 160. Battaglia TC, Miller MD. Management of bony deficiency in revision anterior cruciate ligament reconstruction using allograft bone dowels: surgical technique. Arthroscopy. 2005;21(6):767. 161. Leroux T, Ogilvie-Harris D, Dwyer T, et al. The risk of knee arthroplasty following cruciate ligament reconstruction: a population-based matched cohort study. J Bone Joint Surg. 2014;96(1):2–10. 162. Arianjam A, Inacio MCS, Funahashi TT, et al. Analysis of 2019 patients undergoing revision anterior cruciate ligament reconstruction from a community-based registry. Am J Sports Med. 2017;45(7):1574–1580.

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100  Posterior Cruciate Ligament Injuries Frank A. Petrigliano, Evan E. Vellios, Scott R. Montgomery, Jared S. Johnson, David R. McAllister

The treatment of posterior cruciate ligament (PCL) injuries is a controversial topic in orthopaedic surgery. In contrast to anterior cruciate ligament (ACL) injuries, for which an abundance of basic science and clinical data is available, the PCL has only recently become a topic of intense investigation. PCL injuries are less common compared with ACL injuries, and thus studies on outcomes are underpowered, making it difficult to draw definitive conclusions regarding management. However, recent biomechanical and clinical data have highlighted the importance of the PCL in knee stability and function. Injury to the PCL, which acts as the primary restraint to posterior tibial translation, may lead to instability, pain, diminished function, and eventually arthrosis. The purpose of this chapter is to discuss the evaluation, diagnosis, and management of PCL injuries and to present the relevant historic and recent literature on these topics. After a brief review of the pertinent components of the history, physical examination, and imaging modalities, we discuss important considerations in decision-making and treatment options in patients with PCL injuries, as well as our preferred surgical technique and outcomes of surgical management of PCL injuries. Decision-making in this patient population is largely dependent on the grade of PCL injury and the presence or absence of concomitant ligamentous injuries in the knee. We also focus on the latest evidence regarding transtibial versus the tibial inlay technique, single- versus double-bundle methods of reconstruction, and the outcomes of these various surgical treatment options.

HISTORY The true incidence and prevalence of PCL injuries are unknown and difficult to estimate because many of these injuries, particularly prior to the introduction of magnetic resonance imaging (MRI), were not diagnosed.1 The reported incidence of PCL injuries has differed depending on the population studied. The incidence is as low as 3% in the outpatient setting2 and as high as 37% in the traumatic setting.3 Traumatic injuries and sportsrelated injuries account for the majority of PCL injuries. A prospective analysis of patients presenting with acute hemarthrosis of the knee and diagnosed with a PCL injury demonstrated that 56.5% of patients were trauma victims, whereas 32.9% had a sports-related injury.3 Yet isolated PCL injuries were infrequent in this cohort, with 96.5% being part of a multiligamentous

injury. Similarly, in a retrospective cohort of 494 patients with PCL insufficiency, Schulz et al.4 found traffic accidents (45%) and athletic injuries (40%) to be the most common causes of injury. Among specific sports, the incidence of PCL injury tends to be greater in those involving contact, such as football, soccer, and rugby. In the cohort reviewed by Schulz and colleagues,4 skiing and soccer were the sports with the highest incidence of PCL injuries. Overall, the incidence of PCL injury has been estimated to be relatively low in athletes across a variety of sports.5–8 Important information can be obtained from the history of the patient presenting with acute knee pain or trauma. Any patient with knee pain and swelling with a high-energy mechanism of injury should be suspected of having a PCL injury, another capsuloligamentous injury, or both. Patients commonly report the inability to bear weight, instability, and decreased knee range of motion (ROM). In contrast to ACL injuries, which often result from a noncontact event, PCL injuries are typically due to external trauma. The classic “dashboard injury” pattern results from a posteriorly directed force on the anterior aspect of the proximal tibia with the knee in a flexed position. In patients with a higher energy mechanism of injury, it is possible that a knee dislocation occurred at the time of the injury even if the knee is reduced at the time of the evaluation. In athletics, the typical mechanism of isolated PCL injury is a direct blow to the anterior tibia (Fig. 100.1A) or a fall onto the knee with the foot plantar flexed. When the foot is in a position of dorsiflexion, the force is transmitted to the patella and distal femur, decreasing the risk of injury to the PCL (Fig. 100.2). Noncontact mechanisms of injury, although less common, have also been reported. Most commonly, this mechanism of injury occurs via forced hyperflexion of the knee (see Fig. 100.1B).9 In a small cohort reported by Fowler and Messieh,9 these injuries would often lead to incomplete tearing of the PCL with the posteromedial (PM) fibers intact. Knee hyperextension has also been described as a mechanism of injury, which is usually combined with a varus or valgus force that results in multiple ligament injury (see Fig. 100.1C). Isolated injuries may have more subtle presentations, with patients reporting stiffness, swelling, and pain located in the back of the knee or pain with deep knee flexion (squatting and kneeling). In contrast to acute ACL tears, a “pop” is not usually reported with acute isolated PCL injuries and athletes are often able to continue to play. Reports of anterior knee pain, difficulty ascending stairs, and instability

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CHAPTER 100  Posterior Cruciate Ligament Injuries

Abstract

Keywords

The treatment of posterior cruciate ligament (PCL) injuries is a controversial topic in orthopaedic surgery. In contrast to anterior cruciate ligament (ACL) injuries, for which an abundance of basic science and clinical data is available, the PCL has only recently become a topic of intense investigation. PCL injuries are less common compared with ACL injuries, and thus studies on outcomes are underpowered, making it difficult to draw definitive conclusions regarding management. However, recent biomechanical and clinical data have highlighted the importance of the PCL in knee stability and function. Injury to the PCL, which acts as the primary restraint to posterior tibial translation, may lead to instability, pain, diminished function, and eventually arthrosis. The purpose of this chapter is to discuss the evaluation, diagnosis, and management of PCL injuries and to present the relevant historic and recent literature on these topics. After a brief review of the pertinent components of the history, physical examination, and imaging modalities, we discuss important considerations in decision-making and treatment options in patients with PCL injuries, as well as our preferred surgical technique and outcomes of surgical management of PCL injuries. Decision-making in this patient population is largely dependent on the grade of PCL injury and the presence or absence of concomitant ligamentous injuries in the knee. We also focus on the latest evidence regarding transtibial versus the tibial inlay technique, single- versus double-bundle methods of reconstruction, and the outcomes of these various surgical treatment options.

posterior cruciate transtibial inlay single versus double bundle

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A

B

C

Fig. 100.1  Posterior cruciate ligament injuries are most frequently the result of a blow to the front of the flexed knee.

A

B

C Fig. 100.2  (A) Falling on a flexed knee with the foot in a dorsiflexed position spares injury to the posterior cruciate ligament (PCL) by transmitting the force to the patellofemoral joint. (B) Landing with the foot in a plantar flexed position injures the PCL because the posteriorly directed force is applied to the tibial tubercle. (C) Hyperflexion of the knee without a direct blow is a common mechanism of PCL injury in athletes.

are common when patients present in the chronic phase of an isolated PCL injury.10

PHYSICAL EXAMINATION Posterior Drawer Test The posterior drawer test was described initially by Hughston et al.11 in 1976 and later by Clancy et al.12 in 1983 and is considered the most accurate clinical test to assess the integrity of the PCL, with a sensitivity of 90% and 99% specificity.13,14 The results of this examination also guide treatment recommendations. A posteriorly directed force is placed on the proximal tibia

with the patient lying supine and the knee flexed to 90 degrees. This test can be performed with the tibia in neutral, external, and internal rotation. It is important to remember that with a PCL injury, the tibia subluxes posteriorly. Thus it is important to first apply an anteriorly directed force to reduce the posterior subluxation before applying the posteriorly directed force (Fig. 100.3). In cases of isolated PCL tears, a decrease occurs in posterior tibial translation with internal tibial rotation.15 The superficial medial collateral ligament (MCL) and posterior oblique ligament act as a secondary restraint with the tibia in internal rotation.16 Translation is measured as the change in distance of step-off between the medial tibial plateau relative to the medial femoral condyle. It is critical to examine the contralateral knee, because the normal relationship between the medial tibial plateau and medial femoral condyle is variable, with the plateau normally resting on average 1 cm anterior to the condyle. Understanding this relationship is also critical in avoiding a false-positive anterior drawer test. The presence or lack of a firm end point should also be noted. The amount of posterior translation observed during the posterior drawer test is used to grade the PCL injury. In grade I injuries, 0 to 5 mm of increased posterior translation is observed compared with the contralateral knee, but the anterior step-off of the plateau relative to the condyle is maintained. Grade II injuries are defined as those with 6 to 10 mm of posterior translation, which results in the plateau being flush with, but not posterior to, the medial femoral condyle. In both grade I and II injuries, the PCL is usually partially torn. With grade III injuries, posterior translation exceeds 10 mm and the medial tibial plateau displaces posterior to the medial femoral condyle during the posterior drawer test. This finding usually represents a complete tear of the PCL and could also represent a combined PCL and posterolateral corner (PLC) injury.

Posterior Sag Test (Godfrey Test) and Quadriceps Active Test The posterior sag test may be positive in patients with complete PCL tears or partial tears. The patient lies supine with the hip and knee flexed to 90 degrees and the limb supported at the foot by the examiner. The anterior aspect of the proximal tibia

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Fig. 100.4  A positive Godfrey test. (Modified from Miller MD, Harner CD, Koshiwaguchi S. Acute posterior cruciate ligament injuries. In: Fu FH, Harner CD, Vince KG, eds. Knee Surgery. Vol. 1. Baltimore: Williams & Wilkins; 1994.)

Fig. 100.3  Assessing the tibial step-off before performing the posterior drawer examination. (Modified from Miller MD, Harner CD, Koshiwaguchi S. Acute posterior cruciate ligament injuries. In: Fu FH, Harner CD, Vince KG, eds. Knee Surgery. Vol. 1. Baltimore: Williams & Wilkins; 1994.)

is viewed from the side and compared with the uninjured, contralateral knee. Gravity displaces the tibia posterior to the femur in the case of a complete tear (Fig. 100.4). The quadriceps active test can aid in the diagnosis of complete tears. With this test, the patient lies supine and the knee is placed at 90 degrees of flexion. While the examiner stabilizes the foot, the patient is asked to contract the quadriceps isometrically. In the presence of a complete tear of the PCL (grade III), the patient will achieve dynamic reduction of the posteriorly displaced tibia.

External Rotation of the Tibia (Dial Test) The dial test is performed to evaluate for concomitant injuries to the PLC, which will affect decision-making and treatment options because these patients are more likely to require surgery. The dial test is performed with the patient positioned prone or supine, while an external rotation force is applied to both feet with the knee positioned at 30 degrees and then 90 degrees of flexion. The degree of external tibial rotation is measured by comparing the medial border of the foot with the axis of the femur. It is essential to compare the results with the contralateral

side because wide variability of external rotation is possible at these positions.18,19 More than a 10-degree side-to-side difference is considered abnormal.20 At all degrees of knee flexion, the popliteus complex portion of the PLC is the primary restraint to external rotation, but its effect is maximal at 30 degrees. An increase of 10 degrees or more of external rotation at 30 degrees of knee flexion, but not at 90 degrees, is considered diagnostic of an isolated PLC injury.21 Increased external rotation at both 30 and 90 degrees of knee flexion suggests a combined PCL and PLC injury.

Reverse Pivot-Shift Test The reverse pivot-shift test is also used to assess combined injuries and is performed with the patient supine. The knee is passively extended from 90 degrees of flexion with the foot externally rotated and a valgus force applied to the tibia. A positive result is observed when the posteriorly subluxed lateral tibial plateau is abruptly reduced by the iliotibial band at 20 to 30 degrees of flexion. A positive test typically indicates injury to the PCL and another capsuloligamentous structure, usually the PLC.22

Collateral Ligament Assessment Varus and valgus stress tests are used to assess the lateral collateral ligament (LCL) portion of the PLC. The tests are performed with the knee in full extension and in 30 degrees of flexion. Although an isolated PCL injury does not significantly affect varus or valgus stability, increased varus opening at 30 degrees

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of knee flexion indicates an injury to the LCL and possibly the popliteus complex. If a significant degree of varus opening is noted at full extension, a combined injury of the PLC, PCL, and/or ACL is likely present.24,25

Gait and Limb Alignment The evaluation of gait and limb alignment is particularly important for persons with chronic injury of the PCL or the PLC. In these patients, varus alignment, external rotation, and varus thrust may be observed. Compromised function of the stabilizers of the lateral knee can lead to excessive posterolateral rotation and varus opening (or thrust) in the stance phase of gait.

IMAGING Radiography In the acute setting, plain radiographs of the knee should be performed, including bilateral standing anteroposterior, flexion posteroanterior 45 degrees with weight bearing, and Merchant patellar and lateral radiographs. These views are evaluated for posterior tibial subluxation, avulsion fractures, posterior tibial slope, and tibial plateau fractures. Tibial plateau fractures often indicate a high-energy injury with multiligament involvement. Bony avulsion fractures can be seen at the insertion of the PCL and at the fibular head, medial tibial plateau (medial Segond fracture), or the tibial tubercle.26 Identification of bony avulsion injuries of the PCL, when recognized acutely, may be repaired primarily with superior results compared with late reconstruction.26,27 Identification of tibial tubercle fractures is also critical. The unopposed pull of the hamstrings causes posterior tibial subluxation in this scenario, which can become fixed within a short time, requiring open reduction. Medial Segond fractures represent a medial capsular avulsion in PCL injuries that may be associated with a peripheral medial meniscus tear.28,29 Lastly, long leg hip-to-ankle views are critical to evaluate overall lower extremity alignment, particularly varus, in chronic or revision cases. Stress radiographs are not necessary to diagnose a PCL injury but may be helpful to differentiate between complete and partial PCL tears. However, these radiographs are most commonly used for research purposes. In a retrospective review of 21 patients with partial or complete PCL tears, Hewett and colleagues31 found that stress radiographs were more accurate than KT-1000 measurements in diagnosing PCL tears. With the knee flexed to 70 degrees and an 89-N weight suspended from the tibia at the level of the tibial tubercle, a lateral radiograph was taken. The mean translation of the medial tibial plateau was 12.2 mm in the presence of a complete tear compared with 5.2 mm seen with a partial tear as confirmed with diagnostic arthroscopy. The magnitude of posterior tibial translation during stress radiography has been correlated with the presence of combined ligament injury. In a cadaveric study by Sekiya et al.,32 the authors demonstrated that greater than 10 mm of posterior tibial translation on stress radiography correlated with the presence of a PLC injury in addition to a complete disruption of the PCL. It should be noted that the accuracy of stress radiography may be decreased by patient guarding and partial reduction of the tibia

with quadriceps activation; in addition, this infrequently performed examination is operator dependent. Stress radiographs can also be influenced by tibial rotation, and thus some authors have concluded that physical examination may be equally sensitive to stress radiographs in determining the presence and extent of a PCL tear.33

Magnetic Resonance Imaging MRI has become the imaging modality of choice for confirming the presence of an acute PCL tear and to diagnose associated injuries with a sensitivity of up to 100%.14,34,35 The location and physical characteristics of the tear can also be assessed with MRI and may have implications for prognosis and treatment.36,37 MRI may be less sensitive in the diagnoses of chronic tears. The normal PCL appears dark on T1- and T2-weighted sequences and is curvilinear in appearance.38 In contrast, chronic tears of the PCL can heal and assume the aforementioned curvilinear appearance; thus MRIs are much less sensitive for chronic PCL tears, and the appearance of a normal shape of the ligament should not be used as a criterion for a normal PCL.39,40 Lastly, MRI provides important information on the status of the menisci, articular cartilage, and other ligaments in the knee, because concomitant injuries affect treatment decision-making and prognosis.41 Bone bruises have been found in 83% of grade II and III PCL injuries on MRI, but in contrast to the bone bruise associated with ACL tears, the location is variable.42 The utility of MRI for the diagnosis of associated injuries to the PLC has previously been evaluated. With use of thin-slice coronal oblique T1-weighted images through the entire fibular head, LaPrade and colleagues43 were able to identify injury to the posterolateral structures with an accuracy of 68.8% to 94.4%, depending on the structure. Similarly, Theodorou et al.44 found that MRI has an accuracy of 79% to 100% for the diagnoses of posterolateral injuries confirmed with arthroscopy.

Bone Scan Although a bone scan is not frequently used, it can be useful in the evaluation and management of chronic PCL injuries. In particular, patients with these injuries are predisposed to early medial and patellofemoral compartment chondrosis.12,45,46 In the setting of an isolated PCL-deficient knee with medial or patellofemoral compartment pain and normal radiographs, a bone scan to assess these compartments may be indicated. Increased uptake suggests that surgical intervention may be beneficial,47 although this supposition has not been proven definitively.

DECISION-MAKING Decision-making in the treatment of PCL injuries is dependent on the natural history of the disease, with most treatment recommendations made on the basis of symptoms, activity level, grade of the injury, and associated injuries. As with any orthopaedic ailment, operative intervention should be chosen only if it results in superior outcomes compared with nonsurgical management. Controversy exists regarding PCL treatment because the extent to which posterior laxity causes symptoms or accelerates the development of degenerative joint disease (DJD) is unclear.

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CHAPTER 100  Posterior Cruciate Ligament Injuries

However, a computational knee kinematic study by Kang et al. suggests that PCL deficiency leads to significantly increased contact forces on the patellofemoral joint as well as PLC structures during normal gait.48 Furthermore, it is unknown whether reconstruction sufficiently mitigates laxity to result in clinical improvement and slow the development of DJD. Reducing posterior laxity with reconstruction may improve long-term outcomes in patients with PCL injuries, and yet residual laxity is common even after reconstruction.49,50 Some investigators propose that isolated PCL tears follow a benign course in the short term without reconstruction1,9,47,51 but that diminishing results may be seen at a later point.52 To date, no study has demonstrated that PCL reconstruction can prevent the development of DJD.53 Controversy remains regarding indications for nonoperative versus operative management because few clinical studies have sufficient sample sizes and duration of follow-up to draw definitive conclusions. Additionally, a variety of PCL reconstructions are currently used, and the treatment of isolated PCL injuries is often reported in conjunction with combined injuries, such as PLC injuries, making outcome studies relatively heterogeneous. Currently most studies are retrospective in nature and use various outcome measurements, which make comparisons difficult. Until randomized prospective clinical trials are conducted, this debate will likely continue. The next section reviews the results of nonoperative management of PCL injuries and conclude the section with our decision-making rationale.

Nonoperative Treatment Many studies have found favorable outcomes when isolated PCL injuries are treated conservatively. Parolie and Bergfeld1 evaluated patient satisfaction in 25 persons with isolated PCL tears that had resulted from sporting injuries at a minimum of 2 years of follow-up. These investigators found that 68% of patients returned to their previous level of activity and 80% were satisfied with their knee function. They evaluated laxity and found no correlation with DJD. More recently, Shelbourne and Muthukaruppan54 prospectively evaluated 215 conservatively treated patients with isolated PCL tears. Their study focused on patients with grade II laxity or less. These investigators found that subjective scores did not correlate with the degree of laxity and mean scores did not decrease with time from injury. They were unable to identify any risk factors that would predict which patients would have a decline in knee function over time. Patel et al.,55 in another recent retrospective review of 57 patients with grade A or B PCL tears, a grading system proposed by MacGillivray and colleagues56 also found that functional scores did not correlate with the degree of PCL laxity. Lysholm knee scores were excellent in 40% and good in 52%. Patel et al.55 found grade I medial compartment osteoarthritis (OA) in seven knees, grade II in three knees, and mild patellofemoral OA in four knees at an average of 6.8 years of follow-up. They concluded that most patients with acute, isolated PCL tears do well with nonoperative management at intermediate follow-up. Furthermore, a more recent study by Shelbourne and colleagues showed that at an average of 14.3 years follow-up 89% (39/44) of individuals with isolated grade I or II PCL injuries treated nonoperatively showed full ROM, good quadriceps strength, and minimal OA.57

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Other investigators have also found good initial clinical outcomes with nonoperative treatment but have found deterioration at extended follow-up. Boynton and Tietjens52 observed 38 patients with isolated tears for a mean of 13.4 years. Of these patients, eight had subsequent meniscal injuries and surgery. Of the remaining 30 patients with normal menisci, 24 (81%) had occasional pain, 17 (56%) had occasional swelling, and a positive increase in articular cartilage degeneration was seen on radiographs over time. Fowler and Messieh9 prospectively followed up 13 patients with acute isolated PCL tears that were confirmed by arthroscopy and treated with physiotherapy. All patients had a good subjective functional score according to the Houston criteria, but objective scores were good in only 3 patients and only fair in the other 10 patients. Although relatively good results have been observed with nonoperative treatment, it should be noted that many of the patients in these series had grade II laxity or less and not all patients achieved a normal outcome, especially patients with grade III injuries. The benign course observed may be due to the integrity of the secondary restraints and various portions of the PCL complex remaining intact in persons with less serious injuries. Tibial slope may also affect the stability of the PCL deficient knee. In a cadaveric study, increasing the posterior tibial slope decreased the static posterior instability of the PCL/PLC-deficient knee, whereas decreasing the tibial slope increased posterior instability and the magnitude of the reverse pivot-shift test.58 Despite acceptable clinical results with nonoperative treatment, it is well understood that PCL deficiency alters knee kinematics and the distribution of load during activity. In an uninjured knee, numerous biomechanical studies have shown that the PCL plays a significant role in tibiofemoral joint stability throughout an active and passive ROM especially in the presence of a posteriorly directed tibial force, while it has been shown that the PCL-deficient knee experiences increased contact pressures in the patellofemoral and medial compartments.48,59,60 Logan et al.59 evaluated the effect of PCL rupture on tibiofemoral motion during squatting with use of MRI. They concluded that PCL deficiency is similar to a medial meniscus resection and results in a “fixed” anterior subluxation of the medial femoral condyle (posterior subluxation of the medial tibial plateau). This subluxation changes the kinematics of the knee and may explain the increase in medial compartment OA seen in PCL-deficient knees. Currently more attention is being placed on additional injuries that are commonly associated with grade III tears that lead to greater instability and more severely altered biomechanics. Although it is known that the kinematics of the knee are altered in the presence of a PCL injury, specific prognostic factors that predict outcome have proven elusive. In many studies the time from injury and objective instability have not correlated well with final outcome and radiographic changes. Surgical reconstruction is not recommended for isolated grade I injuries. Because many patients with isolated grade II posterior laxity only improve to grade I laxity with reconstruction, we agree with other authors that operative intervention in these patients may not offer improved outcome when compared with nonoperative treatment.49,54 The treatment of acute isolated grade III PCL injuries is controversial. In these patients, some surgeons

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favor a more aggressive approach involving PCL reconstruction, whereas others recommend nonsurgical treatment. In cases with greater than 10 mm of abnormal posterior laxity, the clinician should remember to have a high index of suspicion for a combined ligamentous injury involving the PLC. Level I evidence does not currently exist to support strong recommendations on the management of PCL injuries. However, based on the previously described data, we recommend nonoperative management for the treatment of acute and chronic isolated grade I and II PCL injuries (Figs. 100.5 and 100.6). Operative management is reserved for chronic isolated grade III PCL injuries with symptoms of pain or instability when an adequate course of conservative treatment has failed. In addition, surgical treatment is usually recommended for acute and chronic combined ligamentous injuries. The treatment of acute grade III PCL tears is controversial, with some surgeons recommending PCL reconstruction and others recommending nonoperative treatment. Lastly, open reduction and internal fixation are recommended for acute avulsion fractures at the PCL tibial attachment site.

TREATMENT OPTIONS Nonoperative Treatment As discussed in the previous section, nonoperative treatment is recommended in patients with acute, isolated grade I or II PCL tears.1,45 Nonoperative management is aimed at counteracting the forces of gravity and the hamstring muscles, which act to sublux the tibia posteriorly on the femur. Pierce and colleagues62 have recently reviewed the literature on rehabilitation protocols for nonoperative and operative treatment of PCL injuries. Based on the finding of the reviewed studies, a three-phase rehabilitation

protocol was recommended. We follow a similar protocol at our institution. In the first 6 weeks after injury (phase I), rehabilitation is focused on partial weight-bearing, hamstring and gastrocnemius stretching to reduce the posterior pull on the tibia, quadriceps strengthening and prone ROM exercises. In this initial phase, a number of immobilization techniques have been described to decrease stress on the healing ligament. These techniques include bracing the knee locked between 0 and 60 degrees of knee flexion,63 use of a cylindrical leg cast with a posterior support to prevent posterior displacement of the tibia,64 and use of a brace with a dynamic anterior drawer to apply an anterior force on the posterior proximal tibia.65,66 In phase II, 6 to 12 weeks after injury, the focus is on progressive strengthening, reestablishment of full ROM, and improving proprioception. In phase III, 13 to 18 weeks after the injury occurred, the patient is allowed to begin running and to perform sports-specific exercises, with return to sports allowed 4 to 6 months after the initial injury, assuming quadriceps strength is comparable to that of the contralateral leg. It is important to note that this time frame can be significantly accelerated in the case of elite athletes with potential return to sport as early as 6 to 8 weeks but with the expected risk of increased residual joint laxity.61

Operative Treatment A number of surgical techniques for PCL reconstruction can be considered. Current surgical treatment options include transtibial and tibial inlay reconstruction techniques with single- or double-bundle reconstruction and a variety of fixation methods. Several biomechanical and anatomic studies have been published recently investigating the benefits and pitfalls of these techniques.

Acute PCL injury

Isolated

Grade I or II

Nonoperative • 4 weeks of extension immobilization • Physical therapy/quadriceps strengthening • Avoid unopposed hamstring excercises for 3 months • Gradual return to activity

Combined • PLC (± LCL) • MCL and medial side injury • ACL (± collaterals) • Knee dislocation

Grade III

Young, athletic patient No

Avulsion injury

Yes

Nonoperative • 4 weeks of full extension • Avoid posterior tibial subluxation • Physical therapy/quadriceps strengthening

Operative • ORIF avulsion • Consider PCL reconstruction in young athlete

Operative • Surgery performed less than 2 weeks, acute repair/reconstruction of collateral injuries • PCL reconstruction

Fig. 100.5  Treatment recommendations for acute injuries of the posterior cruciate ligament (PCL). ACL, Anterior cruciate ligament; LCL, lateral collateral ligament; MCL, medial collateral ligament; ORIF, open reduction, internal fixation; PLC, posterolateral corner.

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Chronic PCL injury

Isolated

Grade I or II

Combined • PLC (± LCL) • MCL and medial side injury • ACL (± collatrals) • Knee dislocation

Grade III

Nonoperative • Physical therapy/quadriceps strengthening • Activity modification

Symptomatic pain or instability?

Malalignment? No

Yes Physical therapy/quadriceps strengthening

Persistent symptoms?

Return to normal activities

No

Operative • Reconstruct all injured components, especially PLC • PCL reconstruction

Yes Malalignment?

No Operative • PCL reconstruction

Yes Operative • Biplanar osteotomy • Staged reconstruction for combined injuries

Yes

Fig. 100.6  Treatment recommendations for chronic injuries of the posterior cruciate ligament (PCL). ACL, Anterior cruciate ligament; LCL, lateral collateral ligament; MCL, medial collateral ligament; PLC, posterolateral corner.

However, no consensus currently exists on the best method of PCL reconstruction.

Transtibial Tunnel Versus Tibial Inlay Techniques The transtibial technique is a commonly used method of PCL reconstruction. In this technique, the tibial and femoral tunnels are drilled and the graft must make a sharp turn around the “killer turn” as it surfaces from the tibial tunnel and changes direction before entering the knee joint. This acute turn has been implicated as the cause of graft abrasion with subsequent thinning of the graft and eventual graft rupture or excessive laxity.65 The residual posterior knee laxity observed clinically after traditional transtibial PCL reconstruction techniques may be related to this acute turn. To address the concern of graft attenuation resulting from this tunnel, the tibial inlay technique was developed and reported by Jakob and Ruegsegger,67 as well as by Berg.68 In this technique, direct fixation occurs at the tibial attachment site of the PCL, preventing an acute turn as the graft passes from the tibia to the femoral tunnel. A number of cadaveric biomechanical studies have compared the transtibial and tibial inlay techniques. Although McAllister et al.69 found no significant differences in mean knee laxities between the tibial tunnel and tibial inlay techniques at time zero, increased laxity was observed with this technique after cyclic loading. Bergfeld et al.70 assessed anteroposterior laxity in cadaveric knees undergoing tunnel reconstruction or inlay reconstruction. Minimal differences in anteroposterior laxity were observed

in the inlay group when compared with the tunnel group from 30 to 90 degrees of knee flexion and after repetitive loading at 90 degrees of knee flexion. However, evaluation of the grafts after testing demonstrated evidence of graft thinning and attenuation in the tunnel group but not in the inlay group. In a detailed cyclic loading analysis, Markolf and colleagues71 also evaluated cadaver knees with tibial inlay and transtibial reconstruction. Ten of 31 grafts in the tunnel group failed at the acute angle before 2000 cycles of testing could be completed, whereas all 31 grafts that had been fixed to the tibia with use of the inlay method survived the testing intact. In addition, a significant increase in graft thinning and stretching out was observed in the remaining tunnel grafts that survived testing compared with the inlay grafts. Thus in vitro analyses comparing the transtibial technique with tibial inlay suggest that although initial knee stability is equivalent, posterior laxity increases with cyclic loading with the transtibial technique when compared with the tibial inlay technique. Attempts have also been made to decrease the effects of the killer turn by reducing the sharp edge at the tibial tunnel exit, but this technique has only been attempted in an animal model.72 Weimann and colleagues72 found that rounding the sharp edge of the tibial tunnel decreased graft damage associated with the killer turn in a porcine model of PCL reconstruction. To date, retrospective studies comparing patients undergoing transtibial versus tibial inlay procedures56,73 have not shown significant differences in subjective outcome or knee laxity measurements.74,75 Thus although the tibial inlay technique may have

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some biomechanical advantages when tested in a cadaveric model, these advantages have yet to be realized in the clinical setting.

Single-Bundle Versus Double-Bundle Reconstruction Controversy also exists regarding the utility of single- versus double-bundle techniques of PCL reconstruction. The native PCL can be divided into an anterolateral (AL) and a PM bundle (Fig. 100.7). The AL bundle is tight in knee flexion and becomes lax in extension, whereas the PM bundle is tight in knee extension and becomes lax in flexion. The AL bundle is larger in cross-sectional area and thus is most commonly reconstructed in single-bundle procedures (Fig. 100.8). Double-bundle PCL reconstructions were proposed to more closely reproduce the anatomy and biomechanical properties of the intact PCL. Biomechanical studies have indicated that the two bundles demonstrate reciprocal tightening during knee ROM and both are active in reducing posterior tibial translation and external tibial rotation, suggesting that both are required for normal knee kinematics.76,77 Single- versus double-bundle PCL reconstruction have been compared in several biomechanical studies, and some investigators have suggested improved biomechanics with double-bundle reconstruction.78,79 Milles et al.80 compared single-bundle versus double-bundle reconstruction in cadaveric human knees using five different surgical techniques and found increased stiffness and decreased laxity in double-bundle reconstructions at numerous flexion angles. Tsukada et al.81 compared single AL bundle reconstruction, single PM bundle reconstruction, and doublebundle reconstruction in cadaveric human knees at different angles of knee flexion. The double-bundle reconstruction resisted posterior tibial load better than the AL single bundle at 0 and 30 degrees of knee flexion and better than the PM single bundle at 30, 60, and 90 degrees of knee flexion under the posterior

A

tibial load, leading the authors to conclude that double-bundle reconstruction reduces laxity in extension. Additional studies have demonstrated potential drawbacks of double-bundle reconstruction, and some studies have been unable to demonstrate a benefit. Whiddon et al.82 compared single- and double-bundle tibial inlay reconstruction in a cadaver

PM

AL

Fig. 100.7  Femoral and tibial insertion sites of the posteromedial (PM) and anterolateral (AL) bundles of the posterior cruciate ligament. (From Chahla J, Nitri M, Civitarese D, et al. Anatomic double bundle posterior cruciate ligament reconstruction. Arthrosc Tech. 2016;5(1):149–156.)

B

Fig. 100.8  (A) Left knee showing both bundles: anterolateral bundle (ALB) and posteromedial bundle (PMB). The trochlear point is easily identifiable on the distal aspect of the trochlea. The more anterior aspect of the ALB is noted by the trochlear point, whereas its more inferoposterior aspect is delineated by the medial arch point. Likewise, the PMB is located along the wall of the notch and distal to the medial arch point. (B) Profile view of a hemi-sectioned left knee showing the tibial and femoral insertion of the posterior cruciate ligament (PCL). (From Chahla J, Nitri M, Civitarese D, et al. Anatomic double-bundle posterior cruciate ligament reconstruction. Arthrosc Tech. 2016;5[1]:e149–e156. Elsevier, Inc.)

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model and found that the double-bundle technique improved rotational stability and posterior translation in knees with a concomitant PLC injury. However, no advantage was seen with a double-bundle reconstruction when compared with a singlebundle reconstruction with regard to posterior translation with the PLC intact. In addition, excessive rotational constraint was observed at 30 degrees. Wiley and colleagues83 also observed that although posterior laxity was reduced compared with singlebundle reconstruction, overconstraint at 30 degrees of flexion was seen with double-bundle reconstruction. In a comparison of single-bundle AL reconstruction with double-bundle reconstruction in cadaver knees, Markolf and colleagues84 found that the addition of a PM bundle reduced laxity from 0 to 30 degrees of flexion but at the expense of increased PCL graft forces. Bergfeld et al.85 compared single- and double-bundle tibial inlay reconstruction in cadaveric knees using Achilles tendon grafts. No differences in translation between the single- and double-bundle reconstruction were observed at any flexion angle. A number of clinical studies have shown no significant differences in subjective and objective results between single- and double-bundle PCL graft reconstructions.86–88 Jain and colleagues performed a retrospective review of 40 patients, 18 of which underwent double-bundle PCL reconstruction and 22 of which underwent single-bundle PCL reconstruction and looked at clinical, functional, and radiologic outcomes at 24 months postoperatively.8 KT-1000 measurements showed an average side-to-side difference in the double-bundle group of 1.78 mm and 2.4 mm in the single-bundle group (P < .04). Stress radiographs showed increased posterior tibial translation in the single-bundle group as compared to the double-bundle group. However, both doublebundle and single-bundle groups showed significant functional improvement in Lysholm and IKDC scores with no statistically significant difference between the groups themselves. Furthermore, Hatayama et al.,88 in a retrospective clinical study comparing arthroscopic single-bundle and double-bundle PCL reconstruction showed that at 2-year follow-up of 3/10 patients who underwent double-bundle PCL reconstruction showed rupture of the PM bundle at second-look arthroscopy.89 Based on the literature to date, we believe evidence is lacking to support the routine use of double-bundle reconstruction. However, this type of reconstruction remains a topic of interest and is undergoing continued investigation in the treatment of PCL injuries.

synergistically with the PCL to prevent posterior tibial translation, is a concern with this graft option, as is the variable length of the tendinous portion.91 Lin et al.92 performed a retrospective review of 59 patients with isolated PCL injuries who either underwent arthroscopic transtibial single-bundle PCL reconstruction using autologous patellar tendon or hamstring tendon grafts looking for differences in clinical outcomes. At an average of 4 years follow-up, patients who underwent single-bundle PCL reconstruction using bone–patellar tendon–bone grafts demonstrated significantly more kneeling pain, anterior knee pain, squatting pain, posterior drawer laxity, and osteoarthritic change on radiography. Allograft tissue has the advantage of avoiding donorsite morbidity, reducing operating time, and offering improved graft diameter with greater collagen tissue when Achilles and tibialis anterior tendons are used. Pitfalls of allografts include a small risk of disease transmission, cost, and availability. In a survey of orthopaedic surgeons, Dennis et al.93 reported that allograft Achilles tendon was the most commonly used graft for acute (43%) and chronic (50%) PCL reconstructions. For the reasons previously discussed, we favor the use of Achilles tendon allografts for PCL reconstruction. A number of biomechanical studies have investigated various graft fixation constructs used in PCL reconstruction. Most recently, Lim et al.94 compared cross-pin fixation in a porcine model with bone blocks, interference screw fixation with bone blocks, crosspin fixation of soft tissue with backup fixation, and interference screw fixation of soft tissue with backup fixation on the tibial side using Achilles allograft PCL reconstruction. Although crosspin fixation with backup fixation had a higher maximum failure load and stiffness, tendon graft displacement was increased compared with bone-block fixation. Gupta and colleagues compared bioabsorbable to metallic screws for inlay fixation and found no difference in failure load or linear stiffness.95 Markolf and colleagues96 demonstrated the importance of bone-block position and orientation within the tibial tunnel; they found that positioning the bone–patellar tendon–bone graft flush with the posterior tunnel opening with the graft oriented so the bone block faced anteriorly in the tibial tunnel was the position with the best biomechanical properties. Margheritini et al.97 found that combining distal and proximal tibial fixation resulted in significantly less posterior tibial translation and more closely restored intact PCL in situ forces at 90 degrees than did reconstruction with distal fixation.

