Essential Sports Medicine: A Clinical Guide for Students and Residents [2 ed.] 3030643158, 9783030643157

Table of contents :
Acknowledgments
Contents
Contributors
Part I: General Concepts in Sports Medicine
1: An Overview of Sports Medicine
References
2: Advances in Sports Medicine
Sports Ultrasound
Introduction
Cardiac Evaluation
Thoracic and Abdominal Evaluation
Ocular Evaluation
Vocal Cord Evaluation
Bone Evaluation
Novel Ultrasound Technologies
Orthobiologics
Introduction
Prolotherapy
Platelet-Rich Plasma
Mesenchymal Stem Cells
Conclusion
Technological Applications for the Athlete
Introduction
Motion Capture
Wearable Devices
Conclusion
References
3: Exercise Prescription
Introduction
Physical Activity and Exercise
Physical Activity Recommendations
Aerobic Exercise
Resistance Exercise
Flexibility Exercise
Neuromotor Exercise
Special Considerations
Physical Inactivity
Cardiovascular Disease (CVD)
Cancer
Obesity
Osteoarthritis (OA)
Conclusion
References
4: Preparticipation Evaluation
Introduction
Goals
Logistics
Timing
Frequency
Format
Examiner
Components of PPE
Past Medical and Family History
Injury and Sport Participation History
Cardiovascular History
Neurologic History
Other Medical Comorbidities and Review of Systems
Physical Exam
Additional Testing
PPE Considerations in Specific Sporting Populations
Athletes with Organ Loss or Impairment
Female Athletes
RED-S
Disabled Athletes
The Pediatric Athlete
Masters Athlete
Clearance
Medicolegal
Implementation Issues
Limitations of the Current PPE Paradigm
Conclusion
Bibliography
5: Hydration and Nutrition in Athletes
Hydration
Physiological Factors
Fluid-Related Problems
Heat Cramps
Heat Exhaustion
Exertional Heatstroke
Hyponatremia
Fluid Intake Before Exercise
Fluid Intake During Exercise
Fluid Intake After Exercise
Macronutrient Requirements
Carbohydrates
Protein
Fat
Micronutrients
B Vitamins: Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Biotin, and Pantothenic Acid
Vitamin D
Calcium
Iron
Zinc
Magnesium
Supplements
Creatine
HMB
Caffeine
Banned Supplements/Ergogenic Aids
References
6: General Medical Problems in Athletes
Cardiology in Sports: Screening
Hypertension
Hypertrophic Cardiomyopathy
Brugada Syndrome
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Venous Thromboembolism
Exercise-Associated Collapse
Exercise-Induced Bronchospasm/Exercise-Induced Asthma
Infectious Disease
Blood-Borne Infections
High-Altitude Illness
Exertional Heat-Related Illness
Cold-Related Illness
References
7: Doping in Sports
References
Part II: Musculoskeletal Injuries
8: Sports-Related Traumatic Brain Injury and Concussion
Introduction
Epidemiology
Risk Factors
Clinical Presentation
Subclassification, Subtypes, and Overlapping Clinical Profile
Pathophysiology
Diagnosis
Sideline Assessment and the In-office Exam
Testing: Sensitivity and Specificity
Return to Play (RTP) Guidelines and Recommendations
Early Exercise and the Subsymptom Threshold
Chronic Traumatic Encephalopathy (CTE)
Prevention and Future Research
References
9: Cervical Spine Injuries
Introduction
Anatomy of Cervical Spine
Bones
Nerves
Intervertebral Discs
Muscles and Ligaments
Biomechanics
Acute Injuries
Preparation and Management of Suspected On-Field Cervical Spine Injury
Pre-event Planning
On-Field Management
Stable Cervical Spine Injuries
Cervical Strain/Sprains
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Acute Cervical Disc Herniation
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Stingers/Burners
Mechanism of Injury/Pathophysiology
Clinical Presentation and Diagnosis
Treatment
Return to Play
Cervical Spinous Process Fracture
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Unstable Cervical Spine Injuries
Unstable Cervical Fractures
Mechanism of Injury/Pathophysiology
Clinical Presentation and Diagnosis
Treatment
Return to Play
Cervical Cord Neurapraxia with Transient Tetraplegia
Mechanism of Injury/Pathophysiology
Clinical Presentation and Diagnosis
Treatment
Return to Play
Blunt Cerebrovascular Injuries
Mechanism of Injury/Pathophysiology
Presentation and Diagnosis
Treatment
Return to Play
Overuse Injuries
Myofascial Pain Syndrome
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Cervical Facet–Mediated Pain/Cervical Facet Arthropathy
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Chronic Cervical Radiculopathy
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Thoracic Outlet Syndrome (TOS)
Mechanism of Injury/Pathophysiology [42, 43]
Neurogenic TOS
Vascular TOS
Clinical Presentation
Diagnosis
Treatment
References
10: Shoulder Injuries
Introduction
Anatomy
Bones
Nerves
Muscles and Ligaments
Biomechanics
Acute Injuries
ACJ Sprain and Separation
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
GHJ Dislocation
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Clavicle Fracture
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Overuse Injuries
Rotator Cuff Tendinopathy
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Bicipital Tendinopathy
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
GHJ Instability
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Glenoid Labrum Tears
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
References
11: Elbow and Forearm Injuries
Introduction
Anatomy and Biomechanics [1]
Bones and Ligaments
Muscles
Nerves
Biomechanics
Acute Elbow Injuries
Fractures and Dislocations [2]
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Olecranon Bursopathy (Bursitis) [5]
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Triceps Rupture
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sports
Distal Biceps Tendon Rupture
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Overuse Elbow Injuries
Lateral Epicondylopathy [2, 9, 10]
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Medial Epicondylopathy
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Triceps Tendinopathy
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Ulnar Neuropathy at the Elbow (UNE)
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Pronator Syndrome
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Anterior Interosseous Nerve Syndrome (Kiloh-Nevin Syndrome)
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Valgus Extension Overload
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Ulnar Collateral Ligament Injuries
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Conclusion
References
12: Hand and Wrist Injuries
Introduction
Anatomy of the Hand and Wrist [1]
Bones and Ligaments
Muscles
Nerves
Biomechanics
Acute Hand and Wrist Injuries [2]
Distal Radius Fracture [3]
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Wrist Sprain
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Scapholunate Ligament Disruption [4]
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Triangular Fibrocartilage Complex (TFCC) Injury
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Scaphoid Fracture [5]
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Hook of the Hamate Fracture
Clinical Presentation
Diagnosis
Treatment
Return to Sport
UCL Tear/First Metacarpophalangeal Instability (Gamekeeper’s Thumb, Skier’s Thumb) [6]
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Metacarpal Shaft/Neck Fracture
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Digital Extensor Tendon Injury (Mallet Finger) [7]
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Flexor Digitorum Profundus Tendon Avulsion Injury (Jersey Finger) [8]
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Finger Dislocations
Clinical Presentation
Diagnosis
Treatment
Overuse Wrist and Hand Injuries [9]
De Quervain’s Tenosynovitis
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Carpal Tunnel Syndrome
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Ulnar Nerve Palsy
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Flexor Tenosynovitis (Trigger Finger)
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Intersection Syndrome (Oarsman’s Wrist)
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Return to Play
Suggested Readings
13: Chest Trauma and Thoracic Spine Injuries
Introduction
Anatomy
Bones
Nerves
Muscles and Ligaments
Lungs
Heart
Acute Injuries
Pulmonary Contusion
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Rib Fractures
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Sternal Fractures
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Pneumothorax
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Commotio Cordis
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Pectoralis Major Tear
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Stress Fracture: Ribs
Overuse Injuries