Graft Choice and Fixation

High Tibial Osteotomy for Chronic PCL Injuries

Graft choice and fixation techniques are also important considerations when discussing treatment options for surgery. Both autograft and allograft tissues have been used for PCL reconstruction. Bone–patellar tendon–bone, hamstring, and quadriceps tendons are common autograft sources. The Achilles tendon, as well as anterior and posterior tibial tendons, are frequently used allografts. Among autografts, bone–patellar tendon–bone grafts have the advantage of bone-to-bone healing in the bone tunnel. In comparison, the tendon portion of the quadriceps graft and both ends of hamstring grafts require tendon-to-bone healing in the bone tunnel, which may have inferior biomechanical properties.90 Weakening of the quadriceps tendon, which acts

A chronic isolated PCL injury results in posterior translation of the tibia and external rotation of the tibia in relation to the femur. These anatomic changes result in increased forces and subsequent development of OA in the medial and patellofemoral compartments.98–100 Additionally, a chronic combined PCL and PLC injury can result in chronic posterolateral instability and varus malalignment associated with bony deformity, lateral soft tissue deficiency, and hyperextension and external rotation as a result of PLC deficiency (i.e., triple varus).101 In cases of chronic PCL or combined PCL/PLC injury with resultant varus malalignment and posterior or posterolateral instability, soft-tissue procedures alone may be insufficient, whereas performance of a

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high tibial osteotomy (HTO) prior to soft-tissue reconstruction may improve outcomes by decreasing forces across the lateral supporting structures of the knee. A medial opening wedge HTO can improve alignment and decrease instability by addressing both coronal and sagittal malalignment. In addition to correcting varus malalignment, a medial opening wedge osteotomy with the anteromedial gap equal or larger than the posterior medial gap increases the posterior tibial slope102 and thus decreases the posterior resting position of the tibia.103 In contrast, a lateral closing wedge osteotomy may decrease posterior tibial slope, consequently increasing the posterior resting position of the tibia,104 and thus may not be appropriate in the knee with a PCL injury. Several investigators have demonstrated a concomitant increase in posterior tibial slope with opening wedge HTO.105,106 Specifically, Noyes et al.102 calculated that for each increase of 1 mm in the anterior gap, an increase of 2 degrees occurs in the posterior tibial slope. In the coronal plane, in the absence of medial compartment OA, the osteotomy should result in the mechanical axis crossing the center of the knee. If medial compartment joint space narrowing is present, some authors have recommended valgus hypercorrection with the mechanical axis crossing lateral to the center of the knee.101

Although satisfactory long-term outcomes have been observed in patients undergoing HTO for medial compartment OA,106 studies reporting results of HTO specifically for chronic PCL deficiency or combined PCL/PLC insufficiency are limited and heterogeneous in patient population, duration of follow-up, and outcomes. In a case series of 17 HTOs for symptomatic hyperextension varus thrust that included four patients with isolated PCL injuries and seven with combined PCL and posterolateral ligament injuries, improved subjective activity scores were observed postoperatively at a mean follow-up of 56 months.105 Similarly, Badhe and Forster107 reported the results of HTO with or without ligament reconstruction in 14 patients with knee instability and varus alignment, including nine patients with PLC or combined PCL injury. The mean time from injury to HTO was 8.3 years. Although the mean Cincinnati Knee Score improved from a mean preoperative score of 53 to a mean postoperative score of 74, no patients were able to participate in competitive sports, and more than 30% had continued knee pain at follow-up. Thus although biomechanical studies suggest that HTO may improve alignment and stability in patients with chronic PCL insufficiency or combined PCL/PLC injury with varus malalignment and instability, data on outcomes in this patient population are currently minimal.

Authors’ Preferred Technique Posterior Cruciate Ligament Reconstruction As discussed previously, many techniques have been described for PCL reconstruction. We prefer the tibial inlay method of reconstruction with an Achilles tendon allograft. The tibial inlay approach avoids the “killer turn” that may predispose the graft to stretch out and failure. We also believe that the acute angle of the graft as it enters the notch in the transtibial technique can make tensioning more difficult. Some surgeons are concerned that the posterior approach to the tibia needed for the open inlay procedure, which may involve a change to the prone position, is more technically demanding. We believe that with experience these challenges are easily overcome and that this technique leads to better biomechanical stability. Previous studies have demonstrated that the AL bundle is the most important component of the native PCL. The AL bundle has a higher cross-sectional area and is stronger than the PM bundle. Therefore the goal of a single-bundle reconstruction is to recreate the native AL bundle. However, it should be remembered that the footprint of the native PCL is much larger than the typical drill used to create the femoral tunnel, and thus the surgeon must choose which portion of the PCL to reconstruct. Clinical studies comparing single- versus double-bundle reconstructions have not found any significant differences in patient outcome scores. Multiple options are available for graft tissue, and no study has conclusively demonstrated a superior graft. We use an Achilles tendon allograft for most of our PCL reconstructions. We prefer to use the Achilles tendon because of its size, strength, and versatility. For the aforementioned reasons, we prefer to use a single-bundle tibial inlay technique with use of an Achilles allograft for PCL reconstruction. This procedure is described in the following sections. Graft Preparation The soft-tissue portion of the Achilles allograft is sized for a 10-mm bone tunnel. The bone plug is then fashioned into a trapezoidal shape 25 mm in length and 13 mm in width. The bone plug is predrilled and tapped for a 6.5-mm cancellous screw. The bone plug is drilled with a 4.5-mm drill from the cancellous to cortical

surface to protect the soft tissue and is then tapped with a 6.5-mm tap. A 6.5-mm cancellous screw, approximately 35 mm in length, and a metal washer are then placed into the bone plug from the soft tissue/cortical surface to the cancellous surface. The screw is placed so that the tip is 5 mm past the cancellous surface to facilitate later tibial fixation. A running locking stitch is then placed along approximately 30 mm of tendon using a no. 2 braided polyester suture, which tabularizes the graft to aid in passage through the femoral tunnel. Arthroscopy/Femoral Tunnel For the arthroscopic portion of the case, the patient is laid supine on the operative table. We recommend that the patient be intubated to protect the airway during position changes. A complete examination is performed after inducement of anesthesia prior to placement of a tourniquet. It is very important to evaluate for both PCL and associated capsuloligamentous injuries at this time. A thigh tourniquet is then placed but not inflated. A routine diagnostic arthroscopy is performed, and any meniscal or chondral injuries are treated at this time. The ACL may appear lax because of posterior tibial subluxation and should tighten with an applied anterior drawer. The PCL is then examined, and often, the ligament is lax or stretched out rather than frankly torn (Fig. 100.9). Once incompetence of the PCL has been confirmed, the residual PCL tissue is removed with a shaver and hand-operated punches. If the ligaments of Humphrey and Wrisberg are present, they are preserved if possible. The native footprint is preserved as a guide for femoral tunnel placement. Our goal of reconstruction is to restore the AL bundle of the PCL. The tunnel is placed in the distal and anterior portion of the native PCL footprint. A small medial incision is made through the skin and then through the medial retinaculum, which facilitates optimal drill-guide placement with the tunnel oriented slightly posteriorly. The medial articular margin is used as a landmark for the guide. An outside-in arthroscopic guide is used to establish the tunnel position, and a femoral guide pin is placed. The femoral tunnel is created with a cannulated drill over the guide pin (Fig. 100.10).

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Authors’ Preferred Technique Posterior Cruciate Ligament Reconstruction—cont’d The drill size is determined by the size of the graft and is typically 10 mm in width. An 18-gauge wire loop is passed through the femoral tunnel from the outside and positioned in the posterior notch to be retrieved later for graft passage.

Fig. 100.9  An arthroscopic view of a posterior cruciate ligament tear.

Fig. 100.10  An arthroscopic view of the femoral tunnel created in the footprint of the native anterolateral bundle with a cannulated drill over a guide pin.

A

Tibial Inlay The patient is then rotated into the prone position in a sterile fashion in preparation for the tibial inlay portion of the case. The extremity is exsanguinated and a tourniquet is inflated. The PM exposure to the tibia, as described by Burks,108 is then performed. The skin incision is a gentle curve with a horizontal end at the medial popliteal crease and vertical limb overlying the medial aspect of the gastrocnemius. Dissection is carried down the investing fascial layer, which is incised over the medial head of the gastrocnemius. The medial sural cutaneous nerve can be at risk but typically perforates the fascia distal to the horizontal limb of the incision. The medial border of the medial gastrocnemius is identified. The interval between the medial gastrocnemius and semimembranosus tendon is developed. Blunt dissection is performed down to the joint capsule. The medial head of the gastrocnemius is then retracted laterally with a blunt-tipped retractor, which protects its motor branch and neurovascular structures. At this point the posterior proximal tibia and posterior femoral condyles are palpated and a vertical incision is made through the posterior capsule. The posterior notch and tibial attachment of the PCL should now be exposed and the tibial insertion site of the native PCL is prepared for placement of the graft. Typically two prominent processes are found on the medial and lateral borders of the PCL that can be palpated. The insertion site is resected using osteotomes, a rongeur, and/or a burr. A graft recipient site is created that will anatomically accommodate the previously prepared graft. The bone graft is then placed into the site and secured with a 6.5-mm cancellous screw and washer (Fig. 100.11). The sutures in the tendinous portion of the graft are shuttled through the femoral tunnel using the previously placed wire loop. After the sutures are passed, the capsule is repaired. The tourniquet is deflated and hemostasis is achieved. The wound is irrigated and closed in layers. Graft Tensioning After wound closure the patient is again returned to the supine position in a sterile fashion. The arthroscope is placed back into the knee and the graft is inspected, entering the femoral tunnel (Fig. 100.12). The knee is cycled several

B

Fig. 100.11  (A) Anteroposterior and (B) lateral radiographs of the knee after completion of single-bundle posterior cruciate ligament reconstruction.

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Authors’ Preferred Technique Posterior Cruciate Ligament Reconstruction—cont’d times, which allows the surgeon to evaluate ROM and helps apply tension to the graft. Tension is applied to the graft in 70 to 90 degrees of flexion with an anterior drawer force placed on the proximal tibia. A 9 × 25-mm soft-tissue interference screw is then used to fix the graft in the femoral tunnel. A staple is then placed over the soft tissue portion of the graft into the medial femoral condyle to augment fixation. The arthroscopic portals and the incision for the femoral tunnel are closed in the standard fashion.

Fig. 100.12  An arthroscopic view of a completed posterior cruciate ligament reconstruction.

Transtibial Technique and Double-Bundle Reconstruction Alternatively, PCL reconstruction can be achieved via an arthroscopic transtibial technique. The patient is positioned supine. A detailed examination is performed after inducement of anesthesia followed by arthroscopic assessment of the knee joint to confirm the extent of the injury and to assist with the repair or reconstructive procedure. The tibial footprint is prepared via an accessory anteromedial portal, and occasionally with use of a 70-degree arthroscope. A tibial tunnel is then created from the anteromedial tibia and directed posteriorly to the native PCL tibial attachment (Fig. 100.13). If a single-bundle procedure is performed, care is taken to place the single guidewire in the center of the tibial footprint via direct visualization and/or radiographic guidance with use of a guide. If a double-bundle reconstruction is performed, two guidewires are placed and confirmed radiographically, with the AL guidewire being more lateral and distal and the PM guidewire being more medial and proximal. The tunnel(s) is (are) reamed under power to the posterior cortex and then completed by hand with direct visualization. After the tibial tunnels are completed, attention is focused on creating the femoral tunnels. The femoral insertion site anatomy is identified, and the appropriate tunnel position is marked for a single-bundle reconstruction or double-bundle reconstruction. The lateral portal is enlarged, and the knee is hyperflexed to drill the femoral tunnel(s) (Fig. 100.14A). One or two grafts are used depending on whether a single-bundle or double-bundle reconstruction is being performed. These grafts are passed anterograde through the tibial tunnel (Fig. 100.15) and subsequently retrograde into the femur. The grafts are fixed on the femoral or tibial side and then tension is applied to the other side of the graft and it is fixed. Tension is applied to the AL bundle and it is fixed at 90 degrees of flexion, whereas tension is applied to the PM bundle and it is fixed at 30 degrees of flexion.

Fig. 100.13  Posterior cruciate ligament tibial guidewire placement and drilling. (Modified from Miller MD, Harner CD, Koshiwaguchi S. Acute posterior cruciate ligament injuries. In: Fu FH, Harner CD, Vince KG, eds. Knee Surgery. Vol. 1. Baltimore: Williams & Wilkins; 1994.)

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Authors’ Preferred Technique Posterior Cruciate Ligament Reconstruction—cont’d

A

B

Fig. 100.14  Positioning of femoral tunnels for double-bundle reconstruction. (A) Femoral tunnel position for anterolateral and posteromedial bundles. Note that the anterolateral bundle is more anterior. (B) Double-bundle reconstruction with tibialis anterior allografts.

1

2

2

A

1

B

Fig. 100.15  Graft placement. (A) The graft for the anterolateral bundle (inset, 1) and a second graft for the posteromedial bundle (inset, 2) are passed in anterograde fashion through the tibial tunnel. (B) The grafts are then fixed to corresponding femoral tunnels. (Modified from Petrie RS, Harner CD. Double bundle posterior cruciate ligament reconstruction technique: University of Pittsburgh approach. Op Tech Sports Med. 1999;7:118–126.)

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POSTOPERATIVE MANAGEMENT Although rehabilitation after ACL reconstruction has been investigated by numerous authors, postoperative management after PCL reconstruction has been studied less extensively. Because PCL reconstruction has not been as successful as ACL reconstruction in restoring objective stability, many surgeons recommend a more conservative postoperative course. No level I studies have been performed to compare different protocols, and in a recent review of the literature, Pierce et al.61 found that currently no consensus exists regarding a set of optimal guidelines. In general, rehabilitation should focus on quadriceps strengthening and regaining ROM while avoiding posterior tibial translation, which places stress on the graft. These goals are usually achieved by initial immobilization and avoidance of active hamstring forces, limited ROM, and progressive weight bearing and strengthening based on the time from surgery and the patient’s progress. The aim of reconstruction and rehabilitation is to help the patient return to previous levels of function. The goal of most protocols is to achieve this goal around 9 months after surgery. Postoperative protocols use functional progression to determine the patient’s advancement. Functional status is determined using a combination of subjective patient assessment and objective data. These data include joint stability, ROM, effusion, proprioception deficits, muscle strength, and gait abnormalities. Careful monitoring of these factors during rehabilitation can help the surgeon identify and manage potential complications early during the postoperative course. It is important for the patient to understand that strict compliance with the postoperative protocol is critical to a good outcome. Traditionally, PCL protocols are divided into specific phases, and advancement is based on time from surgery and patient progression. The nature of these phases varies among surgeons, but many similarities exist. The first phase usually emphasizes protecting the graft from stress, ROM within limits, non–weight bearing, effusion prevention, and reactivation of the quadriceps. The next phase focuses on regaining full ROM, advancement of weight bearing, and low-impact strengthening. The length and method of immobilization have varied among different studies. The initiation of ROM exercises and degrees of motion allowed during the early phases also differs among studies. Progression through the subsequent phases depends on patient function. Factors that influence progression include strength, stability, endurance, and agility. Patients are allowed to return to play when they regain appropriate quadriceps strength and painless active ROM, which, as previously stated, is usually at around 9 months after surgery. To regain strength and proprioception, most protocols include open and closed kinetic chain exercises. For this reason it is important that open- and closed-chain exercises be part of the PCL rehabilitation program. Open-chain knee flexion resulting from hamstring contraction causes significant posterior translational forces across the tibia and should be avoided during early phases of rehabilitation.109 Open-chain knee extension can protect the graft by producing anteriorly directed shear forces across the tibia, and most investigators advocate that these forces

be initiated early.61,109 Closed kinetic chain exercises at low arcs of motion have also been shown to decrease posterior shear forces and are included in PCL rehabilitation. We use the following protocol.

RESULTS OF OPERATIVE TREATMENT Isolated Posterior Cruciate Ligament Injuries The results of isolated PCL reconstruction have been evaluated in many published studies. Although most patients demonstrate

Authors’ Preferred Technique Postoperative Management A  Acute Immediate Postoperative Phase (Early Protection Phase) • Bracing: After surgery, the hinged brace is locked at zero • ROM: passive ROM (initiated after 2 to 3 weeks of immobilization in extension)—patient-assisted tibial lift into flexion (0 to 70 degrees) with passive knee flexion • Exercises: • Quadriceps isometrics, straight leg raise—adduction, abduction proximal weight B  Acute Phase (Maximal Protection Phase) • Goals: • Minimize external forces to protect the graft • Prevention of quadriceps atrophy • Control postsurgical effusion • Weight bearing: weight bearing as tolerated with an assistive device • ROM: as tolerated to 90 degrees • Exercises: • Continue isometric exercises and quadriceps strengthening • Closed kinetic chain mini-squat, shuttle, bike • Open kinetic chain knee extension (60 degrees to 0 degrees) • Proprioception training • Weight shifts • Brace: Fit with a functional brace at 4 to 6 weeks after surgery C  Progressive Range of Motion/Strengthening Phase • Weight bearing: weight bearing as tolerated without an assistive device • ROM: as tolerated to 125 degrees flexion • Exercises: • Continue quadriceps strength training • Begin isotonic quadriceps strength exercises • Leg press (0 to 60 degrees) • Step-ups • Sport-cord progression program • Rowing, NordicTrack • Initiate closed kinetic chain terminal knee extension D  Functional Activity Phase Few scientific data are available to help determine the best method of rehabilitation as the patient transitions into functional stages, and thus progression at this level is determined by the patient’s tolerance to exercise and level of function. The evaluation of power and endurance that have been used for ACL programs should theoretically measure total length, strength, and endurance and can be used for the PCL reconstructed knee. As previously stated, the anticipated return to previous activity after PCL reconstruction is anticipated to take approximately 9 months.

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improvement, some patients report persistent knee symptoms and have residual laxity that may inhibit return to preinjury-level activities.56,65,88,89,110–122 The main limitation of these studies is the low incidence of isolated PCL injury requiring reconstruction, which results in a small sample size. Many of these studies are also retrospective case series that differ in operative technique, outcome measurements, and postoperative treatment, making direct comparison between studies difficult. A summary of these studies can be found in Table 100.1.112,120,121,123–130 Hermans et al.112 evaluated 25 patients who underwent isolated AL bundle PCL reconstructions at an average follow-up of 9.1 years. They used an arthroscopic transtibial, single-bundle approach with use of various graft types. The final International Knee Documentation Committee (IKDC), Lysholm, and functional Visual Analog Scale scores were significantly better than preoperative scores, but only 41% of patients had normal or near-normal clinical findings according to the IKDC guidelines. This finding was mostly attributed to residual laxity with a mean side-to-side difference of 4.7 mm by Telos stress radiographs at final follow-up. Preoperative symptomatic instability greater than 1 year and chondrosis at the time of surgery correlated with poorer subjective outcomes. These findings confirm that although isolated PCL reconstruction often results in improved functional outcome, many patients have residual laxity. Lahner et al.121 prospectively followed up on 33 patients with chronic symptomatic PCL injuries who underwent isolated single-bundle transtibial reconstruction. These patients were followed up over 2 years, and during this time, their IKDC scores improved from 41.8 to 69.5, and 72.8% regained normal to near-normal knee function. In this study, nine patients (27.4%) showed no improvement in knee function postoperatively. Chen and Gao120 evaluated a transtibial double-bundle reconstruction using a suture suspension technique at a minimum follow-up of 2 years. In their series of 19 patients, 78.9% regained normal knee function and 15.8% regained near-normal knee function. These rates are significantly higher than those reported in other studies and may be attributable to higher preoperative scores. The patients in this series had an average preoperative IKDC score of 65.6 and less posterior laxity compared with subjects in other studies.

Transtibial Versus Tibial Inlay Several case series have compared the outcomes of transtibial and tibial inlay methods of PCL reconstruction. No significant difference in clinical outcome scores between the two techniques have been identified. The details of these studies are outlined in Table 100.2. MacGillivray et al.56 evaluated 20 patients who underwent reconstruction of an isolated PCL injury. The mean follow-up was 5.7 years. Thirteen patients underwent transtibial reconstruction and seven underwent tibial inlay, all with a singlebundle graft. These investigators found that the posterior drawer improved in 57% of patients in the inlay group and in 38% in the transtibial group. No significant difference in Tegner, Lysholm, or American Academy of Orthopaedic Surgeons knee scores was found between the two groups. The investigators concluded that neither method predictably restores original laxity and that there was no difference in outcome scores.

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Seon and Song73 retrospectively reviewed 21 isolated transtibial and 22 tibial inlay reconstructions. They found a significant improvement in Lysholm knee scores in both groups but no intergroup differences. Postoperative Tegner scores were also improved in both groups. Final follow-up found normal or grade I laxity on posterior drawer in 19 patients in the transtibial group and in 20 patients in the inlay group. Mean side-to-side differences were also improved, with no significant difference between the two groups. The authors concluded that the transtibial and inlay techniques resulted in relatively good clinical and objective outcomes and are both satisfactory options for reconstruction. Kim et al.115 compared three different PCL reconstruction techniques. Twenty-nine patients underwent single- or double-bundle arthroscopic tibial inlay reconstruction or transtibial single-bundle reconstruction. These investigators found a significant difference in postoperative posterior tibial translation when the doublebundle tibial inlay group was compared with the single-bundle transtibial group, with less translation in the former. Although they noted a difference in translation, they found no significant difference in postoperative Lysholm scores or ROM. Song and colleagues retrospectively reviewed 36 isolated transtibial and 30 isolated tibial inlay reconstructions at an average follow-up of 148 months. Both groups showed no significant differences in terms of Lysholm knee scores, Tegner scores, or residual posterior laxity. Knees from both groups demonstrated development of OA on radiograph with no significant difference in prevalence.75

Single Versus Double Bundle A number of in vivo studies have compared single-bundle and double-bundle PCL reconstructions. Yoon et al.131 prospectively followed up 53 patients who underwent single- or double-bundle reconstruction. All reconstructions were performed with a transtibial approach using Achilles tendon allograft and had a minimum of 2-year follow-up. At final follow-up, patients were evaluated for ROM and posterior stability using stress radiography and by subjective knee scoring. The authors found no significant difference in ROM, Tegner activity scores, Lysholm scores, and IKDC evaluation. The only difference that could be identified was in posterior laxity. Both groups had improved stability postoperatively; however, the double-bundle group had less posterior translation with a difference of 1.4 mm, which was statistically significant. Although they did have less instability on objective testing, the patients’ clinical outcomes as measured by subjective scoring were the same in both groups. These findings were later corroborated by a study by Li et al. who prospectively followed 46 patients who underwent single- or double-bundle PCL reconstructions using tibialis allograft via a transtibial approach. In this study, the authors found no significant difference in Lysholm scores, or Tegner activity scores but the doublebundle group showed a statistically significant difference in residual posterior laxity compared to the single-bundle group (2.2 mm vs. 4.1 mm).132 Several studies to date have shown no significant differences in subjective or objective results between single- and doublebundle PCL graft reconstructions. Wang et al.127 prospectively compared single- and double-bundle PCL reconstruction using

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TABLE 100.1  Results of Isolated Posterior Cruciate Ligament Reconstruction No. of Patients

Age (Years)

Follow-up (Years)

Lahner et al. (2012),114 prospective Hermans et al. (2009),105 retrospective

33

32.5

2

25

30.8

9.1

Chen and Gao (2009)113

19

39

Minimum of 2

Chan et al. (2006),116 prospective

20

29

3.3

Sekiya et al. (2005),117 retrospective

21

38

Ahn et al. (2005),118 retrospective

Group I: 18

Study

Chronicity/Grade

Graft Type

Surgical Technique

Chronic 13 grade II 20 grade III 7 acute, 18 chronic, grade II or more

Hamstring autograft

Transtibial, single bundle

9 BPTB autograft 7 quadrupled hamstring autograft 8 double hamstring autograft

Transtibial, single bundle

Unknown Average time 14 months 15 grade II 4 grade III Unknown Average time 4 months All grade III

8-strand hamstring autograft

Transtibial, double bundle

Quadrupled hamstring autograft

Transtibial

5.9

5 acute 16 chronic All grade III

Achilles allograft

Transtibial

30

2.9

Hamstring autograft

Transtibial

Group II: 18

31

2.3

Achilles allograft

Transtibial

Jung et al. (2004),119 retrospective

12

29

4.3

All chronic 11 grade II 7 grade III 10 grade II 8 grade III Unknown Average time 5.4 months Range 1–10 months

Patellar tendon autograft

Tibial inlay

Wang et al. (2003),120 retrospective

30

32

3.3

13 acute 17 chronic All grade III

Mixed

Transtibial

Deehan et al. (2003),121 prospective

27

27

3.3

Hamstring autograft

Transtibial

Group A (quad tendon): 22

29

2.5

Quadriceps tendon autograft

Transtibial

Group B (hamstring tendon): 27

27

2.2

All chronic (16 patients 4–12 months after injury, 11 patients >1 year) Grade II and III injuries All grade III 12 acute 10 chronic 16 acute 11 chronic

24

26

2.2

Chen et al. (2002),122 retrospective

Mariani et al. (1997),123 retrospective

All chronic

Quadrupled hamstring autograft

Patellar tendon autograft

Transtibial

A, Abnormal; bio, biologic; BPTB, bone–patellar tendon–bone; IKDC, International Knee Documentation Committee; IS, interference screw; KT, KT-1000 testing; N, normal; NA, not available; NN, near-normal; OAK, Orthopädische Arbeitsgruppe Knie; SA, severely abnormal.

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Posterior Drawer

Fixation

Subjective Outcome

Instrumented Laxity

Tibia: bio IS + button Femur: FlippTack Tibia: IS Femur: IS

IKDC: 69, 72.8% N/NN Tegner: 5.9

Telos radiograph: 5 mm

Grade I: 25 Grade II: 8

IKDC: 65 Lysholm 75 Tegner 5.7

KT posterior drawer: 4.7 mm Side-side difference: 2.1 mm

Grade 0: 2 Grade I: 15 Grade II: 5

Suture suspension

Lysholm: 92.1 IKDC: 92.1, 78.9% N, 15.8% NN

Grade 0: 17 Grade I: 1 Grade II: 1

Tibia: bio IS + screw and washer Femur: bio IS + washer Tibia: screw and washer Femur: metal IS

Lysholm: 93 Tegner: 6.3 IKDC: 85% N/NN

KT posterior drawer: 9.4 preoperative to 1.0 postoperative Stress radiograph: 2.0 Average postoperative KT posterior drawer: 3.8 mm

IKDC knee function: 57% N/NN, 43% A/SA IKDC activity level: 62% N/NN, 38% A/SA

KT posterior drawer: 4.5 mm KT side-side difference: 1.96 mm

Femur: IS and screw and washer Tibia: IS and screw and washer

Lysholm: 90 IKDC: 16 N/NN, 2 A

Telos stress radiograph posterior displacement: 2.2 mm 2.0 mm

IKDC acute/ subacute: 75% N/NN Chronic: 40% N/NN NA

Femur: IS Tibia: screw and washer

Lysholm: 85 IKDC: 14 N/NN, 3 A, 1 SA OAK score: 92.5; 7 excellent, 4 good IKDC: 11/11 were N/NN

Grade I: 16 Grade II: 3 Grade III: 1

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Miscellaneous Minor extension deficit 3–5 degrees in only 2 patients 11 patients with residual positive quadriceps active test IKDC N to NN in only 41% Poorer results in chronic injuries Average preoperative IKDC score 65.6

18/20 showed no radiographic deterioration 3 patients had stiffness Acute/subacute group had significantly better IKDC and KT-1000 than chronic group No difference in outcome between groups

NA

Stress radiographs: 3.4 mm side-side difference; KT side-side difference, 1.8 mm NA

NA

Femur: IS; tibia: screw and post

Lysholm: 92 (24 excellent/ good, 6 fair/poor) Tegner: 4.5

Femur: IS Tibia: IS

Lysholm: 94 IKDC: 25 N/NN, 2 A/SA

KT side-side difference 10 mm

NA

Significant correlation between poor results and more chronic injuries

Lysholm: 91.44 IKDC: 22 N/NN, 5 A/SA

Lysholm: 94 Tegner: 5.4 IKDC: 19 N/NN, 5 A/SA

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Grade I: 16 Grade II: 12 Grade III: 3

Significant correlation between poor results and more chronic injuries No correlation between time from injury to surgery and outcome

37

35

Group I (transtibial): 13 Group II (tibial inlay): 7

Group I (transtibial): 36

Group II (tibial inlay): 30

Song et al. (2014),6 retrospective

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31

Unknown/All grade II or greater

Unknown/All grade II or greater

All chronic 5 grade II 8 grade III 3 grade II 4 grade III

All chronic; all grade II or greater

Average time to surgery, 9.4 months; all grade III

Chronicity/ Grade

Mixed

Mixed

Patellar tendon autograft

Hamstring autograft

Achilles allograft in all cases

Graft Type

Tibial inlay

Transtibial

Tibial inlay

Transtibial

Tibial inlay

Transtibial single bundle AS inlay single bundle AS inlay double bundle Transtibial

Surgical Technique

Tibia: two screws/ washers Femur: IS

Tibia: screw/ washer Femur: IS Tibia: IS Femur: ligament anchor screw

Tibia: bio IS and washer Femur: bio IS Tibia: bio IS and washer Femur: bio IS Tibia: bio IS Femur: anchor screw Tibia: screw and washer Femur: bio IS screw Tibia: IS Femur: IS

Tibia: bio IS Femur: bio IS

Fixation

Lysholm: 92.1 ± 10.4 Tegner: 6

Lysholm: 89.9 ± 9.7 Tegner: 5.9

Lysholm: 76 Tegner: 6

Lysholm: 81 Tegner: 6

Lysholm: 92.8 Tegner: 6.1

Lysholm: 91.3 Tegner: 5.6

Lysholm: 84.3

Lysholm: 79.7

Lysholm: 86.9

Subjective Outcome

KT posterior drawer: 83.3% Grade I, 16.7% Grade II KT posterior drawer: 86.7% Grade I, 13.3% Grade II

KT posterior drawer: 5.5 mm

KT posterior drawer: 5.9 mm

Telos side-side difference: 3.7 mm Telos side-side difference: 3.3 mm

3.6 mm

Telos side-to-side difference: 5.6 mm 4.7 mm

Instrumented Laxity

AS, Arthroscopic; bio, biologic; IKDC, International Knee Documentation Committee; IS, interference screw; KT, KT-1000 testing; NA, not available.

1.1

1

6.3

29

3.0

29.4

MacGillivray et al. (2006),55 retrospective

2.6

29.1

I2: 2.5

I1: 3.0

31.9

33.6

3.9

Follow-up (Years)

32.4

Age (Years)

Group A (transtibial): 21 Group B (tibial inlay): 22

Group I2 (inlay): 10

Group T (transtibial): 8 Group I1 (inlay): 11

No. of Patients

Seon and Song (2006),71 retrospective

Kim et al. (2009),108 retrospective

Study

IKDC Guidelines 10% Grade C

3 grade I 6 grade II 4 grade III 3 grade I 3 grade II 1 grade III IKDC Guidelines 16.7% Grade C

19 normal/ grade I 2 grade II 20 normal/ grade I 2 grade II

NA

Posterior Drawer

TABLE 100.2  Results of Isolated Posterior Cruciate Ligament Reconstruction: Transtibial Versus Inlay

Neither method restored anteroposterior stability to the knee

No significant differences between groups

Significant difference in posterior translation between groups T and I2 No significant difference in Lysholm scores

Miscellaneous

1228 SECTION 7  Knee

CHAPTER 100  Posterior Cruciate Ligament Injuries

hamstring autograft. No significant differences were observed between the two groups with regard to functional score, ligament laxity, and radiographic changes of the knee. Hatayama and colleagues88 were also unable to detect a difference in posterior tibial translation between patients treated with single- compared with double-bundle PCL reconstruction. Similarly, in a comparison of bone–patellar tendon–bone in one femoral tunnel compared with hamstring autograft in two tunnels, Houe and Jorgensen87 found no difference in postoperative laxity or Lysholm and Tegner scores. Finally, a study by Deie and colleagues showed that after a mean follow-up of 12.5 years there was no significant difference in Lysholm scores, stress radiography measurements, or knee arthrometry between patients who underwent singlebundle or double-bundle PCL reconstruction with hamstring allograft.133

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different surgical indications and methods of reconstruction that would need to be controlled. Future efforts should focus on overcoming these limitations and thus providing data that could help elucidate the best treatment recommendations for PCL injuries. For a complete list of references, go to ExpertConsult.com.

SELECTED READINGS Citation: Markolf KL, Zemanovic JR, McAllister DR. Cyclic loading of posterior cruciate ligament replacements fixed with tibial tunnel and tibial inlay methods. J Bone Joint Surg Am. 2002;84A(4): 518–524.

Level of Evidence: Biomechanical study

COMPLICATIONS

Summary:

The complications of PCL reconstruction include the more common problems that occur with orthopaedic surgery, such as infection and stiffness. In addition, some complications are associated with the specific nature of the procedure. One of the most common problems after PCL reconstruction is persistent posterior laxity. Hermans et al.112 found that 11 patients in a case series of 25 patients had a positive quadriceps active test after surgery. In addition, four patients required hardware removal because of soreness, and one patient required open capsular release for postoperative arthrofibrosis and decreased ROM. The exact incidence of complication after PCL reconstruction is unknown. Vascular injury during PCL reconstruction is rare but is a known complication. Nemani et al.113 reported on a case involving a popliteal venotomy that occurred during PCL reconstruction in the setting of a previous popliteal artery bypass graft. In this case the patient had sustained a knee dislocation with vascular injury. During the PCL reconstruction, the popliteal vein was found to be adherent to the PCL remnant, and a venotomy was noted after débridement. The authors recommend caution in the setting of previous surgery because the relationship of the neurovascular structures can be altered. Although complications appear to be uncommon, the clinician should have a frank discussion with the patient preoperatively to discuss the potential risks associated with the procedure.

FUTURE CONSIDERATIONS The optimal treatment for the PCL-deficient knee remains unclear. Future studies will help to better define the indications for the different treatment options. These studies will attempt to overcome the limitations of prior investigations. A need exists for randomized and prospectively designed studies with controlled variables that will allow clinicians to draw definitive conclusions. The difficulties encountered in PCL study design have been discussed, but small sample size due to low incidence is probably one of the most significant. Multicenter trials will likely be required to achieve the necessary power to derive treatment recommendations. Conducting multicenter trials is difficult because of

Markolf and colleagues performed a cadaveric study comparing posterior cruciate ligament reconstruction fixed with tibial tunnel and tibial inlay techniques. Knees were subjected to 2000 cycles of tensile force of 50 to 300 N. The authors found that the inlay technique resulted in less graft failure and graft thinning.

Citation: McAllister DR, Petrigliano FA. Diagnosis and treatment of posterior cruciate ligament injuries. Curr Sports Med Rep. 2007;6(5):293–299.

Level of Evidence: Review

Summary: McAllister and Petrigliano reviewed current concepts in the diagnosis and treatment of posterior cruciate ligament injuries.

Citation: Yoon KH, Bae DK, Song SJ, et al. A prospective randomized study comparing arthroscopic single-bundle and double-bundle posterior cruciate ligament reconstructions preserving remnant fibers. Am J Sports Med. 2011;39(3):474–480.

Level of Evidence: II

Summary: Yoon and colleagues compared single- and double-bundle posterior cruciate ligament reconstruction in a prospective, randomized study. Although a small benefit was observed with regard to posterior laxity in the double-bundle group, no difference was seen with subjective outcome measures.

Citation: Song EK, Park HW, Ahn YS, et al. Transtibial versus tibial inlay techniques for posterior cruciate ligament reconstruction. Am J Sports Med. 2014;42(12):2964–2971.

Level of Evidence: IV, cohort study

Summary: Song and colleagues compare transtibial and tibial inlay PCL reconstruction techniques at an average long-term follow-up of 148 months. Clinical and radiographic outcomes were

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SECTION 7  Knee

comparable between the two methods with a significant number of patients demonstrating worsening arthritis.

Citation: Fanelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: part II. Arthroscopy. 1995;11(5):526–529.

Summary: Fanelli and Edson offer one of the few studies on the incidence of PCL injuries in trauma patients with acute hemarthrosis of the knee. More than 200 acute knee injuries with hemarthrosis were reviewed. PCL injuries occurred in 38% of acute knee injuries; 56.5% were trauma patients, and 32.9% were sports related.

Level of Evidence: IV

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CHAPTER 100  Posterior Cruciate Ligament Injuries

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79.

80.

81.

82.

83.

84.

85.

86.

87.

88.

89.

90.

91.

92.

93.

94.

95.

“anatomic” grafts. J Bone Joint Surg Br. 1998;80(1): 173–179. Harner CD, Janaushek MA, Kanamori A, et al. Biomechanical analysis of a double-bundle posterior cruciate ligament reconstruction. Am J Sports Med. 2000;28(2):144–151. Milles JL, Nuelle CW, Pfeiffer F, et al. Biomechanical comparison: single-bundle versus double-bundle posterior cruciate ligament reconstruction techniques. J Knee Surg. 2017;doi:10.1055/s-0036-1593625. Tsukada H, Ishibashi Y, Tsuda E, et al. Biomechanical evaluation of an anatomic double-bundle posterior cruciate ligament reconstruction. Arthroscopy. 2011;28(2):264–271. Whiddon DR, Zehms CT, Miller MD, et al. Double-compared with single-bundle open inlay posterior cruciate ligament reconstruction in a cadaver model. J Bone Joint Surg Am. 2008;90(9):1820–1829. Wiley WB, Askew MJ, Melby A 3rd, et al. Kinematics of the posterior cruciate ligament/posterolateral corner-injured knee after reconstruction by single- and double-bundle intraarticular grafts. Am J Sports Med. 2006;34(5):741–748. Markolf KL, Feeley BT, Jackson SR, et al. Biomechanical studies of double-bundle posterior cruciate ligament reconstructions. J Bone Joint Surg Am. 2006;88(8):1788–1794. Bergfeld JA, Graham SM, Parker RD, et al. A biomechanical comparison of posterior cruciate ligament reconstructions using single- and double-bundle tibial inlay techniques. Am J Sports Med. 2005;33(7):976–981. Wang CJ, Weng LH, Hsu CC, et al. Arthroscopic single- versus double-bundle posterior cruciate ligament reconstructions using hamstring autograft. Injury. 2004;35(12):1293–1299. Houe T, Jorgensen U. Arthroscopic posterior cruciate ligament reconstruction: one- vs. two-tunnel technique. Scand J Med Sci Sports. 2004;14(2):107–111. Hatayama K, Higuchi H, Kimura M, et al. A comparison of arthroscopic single- and double-bundle posterior cruciate ligament reconstruction: review of 20 cases. Am J Orthop. 2006;35(12):568–571. Jain V, Goyal A, Mohindra M, et al. A comparative analysis of arthroscopic double-bundle versus single-bundle posterior cruciate ligament reconstruction using hamstring tendon autograft. Arch Orthop Trauma Surg. 2016;136:1555–1561. Rodeo SA, Arnoczky SP, Torzilli PA, et al. Tendon-healing in a bone tunnel. A biomechanical and histological study in the dog. J Bone Joint Surg Am. 1993;75(12):1795–1803. Hoher J, Scheffler S, Weiler A. Graft choice and graft fixation in PCL reconstruction. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):297–306. Lin YC, Chen SK, Liu TH, et al. Arthroscopic transtibial single-bundle posterior cruciate ligament reconstruction using patellar tendon graft compared with hamstring tendon graft. Arch Orthop Trauma Surg. 2013;133:523–530. Dennis MG, Fox JA, Alford JW, et al. Posterior cruciate ligament reconstruction: current trends. J Knee Surg. 2004;17(3):133–139. Lim HC, Bae JH, Wang JH, et al. The biomechanical performance of bone block and soft-tissue posterior cruciate ligament graft fixation with interference screw and cross-pin techniques. Arthroscopy. 2009;25(3):250–256. Gupta A, Lattermann C, Busam M, et al. Biomechanical evaluation of bioabsorbable versus metallic screws for posterior cruciate ligament inlay graft fixation: a comparative study. Am J Sports Med. 2009;37(4):748–753.

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96. Markolf K, et al. Effects of bone block position and orientation within the tibial tunnel for posterior cruciate ligament graft reconstructions: a cyclic loading study of bone-patellar tendon-bone allografts. Am J Sports Med. 2003;31(5):673–679. 97. Margheritini F, et al. Biomechanics of initial tibial fixation in posterior cruciate ligament reconstruction. Arthroscopy. 2005;21(10):1164–1171. 98. Skyhar MJ, Warren RF, Ortiz GJ, et al. The effects of sectioning of the posterior cruciate ligament and the posterolateral complex on the articular contact pressures within the knee. J Bone Joint Surg Am. 1993;75(5):694–699. 99. Ramaniraka NA, Terrier A, Theumann N, et al. Effects of the posterior cruciate ligament reconstruction on the biomechanics of the knee joint: a finite element analysis. Clin Biomech (Bristol, Avon). 2005;20(4):434–442. 100. LaPrade RF. Wentorf F: Diagnosis and treatment of posterolateral knee injuries. Clin Orthop Relat Res. 2002;402: 110–121. 101. Savarese E, Bisicchia S, Romeo R, et al. Role of high tibial osteotomy in chronic injuries of posterior cruciate ligament and posterolateral corner. J Orthop Traumatol. 2011;12(1):1–17. 102. Noyes FR, Goebel SX, West J. Opening wedge tibial osteotomy: the 3-triangle method to correct axial alignment and tibial slope. Am J Sports Med. 2005;33(3):378–387. 103. Giffin JR, Stabile KJ, Zantop T, et al. Importance of tibial slope for stability of the posterior cruciate ligament deficient knee. Am J Sports Med. 2007;35(9):1443–1449. 104. Hohmann E, Bryant A, Imhoff AB. The effect of closed wedge high tibial osteotomy on tibial slope: a radiographic study. Knee Surg Sports Traumatol Arthrosc. 2006;14(5):454–459. 105. Naudie DD, Amendola A, Fowler PJ. Opening wedge high tibial osteotomy for symptomatic hyperextension-varus thrust. Am J Sports Med. 2004;32(1):60–70. 106. Coventry MB, Ilstrup DM, Wallrichs SL. Proximal tibial osteotomy. A critical long-term study of eighty-seven cases. J Bone Joint Surg Am. 1993;75(2):196–201. 107. Badhe NP, Forster IW. High tibial osteotomy in knee instability: the rationale of treatment and early results. Knee Surg Sports Traumatol Arthrosc. 2002;10(1):38–43. 108. Burks RT, Schaffer JT. A simplified approach to the tibial attachment of the posterior cruciate ligament. Clin Orthop. 1990;254:216–219. 109. Lutz GE, et al. Comparison of tibiofemoral joint forces during open-kinetic-chain and closed-kinetic-chain exercises. J Bone Joint Surg Am. 1993;75(5):732–739. 110. Spiridonov SI, Slinkard NJ, LaPrade RF. Isolated and combined grade-III posterior cruciate ligament tears treated with double-bundle reconstruction with use of endoscopically placed femoral tunnels and grafts: operative technique and clinical outcomes. J Bone Joint Surg Am. 2011;93(19): 1773–1780. 111. Kohen RB, Sekiya JK. Single-bundle versus double-bundle posterior cruciate ligament reconstruction. Arthroscopy. 2009;25(12):1470–1477. 112. Hermans S, Corten K, Bellemans J. Long-term results of isolated anterolateral bundle reconstructions of the posterior cruciate ligament: a 6- to 12-year follow-up study. Am J Sports Med. 2009;37(8):1499–1507. 113. Nemani VM, Frank RM, Reinhardt KR, et al. Popliteal venotomy during posterior cruciate ligament reconstruction in the setting of a popliteal artery bypass graft. Arthroscopy. 2012;28(2):294–299.

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114. Jackson WF, van der Tempel WM, Salmon LJ, et al. Endoscopically-assisted single-bundle posterior cruciate ligament reconstruction: results at minimum ten-year follow-up. J Bone Joint Surg Br. 2008;90(10):1328–1333. 115. Kim SJ, Kim TE, Jo SB, et al. Comparison of the clinical results of three posterior cruciate ligament reconstruction techniques. J Bone Joint Surg Am. 2009;91(11):2543–2549. 116. Ahn JH, Yang HS, Jeong WK, et al. Arthroscopic transtibial posterior cruciate ligament reconstruction with preservation of posterior cruciate ligament fibers: clinical results of minimum 2-year follow-up. Am J Sports Med. 2006;34(2):194–204. 117. Noyes FR, Barber-Westin S. Posterior cruciate ligament replacement with a two-strand quadriceps tendon-patellar bone autograft and a tibial inlay technique. J Bone Joint Surg Am. 2005;87(6):1241–1252. 118. McAllister DR, Miller MD, Sekiya JK, et al. Posterior cruciate ligament biomechanics and options for surgical treatment. Instr Course Lect. 2009;58:377–388. 119. Gill TJ, et al. Tibiofemoral and patellofemoral kinematics after reconstruction of an isolated posterior cruciate ligament injury: in vivo analysis during lunge. Am J Sports Med. 2009;37(12):2377–2385. 120. Chen B, Gao S. Double-bundle posterior cruciate ligament reconstruction using a non-hardware suspension fixation technique and 8 strands of autogenous hamstring tendons. Arthroscopy. 2009;25(7):777–782. 121. Lahner M, Vogel T, von Engelhardt LV, et al. Isolated AL bundle reconstruction of the PCL. Arch Orthop Trauma Surg. 2012;132(3):363–370. 122. Panchal HB, Sekiya JK. Open tibial inlay versus arthroscopic transtibial posterior cruciate ligament reconstructions. Arthroscopy. 2011;27(9):1289–1295. 123. Chan YS, Yang SC, Chang CH, et al. Arthroscopic reconstruction of the posterior cruciate ligament with use of a quadruple hamstring tendon graft with 3- to 5-year follow-up. Arthroscopy. 2006;22(7):762–770.

124. Sekiya JK, West RV, Ong BC, et al. Clinical outcomes after isolated arthroscopic single-bundle posterior cruciate ligament reconstruction. Arthroscopy. 2005;21(9):1042–1050. 125. Ahn JH, Yoo JC, Wang JH. Posterior cruciate ligament reconstruction: Double-loop hamstring tendon autograft versus Achilles tendon allograft-clinical results of a minimum 2-year follow-up. Arthroscopy. 2005;21(8):965–969. 126. Jung YB, Tae SK, Jung HJ, et al. Replacement of the torn posterior cruciate ligament with a mid-third patellar tendon graft with use of a modified tibial inlay method. J Bone Joint Surg Am. 2004;86(9):1878–1883. 127. Wang CJ, Chen HS, Huang TW. Outcome of arthroscopic single bundle reconstruction for complete posterior cruciate ligament tear. Injury. 2003;34(10):747–751. 128. Deehan DJ, Salmon LJ, Russell VJ, et al. Endoscopic singlebundle posterior cruciate ligament reconstruction: Results at minimum 2-year follow-up. Arthroscopy. 2003;19(9):955–962. 129. Chen CH, Chen WJ, Shih CH. Arthroscopic reconstruction of the posterior cruciate ligament: A comparison of quadriceps tendon autograft and quadruple hamstring tendon graft. Arthroscopy. 2002;18(6):603–612. 130. Mariani PP, Adriani E, Santori P, et al. Arthroscopic posterior cruciate ligament reconstruction with bone-tendon-bone patellar graft. Knee Surg Sports Traumatol Arthrosc. 1997;5(4):239–244. 131. Yoon KH, Bae DK, Song SJ, et al. A prospective randomized study comparing arthroscopic single-bundle and doublebundle posterior cruciate ligament reconstructions preserving remnant fibers. Am J Sports Med. 2011;39(3):474–480. 132. Li Y, Li J, Wang J, et al. Comparison of single-bundle and double-bundle isolated posterior cruciate ligament reconstruction with allograft: a prospective, randomized study. Arthroscopy. 2014;30(6):695–700. 133. Deie M, Adachi N, Nakamae A, et al. Evaluation of singlebundle versus double-bundle PCL reconstructions with more than 10-year follow up. Sci World J. 2015;751465.

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101  Medial Collateral Ligament and Posterior Medial Corner Injuries M. Christopher Yonz, Brian F. Wilson, Matthew H. Blake, Darren L. Johnson

Medial ligament injuries of the knee are often assumed to be only medial collateral ligament (MCL) injuries. However, the medial ligament includes not only the MCL but also posteromedial structures that play a vital role in the stability of the knee. The work of LaPrade and colleagues1,2 has demonstrated that the posterior oblique ligament (POL) is an important valgus and rotational stabilizer of the knee. The management of the MCL has evolved during the past 30 years. Most isolated MCL injuries are treated conservatively, with a rare role for surgical intervention. However, the treatment of MCL sprains with anterior cruciate ligament (ACL) injury (or any other concomitant ligamentous injury for that matter), along with the timing of ACL reconstruction, continue to be controversial. This chapter describes the anatomy of the medial knee (including the increasingly important posteromedial corner), the evaluation of the knee, the treatment of medial ligament injuries, and the role of rehabilitation.

HISTORY The history will depend on whether the injury is witnessed by the physician on the sidelines or elicited from the patient in the clinic. Most of these injuries present in the office setting as potentially chronic conditions. A description of the mechanism of injury should be elicited in as much detail as possible. It is important to ascertain when the patient was hurt and how. Typically, the injury is the result of a blow to the lateral aspect of the leg or lower thigh. Up to 70% of MCL injuries in athletes are from contact mechanisms.3,4 The mechanism may be the result of a clipping injury in football or a noncontact injury from cutting, pivoting, or twisting. Skiers are prone to medial side injuries, with 60% of skiing knee injuries affecting the MCL.5,6 The majority of medial-sided knee injuries occur in competition rather than practice.4,7 In addition, it is important to ask the patients about pain, onset of swelling, ability to ambulate, the sensation of a “pop,” and the presence of a deformity necessitating a reduction, such as patellar dislocation or a more severe knee dislocation. In addition, a history of knee injuries or surgeries should be elicited because they can cloud an acute knee injury examination.

PHYSICAL EXAM Ideally, the examination of the knee should occur at the time of injury before the onset of muscle spasm. However, most of these

injuries are examined in the office setting after some time has elapsed after the injury. A thorough knee examination includes observation of the patient’s gait, documentation of the neurovascular status, palpation of the knee for tenderness, swelling, and ecchymosis, and assessment of stability. The physician should follow some basic principles: (1) assess the ligaments and muscles while the patient is as relaxed as possible, (2) perform the physical examination as gently as possible, and (3) examine the uninjured knee before assessing the injured knee. The patient’s gait should be observed as the patient walks into the room or at some point during the examination. However, gait may be misleading because patients with a complete MCL tear may walk with a barely perceptible limp. Hughston and colleagues8,9 found that 50% of athletes with grade III injuries could walk into the office unassisted, and reported that a complete disruption of the medial compartment can occur “without subsequent significant pain, effusion, or disability for walking.” However, patients with an MCL tear may exhibit a vaulting-type gait in which the quadriceps are activated, allowing stabilization of the medial-sided structures during gait. This gait differs from that of a patient with an ACL or meniscus tear who may walk with a bent knee gait because of pain or an effusion. As with any orthopaedic injury, the neurovascular status of the limb should be assessed. Pedal pulses should be palpated and sensation should be assessed over the dorsum, plantar, and first web space of the foot. If a knee dislocation is a possibility, ankle brachial indices should be performed to evaluate for vascular injury. Compartments should be examined to rule out compartment syndrome. The ability to passively and actively dorsiflex and plantarflex the ankle and great toe should be assessed. On the skin, the physician should look for edema, effusion, and ecchymosis to help localize the site of injury. It is important to differentiate between localized edema and an intra-articular effusion. Isolated MCL injuries usually have localized swelling. Hemarthrosis of the knee may indicate intra-articular pathology, such as an ACL or peripheral meniscal tear. Severe medial complex injuries with an ACL tear frequently show no evidence of effusion because the capsular rent is large enough to allow extravasation of fluid and blood. If hemarthrosis is present, the examiner should exclude other injuries such as a torn cruciate, patellar dislocation, an osteochondral fracture, and a peripheral meniscal tear. Along with assessment of swelling, palpation of the anatomic sites of attachment can provide clues to the diagnosis. The entire course of the MCL should be palpated from proximal to distal.

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CHAPTER 101  Medial Collateral Ligament and Posterior Medial Corner Injuries

Abstract

Keywords

The medial collateral ligament (MCL) is the most commonly injured knee ligament. Evaluation of injuries to the MCL includes a thorough history, physical exam, and review of pertinent imaging. The treatment of MCL injuries has evolved with improved understanding of the anatomy and biomechanics of the posteromedial corner. The majority of grade I and II MCL injuries can be treated conservatively. Treatment of grade III injuries is controversial with consideration for surgical treatment based on location of injury, functional demands of the knee, response to a nonoperative course, and/or involvement of the posteromedial corner. The management of combined anterior cruciate ligament and MCL injuries continues to be debated.

MCL posteromedial corner posterior oblique ligament medial knee injury anatomic reconstruction ligament repair

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Pain at the medial femoral epicondyle signifies injury at the femoral insertion of the MCL. With tibial-sided injuries, patients have pain along the proximal tibia around the pes anserine adjacent to the tibial tubercle. Midsubstance tears result in pain at the joint line, and such pain may also present with a medial meniscal injury, posing a diagnostic dilemma. Hughston and colleagues8 showed that point tenderness can accurately identify the location of injury in 78% of cases, and localized edema can identify a tear in the medial meniscus 64% of the time. A valgus injury that disrupts the MCL may also result in lateral meniscus tears or osteochondral fracture to the lateral femoral condyle or lateral tibial plateau. Therefore a thorough examination of the lateral knee should also be performed. Valgus stress testing at 30 degrees of knee flexion is still the gold standard for assessing isolated injury to the MCL. This test should be performed with the foot in neutral rotation because increased laxity will be noted if the knee moves from internal to external rotation. To relax the hamstrings and quadriceps muscles, the thigh should rest on the examination table and the foreleg should move freely off the edge of the table at 30 degrees of flexion. The examiner then grasps the ankle and applies a valgus stress with the other hand resting on the medial side of the knee to assess the amount of opening and the quality of the end point compared with the uninjured side. The laxity of the MCL can be recorded based on a grading system or the amount of opening. The American Medical Association Standard Nomenclature of Athletic Injuries uses the following grading system10: grade I, localized tenderness without laxity; grade II, increased tenderness and gapping but with an endpoint signifying a partial tear; and grade III, laxity without an endpoint indicating a complete tear. Other classification systems are based on the amount of opening with grade I, 0 to 5 mm laxity; grade II, 6 to 10 mm laxity; and grade III, over 10 mm of laxity.11 As described by Noyes, 5 to 8 mm of medial opening signifies a significant collateral ligament injury with “impairment of the ligament’s restraining effect.”12 There is no consensus on which grading system is best. It is important to compare findings to the contralateral knee. After assessing the degree of opening, a repeat valgus stress should be performed with the examiner palpating the medial meniscus to assess if it subluxates in and out of the joint, indicative of injury to the meniscotibial ligament.13 In addition to valgus testing in flexion, opening of the medial joint should be assessed with the knee in full extension. The cruciate ligaments, POL, posteromedial capsule, and MCL all contribute to knee stability in full extension. Asymmetric joint opening in extension compared with the contralateral side should alert the physician to the possibility of a combined MCL/POL injury with a cruciate tear. If any increased laxity is observed in full extension compared with the uninvolved knee, it is unlikely that an isolated MCL injury is present; rather, it is likely that the patient has a concomitant injury to the posteromedial capsule and POL in addition to the MCL lesion. The ACL should be assessed with the Lachman test because the pivot shift is difficult to perform as a result of guarding and the loss of the pivot axis with medial instability. In addition, the posterior cruciate ligament and lateral ligamentous structures should be examined. Along with cruciate injury, patellar instability and tearing of the

vastus medialis oblique are associated with laxity in full extension. Hunter and colleagues14 found 18 of 40 laterally displaceable patellae on stress radiographs in patients with medial-sided injuries and a 9% to 21% incidence of damage to the extensor mechanism with medial ligament injury. In addition to valgus testing at 30 and 0 degrees, the Slocum modified anterior drawer test and an anterior drawer test in external rotation should be performed to assess for medial-sided injuries (Table 101.1). Finally, varus stress testing and dial tests at 30 and 90 degrees should be performed to evaluate for lateral and posterolateral-sided knee injuries. However, it is important to note that dial testing can appear positive in patients with severe medial sided knee injuries.15 In this case, it is important to determine the direction of rotational instability of the tibial plateau in relation to the femoral condyles to distinguish if the positive result is due to a posterolateral knee injury or from anteromedial rotatory instability.10

IMAGING Radiography, arthrography, magnetic resonance imaging (MRI), and arthroscopy can provide information regarding knee injuries. Radiography with anteroposterior (AP), lateral, and sunrise views should be performed for both knees. These radiographs should be evaluated for occult fractures, the lateral capsular sign (Segond fracture), ligamentous avulsions, old Pellegrini-Stieda lesions (i.e., an old MCL injury) (Fig. 101.1), and loose bodies. Stress x-rays must be performed in skeletally immature patients who have medial knee pain associated with a normal x-ray to rule out physeal injury. In addition to ruling out physeal injuries in skeletally immature patients, stress radiography can be used to evaluate the severity of medial-sided knee injuries as well as the presence of concomitant ligament injuries. LaPrade and colleagues have noted that stress radiographs allow better objective measurements of knee instability than traditional physical exam maneuvers.16 However, this modality is often limited by pain in the acute setting and may be more beneficial for the evaluation of chronic injuries. Previous studies have demonstrated that normal, intact knees may have side-to-side gapping differences of up to 2 mm.17 Cadaveric sectioning studies have provided guidelines for expected medial gapping with stress radiographs based to the severity of injury in comparison to the contralateral knee: (1) isolated superficial MCL tear, 3.2 mm gapping at full extension and 20 degrees flexion; (2) superficial MCL and POL injury, 6.8 mm and 9.8 mm gapping at full extension and 20 degrees flexion; (3) complete medial side injury and ACL tear, 8.0 mm and 13.8 mm gapping at 0 and 20 degrees; (4) complete medial side injury and posterior collateral ligament tear, 11.8 mm and 12.6 mm gapping at 0 and 20 degrees; and (5) complete medial side injury and tears to both cruciates, 21.6 mm and 27.6 mm of gapping at 0 and 20 degrees.16 MRI without contrast is the imaging study of choice for evaluating MCL tears because it is less invasive than other studies and provides detail including location of tear, meniscal injury, superficial MCL, POL, posteromedial complex, and semimembranosus tendon (Fig. 101.2). MRI can reveal a Stener-type lesion

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TABLE 101.1  Methods for Examining the Medial Collateral Ligament Examination

Technique

Grading

Significance

Valgus stress at 0 and 30 degrees

Valgus force applied to tibia while stabilizing the femur; this should be done at 0 and 30 degrees of flexion and compared with the opposite leg

Grade I: 0- to 5-mm opening, firm end point Grade II: 5- to 10-mm opening, firm end point Grade III: 10- to 15-mm opening, soft end point

Opening at 30 degrees occurs from isolated MCL injuries; valgus stress at 0 degrees is associated with other ligament tears (anterior cruciate ligament, posterior collateral ligament, or posterior oblique ligament).

The Slocum modified anterior drawer test

Valgus force in 15 degrees of external rotation and 80 degrees of flexion

This test is positive if there is a noticeably increased prominence of the medial condyle compared with the other side.

The disruption of the deep MCL allows the meniscus to move freely and allows the medial tibial plateau to rotate anteriorly, leading to an increased prominence of the medial tibial condyle.

Anterior drawer test in external rotation

Anterior drawer test at 90 degrees of knee flexion with an external rotation applied to proximal tibia

This test is positive if a noticeably increased anterior translation of the medial condyle is present.

A disruption of the MCL alone should not lead to an increased anteromedial translation; an increased anteromedial translation indicates an anteromedial rotatory instability that involves an injury of the posteromedial structures.

MCL, Medial collateral ligament.

A

B

Fig. 101.1  (A) and (B) A Pellegrini–Stieda lesion. (From Pavlov H. Radiology for the orthopedic surgeon. Contemp Orthop. 1993;6:85.)

of the distal MCL with the distal MCL retracted superior to the pes tendons or into the knee joint. In addition, MRI is beneficial in assessing injuries to anterior and posterior cruciate ligaments and osteochondral structures. A 45% incidence of bruising of the lateral femoral condyle of lateral tibial plateau has been identified in isolated medial knee injuries.18 Loredo and associates19 showed that intra-articular contrast may help to highlight and to better define the structures of the posteromedial complex, but still concluded that the assessment of the posteromedial

complex was difficult. They found that the posteromedial complex was best visualized on coronal and axial images. In addition, increased T2 signal extending beyond the posterior border of the superficial MCL may indicate a posteromedial corner injury.11 Indelicato and Linton20 stated that MRI can provide advantages in four circumstances: (1) when the status of the ACL remains uncertain despite physical examination; (2) when the status of the meniscus is in question; (3) when surgical repair of the MCL is indicated and localization of the tear will help limit the

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Fig. 101.2  Magnetic resonance image showing a medial collateral ligament tear.

exposure; and (4) when an unexplainable effusion occurs during rehabilitation. However, MRI does not always provide concrete diagnosis, and the clinical examination becomes the deciding factor. Examination after administration of an anesthetic is another tool the physician can use to assess the injury pattern in patients who present long after an injury has occurred or in patients for whom the office examination and MRI do not provide a diagnosis. Final confirmation and planning must occur at the time of diagnostic arthroscopy, which confirms under direct vision zone of injury as well as amount of opening. Upon examination with use of an anesthetic, Norwood and coworkers21 found that 18% of patients had anterolateral rotatory instability that was not suspected preoperatively. In addition to MRI, arthrograms can be used to evaluate meniscal disease and capsular tearing with extravasation of contrast material. Kimori and colleagues22 found arthrography to be more useful than arthroscopy in diagnosing tears of the meniscotibial and meniscofemoral ligaments. With the increased use of MRI, arthroscopy is used infrequently as a diagnostic tool. ACL and meniscal tears may be identified on MRI. Also, it is rare to find an intrasubstance medial meniscal tear in an isolated MCL rupture because meniscocapsular separation occurs, and thus the fulcrum to load the medial compartment and tear the medial meniscus is lost. However, a series by Ra et al. demonstrated a 27% incidence of medial meniscus posterior root tears in patients with acute, severe medial knee instability.23 Over 30% of those injuries were not diagnosed on MRI and were found only during arthroscopy.

DECISION-MAKING PRINCIPLES When considering treatment of the MCL, one must remember that the majority of MCL injuries heal reliably with conservative management, and treatment decisions should involve the functional demands of the knee. It is also imperative to determine the involvement of the POL in patients with MCL injuries. If the medial sided injury extends past the MCL, involving the POL and the posterior capsule, rotational laxity occurs. While the majority of people, as well as high-performance athletes, can

tolerate small amounts of valgus laxity, rotational laxity is not well tolerated. The debate continues regarding nonoperative versus surgical treatment for primary repair of the MCL/POL with concomitant ACL injury. With most MCL injuries, clinical outcomes will be satisfactory after a period of immobilization and recovery of motion and strength, followed by progressive activities. In the small subset of patients with continued pain, instability, or impaired performance, surgical management must be considered. Surgical treatment should be provided to patients with chronic symptomatic valgus instability, an MCL that is incarcerated in the joint, a distal tibial MCL avulsion that is interposed in the pes tendons (a Stener lesion), and a grade III MCL tear with rotational instability or with grade III valgus laxity in full extension resulting from a complete POL tear.1,2,24,25 Surgical management of chronic laxity of the medial structures can be quite difficult, and therefore anatomic repair of the medial support structures in the acute setting is preferred when indicated. A review of literature for nonoperative versus operative treatment of complete isolated MCL injuries does not delineate the site of injury. The site of injury may have a role in the functional recovery of patients who place a high demand on their knees. In our practice, caring for Division I collegiate athletes, several complete soft tissue avulsions of the MCL/POL complex off the tibial insertion failed to heal reliably with nonoperative treatment. After recovery, athletes may have varying amounts of valgus knee instability preventing return to competitive sports and resulting in dysfunction in activities of daily living. Most MCL sprains should be treated nonoperatively. Complete avulsions of the superficial and deep MCL from the tibia with disruption of the meniscal coronary ligament have a poorer prognosis with nonoperative treatment and may be optimally managed with acute surgical repair for improved valgus stability of the knee. Before proceeding with a treatment plan, it is essential to know the extent of injury. Initially we perform a thorough history and physical examination. With MCL injuries, we assess the grade of injury of the MCL and any associated ligamentous, meniscal, posteromedial corner, or patellar injuries. We obtain radiographs as a routine diagnostic tool to rule out fracture or any signs of chronic medial insufficiency (Pellegrini-Stieda lesion) and chronic ACL deficiency (the deep femoral notch sign, peaked tibial spines, or a cupula lesion). The use of MRI is dependent on the grade of the MCL lesion and associated injury posteriorly. Isolated grade I or II injuries can be diagnosed with clinical examination and do not require MRI. However, in a grade I or II injury with an indeterminate cruciate examination and effusion, we order an MRI. We also obtain MRI for all grade III injuries because the site of involvement—tibia or femur—is important in our decision-making, particularly the extent of injury to the POL and posteromedial capsule. With grade III laxity in full extension and complete involvement of the POL and capsule, avulsion of the posterior horn of the medial meniscus root may be seen (Fig. 101.3) and demands surgical intervention. In addition, most grade III lesions are associated with concomitant ligamentous injuries. Our treatment algorithm is outlined in Fig. 101.4. Management of grade III injuries is controversial. Even with physical examination and advanced imaging, it remains difficult

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CHAPTER 101  Medial Collateral Ligament and Posterior Medial Corner Injuries

to gauge the extent of damage to the POL and the posteromedial capsule in combined injuries. The treatment of grade III MCL sprains has significantly evolved. The general consensus has been to treat isolated grade III injuries conservatively. Generally agreed upon operative indications include: tibial-sided MCL injury with a Stener lesion, joint entrapment of the MCL, a medial meniscal tear requiring repair, persistent instability following a nonoperative trial, and persistent medial instability after ACL reconstruction.26 We believe that the treatment of grade III injury is dependent not only on the specific location of the MCL rupture but also on the degree of laxity on physical examination, as well as the degree of the arthroscopic drive-through sign. It is the posterior extension of the medial-sided injury into the POL and posterior capsule that is critically important in the decision-making in the athletically active patient. Nonoperative management of these

injuries is inferior in this setting and may lead to a rotational instability in addition to valgus laxity, which is not well tolerated by athletes involved in pivoting sports.27,28

TREATMENT OPTIONS Management of the MCL and medial-sided knee injuries can be divided into operative and nonoperative approaches. Numerous factors, including the timing, severity, location, and associated injuries such as an ACL tear need to be considered when formulating a treatment plan. The MCL has the greatest capacity to heal of any of the four major knee ligaments because of its anatomic and biologic properties.29,30 As a result of multiple biomechanical, clinical, and functional studies, the trend has been toward a conservative, nonsurgical method for the majority of MCL injuries. Grade I and II isolated tears of the MCL generally respond well to nonoperative management. Partial tears are treated routinely with temporary immobilization and protected weight bearing with crutches. Once the swelling subsides, range of motion (ROM), resistive exercises, and progressive weight bearing are initiated. Nonsteroidal antiinflammatory drugs can be used to help with pain and swelling. Studies have shown no deleterious effect of nonsteroidal drugs on ligament healing.31 Management of grade III injuries remains much more controversial. Even with physical examination and advanced imaging, it remains difficult to gauge the extent of damage to the POL and posteromedial capsule in combined injuries. Nonoperative management of these injuries may lead to a rotational instability in addition to valgus laxity, which is not well tolerated by athletes involved in pivoting sports. Grade III injuries not only involve complete disruption of its fibers but also are frequently associated with additional ligamentous injuries. Posteromedial corner injuries have been recognized as a separate entity from MCL

MTP

Fig. 101.3  Arthroscopic image of the medial compartment of the knee. The arrow points to the posterior horn of the medial meniscus avulsion injury. MTP, Medial tibial plateau.

Suspected MCL injury? Examine Isolated grade III or MCL with associated injuries

Isolated grade I or II MCL

MRI

Rehab

Isolated grade III MCL

ACL/MCL

Femoral avulsion

Rehab, PT, regain motion

Isolated grade III

Full ROM

Tibial avulsion MCL repair/reconstr

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MCL unstable ACL reconstruction

Fig. 101.4  Algorithm for treatment of medial collateral ligament (MCL) injuries. ACL, Anterior cruciate ligament; MRI, magnetic resonance imaging; PT, physical therapy; ROM, range of motion.

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injuries and may need to be addressed more aggressively because of rotational laxity and instability that can result from their injury.1,2,24 In the last 5 years, multiple surgical techniques have been described for treating Grade III injuries. Surgical options include direct repair,32–34 repair augmented with tendon reconstruction35 or suture,36 and anatomic reconstruction.2,37,38 The most described

reconstruction techniques in the literature include (1) triangular reconstruction of the superficial MCL and POL37,39,40; and (2) the use of two separate grafts and four tunnels to re-create the medial-sided structures.2 For grade III injuries requiring surgery, the reconstruction techniques addressing the POL offer improved clinical stability, restoration of knee mechanics, and lower failure rates.1,39,41–43

Authors’ Preferred Technique Medial Collateral Ligament Injury We treat isolated grade I and II MCL injuries conservatively. In the first 48 hours, we encourage rest and the use of ice, compression, and elevation to help reduce swelling. In addition, we have all patients use a hinged knee brace and provide crutches for protected weight bearing. If patients have significant pain and valgus laxity, initially we lock the brace in extension. Once the swelling subsides and pain is improved, we encourage aggressive range-of-motion (ROM) exercises and straight leg raises with quadriceps exercises. Once the patient has regained full ROM and ambulation without a limp, the use of crutches and the brace can be discontinued. Stationary bicycle and progressive resistive exercises are instituted as tolerated. Once full ROM and 80% strength of the opposite side have been achieved, closed-chain kinetic exercises and jogging are allowed. Once athletes have achieved 75% of the maximal running speed, sport-specific training is allowed. Return to sports is permitted after the patient has strength, agility, and proprioception equal to the other side. We recommend a functional brace for contact or high-risk sports. Patients with grade I sprains usually return to sports in 10 to 14 days; because immobilization is temporary, these patients regain strength and motion quickly. However, return to play (RTP) after grade II sprains is much more variable. With grade II sprains, the period of immobilization can be up to 3 weeks to allow the pain to dissipate. Therefore patients can lose more strength and motion with an increased time of immobilization compared with patients with grade I sprains. Patients are allowed to RTP when they have equal strength of both knees and no pain is experienced with valgus stress.44 The treatment of grade III MCL sprains has significantly evolved during the past 20 years. The general consensus has been to treat isolated grade III injuries conservatively. We believe that the treatment of grade III injury is dependent not only on the specific location of the MCL rupture but also the degree of laxity

A

on physical examination, as well as the degree of the arthroscopic drive-through sign. The extent of injury and laxity of the injury to the POL and posterior capsule is instrumental in our decision-making. Diagnostic arthroscopy is performed initially to evaluate intra-articular injuries. A valgus force is placed on the knee while the knee is flexed at 30 degrees of flexion with the arthroscope viewing from the anterolateral portal. Tibiofemoral widening with valgus stress, which allows the arthroscope to be easily “driven through” to the posteromedial aspect of the knee, is called the “medial drivethrough” sign. This indicates a medial sided injury. One can easily assess, when performing this maneuver, if the MCL injury is primarily based on the femur or tibia, and where it will be necessary to operate and perform a repair. For femoralsided MCL injuries, the medial meniscus remains reduced with the tibia upon valgus opening (i.e., a gap forms above the medial meniscus). On the other hand, tibial-sided MCL injuries demonstrate that the medial meniscus remains reduced with the femur on valgus opening (i.e., a gap forms between medial meniscus and tibia, with the medial meniscus lifting off the tibia). If the medial meniscus elevates off the tibia, the coronary ligament, which attaches the meniscus to the tibia, is torn and should be repaired. An injury with extension to the POL and posterior capsule can also avulse the medial meniscus root from its attachment site. This also is critical to recognize and repair. With valgus opening of the knee during arthroscopic examination, it may be observed whether the knee opens posteriorly to the medial meniscus, particularly as the knee is slowly extended with valgus load. If the capsule is exposed with this maneuver posteriorly, the patient has an injury of the POL and posterior medial capsule, which needs to be addressed at the time of surgical correction (Fig. 101.5).