Mechanism of Injury/ Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Stress Fracture: Sternum
Mechanism of Injury/ Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Slipping Rib Syndrome
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Scapulothoracic Bursitis
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Thoracic Spine Injuries
References
14: Lumbar Spine Injuries
Introduction
Evaluation
Bone
Spinal Variants
Scoliosis
Scheuermann’s Disease
Etiology and Clinical Presentation
Work-Up
Treatment
Acute Traumatic Injuries
Vertebral Fractures
Etiology and Clinical Presentation
Work-Up
Treatment
Spinous Process and Transverse Process Fractures
Etiology and Clinical Presentation
Work-Up
Treatment
Spondylolysis
Etiology and Clinical Presentation
Pedicle Stress Reaction
Work-Up
Treatment
Spondylolisthesis
Etiology and Clinical Presentation
Work-Up
Treatment
Soft Tissue and Nerve
Disc Herniation and Radiculopathy
Etiology and Clinical Presentation
Work-Up
Treatment
Muscle Tendon Complex
Etiology and Clinical Presentation
Work-Up
Treatment
Ligamentous Injury
Etiology and Clinical Presentation
Work-Up
Treatment
Baastrup’s Disease
Etiology and Clinical Presentation
Work-Up
Treatment
Apophysitis
Etiology and Clinical Presentation
Work-Up
Treatment
Zygapophysial (Facet) Joint Pain
Etiology and Clinical Presentation
Work-Up
Treatment
Spinal Stenosis
Etiology and Clinical Presentation
Work-Up
Treatment
SI Joint Complex Pain
Return-to-Play Criteria
Other Causes of Low Back Pain
Conclusion
References
15: Pelvis, Hip, and Thigh Injuries
Introduction
Anatomy
Bone
Nerves
Muscles and Ligaments
Biomechanics
Acute Injuries
Hamstring Muscle Injury
Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Sport
Quadriceps Muscle Injury
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Adductor Strains
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Iliac Crest Contusions
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Overuse Injuries
Femoral Neck Stress Fracture
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Femoroacetabular Impingement
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Greater Trochanteric Pain Syndrome
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Athletic Pubalgia
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Snapping Hip Syndrome
Pathophysiology
Presentation
Diagnosis
Treatment
Return to Sport
Summary
References
16: Knee Injuries
Introduction
Anatomy
Bones
Nerves
Muscle and Ligaments
Menisci
Bursae
Biomechanics
Acute Injuries
Patellar Dislocation
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Anterior Cruciate Ligament
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Lateral Collateral Ligament
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Medial Collateral Ligament
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Posterior Cruciate Ligament
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Meniscal Injuries (Lateral/Medial Meniscus)
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Hamstring/Quadriceps Strain/Tear
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Overuse Injuries
Patellar Tendinopathy
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Patellofemoral Pain
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Knee Apophysitis (Osgood-Schlatter Disease and Sinding-Larsen-Johansson Disease)
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Iliotibial Band Friction Syndrome
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Knee Osteoarthritis (OA)
Mechanism of Injury/Pathophysiology
Clinical Presentation
Diagnosis
Treatment
Return to Play
Conclusion
References
17: Leg Injuries
Anatomy of the Leg [1, 2]
Compartments
Nerves
Sensory Innervation
Motor Innervation
Bones [3]
Acute Injuries of the Leg
Fractures
Tibial Plateau Fractures [4, 5]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Tibial Shaft Fractures [6, 7]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Distal Tibia Fractures [8–10]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Fibula Fractures
Clinical Presentation
Diagnosis
Treatment
Return to Play
Contusions
Clinical Presentation
Diagnosis
Treatment
Return to Play
Neurovascular Injury
Tibial Nerve Injury [11, 12]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Fibular Nerve Injury
Clinical Presentation
Diagnosis
Treatment
Return to Play
Superficial Fibular Nerve
Clinical Presentation
Diagnosis
Treatment
Return to Play
Deep Fibular Nerve
Clinical Presentation
Diagnosis
Treatment
Return to Play
Acute Muscle and Tendon Injuries
Ankle Syndesmosis Injury [13–16]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Gastrocnemius Strain [15, 17–20]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Acute Compartment Syndrome
Clinical Presentation
Diagnosis
Treatment
Return to Play
Popliteus Injury [21–24]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Overuse Injuries (Fig. 17.4, Adapted)
Bone Injuries
Tibial Stress Fractures [25–29]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Medial Tibial Stress Syndrome [30, 31]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Vascular and Ischemic Overuse Syndromes
Chronic Exertional Compartment Syndrome [32–36]
Clinical Presentation
Diagnosis
Treatment
Return to Play
Popliteal Artery Entrapment Syndrome [33, 37, 38]
Clinical Presentation
Diagnosis
Treatment
Return to Play
References
Recommended Reading
18: Ankle and Foot Injuries
Anatomy
Bones
Ligaments
Muscles
Joints
Tarsal Tunnel
Plantar Aponeurosis
Disorders of the Ankle
Ankle Sprains
Clinical Presentation
Diagnosis
Treatment
Return to Play
Achilles Tendinopathy
Clinical Presentation
Diagnosis
Treatment
Return to Play
Achilles Tendon Rupture
Clinical Presentation
Diagnosis
Treatment
Return to Play
Retrocalcaneal Bursitis
Clinical Presentation
Diagnosis
Treatment
Return to Play
Plantar Fasciopathy
Clinical Presentation
Diagnosis
Treatment
Return to Play
Flexor Hallucis Longus Tendinopathy/Injury
Clinical Presentation
Diagnosis
Treatment
Return to Play
Tibialis Anterior Tendinopathy
Clinical Presentation
Diagnosis
Treatment
Return to Play
Tibialis Posterior Tendon Injuries
Clinical Presentation
Diagnosis
Treatment
Return to Play
Fibular Tendon Injuries
Clinical Presentation
Diagnosis
Treatment
Return to Play
Sprain of the First Metatarsophalangeal Joint
Clinical Presentation
Diagnosis
Treatment
Return to Play
Morton’s Neuroma
Clinical Presentation
Diagnosis
Treatment
Return to Play
Sinus Tarsi Syndrome
Clinical Presentation
Diagnosis
Treatment
Return to Play
Metatarsalgia
Clinical Presentation
Diagnosis
Treatment
Return to Play
Heel Fat Pad Contusion
Clinical Presentation
Diagnosis
Treatment
Return to Play
Fractures
References
Part III: Specific Populations
19: Master Athletes
Introduction
Epidemiology
Overall Increase of Master Athletes
Injury Rate in Master Athletes
Age-Related Changes Relevant to Maintaining a High Level of Performance at Older Age
Musculoskeletal System
Cardiovascular System
Gender Differences
Positive Changes in Master Athletes Compared to Sedentary Older Adults
General Principles of Caring for the Master Athlete
Pre-participation
Injury Prevention and Management
Nutrition and Hydration Recommendations
Recovery
Rehabilitation of Injury and Return to Sport
Sports-Specific Considerations
Running
Swimming
Golf
Mountaineering
Triathlons
Summary and Key Points
References
20: The Female Athlete
The Female Athlete Triad and Relative Energy Deficiency in Sport (REDs)
Treatment
Injury Considerations in the Female Athlete: ACL Tears
The Pregnant and Postpartum Athlete
References
21: The Pediatric Athlete
Introduction
Developmental Considerations
Nonlinearity of Growth and the Unique Response to Skeletal Injury
Age- and Maturity-Associated Variation
Acute Injuries
Common Fractures
Common Overuse Injuries
Shoulder Injuries
Elbow Injuries
Wrist Injuries
Lumbar Spine Injuries
Hip Injuries
Knee Injuries
Ankle and Foot Injuries
Sport-Related Concussion
Nutrition and Hydration Considerations
Exercise Prescription in School-Aged Children and Adolescents
Summary
References
22: Adaptive Sport Athlete
Adaptive Sports
A Brief History
Classification
Adaptive Sports Equipment
Wheelchair Technology
Sport-Specific Wheelchair Designs
Adaptive Sports Prostheses
Sport-Specific Prosthesis
Assessment of the Athlete
Pre-participation Examinations (PPE)
Sports Injuries and Medical Complications in Wheelchair Athletes
Upper Limb Injuries
Medical Injuries and Complications of Limb-Deficient Athletes
Sport-Specific Considerations in the Adaptive Athlete
Wheelchair Rugby
Wheelchair Basketball
Running
Sled Hockey
Skiing and Snowboarding
Conclusion
References
Index

Citation preview

Essential Sports Medicine A Clinical Guide for Students and Residents Gerardo Miranda-Comas Grant Cooper Joseph Herrera Scott Curtis Editors Second Edition

123

Essential Sports Medicine

Gerardo Miranda-Comas Grant Cooper  •  Joseph Herrera Scott Curtis Editors

Essential Sports Medicine A Clinical Guide for Students and Residents Second Edition

Editors Gerardo Miranda-Comas Department of Rehabilitation and Human Performance Icahn School of Medicine at Mount Sinai New York, NY USA Joseph Herrera Department of Rehabilitation and Human Performance Icahn School of Medicine at Mount Sinai New York, NY USA

Grant Cooper Princeton Spine and Joint Center Princeton, NJ USA Scott Curtis Princeton Spine and Joint Center Princeton, NJ USA

ISBN 978-3-030-64315-7    ISBN 978-3-030-64316-4 (eBook) https://doi.org/10.1007/978-3-030-64316-4 © Springer Nature Switzerland AG 2021 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

I would like to thank my wife Sandra; my children Alex, Mikhayla, and Andrew; my sister Sacha; and my parents for their unconditional support. I would also like to thank Grant Cooper for his unwavering collaboration. - Joseph Herrera

Acknowledgments

Thank you to all of my co-editors and all of the authors without whose contributions this book would not have been possible. Thank you always to my amazing wife, Ana, and our incredible children, Mila, Lara and Luka. –– Grant Cooper Thank you to all the contributors to this book including co-editors, authors, and the publishing team. Special thanks to my family, including my amazing wife Veroushka and son Matteo, and to all my mentors. –– Gerardo Miranda-Comas Thank you to all of the co-editors and contributing authors for their hard work and dedication. My sincere gratitude to all of the amazing teachers, role models, and mentors who have guided me throughout my career. Special thanks to my wife, Amanda, and our two children, Lily and Ryan, for their endless love and support. –– Scott Curtis

vii

Contents

Part I General Concepts in Sports Medicine 1 An Overview of Sports Medicine������������������������������������������������������������������ 3 Michael Fredericson, Richard Lawley, and Sara Raiser 2 Advances in Sports Medicine���������������������������������������������������������������������� 13 Alexander Lloyd, Andrew Mccoy, and Kentaro Onishi 3 Exercise Prescription ���������������������������������������������������������������������������������� 31 Walter Alomar-Jiménez, Adam Fry, and Gerardo Miranda-Comas 4 Preparticipation Evaluation������������������������������������������������������������������������ 45 William Douglas and Asad Riaz Siddiqi 5 Hydration and Nutrition in Athletes���������������������������������������������������������� 75 Karie Zach 6 General Medical Problems in Athletes������������������������������������������������������ 93 Christine Persaud and Patrick Cleary 7 Doping in Sports���������������������������������������������������������������������������������������� 111 Amy Ann Skaria and Dennis A. Cardone Part II Musculoskeletal Injuries 8 Sports-Related Traumatic Brain Injury and Concussion���������������������� 119 Damion Martins 9 Cervical Spine Injuries������������������������������������������������������������������������������ 151 Jonathan Ramin, Lawrence G. Chang, and Richard G. Chang 10 Shoulder Injuries �������������������������������������������������������������������������������������� 175 Brittany J. Moore and Jacob L. Sellon 11 Elbow and Forearm Injuries�������������������������������������������������������������������� 203 Jonathan Ramin, Jasmin Harounian, and Gerardo Miranda-Comas 12 Hand and Wrist Injuries �������������������������������������������������������������������������� 221 Caroline Schepker ix

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Contents

13 Chest Trauma and Thoracic Spine Injuries�������������������������������������������� 245 Ilya Aylyarov, Kevin Kuo, and Amie Kim 14 Lumbar Spine Injuries������������������������������������������������������������������������������ 273 Vandana Sood and Jonathan S. Kirschner 15 Pelvis, Hip, and Thigh Injuries ���������������������������������������������������������������� 293 Julio Vázquez-Galliano and Gerardo Miranda-Comas 16 Knee Injuries���������������������������������������������������������������������������������������������� 315 William Micheo, Belmarie Rodríguez-Santiago, Fernando Sepulveda-Irizarry, and Brenda Castillo 17 Leg Injuries������������������������������������������������������������������������������������������������ 341 Alexander Lloyd and Daniel Lueders 18 Ankle and Foot Injuries���������������������������������������������������������������������������� 367 Kristina Quirolgico and Christine Townsend Part III Specific Populations 19 Master Athletes������������������������������������������������������������������������������������������ 391 Tiffany Lau and Mooyeon Oh-Park 20 The Female Athlete������������������������������������������������������������������������������������ 413 Eliana Cardozo and Ariana Gluck 21 The Pediatric Athlete �������������������������������������������������������������������������������� 421 Emily Fatakhov and Gerardo Miranda-Comas 22 Adaptive Sport Athlete������������������������������������������������������������������������������ 435 Matthew D. Maxwell, William Berrigan, and Roderick Geer Index�������������������������������������������������������������������������������������������������������������������� 457

Contributors

Walter  Alomar-Jiménez  Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA Ilya  Aylyarov  Department of Emergency Medicine, NYU Medical Center/ Bellevue Hospital, New York, NY, USA William Berrigan  Georgetown School of Medicine, Washington, DC, USA MedStar National Rehabilitation Hospital, Washington, DC, USA Dennis A. Cardone  Department of Orthopedic Surgery, Division of Primary Care Sports Medicine, NYU Langone Health, New York, NY, USA Eliana Cardozo  Icahn School of Medicine at Mount Sinai, New York, NY, USA Brenda Castillo  Department of Physical Medicine and Rehabilitation, MossRehab, Philadelphia, PA, USA Lawrence  G.  Chang, DO, MPH  Department of Physical Medicine and Rehabilitation, Burke Rehabilitation Hospital, White Plains, NY, USA Richard  G.  Chang, MD, MPH  Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA Patrick Cleary  Division of Sports Medicine, SUNY Downstate, Brooklyn, NY, USA William Douglas  Maine Medical Center, Portland, ME, USA Emily  Fatakhov  Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA Michael  Fredericson  Department of Orthopedic Surgery, Stanford University, Redwood City, CA, USA Adam Fry  Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA Roderick Geer  Georgetown School of Medicine, Washington, DC, USA MedStar National Rehabilitation Hospital, Washington, DC, USA Ariana Gluck  Icahn School of Medicine at Mount Sinai, New York, NY, USA xi

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Jasmin Harounian  Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA Amie Kim  Emergency Department, Physical Medicine & Rehabilitation, Mount Sinai Beth Israel Medical Center, New York, NY, USA Jonathan S. Kirschner  Weill Cornell Medicine, New York, NY, USA Hospital for Special Surgery, New York, NY, USA Kevin  Kuo  Emergency Department, Mount Sinai St. Luke’s and West, New York, NY, USA Tiffany  Lau  Burke Rehabilitation Hospital, Department of Rehabilitation Medicine, Albert Einstein College of Medicine, Montefiore Health System, White Plains, NY, USA Richard  Lawley  Department of Orthopedic Surgery, Stanford University, Redwood City, CA, USA Alexander  Lloyd, MD  Department of Sports and Spine Medicine, Swedish Medical Center, Seattle, WA, USA University of Pittsburgh Medical Center, Pittsburgh, PA, USA Daniel Lueders  University of Pittsburgh Medical Center, Pittsburgh, PA, USA Damion  Martins  Orthopedics and Sports Medicine, Atlantic Health System, Morristown, NJ, USA Matthew D. Maxwell  Georgetown School of Medicine, Washington, DC, USA MedStar National Rehabilitation Hospital, Division of Sports Medicine, Washington, DC, USA Andrew  Mccoy, MD  Department of PM&R, University of Pittsburgh, Pittsburgh, PA, USA William  Micheo  Department of Physical Medicine, Rehabilitation and Sports Medicine, University of Puerto Rico School of Medicine, San Juan, PR, Puerto Rico Gerardo Miranda-Comas  Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA Brittany  J.  Moore  Division of Sports Medicine, Department of Orthopedic Surgery; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, USA Mooyeon Oh-Park  Burke Rehabilitation Hospital, Department of Rehabilitation Medicine, Albert Einstein College of Medicine, Montefiore Health System, White Plains, NY, USA Kentaro  Onishi, DO  Department of PM&R, University of Pittsburgh, Pittsburgh, PA, USA