B

Fig. 101.5  A normal appearing medial joint space (A) is actually shown (B) to have a positive medial drive through sign upon valgus stress and tearing of the posterior medial capsule.

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Authors’ Preferred Technique Medial Collateral Ligament Injury—cont’d If the injury is acute, less than 14 days old, primary medial repair is attempted. In this setting particularly in the young athlete, repair is generally successful in the majority of cases with tibial based avulsions. For chronic injuries, the medial structures are repaired and augmented or can be primarily reconstructed. For acute repair, the origins and insertions of the deep and superficial MCL are evaluated. Typically, the lesion is on the tibial side. Isolated femoral-sided lesions often heal reliably without surgical repair. The surgical approach is a fairly easy one in that the incision is similar to a hamstring harvest incision, except the length of the incision is longer in the proximal direction. The surgical incision is longitudinal between the tibial tubercle and the medial aspect of the knee. This exposure is carried from the inferior margin of the superficial MCL and may be taken proximally to the femoral insertion if required. The sartorial fascia is incised to expose the MCL. The hamstrings are retracted for dissection to the distal MCL insertion on the tibia. The initial approach is made from the inferior aspect of the lesion by placing grasping tension sutures in the entire MCL structure. Careful dissection is performed while lifting it off the tibia with a scalpel or periosteal elevator, following its course superiorly and posteriorly. Following the MCL structures superior to the medial joint line and exposing the insertion of the deep MCL results in further dissection. Repair of the deep MCL and coronary ligament that attaches the medial meniscus to the tibia is performed by placing multiple suture anchors from posterior to anterior along the tibial joint line; four anchors with double-loaded nonabsorbable sutures are typically used. Sutures are then passed through the deep and superficial MCL structures and tied down to the tibia while maintaining tension on the grasping sutures placed at the start of dissection. Tying of sutures to the tibial insertion is performed at 30 degrees of flexion with a varus load applied to the knee. The tibial insertion of the superficial MCL is often secured to the tibia with a large fragment screw and spiked-washer construct 6 cm distal to joint line with the grasping sutures. Posteriorly to the repaired MCL structures, the POL and capsular tissue are reefed from multiple posterior to anterior directed sutures, typically figure of 8 sutures or horizontal mattress sutures. The objective is to take the laxity and slack out of the medial POL, which helps tighten the rotational instability caused from the injury. Chronic medial-sided injuries are also initially assessed with arthroscopy. As previously described, the liftoff test is performed in a valgus maneuver to the knee. If the medial meniscus lifts off the tibia with valgus stress to the knee, we approach reconstruction of the tibial side. If the medial meniscus stays to the tibia with valgus stress to the knee, it is a more femoral-based injury. Surgical exposure and approach are the same as stated previously in the acute repair. For chronic MCL injury reconstructions, if postoperative stiffness is not a concern or if the patient has an isolated MCL injury, an autograft hamstring tendon is harvested in the same surgical incision. Otherwise, the allograft tendon is used for reconstruction. The deep MCL structures and capsule are repaired to the anatomic origin and insertion of the femur and tibia with suture anchors that are double-loaded with nonabsorbable sutures, as described previously for the acute injury repair. The tissue is reefed to remove laxity and slack in the injured structures. Augmentation with the autograft or allograft is performed once this maneuver is complete. To augment the repair, autograft semitendinosus hamstring is harvested with an open-ended tendon stripper, leaving the distal attachment intact to the tibia at the pes anserine. The muscle tissue is cleaned from the semitendinosus tendon proximally with a large periosteal elevator, and a nonabsorbable whipstitch suture is placed in the free end of the tendon. All accessory attachments of the semitendinosus distally are carefully freed. A Kirschner wire is inserted at the medial epicondyle. The tendon is looped over the wire and the isometry of

the tendon is evaluated with the knee in flexion and extension. If the excursion is more than 2 mm, the wire is moved to a position of isometry. Once isometry is confirmed, a large fragment screw and spiked washer are placed provisionally in the femur without fully setting the head at that isometric position of the medial femoral epicondyle. A bone trough is made around the screw shank. The tendon is looped around the screw. The screw is then tightened to the femur with the knee in 30 degrees of flexion, and varus stress is applied to the knee. A right-angled hemostat is used to create a window in the direct head semimembranosus tendon attachment of the femur posteriorly. The free end of the semitendinosus tendon autograft is then directed posterior and obliquely and pulled through this window, recreating the central arm of the POL. The autograft is sutured to the semimembranosus tendon with use of a nonabsorbable suture. If an allograft tendon is used, the aforementioned technique is modified, with attachment of the tibial limb of the allograft augment secured to the tibial insertion of the superficial MCL with another large fragment screw and spiked washer fixation. A case example is that of a 16-year-old high school football player who sustained a contact MCL and ACL injury that was treated operatively in a staged fashion (Figs. 101.6–101.8). After treatment, he was allowed full return to contact sports 1 year from injury. Although most femoral-sided tears can be treated successfully with conservative methods, complete tibial-sided avulsions of the deep and superficial MCL, although rare, often heal with residual laxity.24 In athletes who participate in level I sports, we frequently favor operative repair of these tibial-sided complete avulsions that display retraction of the deep or superficial MCL on MRI (Fig. 101.9). Figs. 101.9 and 101.10 highlight a case example of a Division I football player with an isolated tibial-sided complete MCL avulsion with gross laxity and an impressive arthroscopic drive-through sign that was treated surgically. Our rehabilitation protocol for grade III lesions is placement in a long-leg hinged knee brace locked in extension with weight bearing as tolerated on crutches for 2 weeks. After approximately 2 weeks we unlock the brace during weight bearing. In the first 4 weeks, our goal is to have the patient attain nearly full ROM and normal gait pattern with full weight bearing in a hinged knee brace, and begin quadriceps and hamstring strengthening.

Fig. 101.6  Coronal magnetic resonance image shows complete avulsion of the superficial and deep medial collateral ligament with an unattached medial meniscus. Continued

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Authors’ Preferred Technique Medial Collateral Ligament Injury—cont’d In contrast, patients who undergo a repair of the MCL follow a different protocol. Postoperatively, a hinged knee brace is locked from 30 to 90 degrees for 3 weeks, followed by unlimited motion. Weight bearing is limited for 3 weeks with crutches and then progressed to full weight by 4 to 6 weeks. Bracing is discontinued at 6 weeks and nonimpact conditioning is allowed, with running started by 3 months. Chronic laxity of the medial support structures after nonoperative management is difficult to treat. A firefighter we treated after nonoperative management of his grade III medial lesion had chronic medial instability, which for him was a significant safety issue for performance of his professional duties. Fig. 101.11 shows medial reconstruction of his POL and MCL using allograft tissue and performed anatomically as an isolated procedure for chronic medial stability.

Fig. 101.7  Arthroscopy confirms gross laxity of the medial compartment with complete disruption of medial support structures and a free-floating meniscus.

Fig. 101.10  Arthroscopy confirms a drive-through sign with liftoff of the medial meniscus from the tibia, requiring open repair of medial structures.

Fig. 101.8  Open surgery confirms complete avulsion of the medial collateral ligament from the tibia with a free-floating, unattached medial meniscus between the articular cartilage of the medial femoral condyle and the tibial plateau.

Fig. 101.9  A coronal magnetic resonance image shows tibial-sided avulsion of the medial collateral ligament with retraction and a contrecoup bipolar bone bruise lesion laterally, which suggest a high-energy injury pattern.

Fig. 101.11  The medial side of the knee illustrating medial reconstruction of the medial collateral ligament and posterior oblique ligament using allograft tissue and performed anatomically.

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CHAPTER 101  Medial Collateral Ligament and Posterior Medial Corner Injuries

POSTOPERATIVE MANAGEMENT The treatment of MCL injuries initially promotes nonoperative management; thus rehabilitation is pivotal and is the primary modality for treatment. No one perfect rehabilitation protocol exists that will work for every athlete. Upon reviewing the literature, no apparent consensus exists regarding the most efficacious rehabilitation protocol, and protocols are usually based on surgeon preference and experience. Steadman,45 Bergfeld,46 O’Connor,47 and Cox48 have had excellent success with their individual protocols for treatment of MCL injuries. To effectively treat MCL injuries, the grade of the injury must be determined because the parameters of rehabilitation are based on the degree of injury. Table 101.2 shows the general principles for rehabilitation of MCL injuries. Isolated grade I sprains are treated with rest, ice, compression, and elevation for the first couple of days to help reduce swelling. Patients are allowed weight bearing as tolerated with the use of an assistive device if pain is experienced with walking. The only exception is patients with significant valgus deformity, because they will place more stress on the MCL, affecting healing. In these patients, it may be safer to allow partial weight bearing for a couple of weeks. With grade I MCL tears, immobilization in a brace is rarely required, and if patient compliance is of concern, a short-leg hinged brace is used to control valgus and rotational stresses. ROM is begun immediately to prevent arthrofibrosis and stiffness. In addition, quadriceps strengthening and closed chain exercises are started. Once the patient regains full ROM, resistive exercises are begun along with sport-specific drills. Isolated grade II injuries are treated similarly to grade I injuries with rest, ice, elevation, and compression. Because grade II injuries involve a greater degree of damage to the ligament with increased valgus instability, a long-leg hinged brace is usually needed. Patients are allowed to progressively bear weight as tolerated in the brace; however, if the patient is having significant pain, the brace can be locked in extension until the pain subsides, usually in 1 week. Assistive devices are used until the patient has a nonantalgic gait. Active ROM exercises are started immediately. During the early period, quadriceps strengthening is performed TABLE 101.2  Principles for Rehabilitation

of the Medial Collateral Ligament Phase

Goals

Maximal protection phase

Early protected ROM Decrease effusion and pain Prevent quadriceps atrophy Full painless ROM Restore strength Ambulation without crutches Increase strength and power

Moderate protection phase

Minimal protection phase

ROM, Range of motion.

Criteria for Progression No increase in instability No increase in swelling Minimal tenderness Passive ROM at least 10 to 100 degrees No instability No swelling or tenderness Full painless ROM

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in a nonweight-bearing fashion with straight leg raises, quadricepssetting exercises, and electrical stimulation. Once the patient has achieved full ROM and functional strength, proprioceptive and agility drills can be initiated. Isolated grade III injuries usually involve disruption of both the superficial and the deep fibers. Therefore the rehabilitation process is slower, and a longer period of immobilization is required. The treatment of grade III injuries can be divided into stages. In the first phase (for about 4 weeks), the patient should wear a brace locked in extension, and progressively increase weight bearing to attain a normal gait pattern. Also, the patient needs to perform ROM exercises with eccentric strengthening of the quadriceps and hamstrings. Failure to perform ROM exercises and prolonged immobilization results in increased ligament creep and poorer cellular metabolism.50 In phase II, which lasts 4 to 6 weeks, the patient continues to attain full ROM, unlocks the brace, and achieves quadriceps and hamstring strengthening. After 6 weeks, the brace can be discontinued if the patient has a nonantalgic gait and has regained quadriceps strength for daily ambulation. Phase III starts after 6 weeks and includes squatting, light jogging with agility drills, and continued strengthening to return to sports. After surgical repair of an isolated MCL, the brace is locked at 30 degrees and the patient is allowed to perform toe-touch weight bearing for 3 weeks. The patient is encouraged to continue ROM from 30 to 90 degrees. The patient also continues strengthening of the quadriceps and hamstring while wearing a brace. If possible, we prefer to add a compression cryotherapy device (such as a Game Ready, Concord, Georgia, USA) as ACL studies have demonstrated improved knee ROM and functional scores with the use of compression cryotherapy compared to cryotherapy alone.51 After 3 weeks, the patient is allowed to progress to full weight bearing with full-time brace wear to continue to protect the repair. The brace can be worn unlocked to allow free ROM, as well as valgus and rotational stability. From 3 to 6 weeks, the goal is to restore full ROM along with continued strengthening with closed kinetic chain exercises. After 6 weeks, the patient continues to progressively increase activities with resistive and sport-specific exercises. Combined injuries of the MCL and ACL require additional steps compared with the rehabilitation of isolated MCL tears. Upon reviewing the literature on ACL and MCL injuries, as stated previously, conservative treatment of MCL injuries followed by surgical reconstruction of the ACL is the favored management in most patients. Initially the protocol focuses on the severity of the MCL injury. For example, a grade I MCL injury with an ACL injury will proceed with the protocol presented earlier for grade I injuries. The patient will quickly regain ROM and functional strength, and then the surgeon can proceed with reconstruction of the ACL. Conversely, the patient with a grade III injury with an ACL injury will take much longer to heal because of the slower protocol for type III injuries. Regaining ROM and functional strength training may take 8 to 10 weeks, and therefore it will take longer to proceed with ACL reconstruction with a type III injury. The ACL is reconstructed accompanied by conservative treatment of the MCL, following the rehabilitation protocol for an ACL reconstruction. After a combined ACL reconstruction

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BOX 101.1  Return-to-Play Guidelines • Full ROM • No instability • Muscle strength 85% of contralateral side • Proprioception ability is satisfactory • No tenderness over the medial collateral ligament • No effusion • Quadriceps strength; torque/body weight • Use of a lateral knee brace (if necessary) ROM, Range of motion.

and medial-sided repair, the knee is braced in full extension, and a standard ACL protocol is followed with protected weight bearing. In a combined ACL and MCL injury, it is important to remember that ACL rehabilitation takes precedence over medialsided repair. For RTP guidelines, see Box 101.1.

RESULTS Numerous authors have shown excellent results with nonoperative treatment of grade I and II MCL tears.44,52–54 Ellsasser and associates52 looked at 74 knees in professional football players and achieved a 98% success rate with a nonoperative protocol. They had strict inclusion criteria to ensure an isolated MCL injury was present: (1) up to grade II laxity with a firm end point in flexion, (2) no instability to valgus stress in extension, (3) no significant rotatory or AP subluxation, (4) no significant effusion, and (5) normal stress radiograph findings. In this series, patients were treated with crutches, no brace, and progressive weight bearing. Based on their experience, Ellsasser and associates concluded that by 1 week, patients should progress to full extension, have no effusion, and perceive decreased tenderness. The players returned to football in 3 to 8 weeks. The only failure occurred in a patient with an osteochondral fracture that was found at later follow-up. Derscheid and Garrick44 performed a prospective study that examined 51 grade I and grade II MCL injuries in college football players. They used a nonoperative rehabilitation protocol with a knee immobilizer initially. Players with a grade I injury returned to full participation at an average of 10.6 days, and players with a grade II injury returned at an average of 19.5 days. At longterm follow-up, these patients showed slight increases in medial instability. Injured knees had a higher incidence of reinjury than did control knees, but this finding was not statistically significant. Bassett and associates53 and Hastings54 studied the use of a cast brace in treating isolated MCL ruptures. In both studies, early return to athletics was found with the use of the cast brace. Nonoperative treatment varies from casting to functional bracing to no bracing, and good outcomes occur with all three forms of treatment. Fetto and Marshall55 found an 80% incidence of concomitant ligamentous injuries with a grade III MCL tear, with 95% of the associated injuries being an ACL tear. Early authors recommend primary repair for grade III injuries. O’Donoghue56

stressed the importance of immediate repair of complete tears of the MCL. Hughston and Barrett57 supported primary repair of all medial structures, including the superficial MCL and POL. They believed that repair and advancement of the POL was key to restoring medial stability. Their results were good to excellent in 77% to 94% of patients. Muller58 reported 65% good and 31% excellent results in the repair of isolated grade III MCL injuries. He repaired the superficial MCL avulsion with screws and washers and intrasubstance tears with a combination of approximation and tension-relieving sutures. Hughston and Barrett,57 O’Donoghue,56 Muller,58 Collins,59 Kannus,60 LaPrade and Wijdicks1,2 have written that surgical intervention is necessary for complete ruptures of the MCL. Although good results have been demonstrated with surgical repair of the MCL, many studies have focused on the nonoperative management of grade III MCL injuries. Fetto and Marshall55 were among the first to assess outcomes after nonoperative treatment of grade III MCL injuries. They studied 265 MCL injuries and found that patients with grade II injuries did much better than patients with grade III injuries (97% compared with 73%). Initially, in their study, all patients with grade III injuries underwent operative intervention. However, some patients with grade III injuries did not have an operation because of skin lesions and infection. At follow-up, patients with operative treatment of isolated MCL ruptures had no improved outcome compared with the nonsurgical group. This incidental finding led the way for more prospective studies to investigate the role of nonoperative treatment in patients with isolated grade III MCL injuries. Indelicato61 prospectively compared operative and nonoperative treatment of isolated grade III ruptures. All patients underwent examination with the use of an anesthetic and arthroscopy to rule out any other pathology, such as ACL and meniscal tears. Indelicato61 found objectively stable knees in 15 of 16 patients treated operatively and in 17 of 20 patients treated nonoperatively. Both groups followed a rigid rehabilitation protocol including casting at 30 degrees of flexion for 2 weeks and then 4 weeks longer in a cast brace with hinges that allowed motion from 30 to 90 degrees. Subjective scores were higher in the nonsurgical group, with good to excellent results for 90% in the nonsurgical group and 88% in the surgically repaired group, suggesting that surgical intervention offered no benefit. Indelicato also showed that patients treated with early motion returned to football 3 weeks earlier than did immobilized patients. A subsequent study by Indelicato and associates62 showed that a conservative approach in patients with complete MCL ruptures was successful in collegiate football players. All players were managed with a functional rehabilitation program, and 71% had good to excellent results. Similar to Indelicato, both Reider and colleagues63 and Jones and associates64 found excellent outcomes in athletes with isolated grade III medial ligament injuries who were treated conservatively and agreed that nonoperative treatment of these lesions is justified. Reider and colleagues studied 35 athletes who were treated with early functional rehabilitation for isolated grade III tears. Of these 35 athletes, 19 returned to full and unlimited activity in less than 8 weeks. At an average follow-up of 5.3 years, outcomes based on subjective and objective measurements were comparable with earlier investigations using a surgical repair.

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CHAPTER 101  Medial Collateral Ligament and Posterior Medial Corner Injuries

In 1986, Jones et al. reported results for 24 high school football players who returned to competition at an average of 34 days. Management consisted of 1 week of immobilization followed by gradual ROM and strengthening. The knee was tested weekly with valgus stress, and instability was reduced to grade 0 or 1 by 29 days. No increased incidence of reinjury was found the following spring. Although Indelicato,61 Fetto and Marshall,55 Jones et al.,64 and Reider et al.63 found excellent results with nonoperative treatment, Kannus60 studied 27 patients with grade III lesions at an average 9 years of follow-up. Patients were found to have poor outcomes (an average Lysholm score of 66) and degenerative changes on radiographs. Kannus concluded that early surgical repair would prevent deterioration. A careful review of the patients showed that 16 of 27 had greater than a 2+ Lachman score, and 10 of 27 had anterolateral instability. Thus this study did not show that nonoperative treatment has poor outcomes but that associated injuries, such as ACL injuries, need to be addressed to prevent poor long-term outcome. In the last decade, anatomic restoration of the medial knee structures has been found to provide satisfactory outcomes. Lind et al.37 described a technique to reconstruct the MCL and POL. The clinical results they published showed that 98% of their patients treated with this technique had normal or near normal International Knee Documentation Committee (IKDC) measures at follow-up of more than 2 years. LaPrade and associates2 reported their technique and followup at an average of 1.5 years for reconstruction of the MCL and POL. Their outcomes showed improved IKDC measures and decreased valgus opening on stress radiographs. Several cadaveric studies of anatomic MCL reconstruction have been recently performed. Wijdicks and associates35 performed a cadaveric biomechanical study comparing augmented repair versus reconstruction of a completely transected superficial MCL. The MCL was reconstructed via the LaPrade method.2 Compared to the transected state, augmented repair and reconstruction both decreased medial gapping. However, the authors noted that neither technique reproduced the stability of the intact ligament. Gilmer et al.36 performed a cadaveric analysis comparing a repair of the MCL and POL versus a repair with internal bracing versus LaPrade’s allograft reconstruction technique. They found that the mean moment to failure was highest in the intact ligament. Augmentation with internal bracing improved moment to failure and valgus angle at failure compared to repair alone, and was similar in comparison to allograft reconstruction. Finally, Omar and colleagues65 performed a biomechanical analysis of fixation techniques for use in augmented repair. Spiked polyetheretherketone washers (PEEK) reinforced with polyester sutures provided the best results with regard to elongation during cyclic loading and load to failure. Combined injury to the MCL and ACL represents a completely different entity than an isolated MCL injury. The ACL is a primary restraint to anterior displacement and acts as a secondary stabilizer to valgus stress, especially in full extension. Conversely, the MCL is the primary restraint to valgus stress at 30 degrees of flexion. Therefore injury to the MCL and ACL results in both anterior and valgus instability and can significantly compromise

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knee function. Even though the apparent consensus is that a solitary MCL rupture can be treated nonoperatively, the optimal treatment for a concurrent ACL and MCL injury is debated. The extent of involvement of the posteromedial capsule and POL may help to guide treatment strategies. The management of combined ACL and MCL injuries has been a controversial topic in the literature. The first issue pertains to the various surgical options available for managing these injuries. Three principal surgical options exist: (1) surgical reconstruction and repair of both ligaments; (2) ACL reconstruction and nonoperative MCL management; and (3) operative management of MCL with nonoperative ACL treatment. ACL reconstruction with nonoperative management of the MCL remains the most popular option. The second controversial issue regarding combined injuries is whether early or late ACL reconstruction provides better functional and long-term results. In years past, authors recommended surgical intervention for both ligamentous structures in concomitant ACL and MCL ruptures.55,66,67 Fetto and Marshall55 had 79% unsatisfactory outcomes in patients treated operatively for ACL and MCL tears. Even though studies have shown that operative repair of all ligaments results in stable, functional knees, a high incidence of knee stiffness was found.68–70 Other authors have stated that isolated operative MCL repair and nonoperative ACL reconstruction leads to good results. Hughston and Barrett57 reported that 94% of their patients with combined ACL and MCL injury who were treated with only MCL reconstruction returned to their preinjury levels of athletic performance. They stated that the key to obtaining excellent results was reconstruction of the POL and posteromedial structures. Noyes and Barber-Westin71 criticized the method used by Hughston and Barrett to report results, and stated that the results may have been overly optimistic. However, Hughston72 continued to report good results at 22 years of follow-up. In addition to Hughston, Shirakura and associates73 reported excellent results in 14 patients with combined lesions but reconstruction of the MCL only; however, they did not report AP instability. Conversely, Frolke and coworkers74 reported poor results with solitary MCL repair. They performed arthroscopically guided repair of the MCL, which led to functional stability in 68% of knees, but clinical testing of all 22 knees showed abnormal or severe abnormal examination findings. More recently, Pandey and associates75 found higher IKDC scores, higher Lysholm scores, and fewer complaints of instability in patients with combined injuries who underwent repair of the MCL and POL as well as ACL reconstruction compared to patients who underwent repair of medial sided structures only. Most authors suggest that nonoperative treatment of the MCL with reconstruction of the ACL provides good to excellent results. Shelbourne and Porter76 demonstrated good to excellent results in 68 patients with ACL reconstruction and nonsurgical management of an MCL tear. They also showed that these patients achieved a greater ROM and more rapid strength gains than did patients with surgical reconstruction and repair of both ligaments. Similarly, Noyes and Barber-Westin71 demonstrated a higher incidence of motion problems when MCL and ACL were treated operatively, and they recommend arthroscopic reconstruction of the ACL with nonoperative management of the MCL after recovery of

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ROM and muscle function. In a prospective randomized study, Halinen and associates77 treated 47 consecutive patients with combined ACL and grade III MCL injuries. All patients underwent early ACL reconstruction within 3 weeks of injury. The MCL was treated operatively in 23 patients and nonoperatively in 24 patients. All patients were available for follow-up at a mean of 27 months. The nonoperative treatment of the MCL led to results similar to those obtained with operative treatment with respect to subjective function, postoperative stability, ROM, muscle power, return to activities, and Lysholm score. Halinen and colleagues concluded that MCL ruptures did not need to be treated operatively when the ACL was reconstructed early. In a retrospective study, Millett and colleagues78 reported on 19 patients with a complete ACL injury and a minimal grade II MCL tear who underwent early ACL reconstruction and nonoperative treatment of the MCL. At the 2-year follow-up, subjective evaluation showed a Lysholm score of 94.5 and a Tegner activity score of 8.4. Clinical examination revealed good ROM and strength. None of the patients experienced graft failure or required subsequent surgery. More recently, there has been increased interest in anatomic repair or reconstruction of combined injuries. Piatkowski et al.32 examined the primary repair of grade III MCL injuries with delayed reconstruction of ACL tears. Good to very good outcomes were achieved in 63% based on IKDC scores, and good outcomes were achieved in 74% based on the Lysholm scale. They noted that patients over 40 years of age were less likely to have good outcomes. Blanke et al.33 presented a case series of patients who underwent screw and suture repair of grade II MCL injuries at the same time as ACL reconstruction. The chronicity of the injuries was not reported. At the 9-month follow-up, all five patients had grade A IKCD medial instability and postop instability scores. The average Lysholm score was 94.6. Zhang et al.79 also examined simultaneous ACL reconstruction and MCL reconstruction. The patients in their series had a mean time from injury to surgery of 7.6 months. At 40 months follow-up, they noted significant decreases in valgus laxity with normal to near normal mean gapping on stress radiographs. The presence of anteromedial rotatory instability decreased from 71% preoperatively to 0% postoperatively. Patients’ IKDC scores improved postoperatively to a mean of 87.7. One patient had loss of flexion over 15 degrees. Dong and colleagues39 performed a randomized, controlled trial comparing anatomic ligament repair to triangular reconstruction in patients with acute grade III MCL injury and concomitant ACL tears. No significant differences in valgus instability, knee ROM, return to sport, functional scores, or flexion/extension deficit were noted between groups. The reconstruction group had significant decreases in anteromedial rotatory instability (9.4% vs. 34%). The primary repair group had a nonstatistically significant increase in medial knee pain, four ACL re-ruptures, and two patients undergoing revision for continued medial instability. One patient in the reconstruction group underwent revision reconstruction of the MCL secondary to hardware failure, and another patient underwent surgical release for arthrofibrosis. Dong et al.80 also retrospectively reviewed outcomes of triangular ligament reconstruction in patients with isolated grade III MCL injuries and those with concomitant ACL injuries who

had failed 6 months of nonoperative treatment. In both groups of patients, medial instability and the presence of anteromedial rotatory instability significantly improved. A total of 58.9% of patients had Grade A IKDC scores and 35.7% had grade B IKDC scores. However, patients with concomitant MCL and ACL reconstruction were more likely to have extension deficits at final follow-up. Finally, in a systematic review of MCL and posteromedial corner techniques, Delong and associates34 report that 76% of MCL repair cases in the literature had a concomitant ACL reconstruction. A total of 75% of cases in the systematic review had medial laxity less than grade I at final follow-up, and the average Lysholm score was 91.6. Another controversial issue regarding combined ACL and MCL injury is whether early or late ACL reconstruction provides optimal return of function and long-term results. Based on animal studies, MCL healing is adversely affected by ACL insufficiency,81 and therefore it has been proposed that early ACL reconstruction will improve healing of the MCL. Both Halinen and colleagues77 and Millett and associates78 showed good subjective scores and minimal loss of motion complications with early ACL reconstruction (within 3 weeks). Conversely, Petersen and Laprell82 demonstrated poorer results with early ACL reconstruction compared with late ACL reconstruction in combined injuries. All patients underwent nonoperative treatment of MCL injury, with early ACL reconstruction performed within 3 weeks of injury and late ACL reconstruction after a minimum of 10 weeks. The late reconstruction group had a lower rate of loss of motion and higher Lysholm scores compared with the early reconstruction group. The literature supports nonoperative treatment of the MCL tear with surgical reconstruction of the ACL, and most surgeons are currently following this protocol. However, early versus late reconstruction continues to be a subject of debate, with studies supporting both points of view. Other factors, such as preoperative and postoperative rehabilitation protocol along with bracing, may need to be further analyzed to help assess whether early or late reconstruction is more beneficial.

COMPLICATIONS Complications of MCL ruptures are rarely reported in the literature. Failure to diagnose associated ligament injuries, such as ACL, can lead to long-term instability and degenerative problems.12,60 Failure to recognize and repair all injured medial and posteromedial structures can also lead to residual instability.12,13 In addition, missed associated meniscal tears and articular cartilage defects can lead to continued pain. Atrophy and arthrofibrosis are rare complications given the aggressive rehabilitation protocols with early motion and strengthening.13 Infection is a rare complication with surgical reconstruction. Persistent pain and Pellegrini–Stieda lesions can occur after MCL sprains, usually near the femoral origin in the region of the medial epicondyle.83 Treatment consists of a local injection or antiinflammatory medication, and resection of the lesion may be required for relief. In addition to pain, patients with femoral-sided lesions are more prone to have loss of motion and associated stiffness.13,83

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CHAPTER 101  Medial Collateral Ligament and Posterior Medial Corner Injuries

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Citation:

FUTURE CONSIDERATIONS As with most topics within orthopaedic surgery, basic science knowledge is ever increasing. The avenues for future research are vast in the areas of chemistry, biology, and biomechanics. Our understanding of cellular processes allows us to alter the progression of injury or speed up the restoration of health. Collagen healing is currently being investigated for the ligaments of the knee. Enzymatic processes in the inflammatory process of ligament injury and healing are plentiful. Research into the MCL and ACL response to a procollagen growth factor and transforming growth factor-β1 is ongoing.84 In addition, newer research has explored different expressions of lysyl oxidases in ACL and MCL tissue in response to transforming growth factor-β1 and TNF alpha.84,85 This research is furthering the investigation into the role of procollagen processes of ligament healing. The past decade has seen an increase in anatomic and biomechanical studies of the structures of the knee. Data from these and future studies will continue to influence surgical techniques. Finally, the majority of the literature consists of studies level 3 or below in evidence.86,87 Future level 2 and higher studies would help provide answers to many of the controversies regarding medial-sided knee injuries. For a complete list of references, go to ExpertConsult.com.

Tibor LM, et al. Management of medial-sided knee injuries, part 2: posteromedial corner. Am J Sports Med. 2011;39(6):1332–1340.

Level of Evidence: V, clinical review

Summary: In this article the anatomy and biomechanics of medial-sided knee injuries are reviewed. Posteromedial corner and combined posterior cruciate ligament injuries are reviewed.

Citation: DeLong JM, Waterman BR. Surgical techniques for the reconstruction of medial collateral ligament and posteromedial corner injuries of the knee: a systematic review. Arthroscopy. 2015;31(11):2258–2272.e2251.

Level of Evidence: IV, systematic review

Summary: The authors provide a review of outcomes from MCL reconstruction in the literature. Included is a review of the most common reconstruction techniques reported.

Citation: Dale KM, et al. Surgical management and treatment of the anterior cruciate ligament/medial collateral ligament injured knee. Clin Sports Med. 2017;36(1):87–103.

Level of Evidence:

SELECTED READING

V, clinical review

Citation: Wijdicks CA, et al. Structural properties of the primary medial knee ligaments. Am J Sports Med. 2010;38(8):1638–1646.

Level of Evidence:

Summary: The authors discuss the management of combined ACL/MCL injuries, including operative and nonoperative treatment.

Citation:

Cadaveric study

Summary: The two tibial attachments of the superficial medial collateral ligament (MCL) sustain clinically important loads, as do the central arm of the posterior oblique ligament and the deep MCL. Anatomic medial knee reconstructions may allow recreation of the unique stabilizing characteristics of these structures.

Citation: Marchant MH Jr, et al. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102–1113.

LaPrade MD, et al. Anatomy and biomechanics of the medial side of the knee and their surgical implications. Sports Med Arthrosc Rev. 2015;23(2):63–70.

Level of Evidence: V, clinical review

Summary: The authors review the anatomy and biomechanics of key medial knee structures. The article also reviews stress radiography for medial knee injuries.

Level of Evidence: V, clinical review

Summary: In this article the anatomy and biomechanics of medial-sided knee injuries are reviewed. Superficial medial collateral ligament and combined anterior cruciate ligament injuries are reviewed.

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CHAPTER 101  Medial Collateral Ligament and Posterior Medial Corner Injuries

REFERENCES 1. Wijdicks CA, Ewart DT, Nuckley DJ, et al. Structural properties of the primary medial knee ligaments. Am J Sports Med. 2010;38(8):1638–1646. 2. Laprade RF, Wijdicks CA. Surgical technique: development of an anatomic medial knee reconstruction. Clin Orthop Relat Res. 2012;470(3):806–814. 3. Grant JA, Bedi A, Kurz J, et al. Incidence and injury characteristics of medial collateral ligament injuries in male collegiate ice hockey players. Sports Health. 2013;5(3):270–272. 4. Lundblad M, Walden M, Magnusson H, et al. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759–762. 5. Pressman A, Johnson DH. A review of ski injuries resulting in combined injury to the anterior cruciate ligament and medial collateral ligaments. Arthroscopy. 2003;19(2):194–202. 6. Warme WJ, Feagin JA Jr, King P, et al. Ski injury statistics, 1982 to 1993, Jackson Hole ski resort. Am J Sports Med. 1995;23(5):597–600. 7. Swenson DM, Collins CL, Best TM, et al. Epidemiology of knee injuries among U.S. high school athletes, 2005/2006-2010/2011. Med Sci Sports Exerc. 2013;45(3):462–469. 8. Hughston JC, Andrews JR, Cross MJ, et al. Classification of knee ligament instabilities. Part I. The medial compartment and cruciate ligaments. J Bone Joint Surg Am. 1976;58(2): 159–172. 9. Hughston JC, Andrews JR, Cross MJ, et al. Classification of knee ligament instabilities. Part II. The lateral compartment. J Bone Joint Surg Am. 1976;58(2):173–179. 10. Engebretsen L, Lind M. Anteromedial rotatory laxity. Knee Surg Sports Traumatol Arthrosc. 2015;23(10):2797–2804. 11. Elliott M, Johnson DL. Management of medial-sided knee injuries. Orthopedics. 2015;38(3):180–184. 12. Grood ES, Noyes FR, Butler DL, et al. Ligamentous and capsular restraints preventing straight medial and lateral laxity in intact human cadaver knees. J Bone Joint Surg Am. 1981;63(8): 1257–1269. 13. Jacobson KE, Chi FS. Evaluation and treatment of medial collateral ligament and medial-sided injuries of the knee. Sports Med Arthrosc. 2006;14(2):58–66. 14. Hunter SC, Marascalco R, Hughston JC. Disruption of the vastus medialis obliquus with medial knee ligament injuries. Am J Sports Med. 1983;11(6):427–431. 15. Slocum DB, Larson RL. Rotatory instability of the knee. Its pathogenesis and a clinical test to demonstrate its presence. J Bone Joint Surg Am. 1968;50(2):211–225. 16. Laprade RF, Bernhardson AS, Griffith CJ, et al. Correlation of valgus stress radiographs with medial knee ligament injuries: an in vitro biomechanical study. Am J Sports Med. 2010;38(2): 330–338. 17. LaPrade MD, Kennedy MI, Wijdicks CA, et al. Anatomy and biomechanics of the medial side of the knee and their surgical implications. Sports Med Arthrosc. 2015;23(2):63–70. 18. Miller MD, Osborne JR, Gordon WT, et al. The natural history of bone bruises. A prospective study of magnetic resonance imaging-detected trabecular microfractures in patients with isolated medial collateral ligament injuries. Am J Sports Med. 1998;26(1):15–19. 19. Loredo R, Hodler J, Pedowitz R, et al. Posteromedial corner of the knee: MR imaging with gross anatomic correlation. Skeletal Radiol. 1999;28(6):305–311.