Contributors

Christine  Persaud  Division Brooklyn, NY, USA

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SUNY

Downstate,

Kristina Quirolgico  Hospital for Special Surgery, New York, NY, USA Sara  Raiser  Department of Orthopedic Surgery, Stanford University, Redwood City, CA, USA Jonathan  Ramin, DO  Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA Belmarie Rodríguez-Santiago  Department of Physical Medicine, Rehabilitation and Sports Medicine, University of Puerto Rico School of Medicine, San Juan, PR, Puerto Rico Caroline  Schepker  Department of Physical Medicine and Rehabilitation, New York-Presbyterian Hospital of Columbia and Cornell, New York, NY, USA Jacob L. Sellon  Division of Sports Medicine, Department of Orthopedic Surgery; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, USA Fernando Sepulveda-Irizarry  Department of Physical Medicine, Rehabilitation and Sports Medicine, University of Puerto Rico School of Medicine, San Juan, PR, Puerto Rico Asad Riaz Siddiqi  Weill Cornell Medical College, New York City, NY, USA Amy  Ann  Skaria  Department of Pediatrics, Department of Rehabilitation Medicine, Weill Cornell Medicine, New York, NY, USA Vandana Sood  NewYork-Presbyterian Hospital, New York, NY, USA Weill Cornell Medicine, New York, NY, USA Christine  Townsend  Department of Physical Medicine and Rehabilitation, Columbia University Medical Center, New York, NY, USA Julio  Vázquez-Galliano  Department of Rehabilitation Medicine, Montefiore Medical Center/Albert Einstein College of Medicine, Bronx, NY, USA Karie  Zach  Department of Orthopedic Surgery, Medical College of Wisconsin, Milwaukee, WI, USA

Part I General Concepts in Sports Medicine

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An Overview of Sports Medicine Michael Fredericson, Richard Lawley, and Sara Raiser

Sports medicine is a dynamic and far-reaching field that continues to broaden. It incorporates many specialties and encompasses diverse medical topics. Sports medicine physicians provide comprehensive care of a diverse population, including high-level athletes, weekend warriors, and the less active population with musculoskeletal complaints that impede activities of daily living. Based on the care setting, the responsibilities of a sports medicine physician may include prevention, diagnosis, treatment, and rehabilitation of musculoskeletal pathologies and medical illnesses that would otherwise interfere with participation in physical activity. A multidisciplinary team is ideal to thoroughly address this broad spectrum of pathologies and duties. The sports medicine physician is responsible for the coordination of the multidisciplinary team and, in many cases, will be the primary provider for the athlete and will direct return to play. Traditionally, the field of sports medicine has been regarded as largely musculoskeletal medicine. However, in practice, sports medicine involves any condition that limits an athlete’s participation and possibly with activities of daily living. While the presenting athlete may complain of pain, the true deficiency is how the pain or dysfunction affects athletic performance. The two main settings of sports medicine are the outpatient clinic and sideline coverage with complementary training room clinic. While the main goal of improving upon the limiting deficit to allow for return to the desired activity remains the same, there are a multitude of differences regarding the approach to diagnosis, treatment, rehabilitation, and even the healthcare providers involved in the overall care. In the outpatient clinical setting, patient care typically begins by addressing a patient’s complaint of musculoskeletal injury. Workup, diagnosis, and treatment of the underlying etiology subsequently follow. In addition to the sports medicine physician, the outpatient healthcare team commonly includes a nurse and/or medical M. Fredericson (*) · R. Lawley · S. Raiser Department of Orthopedic Surgery, Stanford University, Redwood City, CA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_1

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assistant, physical therapist, occupational therapist, orthopedic surgeon, and other professionals including an athletic trainer, a strength and conditioning specialist, an orthotist, and a chiropractor. The populations treated in the clinical outpatient setting can be rather diverse: from children to the elderly, the infrequent jogger to the professional athlete, and sedentary patients looking to become more active. Further, adaptive sports are becoming more available nationally and internationally as inclusion and accessibility allow for individuals with disabilities to stay active and compete in organized events. The care of the different patient populations requires a variable approach depending on demographic and activity levels. In contrast, as an athletic team physician, the patient age range tends to be more homogenous. The sports medicine healthcare team is multidisciplinary and consists of a wide array of healthcare specialists who are in frequent and close communication with one another. The main point of contact for both the athlete and the team physician is the team’s certified athletic trainer (ATC). The ATC works with the team nearly every day throughout the season. Thus, the ATC is extraordinarily familiar with each athlete, not only regarding health, biomechanics, and performance, but also personality and responsiveness to treatment. This access allows for close contact with the athlete and the ATC can help identify any potential issues even before they arise. The physician-trainer relationship is key to providing optimal care for the team. During sideline coverage, the ATC is generally the first health care professional to evaluate an athlete who requires medical attention and will determine whether the athlete needs assessment by the covering physician. Most sideline evaluations involve a traumatic injury, including lacerations, dislocations, fractures, sprains, strains, contusions, or concussions. However, acute medical conditions can be seen as well, such as asthma exacerbations, ocular foreign bodies, dehydration, hypoglycemia, and heat illness. More serious situations, such as cervical trauma or cardiac emergencies, will require adhering to an emergency action plan (EAP). The sports medicine physician will make the decision whether an athlete can safely return to play for the event, sit out, or even be sent to the emergency room should further resources be needed. To address the widened scope and myriad of issues that can affect athletes’ participation and performance, a diverse multidisciplinary team is needed. The members of this multidisciplinary team typically include, but are not limited to: • • • • • • • • • •

Sports medicine physician Certified athletic trainer Physical therapist, occupational therapist Orthopedic surgery specialist Medical specialist, including cardiology, pulmonology, endocrinology Registered dietician Other professionals including chiropractor and prosthetist/orthotist Coach Sports psychologist Exercise physiologist

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• Strength and performance coach • Agent (for professional athletes) • Athlete’s family (depending on age and capacity) Figure 1.1 demonstrates the typical interaction among members of the team. At the collegiate level, the sports medicine healthcare team will also work closely with academic advisors, counselors, and even professors to ensure the athlete is able to prioritize academics. Musculoskeletal injuries are the most prevalent complaint encountered by the sports medicine physician. Familiarity with the sports as well as the other activities in which the athlete participates can yield many advantages: understanding typical biomechanical loads and requirements, familiarity with common injurious positions and situations the athlete may encounter, developing rapport and trust with the athlete, and having a better understanding of limitations for training as well as an accurate prognosis for return to play. Musculoskeletal injuries can be separated by chronicity: acute and chronic. Acute injuries are typically related to a single traumatic event, whereas chronic injuries are related to overuse and repeated improper or excessive loads over time. The structural components that are commonly injured are evaluated by a sports medicine physician during a full orthopedic and biomechanical functional exam. Not only are the areas of pain fully assessed, but the kinetic chain is explored to determine if the pain is caused by dysfunction in another part of the body – a concept often referred to as “victim and culprit”, in which the painful body part is the “victim” and the dysfunctional body part is the “culprit”. Treatment of an elite athlete differs from that of the average active person. Time missed from training due to workup or rehabilitation can be detrimental to performance and even the athlete’s career. Therefore, a lower threshold is often used for