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20. Indelicato PLR. Medial ligament injuries in the adult. In: DeLee JDD, Miller M, eds. Orthopaedic Sports Medicine: Principles and Practice. Philadelphia: Elsevier; 2003. 21. Norwood LA Jr, Andrews JR, Meisterling RC, et al. Acute anterolateral rotatory instability of the knee. J Bone Joint Surg Am. 1979;61(5):704–709. 22. Kimori K, Suzu F, Yamashita F, et al. Evaluation of arthrography and arthroscopy for lesions of the posteromedial corner of the knee. Am J Sports Med. 1989;17(5):638–643. 23. Ra HJ, Ha JK, Jang HS, et al. Traumatic posterior root tear of the medial meniscus in patients with severe medial instability of the knee. Knee Surg Sports Traumatol Arthrosc. 2015;23(10): 3121–3126. 24. Sims WF, Jacobson KE. The posteromedial corner of the knee: medial-sided injury patterns revisited. Am J Sports Med. 2004;32(2):337–345. 25. Bollier M, Smith PA. Anterior cruciate ligament and medial collateral ligament injuries. J Knee Surg. 2014;27(5):359–368. 26. Dale KM, Bailey JR, Moorman CT 3rd. Surgical management and treatment of the anterior cruciate Ligament/medial collateral ligament injured knee. Clin Sports Med. 2017;36(1): 87–103. 27. Phisitkul P, James SL, Wolf BR, et al. MCL injuries of the knee: current concepts review. Iowa Orthop J. 2006;26:77–90. 28. Woo SL, Vogrin TM, Abramowitch SD. Healing and repair of ligament injuries in the knee. J Am Acad Orthop Surg. 2000;8(6):364–372. 29. Frank C, Amiel D, Akeson WH. Healing of the medial collateral ligament of the knee. A morphological and biochemical assessment in rabbits. Acta Orthop Scand. 1983;54(6): 917–923. 30. Woo SL, Inoue M, McGurk-Burleson E, et al. Treatment of the medial collateral ligament injury. II: structure and function of canine knees in response to differing treatment regimens. Am J Sports Med. 1987;15(1):22–29. 31. Moorman CT 3rd, Kukreti U, Fenton DC, et al. The early effect of ibuprofen on the mechanical properties of healing medial collateral ligament. Am J Sports Med. 1999;27(6):738–741. 32. Piatkowski K, Plominski J, Sowinski T, et al. Results of two-stage operative treatment of anteromedial instability of the knee. Ortop Traumatol Rehabil. 2014;16(1):33–45. 33. Blanke F, Vonwehren L, Pagenstert G, et al. Surgical technique for treatment of concomitant grade II MCL lesion in patients with ACL rupture. Acta Orthop Belg. 2015;81(3):442–446. 34. DeLong JM, Waterman BR. Surgical techniques for the reconstruction of medial collateral ligament and posteromedial corner injuries of the knee: a systematic review. Arthroscopy. 2015;31(11):2258–2272.e2251. 35. Wijdicks CA, Michalski MP, Rasmussen MT, et al. Superficial medial collateral ligament anatomic augmented repair versus anatomic reconstruction: an in vitro biomechanical analysis. Am J Sports Med. 2013;41(12):2858–2866. 36. Gilmer BB, Crall T, DeLong J, et al. Biomechanical analysis of internal bracing for treatment of medial knee injuries. Orthopedics. 2016;39(3):e532–e537. 37. Lind M, Jakobsen BW, Lund B, et al. Anatomical reconstruction of the medial collateral ligament and posteromedial corner of the knee in patients with chronic medial collateral ligament instability. Am J Sports Med. 2009;37(6):1116–1122. 38. Canata GL, Chiey A, Leoni T. Surgical technique: does miniinvasive medial collateral ligament and posterior oblique ligament repair restore knee stability in combined chronic

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47.

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49. 50.

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54.

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56. 57.

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SECTION 7  Knee

medial and ACL injuries? Clin Orthop Relat Res. 2012;470(3): 791–797. Dong J, Wang XF, Men X, et al. Surgical treatment of acute grade III medial collateral ligament injury combined with anterior cruciate ligament injury: anatomic ligament repair versus triangular ligament reconstruction. Arthroscopy. 2015;31(6):1108–1116. Kim SJ, Choi NH, Shin SJ. Semitendinosus tenodesis for medial instability of the knee. Arthroscopy. 2001;17(6):660–663. Miyamoto RG, Bosco JA, Sherman OH. Treatment of medial collateral ligament injuries. J Am Acad Orthop Surg. 2009;17(3): 152–161. Griffith CJ, Wijdicks CA, LaPrade RF, et al. Force measurements on the posterior oblique ligament and superficial medial collateral ligament proximal and distal divisions to applied loads. Am J Sports Med. 2009;37(1):140–148. Coobs BR, Wijdicks CA, Armitage BM, et al. An in vitro analysis of an anatomical medial knee reconstruction. Am J Sports Med. 2010;38(2):339–347. Derscheid GL, Garrick JG. Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med. 1981;9(6):365–368. Steadman JR. Rehabilitation of first- and second-degree sprains of the medial collateral ligament. Am J Sports Med. 1979;7(5):300–302. Bergfeld J. Symposium: functional rehabilitation of isolated medial collateral ligament sprains. First-, second-, and thirddegree sprains. Am J Sports Med. 1979;7(3):207–209. O’Connor GA. Symposium: functional rehabilitation of isolated medial collateral ligament sprains. Collateral ligament injuries of the joint. Am J Sports Med. 1979;7(3):209–210. Cox JS. Symposium: functional rehabilitation of isolated medial collateral ligament sprains. Injury nomenclature. Am J Sports Med. 1979;7(3):211–213. Deleted in review. Logan CA, O’Brien LT, LaPrade RF. Post operative rehabilitation of grade III medial collateral ligament injuries: evidence based rehabilitation and return to play. Int J Sports Phys Ther. 2016;11(7):1177–1190. Schroder D, Passler HH. Combination of cold and compression after knee surgery. A prospective randomized study. Knee Surg Sports Traumatol Arthrosc. 1994;2(3):158–165. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated non-operatively and twenty-four injuries treated surgically. J Bone Joint Surg Am. 1974;56(6):1185–1190. Bassett FH 3rd, Beck JL, Weiker G. A modified cast brace: its use in nonoperative and postoperative management of serious knee ligament injuries. Am J Sports Med. 1980;8(2):63–67. Hastings DE. The non-operative management of collateral ligament injuries of the knee joint. Clin Orthop Relat Res. 1980;147:22–28. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop Relat Res. 1978;132:206–218. O’Donoghue DH. Treatment of acute ligamentous injuries of the knee. Orthop Clin North Am. 1973;4(3):617–645. Hughston JC, Barrett GR. Acute anteromedial rotatory instability. Long-term results of surgical repair. J Bone Joint Surg Am. 1983;65(2):145–153. Muller W. The Knee: Form, Function, and Ligament Reconstruction. New York: Springer-Verlag; 1983.

59. Collins HR. Reconstruction of the athlete’s injured knee: anatomy, diagnosis, treatment. Orthop Clin North Am. 1971;2(1):207–230. 60. Kannus P. Long-term results of conservatively treated medial collateral ligament injuries of the knee joint. Clin Orthop Relat Res. 1988;226:103–112. 61. Indelicato PA. Non-operative treatment of complete tears of the medial collateral ligament of the knee. J Bone Joint Surg Am. 1983;65(3):323–329. 62. Indelicato PA, Hermansdorfer J, Huegel M. Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop Relat Res. 1990;256:174–177. 63. Reider B, Sathy MR, Talkington J, et al. Treatment of isolated medial collateral ligament injuries in athletes with early functional rehabilitation. A five-year follow-up study. Am J Sports Med. 1994;22(4):470–477. 64. Jones RE, Henley MB, Francis P. Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop Relat Res. 1986;213:137–140. 65. Omar M, Petri M, Dratzidis A, et al. Biomechanical comparison of fixation techniques for medial collateral ligament anatomical augmented repair. Knee Surg Sports Traumatol Arthrosc. 2016;24(12):3982–3987. 66. Warren RF, Marshall JL. Injuries of the anterior cruciate and medial collateral ligaments of the knee. A long-term follow-up of 86 cases–part II. Clin Orthop Relat Res. 1978;136:198–211. 67. Larson RL. Combined instabilities of the knee. Clin Orthop Relat Res. 1980;147:68–75. 68. Aglietti P. Operative treatment of acute complete lesions of the anterior cruciate ligament and medial collateral ligament: a 4 to 7 year follow-up study. Am J Knee Surg. 1991;4:186–194. 69. Andersson C, Gillquist J. Treatment of acute isolated and combined ruptures of the anterior cruciate ligament. A long-term follow-up study. Am J Sports Med. 1992;20(1): 7–12. 70. Harner CD, Irrgang JJ, Paul J, et al. Loss of motion after anterior cruciate ligament reconstruction. Am J Sports Med. 1992;20(5): 499–506. 71. Noyes FR, Barber-Westin SD. The treatment of acute combined ruptures of the anterior cruciate and medial ligaments of the knee. Am J Sports Med. 1995;23(4):380–389. 72. Hughston JC. The importance of the posterior oblique ligament in repairs of acute tears of the medial ligaments in knees with and without an associated rupture of the anterior cruciate ligament. Results of long-term follow-up. J Bone Joint Surg Am. 1994;76(9):1328–1344. 73. Shirakura K, Terauchi M, Katayama M, et al. The management of medial ligament tears in patients with combined anterior cruciate and medial ligament lesions. Int Orthop. 2000;24(2):108–111. 74. Frolke JP, Oskam J, Vierhout PA. Primary reconstruction of the medial collateral ligament in combined injury of the medial collateral and anterior cruciate ligaments. Short-term results. Knee Surg Sports Traumatol Arthrosc. 1998;6(2):103–106. 75. Pandey V, Khanna V, Madi S, et al. Clinical outcome of primary medial collateral ligament-posteromedial corner repair with or without staged anterior cruciate ligament reconstruction. Injury. 2017;48(6):1236–1242. 76. Shelbourne KD, Porter DA. Anterior cruciate ligament-medial collateral ligament injury: nonoperative management of medial collateral ligament tears with anterior cruciate ligament

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reconstruction. A preliminary report. Am J Sports Med. 1992;20(3):283–286. Halinen J, Lindahl J, Hirvensalo E, et al. Operative and nonoperative treatments of medial collateral ligament rupture with early anterior cruciate ligament reconstruction: a prospective randomized study. Am J Sports Med. 2006;34(7): 1134–1140. Millett PJ, Pennock AT, Sterett WI, et al. Early ACL reconstruction in combined ACL-MCL injuries. J Knee Surg. 2004;17(2):94–98. Zhang H, Sun Y, Han X, et al. Simultaneous reconstruction of the anterior cruciate ligament and medial collateral ligament in patients with chronic ACL-MCL lesions: A minimum 2-year Follow-up study. Am J Sports Med. 2014;42(7):1675–1681. Dong JT, Chen BC, Men XQ, et al. Application of triangular vector to functionally reconstruct the medial collateral ligament with double-bundle allograft technique. Arthroscopy. 2012;28(10):1445–1453. Woo SL, Young EP, Ohland KJ, et al. The effects of transection of the anterior cruciate ligament on healing of the medial collateral ligament. A biomechanical study of the knee in dogs. J Bone Joint Surg Am. 1990;72(3):382–392.

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82. Petersen W, Laprell H. Combined injuries of the medial collateral ligament and the anterior cruciate ligament. Early ACL reconstruction versus late ACL reconstruction. Arch Orthop Trauma Surg. 1999;119(5–6):258–262. 83. Wang JC, Shapiro MS. Pellegrini-Stieda syndrome. Am J Orthop (Belle Mead NJ). 1995;24(6):493–497. 84. Xie J, Jiang J, Zhang Y, et al. Up-regulation expressions of lysyl oxidase family in anterior cruciate ligament and medial collateral ligament fibroblasts induced by transforming growth Factor-beta 1. Int Orthop. 2012;36(1):207–213. 85. Xie J, Jiang J, Huang W, et al. TNF-alpha induced downregulation of lysyl oxidase family in anterior cruciate ligament and medial collateral ligament fibroblasts. Knee. 2014;21(1): 47–53. 86. Varelas AN, Erickson BJ, Cvetanovich GL, et al. Medial collateral ligament reconstruction in patients with medial knee instability: A systematic review. Orthop J Sports Med. 2017;5(5): 2325967117703920. 87. Grant JA, Tannenbaum E, Miller BS, et al. Treatment of combined complete tears of the anterior cruciate and medial collateral ligaments. Arthroscopy. 2012;28(1):110–122.

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102  Lateral and Posterolateral Corner Injuries of the Knee Ryan P. Coughlin, Dayne T. Mickelson, Claude T. Moorman III

As understanding of the posterolateral corner (PLC) has increased, its significance to overall knee function and biomechanics has become clearer. Although it is a relatively uncommon injury, PLC injuries can have severe consequences for overall knee stability and function. Missed injuries may affect the outcome of surgeries to correct concomitant injuries. This chapter reviews the epidemiology, relevant anatomy, biomechanics, presentation, examination, imaging, and treatment of PLC injuries. Rehabilitation, potential complications, and future considerations for the management of these serious injuries are also discussed. Isolated PLC injuries are relatively rare and have been reported to range from 1.6% to 7% of all knee injuries in persons who present for evaluation.1-6 However, the true incidence is not fully known, because these injuries are believed to be underreported or often missed at the time of evaluation. In a review of 68 persons with PLC injuries, Pacheco et al. found that 72% were not correctly diagnosed at time of presentation to the hospital and 50% were still misdiagnosed by the time they were referred to a knee specialist.7 This misdiagnosis may in part be due to the fact that understanding of the PLC has only recently improved. With recent advances, physicians are developing a better understanding of the anatomy, biomechanics, and mechanism of these injuries. In addition, the effects of chronic deficiency on gait, level of activity, natural progression, and impact on the management of other injuries are becoming clearer. Finally, surgical techniques continue to evolve as the best way to treat these injuries continues to be debated.

ANATOMY An understanding of the PLC begins with an understanding of the relevant anatomy of the region. This anatomy is among the most complex around the knee. The PLC has been characterized by dynamic and static restraints, anatomic layers, and various structures with multiple names in the literature, thus making the use of consistent nomenclature difficult.

Layers of the Lateral Side of the Knee Seebacher et al.8 described the structures on the lateral side of the knee in three anatomic layers. The most superficial layer, layer 1, consists of the lateral fascia, iliotibial (IT) band, and the superficial portion of the biceps femoris tendon. The peroneal nerve, located posterior to the biceps, is located in the deepest aspect of layer 1. The intermediate layer, layer 2, consists of 1244

the retinaculum of the quadriceps and the proximal and distal patellofemoral ligaments. The deep layer, layer 3, includes the lateral part of the joint capsule, the lateral collateral ligament, the fabellofibular ligament, the coronary ligament, the popliteal tendon, and the arcuate ligament. Even when described in layers, Seebacher et al.8 found anatomic variations within their dissected specimens.

Individual Structures Recent descriptions have focused more on specific anatomic structures and their relation to the posterolateral knee, including the IT band, lateral collateral ligament, popliteus tendon, long and short heads of the biceps femoris, and several smaller structures (Fig. 102.1).

Iliotibial Band The IT band, or IT tract, is composed of different layers and has at least four separate attachments at the knee.9-12 The main component, the superficial layer, which covers much of the lateral side of the knee, has a wide attachment to Gerdy tubercle. In addition, it has an anterior component attaching to the patella called the iliopatellar band, which influences patellar tracking. The deep layer, a structure found on the medial aspect of the superficial layer, attaches to the lateral intermuscular septum of the distal femur. Distal to the lateral epicondyle of the femur, the deep layer blends with the superficial layer and attaches to the Gerdy tubercle.12 The capsular-osseous layer, beginning at the lateral intermuscular septum of the femur, receives contributions from the lateral gastrocnemius and biceps femoris before inserting on Gerdy tubercle. This layer also has attachments to the patella and can influence patellar tracking.12 When viewed as a whole, the IT band is the first structure encountered during exposure for PLC reconstruction and serves as a stabilizer of the lateral side of the knee. Fibular Collateral Ligament With attachments on the fibular head and distal femur, the fibular collateral ligament (FCL; also known as the lateral collateral ligament) is a primary restraint to varus stress on the knee. Its fanlike attachment on the femur is in a bony depression 1.3 to 1.4 mm proximal and 3.1 to 4.6 mm posterior to the lateral epicondyle, but it does not actually attach to the epicondyle.13,14 With an average length of 6.3 to 7.1 cm, it traverses distally deep to the superficial layer of the IT band and attaches to the

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CHAPTER 102  Lateral and Posterolateral Corner Injuries of the Knee

Abstract

Keywords

As understanding of the posterolateral corner (PLC) has increased, its significance to overall knee function and biomechanics has become clearer. Although it is a relatively uncommon injury, PLC injuries can have severe consequences for overall knee stability and function. Missed injuries may affect the outcome of surgeries to correct concomitant injuries. This chapter reviews the epidemiology, relevant anatomy, biomechanics, presentation, examination, imaging, and treatment of PLC injuries. Rehabilitation, potential complications, and future considerations for the management of these serious injuries are also discussed.

posterolateral instability knee dislocation reconstruction repair

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CHAPTER 102  Lateral and Posterolateral Corner Injuries of the Knee

1245

Lateral gastrocnemius tendon

Fibular collateral ligament

Lateral gastrocnemius tendon

te

nd

on

Fibular collateral ligament

Po

pl

ite

us

Popliteus tendon

Popliteofibular ligament

Popliteofibular ligament

A

B Fig. 102.1  Image (A) and illustration (B) of the anatomy of the posterolateral corner and the relationships of individual structures to each other. (From LaPrade RF, Ly TV, Wentorf FA, et al. The posterolateral attachments of the knee: a qualitative and quantitative morphologic analysis of the fibular collateral ligament, popliteus tendon, popliteofibular ligament, and lateral gastrocnemius tendon. Am J Sports Med. 2003;31:854–860.)

fibular head.15-18 The tendon narrows as it courses distally to its narrowest point midway between the femoral and fibular attachments, where it measures 3.4 mm in an anteroposterior (AP) plane and 2.3 mm in a medial to lateral plane.16 It then expands into its fanlike attachment on the lateral aspect of the fibular head, covering 38% of the width of the head, and is located 8.2 mm posterior and 28.4 mm distal to styloid process.13,15,16 An understanding of FCL anatomy is essential to anatomic surgical reconstruction for both fibular and femoral tunnel placement.

Popliteus Tendon Complex The popliteus begins on the posteromedial aspect of the tibia and courses proximally to insert in the popliteal sulcus on the lateral femoral condyle. At the level of the popliteal fossa, the muscle gives rise to the popliteus tendon, which then inserts into the popliteal sulcus. It is at this musculotendinous junction that the popliteofibular ligament attaches the popliteus to the fibula.13 The tendon becomes intra-articular and runs medial to the FCL. It then inserts onto the femur typically 9.7 mm distal and 5.3 mm posterior to the lateral epicondyle,14 which represents a distance of 18.5 mm between the femoral attachments of the two structures, a concept to take into consideration when planning a reconstruction.13 In addition to its attachments on the femur and tibia, the popliteus contains popliteomeniscal fascicles that extend to the lateral meniscus, as well as attachments to the posterior capsule.

The popliteofibular ligament, originating at the musculotendinous junction of the popliteus, travels distally and laterally to insert on the fibular head.13,17 With anterior and posterior divisions, the ligament provides a strong connection between the fibula and the popliteus.19 The smaller anterior division attaches to the anteromedial aspect of the fibular styloid 2.8 mm from the tip of the styloid, whereas the larger posterior division attaches to the posteromedial aspect of the fibular styloid 1.6 mm distal to the tip of the styloid.13 The true role of the popliteofibular ligament to overall stability has been debated. Some investigators propose that it is a primary stabilizer to varus stress, external tibial rotation, and posterior tibial translation.20,21 However, others have found that it serves purely as a secondary stabilizer, serving a purpose if the FCL is transected.22

Biceps Femoris Muscle Long head. The long head of the biceps femoris muscle, originating at the ischial tuberosity, travels distally to the knee and forms two tendinous portions, the direct and anterior arms, with the direct arm attaching to the posterolateral fibular head and the anterior arm crossing lateral to the FCL and attaching to the lateral fibular head.19 The anterior arm is separated from the FCL by the FCL-biceps bursa. This bursa, typically measuring 8.4 by 18 mm, is consistently found between the two structures and serves as a surgical landmark for identifying the FCL attachment to the fibular head.18 In addition, the long head has three fascial attachments, the reflected arm and the lateral and anterior

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aponeurosis. The reflected arm travels superficial to the short head of the biceps femoris and inserts on the posterior aspect of the IT tract.10,19 Short head.  The short head of the biceps femoris, originating from the femur, travels distally at a 45-degree angle to the femur, where it splits into six components, including attachments to the long head of the biceps, the posterolateral aspect of the joint capsule, and the IT tract.19 The attachment to the capsule (the “capsular arm”) forms a large fascial sheath that includes the fabellofibular ligament.17 In addition, further distal, the short head attaches just lateral to the tip of the fibular styloid and a separate anterior arm travels proximal to the fibular styloid and medial to the FCL to attach posterior to the Gerdy tubercle.17 The final component, the lateral aponeurotic expansion, attaches to the posteromedial aspect of the FCL.19 The long and short heads of the biceps femoris are innervated by different components of the sciatic nerve. The long head is innervated by the tibial component and the short head by the common peroneal nerve.

Fabellofibular Ligament The fabellofibular ligament represents the most distal aspect of the capsular arm from the short head of the biceps femoris.17 Originating from the fabella or fabella-analog, it courses distally to attach to the fibular styloid. It is thought to provide stability to the knee once it has reached close to full extension.17 Arcuate Ligament Complex The arcuate ligament complex (also referred to as the arcuate popliteal ligament or arcuate complex), one of the more inconsistently referenced structures in the knee, is a Y-shaped structure consisting of medial and lateral limbs. Both limbs originate on the fibular styloid process. The lateral limb ascends proximally along the lateral joint capsule to insert on the lateral femoral condyle at the posterior joint capsule, whereas the medial limb courses over the musculotendinous junction of the popliteus, blends with the oblique popliteal ligament (ligament of Winslow), and then inserts variably onto the fabella, if present, or the posterior joint capsule.8,19,23,24 The arcuate ligament complex, when present, is believed to be more accurately described as a variable confluence of several structures, including the posterior oblique, popliteofibular, fabellofibular, and short lateral ligaments, with the final appearance of a Y-shaped ligament complex.25 It has been shown to contribute to the prevention of varus instability.26 Lateral Gastrocnemius Tendon The lateral gastrocnemius tendon originates at the musculotendinous junction of the lateral gastrocnemius muscle and then courses proximally, first attaching to a fabella or fabella-analog before blending into the meniscofemoral portion of posterior capsule.17 It ultimately attaches to the femur at the region of the supracondylar process 13.8 mm posterior to the fibular collateral attachment and 28.4 mm from the popliteus tendon attachment.13 Mid-Third Lateral Capsular Ligament The mid-third lateral capsular ligament, a thickening of the lateral capsule of the knee, originates on the femur in an area around

the lateral epicondyle and then travels distally and provides a capsular attachment to the lateral meniscus before inserting on the tibia between the Gerdy tubercle and the popliteal hiatus.17,27 It is composed of meniscotibial and meniscofemoral ligaments. Clinically, the meniscotibial ligament is responsible for the Segond fracture, an avulsion of the lateral tibial plateau.28,29 A Segond fracture can easily be seen on radiographs and magnetic resonance imaging (MRI) and is indicative of ligamentous injury to the knee.27,29

Neurovascular Structures The peroneal nerve is intimately related to the structures of the PLC. As a result, the nerve is injured in 13% of PLC injuries.26 In the popliteal fossa, the sciatic nerve splits to form the tibial and common peroneal nerves. The peroneal nerve courses distal and lateral to emerge from under the biceps femoris and then passes behind the fibular neck, ultimately passing deep to the peroneal longus.30 The nerve is located approximately 15 mm from the joint capsule.31 The inferior lateral genicular artery is the main artery associated with the PLC. Originating from the popliteal artery, it is found along the posterior joint capsule proximal to the lateral meniscus. It continues laterally and passes anterior to the fabellofibular ligament and posterior to the popliteofibular ligament before traveling within the lateral capsular ligament along the lateral meniscus.17

Biomechanics With its complex anatomy and its association with the function of other ligaments, the biomechanics of the PLC have proven difficult to determine and remain difficult to understand. In its most basic terms, the PLC serves to resist varus angulation, external tibial rotation, and posterior tibial translation. Through cadaveric sectioning studies, the role of individual structures has become clearer. Previous studies have identified the lateral collateral ligament, popliteus tendon, and popliteofibular ligament as being the key structures contributing to PLC function and stability.32-36 In addition, the PLC structures affect the function and loads seen on the cruciate ligaments (Fig. 102.2).

Role of Posterolateral Corner Structures to Varus Motion The FCL is the primary restraint to varus stress. Sectioning of the FCL causes increases in varus motion in all degrees of knee flexion.37 As long as the FCL remains intact, minimal change occurs in varus translation regardless of what other structures may be torn.38 However, isolated sectioning of the popliteus tendon has shown small but significant increases in varus motion, but to a much smaller degree than isolated sectioning of the FCL.39 Varus stress produces the greatest load on the FCL with the knee in 30 degrees of flexion, and the load subsequently decreases once the knee reaches 90 degrees of flexion, with an ultimate maximum tensile load of 295 to 309 N.40-42 Once the FCL is torn, secondary structures assume the main restraint to varus motion, including the posterior cruciate ligament (PCL), popliteofibular ligament, posterior capsule, mid-third lateral

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30

Posterior translation (mm)

Varus rotation (degrees)

PCL + LCL + deep (n – 9)

LCL + deep (n – 10)

20

10

PCL + LCL + deep (n – 8)

8 LCL + deep (n – 10) 6 4 2 0

Intact (n – 17) 0

0

15

External rotation (degrees)

A

40

30 45 60 Flexion angle (degrees)

75

90

B

0

15

30 45 60 Flexion angle (degrees)

75

90

PCL + LCL + deep (n – 6)

30

LCL + deep (n – 10)

20

10

0

C

Intact (n – 18) –2

Intact (n – 17)

0

15

30 45 60 Flexion angle (degrees)

75

90

Fig. 102.2  Sectioning studies showing motion versus knee flexion angle relative to contribution of the posterolateral structures and posterior cruciate ligament with respect to varus rotation (A), posterior translation (B), and external rotation stability (C). LCL, Lateral collateral ligament; PCL, posterior cruciate ligament; deep, popliteus-arcuate ligament complex. (Modified from Gollehon DL, Torzilli PA, Warren RF. The role of the posterolateral and cruciate ligaments in the stability of the human knee: a biomechanical study. J Bone Joint Surg Am. 1987;69:233–242.)

capsule ligament, IT band, and popliteal tendon.22,39,43,44 This primary function of the FCL is essential to consider during reconstruction to recreate the main contributor to varus stability in the knee.

Role of the Posterolateral Corner Structures in Preventing External Rotation The popliteus tendon and the popliteofibular ligament are the primary restraints to external rotation.20-22 Isolated sectioning of the popliteus leads to significant increases in external rotation, and conversely, a reconstructed popliteus demonstrates significantly decreased external rotation compared with a sectioned specimen.39 However, the FCL appears to have a greater contribution to external rotation stability than previously thought, especially at 30 degrees of knee flexion where the maximal load from external rotation forces is greater on the FCL than on the popliteus and popliteofibular ligament.40 Consequently, it appears that the FCL plays a primary role in external rotation restraint when the knee is closer to full extension, and the popliteus and popliteofibular ligament assume responsibility with increasing degrees of knee flexion.

The PCL also affects external rotation resistance. The PLC and PCL work in concert to resist external rotation stresses. Isolated sectioning of the PCL does not affect external rotation motion of the knee if the PLC is intact.38,43 As noted, the PLC experiences greatest external rotation moments at 30 degrees of knee flexion.38,43 The PCL does not experience external rotation loads until 80 to 90 degrees of knee flexion, when it becomes a secondary stabilizer to external rotation, thus explaining why in the dial test, decreased external rotation at 90 degrees compared with 30 degrees of knee flexion suggests an intact PCL and an isolated PLC injury.45

Role of the Posterolateral Corner Structures in Preventing Anterior/Posterior Tibial Translation Injured PLC structures have little effect on total anterior tibial translation if the anterior cruciate ligament (ACL) is intact.36,38,43 The FCL, popliteus, and popliteofibular ligament each experience negligible force when subjected to an anterior drawer test in a knee with a competent ACL.40 This finding is significant during the physical examination. In persons with an isolated PLC injury, findings of the Lachman test and anterior drawer test will be

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mostly normal because of the minimal impact of the PLC on anterior tibial translation. Slight differences in total translation may be found because sectioning the popliteus can cause up to a 2.6-mm increase of anterior translation.39 However, the test should have a firm end point and very minimal clinical difference, although if the ACL is also torn, the combined ACL/PLC injury leads to significantly increased anterior tibial translation. Combined sectioning of the PLC and ACL causes an additional 7 mm of anterior translation,34 which may lead to a more pronounced Lachman test during the physical examination. Isolated PLC injuries can cause increased posterior tibial translation, even in the setting of an intact PCL.36,38,43 This increase is small but significant, with the greatest increase occurring in the first 45 degrees of knee flexion. In the knee with a deficient PCL, the PLC assumes a major stabilizing role, with increases in force load of six to eight times that of the knee with an intact PCL, especially at higher degrees of knee flexion.46 Total posterior tibial translation increases significantly, up to 20 to 25 mm, when both the PCL and PLC are torn and no longer resist posterior tibial translation.38,47 Clinically, this finding is manifested in a more pronounced posterior drawer test than is found with isolated PCL tears, with a minimum of at least a grade 3 posterior drawer in the combined injury setting.47 Recent biomechanical studies have focused on the reconstruction of the cruciate ligaments in the setting of concomitant PLC injury to better explain the higher failure rate seen after cruciate ligament reconstruction in the knee with multiple ligament injuries. Graft rupture after ACL reconstruction has been reported to range from 1.8% to 10.4%, with an average rate of 5.8% reported in a recent review.48 It is becoming increasingly clear that missed PLC injuries may contribute to a higher failure rate.49-51 In response to varus load, ACL graft forces are increased with isolated FCL sectioning, and this force is further increased with varus and external rotation loads.49 In addition, concomitant reconstruction of the ACL and PLC decreases instability by allowing less anterior tibial translation, and instability was the major reason cited for poor subjective outcomes by patients with residual PLC injury after ACL reconstruction.50,52 In the setting of PCL injury, concomitant injury to the PLC is the most frequently associated injury and occurs in up to 60% of all PCL injuries.53 A missed PLC injury can affect the success of PCL reconstruction.53 In an isolated PCL injury, forces on the PCL graft resulting from external rotation loads, posterior tibial loads, or combined posterior and external rotation loads are similar to the native PCL. However, in the setting of residual PLC injury, forces acting on the PCL graft are increased during all loading conditions, with increases as much 150% on the reconstructed graft.54 The increased load may predispose the PCL reconstruction to failure.

Classification Classification systems have been created on the basis of the amount of instability and the location of the injury (Table 102.1). The American Medical Association initially standardized ligamentous injuries into grades I, II, and III based on the extent of injury and subsequent motion.55 Hughston et al.56 were the first to classify lateral side instability and

TABLE 102.1  Classification Systems to

Describe Posterolateral Corner Injuries System/Grade

Description

AMA I

Injury Severity Minimal tearing of ligament fibers, no increased motion Partial tear of ligament, slight to moderate abnormal motion Complete tear of ligament, loss of function and marked abnormal motion Structures Injured Popliteofibular ligament and popliteus tendon Popliteofibular ligament, popliteus, and fibular collateral ligament Popliteofibular ligament, popliteus, fibular collateral ligament, lateral capsule avulsion, and cruciate ligament disruption Amount of Instability Opening of 0–5 mm to varus stress Opening of 5–10 mm to varus stress Opening of 10+ mm to varus stress

II III Fanelli A B C

Hughston 1+ 2+ 3+

identified six types of lateral compartment instability based on physical examination tests: anterolateral rotatory instability, posterolateral rotatory instability, combined anterolateral and posterolateral rotatory instability, combined anterolateral and anteromedial rotatory instability, combined posterolateral, anterolateral, and anteromedial rotatory instability, and straight lateral instability. These types were graded on the basis of various clinical exams as 1+, or minor, if the joint surfaces separated 5 mm or less; 2+, or moderate, if they separated 5 to 10 mm; and 3+, or severe, if they separated 10 mm or more. A classification system was developed by Fanelli and Feldmann11 based on the location of the injury. Finally, injuries can be classified more simply as either stable or unstable, because it is instability that dictates surgical management.

HISTORY Most PLC injuries are sustained during athletic competitions, motor vehicle accidents, and falls.6,57-60 In one study, 65% of injuries were sports related, with 26% from motor vehicle accidents and 9% from falls.7 A typical mechanism is a posterolaterally directed force to the anteromedial tibia, which leads to hyperextension and a varus force. Additional mechanisms include knee hyperextension or severe tibial external rotation in a partially flexed knee, and both contact and noncontact mechanisms have been reported.61 An emerging mechanism that is increasing in frequency is injury during low-energy knee dislocation in obese persons. Azar et al.62 reported on 17 obese persons with “ultra– low-velocity” knee dislocations, of which 50% had documented injury to the lateral-sided structures. In the United States alone, 35.7% of adults are considered obese, which is not only a major risk factor identified for these ultra–low-velocity knee dislocations but also increases the risk of limb-threatening neurovascular injury during dislocation.62,63

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Concomitant Injury PLC injuries are rarely isolated and are associated with concomitant injuries in 43% to 87% of patients.2,3,35,26,60,64 These associated injuries commonly include ACL and PCL tears, as well as tibial plateau fractures. In the study by Gardner et al.65 of operative tibial plateau fractures, 29% of the fractures had a complete FCL tear and 68% had injuries to the popliteofibular ligament and/or the popliteus tendon. Given that PLC injuries can occur in the setting of knee dislocations, in the case of multiple ligamentous injury, high clinical suspicion should be maintained for spontaneously reduced knee dislocation and subsequent neurovascular injury.