Sports Medicine Physician

Certified Athletic Trainer

Coach Orthopedic Surgeon Other Medical Specialists Chiropractor Physical & Occupational Therapists Prosthetist, Orthotist Registered Dietician Sports Psychologist Exercise Physiologist Strength & Performance Coach

PatientAthlete

Fig. 1.1  Typical interaction dynamic in the multidisciplinary healthcare team. Blue circles and arrows denote healthcare team and flow of health information, gray circle and arrows solely involve play status

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tests that will aid in diagnosis, prognosis, and return to play. Imaging, especially magnetic resonance imaging (MRI) and ultrasound, is used regularly to assess for structural damage. Not only can this information guide the diagnosis and prognosis, but it can also assist orthopedic surgeons in surgical planning, if needed. Knowing the indications for surgical referral, particularly with in-season athletes, is vital to optimal care of an athlete. Recommendations made by the treating physician direct return to play/return to sport for the athlete. Return to play guidelines and consensus statements are rarely concrete due to the many factors that need to be considered. However, knowledge of the variables that contribute to return to play parameters as well as general experience with the rehabilitation process can assist sports medicine physicians in appropriately estimating the time needed for an athlete to return to sport. Medical conditions may also threaten the overall health of the athlete and, at times, can be even more detrimental to athletic performance than musculoskeletal complaints. Infectious pathologies can be easily spread among athletes based on their proximity to other athletes with traveling, competition, and living quarters in athletes and military personnel. Overtraining can also put the athlete at greater risk for frequent infections. Common infections include viral illnesses, such as upper respiratory infection, influenza, mononucleosis, gastroenteritis, and conjunctivitis. Further, dermatologic infections and disease are relatively frequent, especially in athletes engaged in contact sports such as wrestling. The myriad of non-life-­ threatening illnesses can limit an athlete’s participation in training and competition, and the sports medicine physician will determine activity restriction and full return to play planning. Other more serious medical conditions can be found in the athletic population. Sudden cardiac death (SCD) in athletes is a rare but devastating event. This is understandably a priority of physicians to prevent; therefore, any complaints related to cardiopulmonary etiology that may increase the risk of SCD are thoroughly evaluated in the pre-participation exam. Additional cardiopulmonary disorders of note include asthma and exercised-­ induced bronchospasm. Respiratory conditions are particularly common in sports such as indoor swimming, in which athletes have frequent exposure to inhaled chemicals [1]. Monitoring the air quality can be an overlooked but important task to ensure both optimal performance and prevention of respiratory emergencies in athletes with these conditions. During sporting events, the sports medicine physician must be prepared to coordinate the emergency action plan (EAP) should the need arise. As such, the covering physician will need to know the location of the designated ambulance access as well as equipment such as an automated external defibrillator (AED), bag-valve mask, spine board, and bleeding control materials including a tourniquet. Communication with local emergency medical services is paramount in the EAP. A medical bag with supplies for laceration repair, splinting, intravenous access, and medications including an epinephrine injector can be helpful during sideline coverage. Fatigue, particularly in elite athletes, can be a frequent complaint with a wide differential of potential etiologies. It can be seen as a symptom of female athlete triad,

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which is a syndrome that exists on a spectrum and involves low energy availability, menstrual function, and bone health [2]. Male athletes can experience a similar spectrum of disease that likewise involves nutrition, hormonal balance, and bone health [3]. Overtraining syndrome is typically a diagnosis of exclusion; it can interfere greatly with performance but, often overlooked, it can also manifest with mood dysfunction. Recovery from overtraining syndrome can unfortunately be prolonged, requiring months or longer [4]; thus, prevention is key. One of the more disruptive injuries an athlete can sustain is a concussion and the related sequelae. Proper identification of a concussion is vital to prevent second impact syndrome. Concussion testing tools are used to augment the neuromuscular physical exam done by the sports medicine physician. Many concussion testing tools are available, such as the fifth edition of the Sport Concussion Assessment Tool (SCAT5), King-Devick test, ImPACT assessment, Vestibular/Ocular-Motor Screening (VOMS), and the Eye-Sync eye tracking headset. The multidisciplinary health care team coordinates the athlete’s return to play using a progression protocol. Elite sports can take a toll on not only the body, but the mind as well. Sports psychologists are an integral part of the multidisciplinary team. Literature supports that athletes are at risk for developing pathological psychological responses to injuries, which can interfere with the recovery process [5]. Further, the recommendations of sports psychologists can be helpful with management of concussive symptoms as well as school or work accommodations [6]. Sports psychologists also work with athletes who have been diagnosed with mental health disorders, providing valuable insight and advice for care. Adaptive sports are an exciting and evolving focus in sports medicine. Special considerations should be made for medical conditions that are specific to the adaptive athlete. In wheelchair athletes, rotator cuff injuries can be seen in up to 75.7% involved in overhead sports [7]. Additionally, wheelchair athletes with spinal cord injury are at risk for autonomic dysreflexia, hyperthermia, urinary tract complications, and pressure injuries [8]. While the setting of a sports medicine physician generally includes musculoskeletal injuries, there are some diseases that mimic musculoskeletal etiology but in fact are due to another root cause. Therefore, knowledge of rheumatologic, disorders, vascular disorders, regional pain syndromes, and even bone and soft tissue tumors is essential to patient care. The pre-participation exam (PPE) is yet another unique feature of sports medicine. Numerous medical conditions, prior injuries and musculoskeletal conditions, and even suboptimal biomechanics can put an athlete at risk of significant injury. PPEs can be administered in a one-on-one clinic appointment or in a mass athlete physical setting. Depending on the level of participation, an athlete will typically undergo a PPE annually or upon entry into a new level of participation (such as for high school and college). While PPEs are not standardized, they generally include a comprehensive medical history including screening for cardiopulmonary health and female athlete triad, family health history, prior musculoskeletal injuries, and medication/supplement use. A thorough physical examination, including core stability and kinetic chain testing is recommended in order to fully evaluate the athlete

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for risks of high intensity athletic participation. Depending on the institution, an electrocardiogram may also be administered in all or select “at-risk” athletes. At the high school and collegiate levels, baseline concussion assessments are completed during PPEs so that diagnosis and even prognosis of a concussion can be accurate in the case of head trauma during the season. The multidisciplinary sports medicine healthcare team is well-suited to provide the foundation for not only injury prevention and treatment of injuries, but also sports performance optimization. Physicians provide functional assessment and preventative screening through the PPE. Multiple members of the healthcare team may counsel on the importance of sleep hygiene, appropriate hydration, and nutrition habits as well as stress management techniques. Sports psychologists may work with athletes to improve their performance from a mental standpoint. Psychological skills training [9] and mindfulness practice [10] have been shown to improve sports performance. Human performance labs may offer a variety of methods for evaluation including dynamic biomechanical evaluations, maximal oxygen uptake testing, lactate threshold testing, and body composition analyses. Performance testing can be utilized for injury prevention or sports optimization purposes. When it comes to human performance, doping is an unfortunate reality in sports competition. Most elite level sports have anti-doping procedures for testing athletes to discourage the use of substances deemed to be “illegal” in competition by the responsible sport governing body. Anti-doping agencies whose rules and regulations may apply to athletes competing in the United States include the drug-testing program of the National Collegiate Athletic Association (NCAA), U.S. Anti-Doping Agency (USADA), and the World Anti-Doping Agency (WADA). These agencies work to facilitate fair and safe competition. Doping may include use of banned substances, manipulation of blood products, use of intravenous infusions, tampering with a sample collected for doping control, and gene and cell doping. Depending on the governing body, there may also be whereabouts requirements such that an athlete could be randomly tested at any time even outside of competition. Sports medicine teams should be vigilant when it comes to any substances that an athlete may put into their body both to ensure the safety of the athlete and to avoid disqualifying drug tests. Sport substance rules should be taken into consideration when reviewing an athlete’s medications, counseling on illicit substance use, and providing in-season pharmacological treatment recommendations. Athletes must be advised that even over-the-counter vitamins may contain substances which could result in a positive drug test. When medications are required for the treatment of an athlete, they should be chosen carefully and banned substances reported immediately to the appropriate testing board(s) with adequate documentation that includes clear therapeutic justification (such as a Therapeutic Use Exemption). Failure to be mindful of and adhere to these rules may potentially lead to a devastating disqualification from sport. As previously mentioned, sports medicine is growing and becoming more diverse. There are multiple training routes once can pursue in order to practice in sports medicine. For primary care sports medicine, this training includes a residency in family medicine, internal medicine, pediatrics, emergency medicine, or

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physical medicine and rehabilitation (PM&R). For the surgical counterpart, training includes a residency in orthopedic surgery. Some physicians develop competence to practice sports medicine by augmenting their training without a formal sports medicine fellowship, but for those looking to work with higher level teams or pursue a career in academia, the trend is to complete an ACGME-accredited sports medicine fellowship. Physicians can apply for primary care sports medicine fellowships in a variety of specialties: as of 2020, there are 158 family medicine department-based programs, 23  PM&R, 18 pediatric, and 9 emergency medicine participating in the NRMP match1. As one might imagine, the specialty in which the fellowship is based will guide the experience and training background of that fellowship. There are specific requirements a fellowship program must fulfill in order to be ACGME-accredited. These requirements relate to patient care, clinical experience, procedural exposure, sporting event coverage, and scholarly activities. Further, in order to obtain post-fellowship CAQ (certificate of added qualifications), one must successfully complete the one-year ACGME sports medicine fellowship and pass the written sports medicine board examination. There is also maintenance of certification (MOC) that must be completed every 10 years in addition to continuing medical education (CME) credits to maintain the CAQ. Sports medicine organizations provide opportunities for CME, research and networking, and represent the field as advocates in government. The American Medical Society for Sports Medicine (AMSSM) is the largest American organization for sports medicine physicians. The members are described as “physicians for active people and athletes,” and the organization partnered with NATA and AAOS to work on passage of the Sports Medicine Licensure Clarity Act that was signed into law October 5th, 2018 [11]. This law ultimately makes participation safer for athletes by allowing physicians to travel with athletes and provide medical care, even if the travel brings them to states outside of their licensure. The American College of Sports Medicine (ACSM) is an international, multidisciplinary organization with greater than 50,000 members and represents 70 occupations within the sports medicine field. In 2007, the ACSM partnered with the American Medical Association to co-launch the Exercise is Medicine (EIM) initiative in order to promote the ACSM’s physical activity guidelines [12]. A mounting body of evidence supports exercise improving health metrics, reducing risk and/or morbidity of numerous diseases, and reducing overall mortality and morbidity. Some even regard physical activity level as a vital sign that is obtained during a clinical visit [13]. Therefore, utilizing exercise and physical activity as medicine and a path to overall well-being is becoming more commonplace. Sports medicine physicians are viewed as the leaders to bring exercise as medicine to patients. Exercise prescription can lend itself toward engaging to introduce exercise into their schedule as a regular activity, thus promoting adoption and improving the probability of adding its health benefits. 1  For full match statistics of recent years, please see NRMP website http://www.nrmp.org/fellowships/sports-medicine-match

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One of the most prominent changes in sports medicine practice involves the use of bedside or portable ultrasonography. Ultrasound can evaluate tissues including bones, muscles, tendons, ligaments, nerves, and vessels. Compared to MRI, it is less expensive, can show finer superficial detail, and is useful as a point of care diagnostic evaluation [14]. Ultrasound can be used non-invasively for sono palpation and both static and dynamic diagnostic exams. In addition to being used for diagnostic purposes, ultrasound can also be used to facilitate minimally invasive procedures from simple injections to more advanced procedures. These second(tenotomies, peripheral nerve hydrodissections, calcific tendinitis barbotage) and third-generation (A1 pulley releases, muscle compartment fasciotomies) advanced procedures [15] offer diagnostic and therapeutic benefits via minimally invasive techniques. The utilization of outpatient diagnostic musculoskeletal ultrasounds has been increasing tremendously [16], and there is evidence that ultrasound-guided injections provide greater accuracy than landmark-guided or fluoroscopic injections for a number of different procedures [15]. Regenerative medicine is a developing area in sports medicine. Injected biologics have been used since the 1950s [17]. Biologics used today include steroids, prolotherapy, platelet rich plasma (PRP), and mesenchymal stromal cells. Unfortunately, there is a lack of standardization of protocols for indication, injectate preparation, and injection technique. Even nomenclature can be controversial [18]. Though evidence in the literature remains mixed with regard to efficacy, this is a significant focus in current research and is an area expected to continue expansion. Sports medicine healthcare teams constantly seek to improve methods for injury prevention, improved sports performance, and more effective treatment options for injuries. Accordingly, sports medicine physicians are always looking toward the future and anticipating the next advancement in the field of sports medicine.

References 1. Kanikowska A, Napiórkowska-Baran K, Graczyk M, Kucharski M.  Influence of chlorinated water on the development of allergic diseases – an overview. Ann Agric Environ Med. 2018;25(4):651–5. 2. Kraus E, Tenforde AS, Nattiv A, Sainani KL, Kussman A, Deakins-Roche M, et  al. Bone stress injuries in male distance runners: higher modified Female Athlete Triad Cumulative Risk Assessment scores predict increased rates of injury. Br J Sports Med. 2019;53(4):237–42. 3. Tenforde AS, Barrack MT, Nattiv A, Fredericson M. Parallels with the female athlete triad in male athletes. Sports Med. 2016 Feb;46(2):171–82. 4. Meeusen R, Duclos M, Foster C, Fry A, Nieman D, Raglin J, 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. 5. Putukian M. The psychological response to injury in student athletes: a narrative review with a focus on mental health. Br J Sports Med. 2016;50(3):145–8. 6. Guay JL, Lebretore BM, Main JM, DeFrangesco KE, Taylor JL, Amedoro SM.  The era of sport concussion: evolution of knowledge, practice, and the role of psychology. Am Psychol. 2016;71(9):875–87.

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7. Akbar M, Brunner M, Ewerbeck V, Wiedenhöfer B, Grieser T, Bruckner T, et  al. Do overhead sports increase risk for rotator cuff tears in wheelchair users? Arch Phys Med Rehabil. 2015;96(3):484–8. 8. Dutton RA.  Medical and musculoskeletal concerns for the wheelchair athlete: a review of preventative strategies. Curr Sports Med Rep. 2019;18(1):8. 9. Brown DJ, Fletcher D. Effects of psychological and psychosocial interventions on sport performance: a meta-analysis. Sports Med. 2017;47(1):77–99. 10. Bühlmayer L, Birrer D, Röthlin P, Faude O, Donath L.  Effects of mindfulness practice on performance-­ relevant parameters and performance outcomes in sports: a meta-analytical review. Sports Med. 2017;47(11):2309–21. 11. Guthrie B.  Sports Medicine Licensure Clarity Act of 2018 [Internet]. Sect. 12, 115–254 Oct 5, 2018. Available from: https://www.congress.gov/bill/115th-congress/house-bill/302/ text#toc-HE692DB0C6C404FF88442E5AEA82CDE7C 12. Russell E. Exercise is medicine. Can Med Assoc J. 2013;185(11):E526. 13. Liu I-LA, Moy M, Estrada E, Rippberger EJ, Nguyen HQ. An “exercise vital sign” is a valid proxy measure of physical activity in COPD in routine clinical care. Trans Am Coll Sports Med. 2017;2(23):5. 14. Nazarian LN. The top 10 reasons musculoskeletal sonography is an important complementary or alternative technique to MRI. Am J Roentgenol. 2008;190(6):1621–6. 15. Finnoff JT, Hall MM, Adams E, Berkoff D, Concoff AL, Dexter W, et al. American Medical Society for Sports Medicine (AMSSM) Position Statement: Interventional Musculoskeletal Ultrasound in Sports Medicine. PM&R. 2015;7(2):151–168.e12. 16. Sharpe RE, Nazarian LN, Parker L, Rao VM, Levin DC. Dramatically increased musculoskeletal ultrasound utilization from 2000 to 2009, especially by podiatrists in private offices. J Am Coll Radiol. 2012;9(2):141–6. 17. Hollander J.  Intra-articular hydrocortisone in the treatment of arthritis. Ann Intern Med. 1953;39(4):735. 18. Lindner U, Kramer J, Rohwedel J, Schlenke P. Mesenchymal stem or stromal cells: toward a better understanding of their biology? Transfus Med Hemother. 2010;37(2):75–83.