PHYSICAL EXAMINATION In the acute setting, patients present after some form of trauma6,57-60 and report pain, typically at the posterolateral aspect of the knee and at the fibular head.2,61 They will have varying degrees of effusion. In a prospective study, LaPrade et al.3 reported that 9.1% of patients presenting with a knee hemarthrosis had a PLC injury. Initially, depending on the degree of trauma, the basics of trauma care should be followed. First, a thorough primary survey consisting of airway, breathing, and circulation should be performed. During the secondary survey, a more detailed musculoskeletal examination can be completed. Gross deformity may suggest a knee dislocation. Recognizing a vascular injury is of paramount importance, and failure to do so can lead to amputation. In an acute setting, a detailed neurovascular examination should be performed. An ankle-brachial index score should be obtained, and any abnormal finding warrants additional workup and consultation. A thorough neurologic examination is necessary because of the high incidence of peroneal nerve injuries associated with PLC tears.26 Particular attention should be given to peroneal nerve sensation, as well as ankle dorsiflexion, eversion, and great toe extension.59 In the chronic setting, patients often report pain at the medial joint line and/or lateral joint line, as well as at the posterolateral aspect of the knee.26,59 However, with time, swelling and pain subside and instability becomes a primary complaint. This instability is most evident with the knee in extension and often presents as a varus or hyperextension-varus thrust during the stance phase of gait.66 Patients experience difficulty ascending and descending stairs, may be seen walking with the knee in slight flexion or the ankle in equinus to alleviate these symptoms, and report having difficulty with twisting, pivoting, and cutting exercises.35 One must also be mindful of the potential for a steppage gait if a foot-drop occurs from a concomitant peroneal nerve injury.59 For both chronic and acute cases, the physical examination should begin with an evaluation of the entire extremity, looking for areas of tenderness, ecchymosis, and deformity. As stated earlier, a detailed neurovascular examination is essential to evaluate for neurovascular injury. Overall limb alignment should be evaluated because it is important to identify varus malalignment. This malalignment may not only exacerbate the instability but may also predispose a reconstruction to increased risk of failure.57,67-69

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Next, examinations specific for ligamentous injury of the knee should be performed, which includes assessing for ACL, PCL, and medial collateral ligament (MCL) injuries. A thorough evaluation of the PLC is then pursued. In the series by DeLee et al.,2 all patients had tenderness and swelling diffusely over the posterolateral joint. Point tenderness is often found at the fibular head.2,61 Varus stress examination is paramount to a basic physical examination. This test should be performed with the knee in both full extension, as well as at 30 degrees of flexion. Varus instability in full extension is suggestive of a PLC injury and a PCL injury, whereas isolated instability at 30 degrees of flexion is more suggestive of an isolated PLC injury.56 One must be sure that when testing at 30 degrees of flexion, a pure varus directed force is applied without external rotation of the tibia, which could contribute to false-positive examinations.2 In a the series of PLC injuries to the knee reported by DeLee et al.,2 the most sensitive examination technique was varus instability with the knee at 30 degrees of flexion. The frog-leg maneuver is a newly described clinical test for identifying posterolateral knee instability. With the patient lying supine, both knees are abducted and flexed to 90 degrees, bringing the soles of the feet together (frogleg position). A varus stress is applied, and the index or middle fingers of each hand are used to palpate the lateral joint lines to assess for lateral compartment gapping. When combined with the frog-leg test, the sensitivity of the conventional varus stress test has been found to increase from 83.3% to 90.0%.70 Other more specific tests for a PLC injury exist, including the posterolateral drawer test, the external rotation recurvatum test, the dial test, the standing apprehension test, and the reverse pivot shift. The posterolateral drawer test has been described by having the physician flex the hip to 45 degrees and the knee to 80 degrees. The tibia is held in mild external rotation (approximately 15 degrees). With the examiner’s thumbs on the tibial tubercle (Fig. 102.3), a posterior directed force on the proximal tibia will cause the tibial plateau to rotate posterolaterally on the femur.2 The examiner should feel the posterolateral rotation.

Fig. 102.3  Posterolateral drawer test.

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B

A

Fig. 102.4  Dial test performed in the prone position. (A) Test performed with knees bent at 90 degrees showing symmetric external rotation. (B) Test performed with knees bent at 30 degrees showing increased external rotation on the right side consistent with a posterolateral corner injury.

The dial test is performed by positioning the patient either prone or supine with the knee at the edge of the examination table. If the patient is supine, an assistant must stabilize the knees to hold the patella in line.71 The knees are flexed to 30 degrees, and both feet are externally rotated. The same maneuvers are then performed at 90 degrees of knee flexion. A difference in external rotation of 10 to 15 degrees or more compared with the contralateral side is a positive test.72 Increased external rotation at 30 degrees of flexion indicates an isolated PLC injury (Fig. 102.4).72 A positive examination finding at both 30 degrees and 90 degrees of flexion raises suspicion for a PCL injury in addition to the PLC injury.72 Tibial positioning during testing is important because reduced tibial external rotation will be found on the dial test with a posteriorly subluxated tibia.73,74 Therefore when performing the dial test, an anterior force should be applied to the tibia if a concomitant PCL injury is suspected.73,74 This full reduction of the tibia will allow for a more accurate estimate of tibial external rotation with dial testing. The external rotation recurvatum test, described by Hughston and Norwood,75 is performed by lifting the great toe of a patient in the supine position to observe the quantity of genu recurvatum (Fig. 102.5). The amount of recurvatum can be measured with a goniometer or the distance from the heel to the examination table.26 One should also note differences in varus alignment and tibial external rotation.71 The external rotation recurvatum test is less sensitive for PLC injuries because it has been proposed that the intact anteromedial bundle of the ACL provides some stability with this maneuver.2 For this reason, this test can be useful in identifying PLC injury with an ACL tear.13,75 For identifying combined ACL/PLC injuries, this test has sensitivity of 100% but specificity of 30%.13 One must be aware that this test has a high rate of false-negative findings in the setting of PLC injuries with intact ACLs.13 It is seldom useful for isolated PLC injuries or combined PLC/PCL injuries.76 Finally, an important consideration is that the posterolateral drawer test demonstrates instability in flexion, whereas the external rotation recurvatum test demonstrates instability in extension.75 The standing apprehension test (Fig. 102.6) is performed by having the patient stand with the knee at almost full extension.

Fig. 102.5  An example of the external rotation recurvatum test showing severe posterolateral corner injury.

Fig. 102.6  The standing apprehension test. As force is directed medially, the patient experiences instability and the examiner can feel the femur rotate on the tibia.

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A force is the directed medially across the anterolateral femur.59 To consider this test positive, the patient must feel an unstable sensation and rotation of the femur on the tibia must occur.6 The utility of this examination should be placed in context with the remainder of the history and examination because it has the potential to be nonspecific. The reverse pivot shift is another specific test for the PLC that is specific for the FCL, mid-third lateral capsular ligament, and popliteus complex.26 To perform this maneuver, the knee is flexed to 45 degrees with a valgus stress transmitted through the externally rotated foot.26 With subsequent extension of the leg, a subluxation is felt at approximately 25 degrees of flexion.59 Biomechanically, the posteriorly subluxated lateral tibial plateau reduces at 20 to 30 degrees of flexion because the IT band changes from knee flexor to extensor.35,77 False-positive rates have been reported to be as high as 35%, and thus careful comparison with the unaffected limb is essential. Gait examination is more useful in the chronic injury setting. During ambulation, the patient may have the appearance of a varus thrust with a lateral tibial shift. These findings can be attributed to external rotation of the tibia during full extension in the stance phase of the gait cycle. Previous authors liken this gait examination to a standing external rotation recurvatum test.35 Furthermore, a hyperextension thrust gait can be present when loading the lower extremity during the early stance phase.59 For this reason, some patients walk with a flexed knee. The physical examination is critical in the detection of PLC injuries. Although modern imaging modalities are highly accurate for detecting injury to these structures, it is believed that they may be oversensitive for these injuries. In addition, imaging cannot replace the physical examination for assessing clinical instability resulting from injury. Therefore the physical examination is the most important part of the workup to determine the need for operative intervention of PLC injuries. In essence, the examiner should trust the physical examination during the decision-making process.

IMAGING Radiographs Imaging initially begins with radiographs and may include standard AP, lateral, sunrise, and posteroanterior-flexion views. Radiographs are helpful in identifying tibial plateau fractures, Segond fractures, and avulsions of the fibular head. In addition, they may reveal proximal tibiofibular joint dislocations, widening of the lateral joint surface, and arthritis. Evaluating for medial compartment arthritis is especially useful in the chronic setting. The “arcuate sign” refers to the radiographic finding of avulsion of the fibular styloid where the popliteofibular, fabellofibular, and arcuate ligaments attach, or it can represent a larger avulsion involving more of the fibular head that results from the pull of the biceps femoris and FCL, and it may be seen on a radiograph or MRI (Fig. 102.7).78 Stress radiographs have been shown to aid in the diagnosis of PLC injuries.79,80,81 Specifically, varus-stress radiographs with increased lateral joint space widening of 4.0 mm suggest isolated grade III PLC injury, widening of 6.6 mm suggests a combined PLC and ACL tear, and widening of 7.8 mm suggests PLC, ACL, and PCL injuries.81 In a separate clinical

A

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B

C Fig. 102.7  The arcuate sign as seen on anteroposterior (A) and lateral (B) radiographs. (C) The arcuate sign (arrow) seen on coronal magnetic resonance imaging.

study, lateral widening from varus stress totaled 18.6 mm for a complete injury and an average of 12.8 mm in partial injuries.82 Therefore side-to-side comparisons can provide evidence of clinical laxity and warrant further clinical correlation to determine the need for surgical reconstruction. In addition, in the chronic setting, AP full-leg radiographs (hip to ankle) should be obtained to evaluate for varus malalignment.

Magnetic Resonance Imaging MRI allows visualization of individual components of the PLC, including the IT band, FCL, biceps femoris tendon, and popliteus (Fig. 102.8).23,83 LaPrade et al.84 found that the accuracy of identifying torn individual structures ranges from 68% for the popliteofibular ligament to 95% for the FCL. Other studies have reported an ability to detect PLC injuries in 80% to 100% of the cases, especially if the MRI is performed in the acute setting.8,85,86 MRI also identifies concomitant injuries such as tears of the cruciate ligaments, because isolated tears of the PLC are rare and most often occur in the setting of additional ligamentous injury (Fig. 102.9).3 In addition, similar to other ligamentous injuries, characteristic bone bruise patterns have been reported with PLC injuries, with the most common location being the anteromedial femoral condyle.87 Although the complex anatomy of the PLC is better visualized on MRI, it remains difficult to determine clinically significant instability based on MRI

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A

B

Fig. 102.8  Coronal magnetic resonance imaging of the fibular collateral ligament and biceps femoris inserting on the fibula (A) and the popliteus and biceps femoris (B).

A

B

C

D

Fig. 102.9  (A) A tear of fibular collateral ligament near its femoral attachment with retraction of the ligament. (B) The popliteus is torn and retracted. (C) A tear of the biceps femoris. (D) The fibular collateral is torn from its fibular insertion.

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findings alone. In an effort to simplify this diagnosis, it has been suggested that MRI evidence of injury to at least two structures, especially the popliteus, FCL, or posterior lateral joint capsule, is indicative of posterolateral rotatory instability and warrants a thorough clinical evaluation.88

Ultrasound Ultrasound has emerged as an additional imaging modality for the evaluation of PLC injuries. This technique, which can be performed quickly and is noninvasive and inexpensive, has been shown to be useful in identifying the structures of the PLC.89,90 Static ultrasound imaging has an overall sensitivity of 92% and a specificity of 75%, and dynamic ultrasound testing revealing greater than 10.5 mm of total lateral joint line width has sensitivity of 83% and a specificity of 100%.91 In addition, ultrasound has the ability to visualize dynamic processes and oblique structures, which are sometimes poorly visualized on MRI.

DECISION-MAKING PRINCIPLES The decision on how to ultimately treat a particular PLC injury depends on a number of factors, including the timing of the diagnosis, the extent of the injury, and the degree of subsequent instability.

Timing of Diagnosis PLC injuries are classified as either acute or chronic. Typically, acute refers to treatment within 3 weeks from the time of injury, but some investigators include up to 6 weeks. Studies have shown that efforts should be made to treat PLC injuries acutely, assuming the patient and the knee are in a suitable condition for surgery, because acutely treated injuries have better outcomes than do chronically managed injuries.6,35,59,64,80,92 Within the acute stage, structures are more easily visualized, scarring is not as prominent, and the tissue is more amenable to repair, if primary repair is to be attempted. However, as reconstructive techniques continue to improve, the timing of treatment is becoming less important, because reconstruction can effectively be performed in both the acute and chronic settings.

Nonoperative Management The decision to treat a PLC injury nonoperatively must take into consideration the extent of the injury and the overall stability of the joint.

Grade I Injuries Isolated grade I injuries are stable, and nonoperative treatment consistently produces good results.6,57,61,64,93,94 The true outcome of these injuries is difficult to determine, because it is likely that many people do not seek treatment for isolated grade I injuries. These injuries are treated symptomatically. Physical therapy directed at quadriceps strengthening and range of motion (ROM) exercises can begin almost immediately. Grade II Injuries The decision of how to treat grade II injuries is more difficult. Isolated grade II injuries with only mild abnormal joint motion

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typically respond well to nonoperative management but may result in some degree of residual instability.6,57,61,64,93,94 For stable grade II injuries, management is similar to grade I injuries, and they are treated symptomatically. A similar physical therapy protocol may be used, but the patient should progress more slowly. For more severe grade II injuries and grade II injuries with concomitant ligamentous injuries, surgical intervention should be considered, which includes cases with concomitant ACL or PCL reconstruction because of the increased failure rate of these reconstructions in the setting of untreated PLC injuries.49,50,52

Grade III Injuries Grade III injuries (those with significant instability) have universally inferior outcomes when treated conservatively compared with those treated surgically.93-95 In each of these studies, conservatively managed grade III injuries were reported to have persistent instability, only fair outcomes, and increased rates of osteoarthritis. Similar to grade II injuries, concomitant cruciate ligament reconstructions have inferior outcomes in conservatively managed grade III PLC injuries.49,50,52 For this reason, as in severe grade II injuries, surgical treatment is recommended to produce a more stable knee.

Repair Versus Reconstruction Historically, it had been believed that primary repair within the acute setting produced good results and should be the primary treatment.2,6,64,96 Repair consisted of identifying individual structures and securing avulsed structures to bone or performing side-to-side repair. However, recently, studies have started to cast doubt on the benefits of primary repair. Stannard et al.97 found a 37% failure rate in acutely repaired knees. Levy et al.98 identified a 40% failure rate of repair compared with 6% for reconstruction, and Geeslin and LaPrade99 found superior results of combined repair and reconstruction. It has also been shown that the FCL and popliteus tendon have little healing potential, thus making primary repair less likely to be successful.95 As a result, attempts at primary repair should be limited to the acute setting for structures with easily identified avulsions from bone without evidence of midsubstance injury and that are easily anatomically reduced with the knee in full extension.57,100 Otherwise, reconstruction should be performed. Proponents of acute reconstruction also point out the ability for accelerated therapy and ROM exercises compared with the need for longer immobilization for the repaired structures to heal.

TREATMENT OPTIONS Treatment is determined by the timing of the diagnosis, the extent of the injury, and the degree of subsequent instability.

Nonoperative Management The decision to treat PLC injuries conservatively is based on the extent of injury and the presence of instability. Unstable joints warrant surgical intervention. Truly stable joints, which are based on examination after administration of an anesthetic, may be treated nonoperatively.

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Surgical Considerations The timing of surgery and the appropriate procedure for operative PLC injuries have long been debated. Treatment options consist of primary repair and reconstruction, whether “anatomic” or “nonanatomic” reconstruction techniques are used.

Diagnostic Arthroscopy Diagnostic arthroscopy may assist in the diagnosis of PLC injuries, as well as any concomitant injuries in the knee. Arthroscopy is successful at identifying most injuries to the popliteus, coronary ligament, lateral meniscus, mid-third lateral capsular ligament, articular cartilage, and the cruciate ligaments, but it has less capability of identifying injuries to the popliteofibular ligament.101,102 However, not all injuries to the popliteus identified during open dissection were visualized during arthroscopy.102 Various arthroscopic findings have been described to suggest PLC injuries. The “lateral gutter drive-through” sign, signified as the ability to advance the arthroscope into the posterolateral compartment between a lax popliteus tendon and the lateral femoral condyle, suggests an avulsion of the popliteus off the femur.103 The “drive-through sign,” signified as greater than 10 mm of lateral compartment joint opening (Fig. 102.10), also suggests injury to the PLC.101 The visualization of torn structures on diagnostic arthroscopy or the presence of either the drive-through sign or the lateral gutter drive-through sign should prompt close examination of the PLC to avoid missing subtle injuries. Primary Repair Debate continues over the merits of primary repair of structures. Historically, primary repair has been shown to be adequate for acute PLC injuries if performed in the first 3 weeks after an injury is sustained.64,92 In this technique, avulsed structures are repaired directly to bone using suture anchors, nonabsorbable suture, bone tunnels, screw and washer constructs, or other fixation devices. However, recent studies have found that repair carries significantly inferior results compared with reconstruction, with up to a 40% failure rate in the setting of isolated repair.97,98 Some experts advocate repair only if the injury is truly

Fig. 102.10  The lateral compartment “drive-through sign” consistent with a posterolateral corner injury. An opening greater than 10 mm is present between the tibia and femur (the femoral condyle is not visualized).

an isolated avulsion and no evidence is found of midsubstance injury.100 In addition, repair of avulsed structures can help to augment the reconstruction procedures.99

Repair Techniques For acute avulsions of the popliteus or FCL from their insertion on the femur (Fig. 102.11), repair may be performed by the recess procedure.92 Originally described by Hughston, this technique uses small bone tunnels drilled at the anatomic insertion site of the avulsed structure. Initially, the structure is freed of adhesions, and its ability to be anatomically reduced is confirmed. Its proximal end is prepared with suture, which is then passed through the bone tunnel and tied on the medial side of the femur. Various techniques may be used for suture passing through bone, including cruciate ligament guides, Beath needles, or freehand drilling. A second incision is made medially, and the suture is tied over a button and against the medial cortex of the femur. For concomitant injury, care must be taken to avoid interfering with cruciate ligament reconstruction tunnels.104 A similar technique may be used to repair structures back to their insertion on the fibular head. Whether the biceps femoris, the popliteus, or the FCL, the structure’s insertion is initially identified and anatomic reduction is confirmed. Bone tunnels or suture anchors are used to secure the structure into its anatomic position. The popliteofibular ligament may be primarily repaired if the popliteus or FCL is uninjured.100 For fibular head fractures, anatomic reduction and fixation is performed, addressing any concomitant avulsion injuries at the same time. Reconstruction Techniques Biceps tenodesis.  Initially described by Clancy, the biceps tenodesis attempts to recreate the FCL and popliteofibular ligament and to reinforce the posterolateral joint capsule.105,106 A 12-cm lateral incision is made from 6 cm proximal to the lateral epicondyle down past the Gerdy tubercle. The lateral epicondyle is palpated, and the IT band is split longitudinally over the epicondyle. The biceps tendon is freed of attachments to the lateral

Fig. 102.11  Preparing the fibular collateral ligament (arrow) for primary repair back to the femoral condyle. (Courtesy Dean Taylor, MD.)

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gastrocnemius muscle. Distally, the peroneal nerve is identified and freed of attachments to the biceps tendon to prevent tethering once the biceps is rerouted. Proximal excess muscle is removed from tendon to create a 6-cm tendinous portion at the level of the epicondyle. The lateral epicondyle is freed of soft tissue. The origin of the FCL is identified. A trough is made in the bone, and a point 1 cm anterior to the lateral epicondyle is selected for drilling.105,106,107 A 3.2-mm drill hole is made, and a 6.5-mm screw and washer construct is selected. The proximal biceps tendon that had been freed of muscle is brought under the IT band and placed around the screw. The screw and washer are tightened to attach the tendon to the lateral femoral condyle. It is important to plan bone tunnels appropriately in the setting of multiligament reconstruction.104 This nonanatomic technique requires that the distal biceps attachment to the fibula remains intact for tensioning purposes. Split biceps tendon transfer.  In a modification to the technique described by Clancy, a portion of the biceps tendon is rerouted and attached via tenodesis to the epicondyle. This technique requires a stable proximal tibiofibular joint and an intact attachments between the biceps tendon and the posterolateral capsule, and, as previously described, the biceps attachment to the fibular head remains intact.108 A lateral-based incision is made for exposure from the lateral epicondyle down to the fibular head. The peroneal nerve is identified, freed of adhesions, and protected throughout the repair. The IT band is split longitudinally over the epicondyle to expose the origin of the FCL and popliteus. The long head of the biceps is isolated, and the anterior two-thirds of the tendon is separated. This portion of the tendon is detached proximally, freed of excess muscle, brought medial to the IT band, and attached via tenodesis to an area 1 cm anterior to the lateral epicondyle using a screw and washer construct similar to that previously described. Tendon remaining after the tenodesis can be secured to the fibular head for additional reinforcement. The posterolateral capsule is then incised and attached to the newly rerouted tendon to augment the reconstruction with a posterolateral capsular shift. Posterolateral corner sling procedure.  The PLC sling procedure, using autograft or allograft, creates an extraarticular sling extending from the posterior tibia to an area anterior and superior to the lateral femoral epicondyle.109 With the knee flexed 45 degrees, an incision is made along the IT band from mid femur to a point distal to the Gerdy tubercle. The peroneal nerve is identified and protected. A plane between the lateral head of the gastrocnemius and the FCL is created, and the gastrocnemius is retracted posteriorly. The popliteus and joint capsule are then identified, and the popliteus is mobilized and retracted posteriorly. A retractor is placed along the posterolateral aspect of the tibia. A 6- to 8-mm bone tunnel is created 1 to 1.5 cm below the articular surface of the tibia and medial enough to avoid violating the proximal tibiofibular joint. An allograft or autograft is passed through this tunnel from anterior to posterior and secured. The graft is brought proximal and secured to a point 1 cm anterior to the lateral femoral epicondyle using bone tunnels, suture anchors, or screw and washer constructs to complete the sling. An all-arthroscopic sling reconstruction of the popliteus tendon has been described.110

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Fig. 102.12  After presenting because of a failed posterolateral corner reconstruction, a proximal tibial osteotomy was performed and no additional reconstruction was required.

Proximal tibial osteotomy.  In the setting of genu varum and a chronic PLC injury, a proximal tibial osteotomy (Fig. 102.12) has been shown to improve stability and, in the right patient population, can serve as the primary treatment for chronic posterolateral instability.111 In addition, it may serve as the initial procedure to correct malalignment in a two-stage approach to reconstruction. Both opening and closing wedge osteotomies have been described.111,112 The goal of the osteotomy is the restore the mechanical axis to neutral or a slightly valgus position. Standard osteotomy techniques are used based on the surgeon’s preference and experience. Arthur et al.111 found that correction of the varus malalignment was sufficient to restore stability in 38% of their total study population (patients with PLC and other ligamentous injuries) and 67% of patients with isolated PLC injury, and thus a secondary procedure was not necessary. Proximal tibial osteotomy has the potential to not only correct coronal malalignment but can also influence tibial slope (sagittal alignment). An osteotomy to change coronal alignment has been used in the ACL- and PCL-deficient knee to affect stability. However, the impact of altering tibial slope to treat PLC injuries and instability remains controversial. It has been reported that, in the combined PCL- and PLC-deficient knee, increasing tibial slope better stabilizes the joint and decreases forces on the PLC structures.113 However, a biomechanical study showed that increasing the tibial slope in a knee with a combined PCL and PLC injury had no impact on stability during dial testing at 30 and 90 degrees and did not alter the reverse pivot shift test.114

Anatomic Reconstructions Isolated structure reconstruction.  Various techniques have been described for reconstructing individual structures, including the FCL, popliteus tendon, and popliteofibular ligament. In each case, an autograft or allograft may be used. Each procedure

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relies on a precise understanding of the anatomy of the PLC to accurately reconstruct the injured structure. A standard exposure is performed. The peroneal nerve is identified and protected. For the popliteus, the femoral origin of the popliteus is identified and cleared of soft tissue. A bone tunnel is created, and an interference screw is used to secure the graft into the femur. The graft is passed distally to the posterolateral aspect of the tibia. Similar to the sling procedure previously described, an anteriorto-posterior bone tunnel is made in the tibia and the popliteus is passed from posterior to anterior and secured with interference screws. For the FCL, the femoral origin for the FCL is identified, a bone tunnel is created, and the graft is secured with an interference screw. A bone tunnel is then made in the proximal fibula (while protecting the peroneal nerve) and the graft is passed through this tunnel and brought back up to the femoral origin of the graft for additional fixation. The popliteofibular ligament can be reconstructed by extending the graft used to reconstruct the FCL through the same tibial tunnel that would be made for popliteus reconstruction after it exits the fibular tunnel.115,116 When securing grafts in a fibular tunnel, the leg is placed in 30 degrees of knee flexion and a slight valgus stress is applied during fixation. Grafts in the tibial tunnel are secured with the knee in 60 degrees of flexion and with a similar valgus load applied.

Anatomic Reconstruction Technique The anatomic reconstruction technique has been popularized by LaPrade et al.116,117 In the orthopaedic literature, the “anatomic” technique has come to mean the inclusion of a tibial tunnel. After an initial lateral hockey stick incision is made, dissection is carried down to the IT band and the long head of the biceps femoris. The peroneal nerve is identified, and a neurolysis performed. A small incision is made through the anterior arm of the biceps femoris and dissection is carried down to the FCL, and its anatomic attachment to the fibula is identified and cleared from the bone. With use of a cruciate ligament tunnel guide, a 7-mm tunnel is made in the fibular head while protecting the peroneal nerve. The tibial tunnel is then drilled by first identifying relevant landmarks, including the starting point, which is an area just medial and distal to Gerdy tubercle and the exit point of the tunnel, which is a small sulcus on the posterolateral tibial plateau at the level of the musculotendinous junction of the popliteus.117 With use of a cruciate ligament tunnel guide and a guide pin, the tibial tunnel is drilled while protecting neurovascular structures. The IT band is then split over the lateral epicondyle of the femur. Dissection is carried down to the femoral attachment of the popliteus and FCL. Guide pins are placed through the attachment sites of each structure, and 9-mm tunnels are reamed. Previous prepared grafts with bone plugs are passed into these tunnels by using a passing stitch in the guide pin and bringing the pins out medial, and the plugs are secured with interference screws. The tendinous portion of the grafts have been tubularized and prepared for passage through the tunnels. One graft is then passed along the anatomic path of the popliteus and brought through the tibial tunnel in a posterior-to-anterior fashion. The second graft is passed along the anatomic path of the FCL and brought through the femoral tunnel from lateral

to medial and then through the tibial tunnel from posterior to anterior. Interference screws are used for fixation in the tibia and fibula. Fibula-based reconstruction.  The focus of the fibula-based technique is reconstruction of the lateral collateral ligament and the popliteofibular ligament. This technique offers several advantages, including needing only a single hamstring autograft tendon, allowing for remaining native tissue to be preserved and incorporated into the reconstruction, and avoiding tunnels that could threaten a femoral tunnel created for ACL reconstruction in cases of concomitant injury. In addition, it is relatively easy to perform and can be used in all settings of PLC injuries, including instances of associated tibiofibular dislocation. In this case, the tibiofibular joint is simply stabilized prior to proceeding with reconstruction. The fibula-based reconstruction is described in the Authors’ Preferred Technique section.

POSTOPERATIVE MANAGEMENT A four-phase rehabilitation protocol is used (Table 102.2). In phase I, typically in postoperative weeks 0 to 8, the goals are to protect the reconstructed structures, decrease inflammation and swelling, and carefully advance ROM of the joint. Initially, the patient performs only toe-touch weight bearing for at least 6 weeks. The extremity is protected in a hinged knee brace locked in extension for 2 weeks. After 2 weeks, passive ROM is begun as symptoms allow. Quadriceps sets are allowed, and patella mobilization is performed. Hamstring contractions and stretching are avoided. Precautions are taken to specifically prevent tibial external rotation and varus stress. After 8 weeks, the brace is unlocked and active and passive ROM is advanced as tolerated. In phase II, typically during postoperative weeks 9 to 12, attempts are made to eliminate inflammation and swelling, obtain full ROM, restore normal gait, and improve lower extremity strength. During this phase, more aggressive ROM exercises are performed until full ROM is achieved, which includes the use of a stationary bicycle. Closed kinetic chain quad strengthening begins, and cross-training machines may be used for conditioning. Gait mechanics are restored and proprioceptive exercises are performed. In phase III, typically during postoperative weeks 13 to 24, attempts are made to increase strength to at least 85% of the contralateral limb, improve aerobic endurance, initiate plyometric exercises, and begin a running program. Modalities include using a spin bike, Cybex training, agility drills, and advanced proprioception exercises. Strengthening is continued. A return to running is initiated, initially using a treadmill, and is advanced to level, outdoor surfaces. Phase IV is started once the extremity has reached greater than or equal to 85% of the strength of the contralateral limb and has results of a single-leg hop test greater than or equal to 85% of the contralateral limb, when no pain is experienced with forward running, agilities, jump training, or strengthening, and when the patient demonstrates good knee control with single-leg dynamic proprioceptive activities. This phase attempts to return the patient to full sport activities, to create equal strength, balance,

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Authors’ Preferred Technique For injuries that produce an unstable joint based on physical examination, we prefer a fibula-based reconstruction technique in both the acute and chronic settings.118 The procedure is performed with the patient supine on the operating table. Initially, an examination is performed after administration of an anesthetic to confirm the diagnosis and recognize concomitant ligamentous injury. A tourniquet is placed on the upper thigh. A diagnostic arthroscopy is performed and intra-articular pathology is addressed, including articular cartilage injuries and meniscus tears. Typically, cruciate ligament reconstruction is performed at this time. After arthroscopy, the extremity is exsanguinated and the tourniquet is inflated. A semitendinosus tendon is harvested and prepared on the back table by tubularizing it and preparing each end with no. 2 nonabsorbable suture to facilitate graft passage. A longitudinal incision is made on the lateral side of the knee centered on the lateral epicondyle proximally and between Gerdy tubercle and the fibular head distally (Fig. 102.13). The incision is carried down to the IT band with thick softtissue flaps preserved. The peroneal nerve is identified behind the biceps femoris, marked with a vessel loop, and protected throughout the procedure. Next, exposure of the deep structures is performed through the three windows described by Terry and LaPrade.19 In an acute injury, primary repair of individual structures can then be performed before proceeding with reconstruction with the use of direct sutures to bone, suture anchors, or screws and washers.

The femoral attachment of the FCL and the insertion of the popliteus are visualized. A point equidistant between these two structures is identified, and the soft tissue in this area is elevated off of bone (Fig. 102.14). A 6.5-mm screw and an 18-mm washer construct is used as an anchor and drilled appropriately. A countersink attached to the drill removes additional soft tissue and creates a bleeding bone bed to facilitate healing. An 18-mm washer is specifically chosen to help maintain the anatomic relationship of the femoral attachments of the popliteus and FCL, because they are 18.5 mm apart.13 The screw, usually 30- to 35-mm long, is inserted until just enough protrudes to allow graft passage. The peroneal nerve is then identified distally, and a neurolysis is performed if necessary. It is protected with retractors, and a tunnel is drilled anterior to posterior through the fibular head using a 6- to 7-mm acorn reamer over a guidewire 1 to 1.5 cm distal to the proximal tip of the fibular head (Fig. 102.15). The prepared semitendinosus graft is passed through this tunnel. A posterior limb is passed under the biceps femoris and under the IT band up to the screw on the femur. The anterior limb is passed under the IT band and up to just below the screw. The anterior limb does not pass around the screw so as to avoid excess soft tissue causing a more prominent screw and washer. The anterior limb is sutured to soft tissue just distal to the screw. The posterior limb is made longer than the anterior limb. The knee is flexed 30 degrees, valgus and internal rotatory forces are placed on the knee, and the screw and washer are tightened. The posterior limb is passed back through the tunnel in the fibular head. The passing sutures are then tied to each other and the graft limbs are sewn together for additional support. The area is copiously irrigated. The tourniquet is let down and hemostasis is maintained. The incisions in the lateral capsule and IT bands are closed. The skin is closed, and a bandage is applied. A hinged knee brace, locked in extension, is applied. Surgical Pearls • Use an 18-mm washer to restore the anatomic arrangement of the popliteus and FCL on the femur. • In case of tibiofibular joint instability, drill a fibular tunnel for a graft before stabilizing the joint to avoid cutting the fixation device with the drill through the fibula. • Minimize the amount of the graft under the washer to avoid prominent hardware. • For obese patients, consider external fixation for added stability in the early postoperative period. • When drilling for a femoral screw, dropping the hand slightly toward the ankle to allow a proximally directed screw will limit interference with ACL tunnels. • Protection of the peroneal nerve is imperative during fibular tunnel preparation.

Fig. 102.13  Surface anatomy for planning the incision to perform a posterolateral corner reconstruction on a left knee.

A

B

Fig. 102.14  (A) Graft passage through the fibular tunnel. (B) Graft passage around the femoral washer. Continued

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Authors’ Preferred Technique—cont’d Biceps femoris (short head) Lateral epicondyle

Biceps femoris (long head)

Iliotibial band

1st window

3rd window Fibular head

Gerdy’s tubercle

A

B

C

D

E

F

Common peroneal nerve

2nd window

Fig. 102.15  (A) The longitudinal skin incision crosses the lateral epicondyle proximally and bisects the Gerdy tubercle and the fibular head distally. (B) The lateral side of the knee is exposed through the three windows. (C) The position of the femoral drill hole is at “ground zero,” which is a point equidistant from the femoral attachment of the lateral collateral ligament and the insertion of the popliteus tendon. (D) A 7-mm tunnel is drilled through the fibular head 1 to 1.5 cm from the proximal tip and superior to the point where the peroneal nerve crosses the neck of the fibular. (E and F) The graft is passed through the fibula and around the washer and back through the tunnel (if length allows). (From Larson MW, Moinfar AR, Moorman CT, III. Posterolateral corner reconstruction: fibular-based technique. J Knee Surg. 2005;28[2]:163–166.)

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CHAPTER 102  Lateral and Posterolateral Corner Injuries of the Knee

Authors’ Preferred Technique

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Authors’ Preferred Technique

Proximal Tibial Osteotomy

Proximal Tibiofibular Joint Instability

In the setting of chronic varus malalignment, we perform an opening wedge osteotomy for deformity correction. Similar to the findings of Arthur et al.,111 we have found that osteotomy alone can restore stability and PLC reconstruction is not always necessary (Fig. 102.16).

Proximal tibiofibular joint instability should be considered in the setting of PLC injury. Acute anterolateral dislocation, the most common form of instability, is frequently associated with injury to the FCL and biceps femoris tendon and results from injury to the anterior and posterior capsular ligaments.119,120 The diagnosis can be made clinically and radiographically, with various tests and radiographic measures described.120 Proximal tibiofibular joint instability does not prevent a fibula-based reconstruction. The key is to identify the injury and stabilize the joint. Various techniques have been described throughout the literature. We use a suture fixation device technique for stabilization (Fig. 102.17). The incision created for PLC reconstruction is used. Dissection is carried down to the peroneal nerve. The nerve is identified and protected throughout. The suture device is passed across the fibula and into the tibia and finally deployed on the medial side of the tibia. It is tightened to the appropriate tension and tied over the fibula. A second device is deployed in a similar fashion. The knots are buried in soft tissue to avoid irritation of the peroneal nerve, or newer knotless devices may be used.

A

B

Fig. 102.16  Final anteroposterior (A) and lateral (B) radiograph appearance of a completed high tibial osteotomy.

A

B

Fig. 102.17  Anteroposterior (A) and lateral (B) radiographs showing proximal tibiofibular joint stabilization.

TABLE 102.2  Four-Phase Rehabilitation Protocol Used After Posterolateral Corner

Reconstruction

Phase 1 (Weeks 0–8)

Phase 2 (Weeks 9–12)

Phase 3 (Weeks 13–24)

Phase 4 (Weeks 24+)

Restricted motion to promote healing (knee locked in extension for 2 weeks and then passive ROM 0–90 degrees with therapy after 2 weeks) Toe-touch weight bearing for 6 weeks, and then gradual progression of weight-bearing status Quadriceps strengthening/patella mobilization

Obtain full knee ROM

Improve aerobic endurance, initiate plyometric exercises

Begin sport-specific functional motions

Restore normal gait, initiate proprioception exercises

Initiate running program on level surfaces

Continue strengthening, including closed kinetic chain exercises Eliminate residual swelling/ inflammation

Increase strength to at least 85% of the contralateral limb Have no pain with running, agility exercises, jumping, or strengthening

Obtain equal balance and proprioception, gradually increase level of participation in sports Obtain equal bilateral lower extremity strength

Avoid hamstring stretches and external rotation/varus stress on the tibia ROM, Range of motion.

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proprioception, and power bilaterally, and to achieve a 100% global function rating. Exercises started in phase III are advanced, with a gradual increase in the level of participation in sportspecific activities, and the patient progresses to running on all surfaces without restriction.

RETURN TO PLAY Once the athlete has progressed to stage IV of the rehabilitation protocol, he or she begins sport-specific rehabilitation, conditioning, and training. Minimal data exist on PLC injuries in elite athletes, given their rare diagnosis.121-123 In a retrospective review of National Football League players, Bushnell et al.121 found that nine players over a 10-year period were diagnosed with isolated grade III FCL tears, and the four who underwent operative treatment and the five who were treated nonoperatively all returned to play in the NFL. In general, it may take at least a year for an athlete to return to a preinjury level of play. Extensive rehabilitation is required, and clearance from the treating physician must be obtained before returning to competitive training and sports. This decision is based on functional screening measures, strength testing, the knee’s ROM, absence of swelling, and painless sport-specific activities. Preoperatively, it is important to discuss the expected time frame for returning to sporting activities so the athlete has realistic expectations during the rehabilitation process.

RESULTS Numerous studies demonstrating the results of various techniques used to treat PLC instability have been published. Without a standardized outcome measure, it is difficult to truly compare these various techniques. In addition, the length of follow-up varies between the different studies, which can make one technique appear superior to another. Also, authors often use similar descriptive terms for techniques but offer a modification to a previously described technique of the same name. For example, within the

literature, multiple authors describe an anatomic reconstruction, but great variability exists between the different anatomic techniques. In Tables 102.3116,124-128 and 102.4,67,93,97,98,111,129-136 studies indicating “fibular based” imply isolated tunnels in the fibula and femur, whereas studies indicating “anatomic” imply an additional tibial tunnel.

COMPLICATIONS Complications may be separated into two categories: those resulting from the injury and those resulting from the surgery. As with any surgery, the risk of bleeding, infection, deep venous thrombosis, and prominent/painful hardware are associated with reconstruction of PLC injuries. Because injuries to the PLC more commonly occur with additional ligamentous injuries, they are often seen in the setting of knee dislocations and therefore may carry many of the same risks. In the setting of significant soft tissue injury or open wounds, infection and soft tissue healing can become a problem, and infection occurs in up to 43% of open knee dislocations.139 With its close proximity to the lateral joint capsule, common peroneal nerve injury is common and has been documented in 13% of patients with PLC injuries.26,140 The rates of nerve recovery for complete disrupted injury, complete stretched injury, and partial injury are found to be 0%, 50%, and 100%, respectively, with an overall rate of recovery of 50%.141 Nerve injury appears to be related to disruption of the distal attachment of the biceps tendon to the fibular head, causing the nerve to be displaced into an abnormal position, thus making it vulnerable to injury.142 In the chronic setting, the risk of iatrogenic peroneal nerve injury may be increased because of the presence of more scar tissue, and subsequently, a more difficult neurolysis procedure (Fig. 102.18). Vascular injury, which requires immediate recognition and treatment, has been reported to occur in 12% to 64% of knee dislocations.143,144 The presence of normal distal pulses cannot completely rule out arterial injury due to collateral circulation. The ankle-brachial index (ABI) is a reliable, noninvasive screening tool for diagnosing vascular injury

TABLE 102.3  Biomechanical Studies of Posterolateral Corner Reconstruction Study

Year

No. of Knees

Technique

Outcome

Kang et al.127

2017

3D-computational model

TBR vs. mFBR vs. cFBR

Plaweski et al.128

2015

8 cadaveric knees

mFBR

Rauh et al.124

2010

10 cadaveric knees

Fibula based vs. anatomic

Apsingi et al.125

2009

10 cadaveric knees

Fibula based vs. anatomic

Nau et al.126

2005

10 cadaveric knees

Fibula based vs. anatomic

LaPrade et al.116

2005

10 cadaveric knees

Anatomic

Cruciate ligament forces greatest in cFBR model, with no difference between the TBR and mFBR models; joint contact stresses of the three surgical models were greater than those of the intact model Restoration of external varus rotation in extension and translation of the lateral tibial plateau at 90-degree flexion similar to intact knee No difference in stability observed between either reconstruction technique No difference in stability observed between either reconstruction technique No difference in stability observed between either reconstruction technique No difference in external rotation stability between intact knee or reconstructed knee

3D, Three-dimensional; cFBR, conventional fibular-based; mFBR, modified fibular-based; TBR, tibial-based.

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TABLE 102.4  Results of Various Techniques for Posterolateral Corner Reconstruction Year

N

Mean Follow-Up and Range (Months)

93

Kannus

1989

23

99 (72–126)

Levy et al.98 Stannard et al.97 Arthur et al.111

2010 2005 2007

10 57 21

Yoon et al.137

2011

Zorzi et al.136

Study

Mean Age and Range (Years)

Technique

Outcome

34 (14–61)

Nonoperative management

34 (24–49) 24 (24–59) 37 (19–65)

Not reported 33 (17–57) 32 (18–49)

Repair (acute) Repair (acute) High tibial osteotomy (chronic)

32

35 (24–63)

35 (20–54)

Fibular sling (chronic)

2013

19

38 (–)

29 (17–41)

Fibular sling (chronic)

Ibrahim et al.156

2013

20

44 (24–52)

26 (18–48)

Fanelli et al.135

2014

34

32 (24–84)

27 (15–53)

Kim et al.106

2003

46

40 (24–93)

35 (16–62)

Yoon et al.129

2006

21

22 (12–41)

34 (21–64)

LaPrade et al.130

2010

64

53 (24–86)

32 (18–58)

Fibular sling (acute) Sling; capsular imbrication (chronic) Biceps tenodesis (chronic) Anatomic (acute and chronic) Anatomic (chronic)

Grade I and II: 82% returned to preinjury level of activity Grade III: 25% returned to preinjury level of activity 40% failure rate 37% failure rate 38% of patients stable after high tibial osteotomy only (no reconstruction needed) Mean postoperative Lysholm and IKDC 86.4 and 75.3, respectfully; 1 failure with persistent laxity Mean postoperative IKDC 86; 11% persistent laxity Mean postoperative Lysholm 90; 6% persistent laxity Mean postoperative Lysholm 91.8; 1 patient with persistent laxity 17% with loss of stability at final follow-up

Jakobsen et al.131 Gormeli et al.134

2010

27

46 (24–86)

28 (13–57)

Anatomic (chronic)

2015

21

40.9 ± 13.7

31.1 ± 9.2 years

Anatomic (chronic)

Kim et al.138

2013

65

34 (–)

37.2 (16–64)

Anatomic (chronic)

Camarda et al.67

2010

10

28 (18–40)

27 (16–47)

Fibular based (chronic)

Schechinger et al.132

2009

16

30 (24–75)

30 (19–61)

Khanduja et al.133

2006

19

67 (24–110)

30 (21–47)

Fibular based + capsular shift (chronic) Fibular based (chronic)

19% with greater than 1+ excess laxity Mean postoperative IKDC 62.6; 5% recurrent instability requiring revision surgery 5% with rotatory instability and 5% varus instability Mean postoperative Lysholm, IKDC and Tegner 80, 64, and 4, respectfully. No differences between isolated PLC and multi-ligament reconstruction Mean postoperative Lysholm 86.3; 18% failures on varus stress radiographs 0% loss of stability, 10% overconstrained compared with uninjured side Mean postoperative Lysholm and IKDC 89.9 and 81.3, respectively; No functional instability, 25% with 1+ varus laxity 26% with “residual minimal posterolateral instability” but not further defined

IKDC, International Knee Documentation Committee; PLC, posterolateral corner.

following knee dislocations. An index greater than 0.90 was found to have a 100% negative predictive value of arterial injury, and in this situation the patient can be monitored with serial clinical examinations.145 However, an ABI less than 0.90 requires further investigation with either an arterial duplex ultrasound or CT angiography. A detailed neurovascular examination is imperative, not only to identify limb-threatening emergencies, but to also identify neurologic deficit prior to surgical intervention, given the proximity of the peroneal nerve to the surgical field. Posttraumatic joint space narrowing after PLC reconstruction was reported to occur in 29% of patients followed up 4 years postoperatively, with most of those patients having evidence of

early chondrosis at the time of initial surgery.146 Joint stiffness, or arthrofibrosis, may also occur after these injuries and their reconstruction. Some period of immobilization is required to promote healing, which places the knee at risk for the development of arthrofibrosis. This risk can be decreased by determining, intraoperatively, a safe degree of flexion to allow in the early postoperative period and to perform patellar mobilization.59 Iatrogenic fracture of the fibular head can occur during bone tunnel preparation if the guide pin is not appropriately placed prior to reaming. Painful hardware has been a problem with the tibial screw and washer construct in the past. Lower profile hardware may minimize this concern.

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SELECTED READINGS Citation: Larson MW, Moinfar AR, Moorman CT III. Posterolateral corner reconstruction: fibular-based technique. J Knee Surg. 2005;18(2):163–166.

Level of Evidence: IV

Summary:

Fig. 102.18  A peroneal nerve avulsion injury (black arrow) after a posterolateral corner injury. (Courtesy Katherine Coyner, MD.)

FUTURE CONSIDERATIONS Pediatric Posterolateral Corner Injuries As the number of children playing sports increases and as more demands and expectations are placed on these adolescent athletes, the rate of injury is going to increase and may include a higher incidence of PLC injuries. Purely ligamentous injury is uncommon in the pediatric population, which is most often attributed to the ligament being stronger than the adjacent growth plate.147,148 PLC injuries appear to be especially rare. In a review of 39 adolescents undergoing ACL reconstruction, despite 67% having concomitant injuries, none were diagnosed as having PLC injuries.149 Case series have described isolated avulsions of the popliteus tendon and injuries to both the popliteus and FCL.150-154 Von Heideken et al.154 identified 23 reported cases of isolated pediatric PLC injuries in the literature, with most involving avulsion fractures at the femoral attachment of the popliteus and FCL. However, no extensive report on pediatric PLC injuries was found in the literature. Given its rare incidence, treatment of isolated pediatric PLC injuries is not clear. Kannus and Jarvinen155 reported on the nonoperative treatment of 33 adolescents with grade II and III ligament injuries, including five grade II and two grade III FCL injuries. The findings, which were not just specific to the LCL injuries, resembled those found in adults, with the grade II injuries doing well and the grade III injuries having poor results and persistent instability. It was recommended that the grade III injuries be treated surgically. However, the best way to surgically treat these injuries remains unclear. In addition, surgical treatment in adolescents poses the additional risk of operating around the physis and risking growth disturbance. Complicating this situation is the fact that the one patient in the case series by Von Heideken et al.154 who was treated nonoperatively was the only patient in whom a growth disturbance and angular deformity of the injured extremity developed. More research is necessary to better determine the best way to treat these rare injuries. For a complete list of references, go to ExpertConsult.com.

The fibula-based technique for both acute and chronic posterolateral corner reconstruction is a successful way to restore stability, preserve native tissue to incorporate into the reconstruction, and minimize bone tunnels during combined reconstructions, and it is relatively easy to perform. The technique is thoroughly described.

Citation: LaPrade RF, Ly TV, Wentorf FA, et al. The posterolateral attachments of the knee: a qualitative and quantitative morphologic analysis of the fibular collateral ligament, popliteus tendon, popliteofibular ligament, and lateral gastrocnemius tendon. Am J Sports Med. 2003;(31):854–860.

Level of Evidence: Cadaveric study

Summary: The femoral and tibial attachments for the major structures of the posterolateral corner have a consistent anatomic relationship to each other with consistently measurable distances between the various structures. It is important to consider these relationships and restore this anatomic relationship during reconstruction techniques.

Citation: Levy BA, Dajani KA, Morgan JA, et al. Repair versus reconstruction of the fibular collateral ligament and posterolateral corner in the multiligament-injured knee. Am J Sports Med. 2010;38(4):804–809.

Level of Evidence: III

Summary: Comparing the acute repair of structures with the reconstruction of the posterolateral corner revealed a much higher failure rate in the acute repair group, in which 40% failed compared with 6% in the reconstruction group. Reconstruction should be considered, even in the acute setting, because of the much higher rate of failure in the primary repair group.

Citation: LaPrade RF, Resig S, Wentorf F, et al. The effects of grade III posterolateral knee complex injuries on anterior cruciate ligament graft forces. Am J Sports Med. 1999;27(4):469–475.

Level of Evidence: Cadaveric study

Summary: Untreated grade III posterolateral corner injuries lead to significantly higher forces on the anterior cruciate ligament. Therefore in the setting of combined injury, untreated grade III posterolateral corner injuries contribute to ACL graft failure because of this higher force experienced by the graft.

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CHAPTER 102  Lateral and Posterolateral Corner Injuries of the Knee

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Citation:

Summary:

LaPrade RF, Wentorf FA, Fritts H, et al. A prospective magnetic resonance imaging study of the incidence of posterolateral and multiple ligament injuries in acute knee injuries presenting with a hemarthrosis. Arthroscopy. 2007;23: 1341–1347.

Out of 331 patients with acute knee injuries presenting with a hemarthrosis, 9.1% of the entire group and 16% of the group diagnosed with ligament tears were found to have a posterolateral knee injury, and in more than 50% of these injuries, more than one posterolateral corner structure was involved. Posterolateral corner injuries may be more common than previously reported, and when present, they are usually associated with additional ligamentous injury.

Level of Evidence: II

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CHAPTER 102  Lateral and Posterolateral Corner Injuries of the Knee

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117. LaPrade RF. Anatomic reconstruction of the posterolateral aspect of the knee. J Knee Surg. 2005;18(2):167–171. 118. Larson MW, Moinfar AR, Moorman CT III. Posterolateral corner reconstruction: fibular-based technique. J Knee Surg. 2005;18(2):163–166. 119. Ogden JA. Subluxation and dislocation of the proximal tibiofibular joint. J Bone Joint Surg Am. 1974;56:145–154. 120. Sekiya JK, Kuhn JE. Instability of the proximal tibiofibular joint. J Am Acad Orthop Surg. 2003;11:120–128. 121. Bushnell BD, Bitting SS, Crain JM, et al. Treatment of magnetic resonance imaging-documented isolated grade III lateral collateral ligament injuries in National Football League athletes. Am J Sports Med. 2010;38(1):86–91. 122. Gabbett TJ. Incidence of injury in semi-professional rugby league players. Br J Sports Med. 2003;37(1):36–44. 123. Pluim BM, Staal JB, Windler GE, et al. Tennis injuries: occurrence, etiology, and prevention. Br J Sports Med. 2006;40(5):415–423. 124. Rauh PB, Clancy WG, Jasper LE, et al. Biomechanical evaluation of two reconstruction techniques for posterolateral instability of the knee. J Bone Joint Surg Br. 2010;92-B:1460–1465. 125. Apsingi S, Nguyen T, Bull AM, et al. A comparison of modified Larson and ‘anatomic’ posterolateral corner reconstructions in knees with combined PCL and posterolateral corner deficiency. Knee Surg Sports Traumatol Arthrosc. 2009;17(3):305–312. 126. Nau T, Chevalier Y, Hagemeister N, et al. Comparison of two surgical techniques of posterolateral corner reconstruction of the knee. Am J Sports Med. 2005;33(12):1838–1845. 127. Kang KT, Koh YG, Son J, et al. Finite element analysis of the biomechanical effects of the 3 posterolateral corner reconstruction techniques for the knee joint. Arthroscopy. 2017;doi:10.1016/ j.arthro.2017.02.011. pii: S0749-8063(17)30178-0. 128. Plaweski S, Belvisi B, Moreau-Gaudry A. Reconstruction of the posterolateral corner after sequential sectioning restores knee kinematics. Orthop J Sports Med. 2015;3(2):2325967115570560. 129. Yoon KH, Bae DK, Ha JH, et al. Anatomic reconstructive surgery for posterolateral instability of the knee. Arthroscopy. 2006;22:159–165. 130. LaPrade RF, Johansen S, Agel J, et al. Outcomes of an anatomic posterolateral knee reconstruction. J Bone Joint Surg Am. 2010;92:16–22. 131. Jakobsen BW, Lund B, Christiansen SE, et al. Anatomic reconstruction of the posterolateral corner of the knee: a case series with isolated reconstructions in 27 patients. Arthroscopy. 2010;26(7):918–925. 132. Schechinger SJ, Levy BA, Dajani KA, et al. Achilles tendon allograft reconstruction of the fibular collateral ligament and posterolateral corner. Arthroscopy. 2009;25(3):232–242. 133. Khanduja V, Somoyaji HS, Harnett P, et al. Combined reconstruction of chronic posterior cruciate ligament and posterolateral corner deficiency. A two- to nine-year follow-up study. J Bone Joint Surg Br. 2006;88-B:1169–1172. 134. Gormeli G, Gormeli CA, Elmali N, et al. Outcome of the treatment of chronic isolated and combined posterolateral corner knee injuries with 2- to 6-year follow up. Arch Orthop Trauma Surg. 2015;135:1363–1368. 135. Fanelli GC, Fanelli DG, Edson CJ, et al. Combined anterior cruciate ligament and posterolateral reconstruction of the knee using allograft tissue in chronic knee injuries. J Knee Surg. 2014;27(5):353–358. 136. Zorzi C, Alam M, Iacono V, et al. Combined PCL and PLC reconstruction in chronic posterolateral instability. Knee Surg Sports Traumatol Arthrosc. 2013;21(5):1036–1042.

137. Yoon KH, Lee JH, Bae DK, et al. Comparison of clinical results of anatomic posterolateral corner reconstruction for posterolateral rotatory instability of the knee with or without popliteal tendon reconstruction. Am J Sports Med. 2011;39(11): 2421–2428. 138. Kim SJ, Kim SG, Lee IS, et al. Effect of physiological posterolateral rotatory laxity on early results of posterior cruciate ligament reconstruction with posterolateral corner reconstruction. J Bone Joint Surg Am. 2013;95(13):1222–1227. 139. King JK, Blair JA, Tom JA. Surgical outcomes after traumatic open knee dislocation. Knee Surg Sports Traumatol Arthrosc. 2009;17:1027–1032. 140. Niall DM, Nutton RW, Keating JF. Palsy of the common peroneal nerve after traumatic dislocation of the knee. J Bone Joint Surg Br. 2005;87-B:664–667. 141. Ridley TJ, McCarthy MA, Bollier MJ, et al. The incidence and clinical outcomes of peroneal nerve injuries associated with posterolateral corner injuries of the knee. Knee Surg Sports Traumatol Arthrosc. 2017;doi:10.1007/s00167-016-4417-2. 142. Bottomley N, Williams A, Birch R, et al. Displacement of the common peroneal nerve in posterolateral corner injuries of the knee. J Bone Joint Surg Br. 2005;87-B:1225–1226. 143. Boisrenoult P, Lustig S, Bonneviale P, et al. Vascular lesions associated with bicruciate and knee dislocation ligamentous injury. Orthop Traumatol Surg Res. 2009;95:621–626. 144. Hoover NN. Injuries of the popliteal artery associated with fractures and dislocations. Surg Clin North Am. 1961;41: 1099–1112. 145. Mills WJ, Barei DP, McNair P. The value of the ankle-brachial index for diagnosing arterial injury after knee dislocation: a prospective study. J Trauma. 2004;56(6):1261–1265. 146. Corten K, Bellemans J. Cartilage damage determines intermediate outcome in the late multiple ligament and posterolateral corner-reconstructed knee. A 5- to 10-year follow-up study. Am J Sports Med. 2008;36(2):267–275. 147. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J Bone Joint Surg Am. 1963;45-A:587–622. 148. Bradley GW, Shives TC, Samuelson KM. Ligament injuries in the knees of children. J Bone Joint Surg Am. 1979;61-A(4):588–591. 149. Millet PJ, Willis AA, Warren RF. Associated injuries in pediatric and adolescent anterior cruciate ligament tears: does a delay in treatment increase the risk of meniscus tear? Arthroscopy. 2002;18(9):955–959. 150. Nakhostine M, Perko M, Cross M. Isolated avulsion of the popliteus tendon. J Bone Joint Surg Br. 1995;77-B(2):242–244. 151. Mirkopulos N, Myer T. Isolated avulsion of the popliteus tendon: a case report. Am J Sports Med. 1991;19(4):417–419. 152. Wheeler LD, Lee EYP, Lloyd DCF. Isolated popliteus tendon avulsion in skeletally immature patients. Clin Radiol. 2008;63:824–828. 153. Kovack TJ, Jacob PB, Tesner R, et al. Periosteal avulsion of the posterolateral corner of the knee in an adolescent: an unreported case. Orthopaedics. 2011;34(10):791–794. 154. Von Heideken J, Mikkelsson C, Windhamre HB, et al. Acute injuries to the posterolateral corner of the knee in children: a case series of 6 patients. Am J Sports Med. 2011;39(10): 2199–2205. 155. Kannus P, Jarvinen M. Knee ligament injuries in adolescents. J Bone Joint Surg Br. 1988;70-B(5):772–776. 156. Ibrahim SA, Ghafar S, Salah M, et al. Surgical management of traumatic knee dislocation with posterolateral corner injury. Arthroscopy. 2013;29(4):733–741.

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103  Multiligament Knee Injuries Samantha L. Kallenbach, Matthew D. LaPrade, Robert F. LaPrade

Knee ligaments are responsible for providing the static stability of the knee, control of kinematics, and prevention of abnormal rotation and/or displacement that may damage the articular surfaces or the menisci. Knee dislocations are rare and are estimated to account for 0.02% to 0.2% of orthopaedic injuries1; however, it is generally accepted that multiligament injuries may occur at a higher rate because some knees spontaneously reduce before presentation.2,3 These injuries may spontaneously reduce or may present as an acutely dislocated knee requiring reduction. The diagnosis and management of multiligament injuries pose unique challenges to orthopaedic surgeons, and a wide spectrum of injury exists, ranging from two-ligament injuries such as a cruciate and collateral ligament rupture to a grossly unstable knee that requires spanning external fixation. Although the immediate concerns should be to determine the integrity of the neurovascular structures, other essential concepts include accurate identification of all injured structures, repair versus reconstruction, management of acute versus chronic injuries, single- versus two-stage surgery, and postoperative rehabilitation. During the past three decades, clinical outcome studies along with anatomic and biomechanical investigations have greatly improved the management of these complex injuries.

HISTORY In evaluating a patient who presents with knee pain or instability, the clinician must obtain a careful history of symptom onset, mechanism of injury, history of prior knee injuries, and previous operative and nonoperative treatments. Multiligament injuries associated with sports are considered low-energy and are often isolated to the involved extremity, whereas those associated with automobile or motorcycle crashes are considered high-energy4 and may be combined with other life-threatening injuries. Acutely injured patients may be unable to ambulate because of swelling, pain, and instability. Determination of the time since the injury occurred is crucial in patients who present with persistent dislocation because of the possibility of vascular injury and limb ischemia. Patients with chronic injuries may report mechanical symptoms, including clicking, catching, or locking or they may report instability on uneven ground, with cutting motions, and during activities of daily living. Neurologic deficits may be reported, including the presence of paresthesias in the common peroneal nerve distribution and a foot drop. Synthesis 1264

of this information will guide the clinician in the physical examination and selection of imaging studies.

PHYSICAL EXAMINATION Examination of a patient with a suspected multiligament injury in the acute setting must include the assessment of vascular status. If an arterial injury is suspected, an ankle-brachial index score should be determined; a score of less than 0.9 is an indication that advanced arterial imaging should be obtained.5 Serial neurovascular examination and selective computed tomography angiography has been recommended; “hard signs” of ischemia warrant emergent vascular consultation.6 The neurologic status must also be assessed. The common peroneal nerve supplies motor innervation to the anterior (deep peroneal) and lateral (superficial peroneal) compartments of the leg, as well as the extensor hallucis brevis and extensor digitorum brevis (deep peroneal) on the dorsum of the foot. A 25% to 35% nerve injury rate has been reported in the population with high-velocity knee dislocations.7 In a series of acute isolated or combined posterolateral corner (PLC) knee injuries in an orthopaedic sports medicine referral practice, 4 of 29 patients had a complete palsy of the common peroneal nerve and an additional 7 of 29 had a partial motor/sensory deficit.8 A recent study by Moatshe et al. found that peroneal nerve injury was significantly associated with vascular injury; thus injury to the peroneal nerve should raise suspicion of a vascular lesion.2 Tibial nerve injuries may also occur in knee dislocations; although these injuries occur less frequently. Physical examination of knee stability is a repeatable method of predicting intra-articular pathology but may be more difficult in patients with acute injuries. It is important to examine both legs to assess for pathologic instability versus physiologic laxity. Multiligament injuries are not subtle on examination; however, attention to subtle findings will aid the clinician in determining which specific structures are injured. Anteroposterior (AP) stability should be assessed with the Lachman, pivot shift, and posterior drawer tests. The posterior sag and quadriceps active tests also aid in the evaluation of the posterior cruciate ligament (PCL). Lateral and posterolateral knee injuries are typically combined with an injury to one or both of the cruciate ligaments.8-10 In acute injuries, the patient may have tenderness upon palpation of the fibular head. Examination maneuvers should include varus stress11 at 0 and 20 degrees, reverse pivot shift, external rotation

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CHAPTER 103  Multiligament Knee Injuries

Abstract

Keywords

Knee ligaments are responsible for providing the static stability of the knee, control of kinematics, and prevention of abnormal rotation and/or displacement that may damage the articular surfaces or the menisci. Knee dislocations are rare and are estimated to account for 0.02% to 0.2% of orthopaedic injuries; however, it is generally accepted that multiligament injuries may occur at a higher rate because some knees spontaneously reduce before presentation. These injuries may spontaneously reduce or may present as an acutely dislocated knee requiring reduction. The diagnosis and management of multiligament injuries pose unique challenges to orthopaedic surgeons, and a wide spectrum of injury exists, ranging from two-ligament injuries such as a cruciate and collateral ligament rupture to a grossly unstable knee that requires spanning external fixation. Although the immediate concerns should be to determine the integrity of the neurovascular structures, other essential concepts include accurate identification of all injured structures, repair versus reconstruction, management of acute versus chronic injuries, single- versus two-stage surgery, and postoperative rehabilitation. During the past three decades, clinical outcome studies along with anatomic and biomechanical investigations have greatly improved the management of these complex injuries.

multiligament knee dislocation knee injury knee reconstruction PLC PCL

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CHAPTER 103  Multiligament Knee Injuries

recurvatum,12 and the dial test at 30 and 90 degrees. In a patient with a positive varus stress test at 30 degrees and negative findings at 0 degrees, an isolated fibular collateral ligament (FCL) tear is suspected. However, with multiligament injuries, the varus stress test will also be positive at 0 degrees. A positive dial test at both 30 and 90 degrees suggests a combined PCL and PLC injury.13,14 A positive posterolateral drawer test reinforces findings consistent with a PLC injury but must be interpreted with caution, as discussed further on. Medial structures are evaluated with the valgus stress test at 0 and 20 degrees of flexion15; instability at full extension is indicative of a combined cruciate ligament injury. Assessment of medial compartment gapping at 20 degrees under a valgus stress primarily isolates the superficial medial collateral ligament (MCL). Evaluation of associated rotational abnormalities is assessed with anteromedial tibial rotation at 90 degrees of flexion and the dial test at 30 and 90 degrees of flexion.16 Increased anteromedial rotation suggests a more extensive knee injury that includes the superficial MCL as well as the posterior oblique ligament (POL) and deep MCL. The examiner must be careful to differentiate anteromedial from posterolateral tibial rotation during the dial test by palpation and visualization of tibial subluxation with the patient in the supine position.16 Gait assessment is an important component of the physical examination but may be compromised because of pain in persons with acute injuries. In subacute or chronic injuries, a varus thrust gait or foot drop may be observed in patients with combined lateral injuries. Patients with medial knee injuries may demonstrate a valgus thrust during the stance phase of gait, but this manifestation is less common and usually occurs in patients with genu valgus alignment.

IMAGING Radiographic examination for patients with a suspected multiligament knee injury should include standard AP and lateral views (Fig. 103.1) as well as weight-bearing flexion (Rosenberg)

A

B

Fig. 103.1  Anteroposterior (A) and lateral (B) radiographs demonstrating an acute left knee dislocation. An arcuate fracture is also visible on the anteroposterior radiograph (arrow).

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views.17 These views allow visualization of tibial plateau, femoral condyle, or osteochondral fractures. Segond18 and/or arcuate19 fractures may be visualized with lateral/posterolateral injuries, and calcification near the MCL origin (Pellegrini-Stieda ossification) may be visualized in chronic medial-sided injuries. Baseline bilateral standing long-leg radiographs allow the clinician to determine the mechanical axis of the injured and contralateral extremities, which may have a significant impact on treatment decisions for chronic multiligament injuries.20,21 Preoperative stress radiographs provide quantitative objective information on the stability to valgus and varus stress and should also be routinely obtained postoperatively. Biomechanical studies were performed to objectively quantify the amount of joint opening with varus11 and valgus15 stress; radiographic techniques were developed and tested by sequential sectioning in cadaveric knees with intact cruciate ligaments. Isolated sectioning of the FCL (simulating a grade III injury) resulted in an increase of 2.7 mm of lateral joint gapping at 20 degrees of flexion when compared with the contralateral knee. Sectioning of the FCL, popliteus tendon (PLT), and PFL (simulating a complete grade III PLC injury) was associated with lateral joint gapping of 4 mm at 20 degrees of flexion. Isolated sectioning of the superficial MCL (simulating a grade III injury) resulted in 3.2 mm of increased medial joint gapping at 20 degrees of flexion when compared with the contralateral knee. Increased medial joint gapping of 6.5 and 9.8 mm at 0 and 20 degrees of flexion, respectively, was associated with sectioning of the superficial MCL, deep MCL, and POL (simulating a complete medial knee injury). Several imaging techniques have been developed to allow quantitative assessment of the integrity of the PCL; these are especially useful in persons with chronic injuries. Stress radiographs have been described using the kneeling knee technique22 and Telos device (Telos GmbH, Marburg, Germany)23; these two techniques have been reported to allow the quantification of posterior displacement of the tibia and are superior to a physical examination and use of the KT-1000 arthrometer.24 Magnetic resonance imaging (MRI) has become part of the standard of care for the evaluation of knee instability, especially in persons with acute injuries for whom examination may be limited by pain and swelling (Fig. 103.2). With high sensitivity and accuracy, MRI allows visualization of the cruciate and collateral ligaments, posteromedial corner and PLC,25 bone marrow edema,9,26,27 meniscal injuries, and cartilage lesions. Anteromedial femoral condyle bone bruises should alert the physician to a possible PLC injury.9 In addition, lateral-sided tibial or femoral bone bruises have also been associated with MCL injuries.28 It is important to recognize common imaging findings associated with multiligament knee injuries. Plain radiographs may be negative in the acute setting if the patient is lying supine, and it may be difficult to obtain weight-bearing films. In chronic injuries, weight-bearing films may reveal varus or valgus gapping or loss of joint space and early findings of degenerative disease. Stress radiographs are especially useful to quantitatively assess stability of the PCL, medial complex, and posterolateral complex. In patients with acute injuries, MRI will usually reveal the status of the cruciate ligaments and allow assessment of the collateral

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whereas in early reports nonoperative treatment was often recommended for “uncomplicated” cases (i.e., absence of vascular injury or fracture).38,39 A recent review indicates improved outcomes in multiple subjective and objective facets for patients treated with an operation compared with those treated conservatively with immobilization.37

Surgical Timing

Fig. 103.2  A coronal magnetic resonance image of a left knee injury with bicruciate rupture and a complete posterolateral corner injury including arcuate fracture (arrow) and grade III injury of the fibular collateral ligament, popliteus tendon, and popliteofibular ligament.

structures if appropriate cuts and slice thicknesses are obtained. Classic bone bruises associated with ACL ruptures may be seen, as well as those associated with PLC injuries.

DECISION-MAKING PRINCIPLES Patients with multiligament injuries are a heterogeneous group and may present with a variety of skin, bony, neurovascular, and ligamentous injuries. Although several general treatment algorithms have been developed, individualized treatment for the patient’s specific knee injuries and concomitant injuries is necessary. Meniscus injuries should ideally be repaired, especially in the young patient, but this may require a partial meniscectomy. Management of vascular injuries, open injuries, skin coverage, fracture treatment, and meniscus injuries is not specifically discussed here. Important considerations for the treatment of multiligament injuries include operative versus nonoperative treatment, surgical timing, single- versus two-stage cruciate ligament reconstruction techniques, and repair versus reconstruction of collateral structures. Knee ligament injuries have historically been classified with the use of a grading scale that assesses sagittal (AP) and coronal (varus/valgus) plane16,29 stability. Rotational stability does not have a formal classification system, although many injury types have been described.30-32 Treatment must be based on the extent of injury to individual structures and the number of structures injured. Knee ligament injuries are often subjectively classified according to the original American Medical Association guidelines, rated as grade I, II, or III.33 An additional classification system is based on the number and location of torn ligaments.34

Nonoperative Versus Operative Treatment It must be recognized that multiligament knee injuries are rare and that few studies have been conducted that compare treatment strategies with a high level of evidence. Current literature favors surgical management of multiligament knee injuries,35-37

Several studies have evaluated the impact of surgical timing. However, interpretation of outcomes of surgically treated multiligament injuries is difficult because of the wide range of pathology within individual studies.36 Irreducible knee injuries, open injuries, and popliteal vascular injuries necessitate emergent management. If the multiligament injury is associated with a high-energy trauma, the patient’s overall medical status and serious concomitant extremity, torso, and head injuries may delay definitive treatment. Overlying skin injuries and associated plateau or femoral condyle fractures may necessitate delayed ligament reconstruction. These complicating factors are not specifically evaluated; rather, the focus here is on single-extremity multiligament injuries without concomitant injuries. Timing of surgery is typically divided into one of the following three categories: acute (often defined as surgery within 6 weeks), chronic (often defined as surgery after 6 weeks), or staged (the index procedure is performed within 3 to 6 weeks of injury and second-stage surgery is delayed).36 Harner et al.40 reported improved subjective outcomes in acutely treated patients and no ultimate difference in range of motion (ROM); however, 4 of 19 patients with acutely reconstructed knees required manipulation for loss of flexion. Fanelli and Edson41 reported on 35 patients with multiligament injuries and found no subjective differences (according to Tegner, Lysholm, and Hospital for Special Surgery knee ligament rating scales) or objective differences (according to use of the KT-1000 arthrometer) between the acute and chronic cohorts. A recent systematic review of surgical treatment for multiligament injuries found increased anterior instability for patients treated acutely but no difference in posterior, varus, or valgus instability when compared with chronically treated injuries.36 Additionally, flexion loss (>10 degrees) as well as the need to undergo a subsequent repeat operation for stiffness were more frequent in acutely treated patients; no difference was found for extension. Last, patients treated with staged reconstructions had more “excellent” or “good” outcomes than did those treated acutely. As described later in this chapter, these findings may be difficult to interpret because many of these patients were treated with acute PLC repairs (which have been found to frequently fail) rather than reconstructions. Patients with chronic multiligament injuries may present to the orthopaedic surgeon because of a failed index procedure, failed nonoperative management, or concomitant injuries that precluded acute surgical management of the multiligament injury. These patients may have varus malalignment, and a high-tibial osteotomy may be required to correct the mechanical axis prior to ligament reconstruction because a failure to correct varus malalignment with a chronic PLC injury has been reported as a cause of PLC reconstruction graft failure.42,43

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CHAPTER 103  Multiligament Knee Injuries

Cruciate Ligament Reconstruction It is widely accepted that cruciate ligament injuries in patients with multiligament injuries require reconstruction. A biomechanical study by Veltri and colleagues44 demonstrated the importance of reconstructing the cruciate ligaments in multiligament injuries. Options for anterior cruciate ligament (ACL) reconstruction in multiligament injuries include transtibial versus transportal drilling for femoral tunnels and autograft versus allograft; no known studies recommend double-bundle ACL reconstruction in these patients. The debate regarding the best PCL reconstruction technique to use in persons with multiligament injuries is similar to the debate for isolated injuries; graft fixation techniques, single- versus double-bundle technique, and transtibial tunnel versus tibial inlay technique. Few studies have been performed to compare cruciate ligament reconstruction techniques in the multiligament injury patient population; therefore surgeons must apply the principles used for the reconstruction of isolated cruciate ligament injuries to this unique patient group.