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Advances in Sports Medicine Alexander Lloyd, Andrew Mccoy, and Kentaro Onishi

Sports Ultrasound Introduction Musculoskeletal ultrasound (MSK US) use has increased dramatically over the last decade [1]. The largest increases are among non-radiologists, who perform almost two thirds of MSK US exams in the United States [1, 2]. This interest results from US’s portability, superb resolution, lack of radiation, low patient cost, and high patient satisfaction relative to other modalities such as MRI or CT [1–4]. Recently, sports physicians have begun to pursue the use of US beyond the MSK system. This has included evaluation of the heart, abdomen, lungs, and eyes. The use of US for both MSK and non-MSK uses has given rise to the term “sports ultrasound” (SUS) to encompass the sports-related diagnoses discussed in this section [2–5]. MSK US has several advantages over other imaging modalities when used as a diagnostic modality. Compared to MRI, US offers superior spatial resolution, allowing for more detailed visualization of tissues like tendons or ligaments that are commonly injured in sports [2, 4]. US is real-time and capable of evaluating pathology dynamically. US is also cost-effective. A 2008 study found a potential healthcare cost savings of almost $7 billion if MSK US was substituted for musculoskeletal MRI in areas where US use was appropriate [6]. It is important to note that there are several disadvantages of US use. Among the major limitations are its inability to

A. Lloyd Department of Sports and Spine Medicine, Swedish Medical Center, Seattle, WA, USA A. Mccoy Department of PM&R, University of Pittsburgh, Pittsburgh, PA, USA e-mail: [email protected] K. Onishi (*) Department of PM&R/Orthopedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_2

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detect osseous abnormalities beyond bony cortex, its narrow field of view, and the fact that it is operator dependent. For this reason, US is most effective as an extension of the clinical history and exam to narrow the differential diagnosis. Among structures commonly visualized with US are muscles, tendons, ligaments, nerves, fascia, subcutaneous tissue, articular cartilage, and joint spaces. Imaged pathology may include tendinosis, tendon/ligament/muscle tears, effusions, hematomas, cysts, arthritic changes, synovitis, nerve compression, and nerve transection [7]. US is now a common way to guide office-based procedures for the treatment of sports injuries. Many injections are still performed with palpation guidance using anatomic landmarks, but studies show that landmark-guided injections are imprecise and pose a risk of inadvertent needle placement into or through sensitive structures [5]. US offers improved accuracy through direct visualization of needle placement [5]. For newer office-based procedures that go beyond conventional injections, US guidance is of paramount importance. Examples include percutaneous tenotomy/fasciotomy, nerve hydrodissection, and neovessel ablation that pose significant risk of injury if done without guidance [5]. Experimental microsurgical procedures, such as carpal tunnel release and tenotomy/fasciotomy that can debride damaged tissues, require US guidance to be done safely [5].

Cardiac Evaluation SUS can be used to screen for cardiac causes of sudden death during sports [8]. While the history and physical exam (H&P) and EKG are typically used as screening tools in the preparticipation evaluation (PPE), their effectiveness has been questioned. While the H&P is the most common screen before sports participation, it lacks the sensitivity needed to be used as a screening tool [9]. A comprehensive review by Harmon et al. found that the pooled sensitivity for the history was 20% (range 7–44%) and 9% for the physical exam (range 3–24%), but both together were far more specific at 94% and 97%, respectively [9]. EKG was both sensitive and specific at 94% (79–98%) and 93% (90–96%), respectively [9]. Unfortunately, EKG lacks portability and takes time to set up. US is portable and amenable to rapid evaluation, making echocardiography a possible adjunct to improve the PPE. While no study has made systematic claims about its sensitivity and specificity as a screening tool, echocardiography may decrease the false-positive rate when combined with EKG and reduce cardiology referrals [10, 11]. A study by Rizzo et al. using echocardiography to screen 3100 male soccer players found cardiac anomalies missed by H&P and EKG [12]. Mild valvular abnormalities were the most common and included bicuspid aortic valves, atrial septal defects, and mitral valve prolapse. Almost all cases had a normal H&P and only one had an abnormal EKG, although the clinical significance of these mild anomalies is open to question. Severe abnormalities were rare, and all had abnormal EKG findings. These severe abnormalities included two cases of hypertrophic cardiomyopathy, one case of aortic root dilation related to bicuspid aortic valve, and one large PFO. None of these abnormalities was previously symptomatic, and none were detected on physical exam except for fixed splitting of the heart sounds in the athlete with a PFO [12].

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The Early Screening for Cardiac Abnormalities with Preparticipation Echocardiography (ESCAPE) protocol is the most commonly used protocol for screening for cardiac anomalies in athletes. It examines the end-diastolic interventricular septal thickness, left ventricular diameter, left ventricular wall thickness, and aortic root diameter [9, 13–14]. Initial studies done by Yim et al. showed similar rates for detection of anomalies between cardiologists and non-cardiologists [14, 15]. However, all non-cardiologist evaluations were performed by individuals trained by the research team and their findings were all independently validated. At this time, echocardiography can be trialed with the PPE in trained hands, but should not replace the H&P or EKG.

Thoracic and Abdominal Evaluation The Focused Assessment with Sonography in Trauma (FAST) was developed in the 1990s for trauma assessment in blunt thoracoabdominal trauma. It was designed to identify hemoperitoneum, liver injury, hemopericardium, pericardial or cardiac injury, and splenic or renal injury [16]. The subsequently developed extended FAST exam (eFAST) added identification of pneumothorax and hemothorax and is more sensitive than the AP radiographs for these diagnoses [17, 18]. These exams were designed for rapid evaluation in emergency situations and should take experienced examiners 5 minutes or less. The eFAST is not routinely used on the sidelines, but could be used to evaluate athletes awaiting hospital transfer after significant thoracoabdominal trauma [3]. Doing so could help triage athletes based on severity of injury, but at this time, sideline use of the eFAST has not been studied. Further research is needed to determine if eFAST use can reduce unnecessary transfers to the emergency room or reduce the door-to-intervention time when transport is indicated.

Ocular Evaluation US has been used for ocular evaluation by ophthalmologists for decades. However, the use of ocular US by sports physicians started only recently [3]. Sports-­related eye injuries are common and account for approximately 1.5% of all sports injuries with higher rates in sports like baseball and basketball [19, 20]. Retinal detachment is a common injury both amenable to US evaluation and sensitive to rapid diagnosis and intervention [21]. Untreated, symptomatic retinal detachment can progress to complete detachment within days, resulting in complete loss of vision. Nonradiology specialists can reliably use US to identify retinal detachment with sensitivity ranging from 97% to 100% and specificity from 83% to 100% [22]. Optic nerve sheath diameter (ONSD) can also be measured using US and may be helpful in evaluating athletes after acute head injury. Increased values can indicate severe intracranial pathology that warrants emergent transfer [23, 24]. ONSD evaluation with US is 86–100% sensitive and 63–100% specific for increased intracranial pressure [23, 24]. In addition, ONSD can be 60–84% sensitive and 73–100%

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specific for any intracranial abnormality [23, 24]. While more research is needed to validate this measurement in a sports setting, ONSD offers a promising way to triage acute, sports-related head injury.