Collateral Structures Until recently it was believed that PLC structures could be successfully repaired if treated acutely. This practice has been challenged by outcomes studies that compared repairs versus reconstructions.45,46 It has been biomechanically demonstrated that a deficient PLC leads to increased ACL47 and PCL48,49 graft forces; interestingly, Mook et al.36 reported that more patients treated acutely for multiligament injuries underwent repairs rather than reconstructions of the PLC and suggest that repairs may have been insufficient to protect the ACL graft during healing. These findings may provide clinical evidence that reinforces the biomechanical principles of secondary stabilization between cruciate and collateral ligaments and may support the trend toward acute reconstruction rather than repair of PLC structures.50 As discussed later in this chapter, a gradual trend has occurred from local tissue transfers and acute repairs toward several different autograft or allograft tissue reconstruction techniques. A well-defined and successful treatment algorithm for isolated grade III MCL injuries and those combined with ACL ruptures includes a short period of rest and edema control followed by physical therapy.16 However, treatment of MCL injuries associated with bicruciate injuries is less well defined. Some authors advocate delayed cruciate reconstruction while the medial structures are protected with a brace and allowed to potentially heal. Other authors recommend acute repairs or reconstruction of medial structures, although a higher risk of arthrofibrosis is reported.

Graft Choice Graft choice in multiligament injury reconstruction is determined by injury pattern, graft availability, and surgeon preference. Often surgeons prefer to use allografts when treating multiligament injuries because of multiple graft size options and the ability to avoid the increased operative time and donor site morbidity associated with harvesting the patellar and hamstring tendon and possibly quadriceps tendon grafts. Because of the heterogeneity of multiligament injuries, no conclusive studies are

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available to recommend a particular graft choice. Several techniques are discussed in the Treatment Options section, further on, along with graft choices.

Special Considerations Pediatric patients with multiligament injuries require special consideration because of their open physes and the potential risk of growth alteration with traditional ligament reconstruction. Physeal sparing techniques for ACL51 and PCL52 reconstruction have been described. Recently a modified physeal sparing technique was described for PLC/FCL injuries in pediatric patients.53 Lateral and medial structures may be repaired via augmentation or recess procedures8 or with use of suture anchors. A recently defined type of knee dislocation described by Azar and colleagues has been termed ultra–low velocity.54 These injuries are sustained by patients with a high body mass index as a result, for example, of falling from a standing height or tripping on an object. Patients who sustain ultra–low velocity multiligament knee injuries have higher rates of neurovascular injuries as well as a higher incidence of postoperative complications compared with patients who suffer low- or high-velocity multiligament injuries.55 Their treatment must be individualized based on medical comorbidities, patient expectations, preinjury activity level, and ability to comply with rigorous rehabilitation. Conservative therapy with immobilization may be the only treatment suitable for elderly patients with multiligament injuries who have preinjury medical comorbidities.56 Additionally, the presence of arthritis is a relative contraindication to multiligament reconstruction; in fact, most studies exclude patients with preexisting arthritis.

TREATMENT OPTIONS Treatment recommendations for specific ligament injuries in this patient population are limited by the lack of comparative studies. No known studies have evaluated the impact of a specific cruciate ligament reconstruction technique on the outcomes of multiligament injuries. Repair versus reconstruction of collateral ligaments has been debated, but specific reconstruction methods have not been directly compared in clinical studies.

Acute Management Every multiligament knee injury is unique, and a wide range of pathology exists. Most injuries are adequately stabilized in a knee immobilizer. However, some knees associated with a highenergy injury may remain subluxed in a knee immobilizer and require a spanning external fixator to achieve stability in the acute setting.

Anterior Cruciate Ligament Although ACL reconstruction is recommended, the specific technique receives relatively little discussion in the context of multiligament injuries. Many authors have described single-bundle reconstruction using an allograft or autograft with femoral tunnels created via a transtibial technique. Levy et al.45 prefer to use a tibialis anterior allograft, Strobel et al.57 recommended use of a hamstring autograft. Engebretsen et al.1 initially preferred

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allografts for ACL reconstruction but changed their graft choice to a bone–patellar tendon–bone autograft. Harner et al.40 prefer allograft bone–patellar tendon–bone but use an anteromedial portal drilling technique for ACL femoral tunnels rather than the transtibial technique as utilized by previous authors.

tendon allograft, split longitudinally, to reconstruct the ALB and PMB. Cooper and Stewart64 described a single-bundle tibial inlay PCL reconstruction using either a bone–patellar tendon–bone autograft or allograft to reconstruct the ALB.

Posterior Cruciate Ligament

In a recent review, LaPrade and colleagues16,65 underscored the importance of completely evaluating and treating the three main structures of the medial/posteromedial knee: the superficial MCL, deep MCL, and POL. When associated with multiligament injuries, most authors agree that grade III MCL injuries require treatment, often repair or reconstruction. A systematic review reported an absence of sufficient studies to allow formulation of evidence-based recommendations for the treatment of MCL injuries in the multiligament injury population.66 A general trend has been noted in the literature toward repair and/or reconstruction of medial knee injuries, which may be due to a better understanding of the anatomy and availability of biomechanically validated reconstruction techniques. In early reports, Fanelli et al.67 compared valgus stability in patients with bicruciate ruptures and medial-sided injuries. Bicruciate reconstructions were performed in all patients; two acutely presenting patients were treated with primary surgical repair of the MCL tears and seven were treated with bracing to allow the MCL injury to heal with nonoperative treatment followed by subsequent bicruciate ligament reconstruction. More recently, Fanelli and Edson41 describe an anterosuperior shift of the posteromedial capsule for the repair of MCL injuries; when lesions are not amenable for repair, an autograft semitendinosus or allograft is used to reconstruct the superficial MCL and is accompanied by a capsular shift. Lind et al.68 described a rerouting of the ipsilateral semitendinosus tendon to reconstruct the superficial MCL and posteromedial structures in patients with multiligament injuries. The semitendinosus tendon was identified and harvested proximally but left intact at the pes insertion. A blind femoral tunnel, located at the isometric point of the MCL insertion, was created with a diameter equal to the size of the double-looped tendon. Additionally, a transtibial tunnel exiting 10 mm below the tibial plateau and posterolateral to the semimembranosus was drilled through the medial tibial plateau from anterior to posterior and reamed to the diameter of the semitendinosus tendon. The double-looped tendon was secured using interference screw fixation in the femur, pulled through the tibial tunnel, and secured with an additional interference screw. LaPrade and colleagues65 described an anatomically based and biomechanically validated69 reconstruction of the medial knee structures.70 Their technique reconstructs the POL and both the proximal and distal divisions of the superficial MCL. Two femoral and two tibial tunnels are created, and grafts are fixed in the tunnels with use of interference screws. In a series of patients with knee dislocations, Harner et al.40 described repair or reconstruction of MCL injuries. Avulsions and midsubstance injuries were repaired with suture anchors and nonabsorbable sutures, respectively. Chronic injuries were treated with a reconstruction of the MCL using a semitendinosus autograft or Achilles tendon allograft.

A review of treatment options for addressing PCL insufficiency in this patient population follows. It is generally accepted that PCL tears should be reconstructed in these patients, although the optimal technique has not yet been defined. A review of the causes of failure of a series of PCL reconstructions identified the importance of tunnel positioning and addressing concomitant collateral ligament instability.21 However, investigators have not yet determined the role for the single- versus double-bundle technique and for transtibial versus tibial inlay graft placement. Some studies have demonstrated that double-bundle PCL reconstructions restore native biomechanics48,58; however, relatively few studies have specifically described the detailed technique and associated outcomes of double-bundle PCL reconstructions in the multiligament injury population. Spiridonov et al.59 recently described a double-bundle PCL reconstruction in 7 patients with isolated PCL ruptures and 32 with multiligament injuries. Their technique includes two femoral tunnels and a single transtibial tunnel to anatomically reconstruct the anterolateral bundle (ALB) and posteromedial bundle (PMB). Because of the morbidity of graft harvest and the need for large collagen volume, the authors used allografts, specifically Achilles tendon, for the ALB and a semitendinosus tendon for the PMB. Several authors have described single-bundle PCL reconstructions in patients with multiligament injuries. Fanelli and Edson41 recommended a single-bundle transtibial PCL reconstruction and reported using either an autograft or allograft. Engebretsen et al.1 described a single-bundle transtibial PCL reconstruction; during the time of data collection, the investigators changed their graft source from allograft to hamstring autograft. Chhabra et al.60 reported that approximately one-third of patients with an acute multiligament injury have an intact PMB and meniscofemoral ligaments. They attempted to preserve these bundles and performed a reconstruction of the ALB using an Achilles tendon allograft via a transtibial tunnel. In patients with complete ruptures of the entire PCL and those with chronic injuries, the authors recommend double-bundle PCL reconstruction using an Achilles tendon allograft for the ALB and a tibialis anterior allograft for the PMB. A recent systematic review on the topic of transtibial versus tibial inlay technique for PCL reconstruction revealed a paucity of comparative outcomes studies and recommended surgeon preference as a reasonable consideration in technique choice until further evidence is available.61 Biomechanical studies have compared the two techniques but it is difficult to apply their results to the multiligament injury population. Some investigators have recommended that the tibial inlay technique not be used for patients with multiligament injuries; however, this evidence is level V.62 Stannard et al.63 described a technique for double-bundle PCL reconstruction with a tibial inlay technique in patients with multiligament injuries. Their technique requires a single Achilles

Medial/Posteromedial Structures

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CHAPTER 103  Multiligament Knee Injuries

Lateral/Posterolateral Structures In contrast to the extra-articular medial structures, it is well recognized that grade III PLC injuries do not heal with bracing and, without operative treatment, can lead to significant morbidity. Recently reconstruction rather than repair of PLC injuries has been emphasized because of results of comparative outcomes studies. Early investigators reported good results with acute anatomic repair of PLC injuries; however, these patients were immobilized in a cast for 6 weeks postoperatively, and subjective outcomes scoring tools were not available.71-73 More recently, Stannard et al.46 and Levy et al.45 performed a mix of single- and dual-stage operations and found lower failure rates with reconstructions when compared with repairs of the PLC. Stannard et al.46 performed a modified two-tailed technique with a tibialis anterior or posterior allograft for PLC reconstructions. This technique uses a single femoral tunnel at the isometric point along with a single fibular and tibial tunnel.

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Levy et al.45 used a fibula-based technique with an Achilles tendon allograft, along with an anterodistal shift of the posterolateral capsule, to reconstruct the PLC. LaPrade and colleagues recently reported on the acute8 and chronic20 treatment of isolated and combined PLC injuries. All PLC and concomitant cruciate ligament tears were treated with a single-stage surgery. Acute avulsions of PLC structures were repaired with suture anchors or recess procedures; however, most acute PLC injuries were not amenable to repair and were treated with a complete anatomic PLC reconstruction of the FCL, PLT, and/or PFL. A minority of the patients in the chronic PLC injury study were found to have varus malalignment and required an opening wedge proximal tibial osteotomy to correct the mechanical axis before undergoing a soft tissue reconstruction. The remainder of the patients were treated with an anatomic reconstruction of the PLC with single-stage reconstruction of coexistent cruciate ligament tears.

Authors’ Preferred Technique Ligamentous Injuries Our preferred technique for the treatment of multiligament injuries is an anatomic single-stage reconstruction of the cruciate ligament(s) with concurrent treatment of medial/posteromedial and lateral/posterolateral supporting structures with anatomically based and biomechanically validated techniques. Grade III injuries to the medial and lateral structures require surgical treatment for patients with multiligament injuries with a repair and/or reconstruction when indicated. A repair of some structures may be possible in acute injuries with avulsions directly off bone; however, a reconstruction is required for acute injuries with midsubstance tears or inadequate tissue quality and for chronic injuries. It is the preference of the senior author to operate on patients with acute injuries within 3 weeks of injury so as to allow identification of injured structures and repair of meniscal pathology and extra-articular structures. Preoperative Planning Preoperative planning for the treatment of multiligament injuries is critical because of the inherent complexity of these procedures. The injury history, physical examination, and imaging studies will allow the surgeon to plan the details of the operation. The surgeon must be certain that all required equipment is available, including surgical instruments and any required allograft materials. Standard cruciate ligament reconstruction instruments including cannulated drill guides, eyelet-tipped passing pins, suture anchors, and cannulated interference screws (metallic or bioabsorbable) will be necessary. Appropriate graft harvesting instruments will be needed if the surgeon plans to use autografts; a graft preparation station will also be needed. A standard arthroscopic setup with 30- and 70-degree arthroscopes will be necessary for the evaluation and treatment of intra-articular injuries.

Lateral and Posterolateral Knee An incision in a hockey-stick shape centered over the posterior to midportion of the iliotibial band is used to expose the lateral/posterolateral knee. The incision is positioned more posteriorly in patients with a planned autogenous patellar tendon graft harvest for a concurrent ACL reconstruction to maintain a minimum of 6 cm between the two incisions. This incision is continued down through the skin and superficial tissues to the superficial layer of the iliotibial band. Posteriorly, the long and short heads of the biceps femoris are identified; palpation approximately 2 to 3 cm distal to the long head will usually allow identification of the common peroneal nerve. A neurolysis is then performed to release the nerve from scar tissue entrapment and safely isolate it from the surgical site (Fig. 103.3). Avulsions of the biceps tendon are repaired with use of suture anchors with the knee in full extension. Arcuate avulsion fractures may be repaired with No. 5 nonabsorbable sutures passed through the proximal tendon and bony fragment and tied through drill holes in the fibula.8

Patient Positioning The patient is placed supine on the operating table and, after administration of an anesthetic, an examination is performed to confirm the suspected ligamentous pathology. A leg holder is placed to allow sufficient access to the medial and lateral aspect of the injured extremity. A well-padded proximal thigh tourniquet is set in place. The operative leg is prepped and draped free in the usual sterile fashion. Extra-Articular Injury Identification and Treatment We recommend that open dissection for lateral and/or medial injuries be performed prior to arthroscopic examination, which will allow the identification of injuries and assessment of tissue quality prior to arthroscopic fluid extravasation.

Fig. 103.3  The open surgical approach to the posterolateral aspect of a left knee. The common peroneal nerve is elevated by the Metzenbaum scissors. Continued

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Authors’ Preferred Technique Ligamentous Injuries—cont’d Blunt dissection between the soleus and the lateral head of the gastrocnemius muscle will expose an interval through which the posteromedial aspect of the fibular head can be palpated. In this region the popliteofibular ligament (PFL) and musculotendinous junction of the PLT are found. Next, an incision 1 cm proximal to the fibular head is made through the anterior arm of the long head of the biceps and the underlying biceps bursa. The distal aspect and insertion of the FCL can be identified through this incision, and a traction stitch is placed for upcoming identification of the proximal aspect of the ligament. Acute avulsions of the FCL directly from bone without intrasubstance stretch injuries, which usually occur in skeletally immature patients, may be repaired with use of suture anchors; however, the majority of FCL injuries are not amenable to repair and require a ligament reconstruction. A fibular tunnel is drilled with use of a cruciate ligament aiming guide. The desired trajectory for anatomic graft placement is from the FCL attachment site of the lateral aspect of the fibular head to the posteromedial downslope of the fibular styloid. A retractor is placed medially to prevent iatrogenic injury to deep structures, and a guide pin is advanced; the tunnel is overreamed with a 7-mm reamer, and the entry and exit apertures are chamfered with a rasp. Next, a tibial tunnel is created for passage and fixation of the PFL and PLT reconstruction grafts. The anterior tunnel aperture is located at the flat spot between Gerdy’s tubercle and the tibial tubercle; an elevator is used to release the soft tissues from this region. The posterior tunnel aperture is located at the posterolateral aspect of the proximal tibia, slightly distal to the plateau. The previously identified popliteus musculotendinous junction, located 1 cm medial and 1 cm proximal to the fibular head reconstruction tunnel, is the landmark for the posterior aperture of the reconstruction tunnel. A cruciate ligament reconstruction aiming guide is used to create this tunnel; a retractor is placed posteriorly to protect against an erroneously placed guide pin. Accurate placement of the guide pin is confirmed by palpating posteriorly while cross-referencing with a blunt probe placed through the fibular tunnel. Tension is then applied to the traction stitch in the FCL remnant to identify and evaluate the FCL femoral origin.74 To allow direct visualization of the FCL and PLT attachment sites on the femur and prepare for potential tunnel drilling, a splitting incision is placed through the superficial layer of the iliotibial band from a point proximal to the lateral epicondyle and extended distally to Gerdy’s tubercle. Next, a vertical incision through the lateral capsule allows identification of the femoral insertion of the PLT. Avulsions of the PLT directly from the femur without intrasubstance stretch injury or musculotendinous avulsion may be amenable for a recess procedure performed with the knee in full extension.75 The creation of femoral tunnels for reconstruction of the FCL and PLT requires a thorough understanding of the anatomy (Fig. 103.4)74 and is performed according to previously described techniques.76 With use of a collateral ligament aiming guide, two eyelet-tipped guide pins are aimed anteromedially to the adductor tubercle from the FCL and PLT attachment sites and advanced in a parallel fashion; tunnel orientation is important to avoid collision of the PLC tunnels with ACL reconstruction tunnels. The tunnels are then overreamed to a depth of 20 mm and a diameter of 9 mm (Fig. 103.5). A split Achilles tendon allograft is prepared for the two limbs of the PLC reconstruction, and the grafts are secured in their femoral tunnels with 7- by 20-mm cannulated interference screws (Fig. 103.6). The FCL graft is passed through the fibular tunnel, but final fixation is delayed until the end of the procedure. Treatment of associated PLC structures is performed when indicated. Popliteomeniscal fascicle and coronary ligament tears are repaired with mattress sutures. Bony (Segond)18 or soft tissue avulsions of the tibial attachment of the lateral capsular ligament25 are repaired with suture anchors.8

Medial and Posteromedial Knee The treatment of combined ACL/MCL injuries is well defined and is not specifically discussed here. The focus of this discussion is our preferred treatment of severe grade III medial ligamentous injuries combined with PCL or bicruciate ruptures as well as possible associated lateral injuries. Surgical treatment is delayed until knee swelling decreases; medial tissues may be amenable to repair with augmentation, or a reconstruction may be required. Concurrent, rather than staged, cruciate ligament reconstruction is performed in all patients. Exposure of the medial knee is performed via an anteromedial incision that extends distally from the region between the medial border of the patella and the medial epicondyle to the region overlying the pes anserine tendons.70 Next, the gracilis and semitendinosus tendon attachments are identified by incising the anterior border of the sartorial fascia. The semitendinosus tendon is removed with use of a standard tendon harvester and sectioned to create grafts of 16 and 12 cm for reconstruction of the superficial MCL and POL, respectively. Nonabsorbable sutures are used to tubularize each end, and the tendons are sized for 7-mm tunnels. Within the pes anserine bursa, the superficial MCL distal tibial attachment is identified. Next, the superficial MCL is followed distally, and the tibial attachment is identified at the anteromedial proximal tibia. The superficial MCL has both proximal and distal tibial attachments; the distal attachment is approximately 6 cm distal to the joint line.65 The tendon of the sartorius muscle is retracted distally and the largest portion of the POL, the central arm, is identified. The tibial attachment site of the POL central arm, with an underlying small bony ridge, can be found near the direct arm of the semimembranosus tendon.

LGT origin

18.5 mm

FCL-femur Lateral epicondyle

PLT

Popliteus sulcus

Fibular styloid FCL-fibula

Fig. 103.4  Attachments of key posterolateral knee stabilizing structures and associated bony landmarks. FCL, Fibular collateral ligament; LGT, lateral gastrocnemius tendon; PLT, popliteus tendon.

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CHAPTER 103  Multiligament Knee Injuries

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FCL-femur FCL-femur PLT-femur

PLT-femur

PFL/PLTtibia

PFL-fibula

PFL/PLTtibia FCL-fibula

A

B

Fig. 103.5  Lateral (A) and posterior (B) aspects of the knee demonstrating the position of bone tunnels for a complete reconstruction of the posterolateral corner of the knee. FCL, Fibular collateral ligament; PFL, popliteofibular ligament; PLT, popliteus tendon.

Fig. 103.6  The intraoperative posterolateral aspect of the right knee demonstrating fixation of the posterolateral corner grafts in the femoral tunnels. An iliotibial band–splitting incision is visualized and an interference screw is advanced into the popliteus tendon femoral tunnel.

Identification of the femoral attachments of the medial knee structures is often difficult because the bony and soft tissue landmarks are not as obvious as those on the posterolateral knee. The initial step is to identify the adductor magnus tendon and its distal attachment to the adductor tubercle (Fig. 103.7). The senior author calls the adductor magnus tendon “the lighthouse of the medial aspect of the knee.” This step will allow the surgeon to more accurately identify the medial epicondyle, the gastrocnemius tubercle, and the anatomic attachment sites of the superficial MCL and the POL (Fig. 103.8). The femoral attachment of

Fig. 103.7  The open surgical approach for the medial aspect of a left knee. The adductor tendon is elevated by the hemostat and a gloved finger is shown palpating the medial epicondyle. The vastus medialis obliquus muscle is also visible.

the superficial MCL is approximately 12 mm distal and 8 mm anterior to the adductor tubercle, and the POL femoral attachment is approximately 11 mm posterosuperior to the superficial MCL.65 After identification of the femoral and tibial attachments of the superficial MCL and POL, guide pins are inserted and overreamed with a 7-mm cannulated drill and advanced to a depth of 30 mm. Allografts or semitendinosus autografts are prepared (16 cm for the superficial MCL and 12 cm for the POL) and are fixed into the femoral tunnels using 7-mm bioabsorbable interference screws. Graft fixation in the tibial tunnels is delayed until the end of the procedure. Continued

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Authors’ Preferred Technique Ligamentous Injuries—cont’d

POL sMCL (proximal)

sMCL (distal)

Fig. 103.8  Anatomy of the medial aspect of the left knee. The posterior oblique ligament (POL) and superficial medial collateral ligament (sMCL) are demonstrated. (From Coobs BR, Wijdicks CA, Armitage BM, et al. An in vitro analysis of an anatomical medial knee reconstruction. Am J Sports Med. 2010;38[2]:339–347.)

Fig. 103.9  A lateral compartment “drive-through sign” is seen in this arthroscopic photograph in a patient with a posterolateral corner knee injury.

Intra-Articular Injury Identification and Treatment The arthroscopic portion of the surgery is delayed until after open dissection and injury identification to prevent arthroscopic fluid extravasation. Vertical inferomedial and inferolateral parapatellar portals are created and a standard arthroscopic assessment of the knee is performed. Varus and valgus stress is applied and the lateral and medial compartments, respectively, are observed for gapping (Fig. 103.9). The articular cartilage surfaces are examined for lesions, and the meniscal roots and bodies are similarly assessed; meniscal tears are repaired if possible. Cruciate ligament injuries are addressed as discussed in the following sections.

Posterior Cruciate Ligament An endoscopic double-bundle PCL reconstruction is preferred in patients with multiligament injuries. An Achilles tendon allograft is used for the ALB reconstruction and a tibialis anterior allograft is used for the PMB reconstruction. The femoral attachments of these two bundles are identified with an arthroscopic coagulator. An additional portal is created through the posteromedial capsule to allow evaluation and debridement of the PCL tibial attachment. Debridement is continued until the popliteus muscle fibers are visualized. With use of a PCL guide, a guide pin is drilled from the anteromedial tibia, approximately 6 cm distal to the joint line, and exits at the PCL tibial attachment approximately 1 cm distal to the joint line at the PCL bundle ridge; pin placement is verified with intraoperative radiographs or fluoroscopy. Femoral tunnel creation for the PCL reconstruction is performed according to previously described techniques.59 The ALB is positioned so that the aperture edge is adjacent to the articular cartilage margin at the top of the intercondylar roof and along the anterior aspect of the medial femoral condyle. An 11-mm tunnel is drilled to a depth of 25 mm. Similarly, a 7-mm PMB tunnel is created at the previously described location and reamed to a depth of 25 mm; a minimum 2-mm bone bridge is maintained between the two tunnels. After creation of the femoral tunnel, the tibial tunnel is reamed. The previously placed tibial guide pin is used to advance a 12-mm headed reamer to create a complete tunnel exiting at the posterior tibia. The posterior tissues are protected against iatrogenic injury via retraction with a large curette placed through the posteromedial portal. To minimize the potential for cyclic graft failure due to friction against the tibial tunnel aperture, a “smoother” is passed through the tibial tunnel and out the anteromedial portal and cycled several times to clean out the posterior tibial aperture. The grafts are then passed into their respective femoral tunnels endoscopically via the anterolateral arthroscopic portal. A 7-mm titanium screw is used to fix the ALB graft bone plug into its femoral tunnel, and a 7-mm bioabsorbable interference screw is used to fix the PMB soft tissue graft into its femoral tunnel. The ALB and PMB grafts are then pulled distally through the tibial tunnel, and the knee is cycled; tibial graft fixation is delayed until the end of the procedure. Anterior Cruciate Ligament Reconstruction A single-bundle anatomic ACL reconstruction is preferred for patients with multiligament injuries. A bone–patellar tendon–bone autograft or allograft is chosen based on the preference of the patient/surgeon and availability. The tibial attachment is identified, and residual tissue is debrided with the shaver. Next, the femoral attachment is similarly identified and debrided to identify the lateral intercondylar ridge. A burr hole is made to mark the midpoint of the ACL femoral attachment between the anteromedial and posterolateral bundles. The femoral tunnel is created via the anteromedial portal technique. This closed socket femoral tunnel is created with a low-profile reamer prior to tibial tunnel reaming. This sequence allows for identification of the important regional anatomy of this tunnel prior to significant fluid extravasation from the joint. If there was no concurrent medial knee reconstruction incision or if an allograft was used, a 2-cm anteromedial tibial incision is centered approximately 35 mm distal to the joint and 10 mm anterior to the MCL. An ACL reconstruction guide is placed into the joint and centered over the native ACL attachment site; a guide pin is then advanced and the tunnel is reamed. The ACL graft is passed and fixed in the femoral tunnel. Tibial fixation is delayed until the end of the procedure. Final Graft Fixation The order of final graft fixation is important. To restore the central pivot of the knee, tibial fixation of the PCL grafts is performed according to previously defined techniques59 once all associated ligament reconstruction grafts have been fixed

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CHAPTER 103  Multiligament Knee Injuries

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Authors’ Preferred Technique Ligamentous Injuries—cont’d

Semimembranosus muscle

FCL

PLT FCL

PLT

POL (graft)

PFL

sMCL (graft)

B A Fig. 103.10  The lateral (A) and posterior (B) views of a posterolateral corner knee reconstruction are demonstrated in this illustration. The fibular collateral ligament (FCL), popliteus tendon (PLT), and popliteofibular ligament (PFL) grafts are shown.

in their femoral tunnels. PLC grafts are secured next; care is taken to avoid overreducing the knee in patients with an associated medial knee injury. The FCL graft is passed through the fibula and fixed in its reconstruction tunnel at 20 degrees of knee flexion, in neutral rotation, and with a valgus reduction force on the knee. Next, the PLC grafts are passed anteriorly through the tibial tunnel, slack is removed from the grafts, and fixation of the PLT and PFL grafts is performed at 60 degrees of knee flexion, in neutral rotation, and with traction applied to the grafts (Fig. 103.10). ACL graft tibial fixation is performed once the PLC grafts have been secured because of biomechanical evidence that fixation of the ACL graft prior to the PLC grafts can result in an external rotation deformity of the knee.77 An interference screw is used in the tibial tunnel for fixation.

POSTOPERATIVE MANAGEMENT An important consideration in the treatment of multiligament injuries is postoperative rehabilitation and eventual return to play. These topics have received great attention for isolated ligament injuries, but less information is available for patients with multiligament injuries; therefore principles from the former must be applied to the latter. Two general approaches to postoperative care in multiligament injuries are immobilization versus early mobilization. A balance must be achieved between immobilization aimed at preventing the development of instability and early mobilization to minimize scar tissue and resultant rangeof-motion deficits. Although a full discussion of various rehabilitation protocols is beyond the scope of this chapter, the basic preferences of several investigators are described here. Noyes and Barber-Westin described a program of early protected ROM in an attempt to limit arthrofibrosis.78 They

Fig. 103.11  The medial aspect of the left knee with reconstruction grafts fixed in the femoral and tibial tunnels with interference screws. POL, Posterior oblique ligament; sMCL, superficial medial collateral ligament. (From Coobs BR, Wijdicks CA, Armitage BM, et al. An in vitro analysis of an anatomical medial knee reconstruction. Am J Sports Med. 2010;38[2]:339–347.)

Graft fixation in the tibial tunnels is performed next for patients who underwent reconstruction of medial knee injuries (Fig. 103.11). The superficial MCL graft is passed into the tibial tunnel and tension is held while a varus moment is applied with the knee flexed to 20 degrees and in neutral rotation. At this position, the superficial MCL graft is secured with the interference screw. In a similar fashion, tension is applied to the POL graft via traction in full knee extension. The interference screw is inserted as a varus moment is applied with the knee held in extension and neutral rotation. A suture anchor is then used to recreate the proximal tibial superficial MCL attachment.

prescribed active assisted motion from 10 to 90 degrees six to eight times daily along with patellar mobilization for the first 4 weeks postoperatively. Between therapy sessions, the patient’s knee was immobilized in a split cylinder cast to protect the reconstructed structures. After 4 weeks, the cast was changed to a hinged-brace and gradual increase in motion along with progression of weight bearing was then allowed. A recent review of rehabilitation after the reconstruction of multiligament injuries recommended complete immobilization with the knee locked in extension for the first 5 weeks after surgery.79 For the first 6 weeks, the authors allow the patients to bear full weight while standing statically on both legs, but they must use crutches for ambulation and abstain from bearing weight on the operative leg. From postoperative weeks 5 to 10, the brace is unlocked and patients are allowed to perform passive knee flexion; isolated hamstring strengthening is strictly avoided during this period.

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Harner et al.40 also described their preferred surgical treatment and rehabilitation for patients with multiligament injuries. For the first 4 weeks, the knee is held in full extension via a locked knee brace except during passive ROM exercises at up to 90 degrees of flexion. Isolated hamstring contraction is avoided until 6 weeks after surgery. Partial weight bearing is allowed with the brace in full extension for the first 4 to 6 weeks and progresses thereafter. In a recent systematic review, Mook et al.36 evaluated the impact of postoperative rehabilitation on multiligament injury outcomes. Their findings indicate that early mobilization in acutely treated patients is associated with less posterior instability, varus/valgus laxity, and ROM deficits as compared with immobilization after surgery. The apparent influence of early mobilization underscores the importance of a strong anatomic repair and/or reconstruction of posterolateral structures. Wilkins80 provided a detailed description of rehabilitation principles based on work by LaPrade and colleagues and describes early-phase rehabilitation (0 to 12 weeks) and late-phase rehabilitation (4 to 12 months). Similar to other authors, Wilkins recommends non–weight bearing for the first 6 weeks postoperatively, with occasional toe-touch weight bearing during showering and dressing activities; weight bearing is thereafter increased according to the protocol. For the first 2 weeks the brace is locked in full extension with the exception of therapy sessions, where the patient is allowed knee motion within the “safe zone” as defined intraoperatively. ROM is then increased to 90 degrees until 4 weeks postoperatively and thereafter gradually progressed to the goal of greater than or equal to 125 degrees. Because of posterior tibial translation associated with increasing flexion, isolated hamstring exercises are avoided for the first 4 months. Late-phase rehabilitation focuses on high-level balance training, sport-specific drills, and plyometric exercises and is initiated at approximately 4 months after surgery, when the patient has regained full active ROM, has resumed a normal gait, and has no signs of swelling.

RESULTS No level I studies are available on the topic of treatment and associated outcomes of surgical reconstruction of multiligament injuries. Most available studies are level III or IV, and unfortunately evaluation of the results of some studies is limited by the heterogeneous patient mix. Often isolated injuries were included in the analysis with multiligament injuries, and high-energy injuries in polytrauma patients may be reported along with lowenergy injuries associated with sports. A summary of selected literature is provided in Table 103.1.

COMPLICATIONS Complications can be discussed within the context of the initial injury or those associated with treatment. Vascular injuries are not infrequent in the setting of multiligament injuries, and although the reported incidence varies, a commonly referenced number is 32%.81 Urgent vascular surgery consultation is required for suspected large vessel injury because prolonged ischemia

may necessitate limb amputation. Peroneal nerve injuries are also common with multiligament injuries, especially when they are combined with PLC injuries, and are estimated to occur at a rate of 25% to 35%.7 A poor prognosis is associated with complete lesions, whereas most persons with incomplete nerve palsies can often be expected to recover. Treatment options include physical therapy with an ankle-foot orthosis, neurolysis, primary nerve repair, nerve grafting, and tendon transfers.82 With highenergy injuries, infection and skin compromise may also occur; inevitably definitive surgery will be delayed while skin concerns are addressed. Complications may also be associated with treatment, whether nonoperative or operative. In both cases, persistent pain and instability may occur. If the initial treatment was nonoperative, the treatment is deemed a failure, and if the patient is a candidate, a chronic reconstruction may be required. If the initial treatment was operative, the patient may require revision reconstruction of all failed components. Infection and bleeding can also occur with operative treatment. Incision and debridement with antibiotics and staged reconstruction may be necessary for infected cases. Bleeding may be the expected result of a difficult exposure, but attempts at adequate hemostasis must be obtained prior to closure. Bleeding may also occur because of iatrogenic injury to large vessels such as the popliteal artery that necessitates immediate intervention by a vascular surgeon. Iatrogenic injury to the common peroneal nerve may occur during neurolysis or as a failure of an adequate neurolysis prior to ligament reconstruction. However, adequately exposed and carefully handled nerves may still be associated with foot drop if the initial injury was severe. As with any surgery, deep venous thrombosis may occur; adequate prophylaxis is essential, especially in older and obese patients. General causes of ligament reconstruction failure may include lack of incorporation of allografts, unrecognized or untreated ligament lesions, or technical concerns due to the repair technique or reconstruction tunnel placement. A persistent postoperative effusion may occur in some patients and will necessitate delaying progression of the rehabilitation protocol.

FUTURE CONSIDERATIONS Because of the rarity of multiligament injuries and the variation of severity and presence of concomitant injuries, studies with a high level of evidence are limited. Additional clinical studies are necessary to make definitive recommendations on operative timing, surgical technique, and rehabilitation. Level I studies with randomization of surgical treatment may seem impractical because of the complexity of these injuries and the treatment preferences of particular surgeons. However, prospective multicenter studies with treatment outcomes assessed by a standardized method with validated subjective evaluations and unbiased objective measurements of stability and function would significantly benefit the multiligament injury evidence base. In the past one to two decades, several ligament reconstruction techniques have been developed and tested in persons with isolated ligament injuries. However, few studies address the biomechanics of multiligament injuries and subsequent ligament

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2004

2002

Harner

Fanelli

35

31

57

17

85

28

74

*

63

76

53

Not given

Male (%)

(2–10)

3.7 (2–6)

2.8 (2–4.9)

(2–5.5)

5.3 (2–9.9)

Repair: 2.8 (2–4.1) Reconstruction: 2.3 (2–3.4)

Years of Follow-Up, Average (Range)

A: 19 (