Vocal Cord Evaluation Vocal cord dysfunction (VCD) also known as exercise-induced laryngeal obstruction (EILO), is an uncommon sports diagnosis that can present similarly to asthma. However, it has a different pathophysiology and can confuse practitioners attempting to treat athletes on the sidelines [25]. VCD likely has several causes, but all lead to paradoxical movement of the vocal folds with inspiration during exercise, causing wheezing, shortness of breath, stridor, and exercise intolerance [25]. Unlike asthma, VCD will not respond to beta agonists and often resolves rapidly with the cessation of exercise. Laryngoscopy can confirm the diagnosis, but doing so during or soon after exercise can be challenging and often requires specialized equipment [25]. US allows for rapid sideline evaluation while symptoms are occurring, facilitating an accurate diagnosis [26]. However, vocal fold evaluation can be difficult for untrained clinicians, and this technique is currently experimental rather than standard of care.

Bone Evaluation Ultrasound can be sensitive to certain types of bone injury and help with evaluation and diagnosis when traditional imaging modalities are not available [27]. Long, linear bone with little intervening tissue is ideal for ultrasound evaluation because the ultrasound beam is perpendicular to the area of interest. Small cortical irregularities scatter the sound waves and readily demonstrate abnormal areas [27]. Fractures can be viewed as an interruption of the smooth cortical surface and may be accompanied by edema, hyperemia, and periosteal thickening [27]. US is also useful for detecting bony stress injury, which is notoriously difficult to identify on plain films and often requires a costly MRI to diagnose [28]. Elastography, an emerging ultrasound technology discussed below, may also aid in US diagnosis and allow for following fracture healing over time [29].

Novel Ultrasound Technologies Elastography, ultrasound tissue characterization (UTC), and glycogen measurement are new US technologies that may prove useful for sports physicians with more research. Elastography measures tissue stiffness calculated using two different methods. The first, termed strain elastography (SE), monitors tissue resistance to external compression performed by the ultrasonographer [30]. A color-coded overlay (elastogram) is then superimposed over the image reflecting resistance to strain. While this measure of elastography is available on many new machines, reliability has been questioned because the measure is dependent on non-standardized strain generated by the examiner [30]. The second, termed shear wave elastography (SWE), uses ultrasound pulses to shear tissues beneath the probe and provides a more objective measure of elasticity [31]. Tendon stiffness may differ between healthy and diseased states, making elastography a possible future method to predict at-risk or healing tendon.

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Ultrasound tissue characterization (UTC) uses a motor-driven device connected to the ultrasound transducer to comprehensively examine a tissue of interest [32]. Images are taken every 0.2 mm and compiled into a three-dimensional block. The data from this evaluation can characterize the tissue based on echo signal stability or “pattern” [32]. These echo patterns reflect specific tissue interactions with the sound waves that reflect off of or pass through them. Type I and II echo patterns represent stable echo signals, while type III and IV are unstable and often characteristic of tendinopathy [32]. However, the use of UTC is still exploratory and the normal appearance of tendons for athletes is still under investigation. Finally, US is being applied to assess muscle glycogen content. Muscle glycogen content is tied to performance through time to fatigue and muscle contractility and force, making it potentially a useful measure in athletic performance. However, glycogen content is often measured with invasive muscle biopsy, making routine monitoring for performance optimization impractical. US can indirectly measure muscle glycogen by analyzing the water content of the muscle, some of which is bound to glycogen within the muscle [33, 34]. Monitoring glycogen content could give athletes and coaches the ability to monitor how diet and training programs affect overall glycogen stores. This technology is still under development and its long-term clinical utility remains unknown at this time.

Orthobiologics Introduction Corticosteroid injection has long been the standard injectable treatment for musculoskeletal injuries, but may be harmful to tendons, ligaments, and intra-articular cartilage in certain situations [35–39]. As a result, clinicians have sought alternative agents that may provide relief or healing for common MSK complaints. This section will focus on the role and efficacy of prolotherapy and a group of injectables referred to as “orthobiologics” that include platelet-rich plasma (PRP) and mesenchymal stem cells (MSCs) in the treatment of MSK injuries.

Prolotherapy Prolotherapy is one of the original regenerative injectables first described in the 1930s. It came to prominence in the 1950s when Dr. George S. Hackett formalized its use as a method for treating MSK conditions [40]. Prolotherapy agents traditionally included hypertonic dextrose (most common), morrhuate sodium, and phenol-­ glycerine-­glucose [40].

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In spite of being a chemical compound, dextrose is commonly considered for similar indications as the orthobiologics discussed later in this chapter. The precise mechanism of action is unknown, but several theories have been proposed. One possible mechanism is that injecting a small amount of an irritant compound into a chronic injury converts it into an acute injury, promoting normal healing and regeneration [41]. Another is that prolotherapy acts as a vessel sclerosant that disrupts pathologic blood flow seen in chronic tendon and ligament injuries [41]. Dextrose may also have a modulatory effect on pain sensation when applied in the vicinity of peripheral nerves [41]. Prolotherapy has also been used to treat tendinopathy including tendinopathies at the common extensor tendon of the lateral elbow, patellar and rotator cuff tendons, Osgood-Schlatter disease, chronic groin pain, and plantar fasciopathy. Prolotherapy has also been studied as a treatment for osteoarthritis. Treatment of knee osteoarthritis is the most studied use for joint pathology with several level 1 studies, but injection of the temporomandibular joint, carpal, carpometacarpal, and interphalangeal joints has also been studied and has shown improvements in pain, function, rangeof-motion, and articular cartilage measures [41]. Research has generally shown prolotherapy to be effective for management of these disorders. In addition, prolotherapy has the benefit of being both significantly less expensive and more available than other regenerative treatments, making it a good option for management of these conditions [41]. In spite of these promising results, the data for these uses is limited and further research is needed before making stronger recommendations. Ligament effects are not as well studied as tendon and joint effects. Reeves and Hassanein have found positive effects of prolotherapy for improving anterior cruciate ligament laxity [42]. Jensen et al. also studied the effects of prolotherapy on medial collateral ligaments in rats and found that treatment increased MCL cross-­ sectional area, but did not alter ligament laxity [43].

Platelet-Rich Plasma Platelet-rich plasma (PRP) is broadly defined as autologous blood containing a higher concentration of platelets as a derivative of whole blood produced through centrifugation [39]. A portion of the centrifuged blood is removed and used as the therapeutic injectate in the location of interest. It was first used in oral surgery and subsequently in orthopedic procedures with the goal of stimulating bone and soft tissue healing. In spite of its surgical origins, it has been increasingly adopted as a nonsurgical treatment for soft tissue injuries. Its use has been driven by mounting evidence that it may accelerate tissue healing [44]. While research continues on the use of PRP and related compounds as biological augmentation for surgical interventions, this review will focus on PRP as monotherapy in nonoperative management of MSK disease. There are multiple proposed mechanisms for the efficacy of PRP, although the exact mechanism is unknown. One proposed mechanism is that alpha granules within platelets containing multiple growth factors normally involved in healing increase angiogenesis and facilitate allocation of blood supply to the area of injury [39]. PRP may also help with differentiation of local stem cells into lineages needed for repair of local tissues. It has also been proposed that PRP modulates the local inflammatory response to attract cells involved in healing of the injured area [39].

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Clinical studies on PRP have produced variable results, and definitive conclusions are difficult to make for several reasons. One core problem is that definition of what constitutes PRP is difficult to elucidate because the methods used to create the injectate vary [45]. Preparation variation, along with the host factors, results in different PRP products. The concentrations of red blood cells, white blood cells, and platelets have all been debated regarding their influence on PRP’s effectiveness and are used in variable concentrations in the literature. In many cases, these concentrations are not reported. Platelet activation has also been used by some as a way to maximize the benefits of the injection, but whether this is helpful and which activators should be used is a point of contention. Additionally, many studies do not adequately report details about the pathology being studied, including information about the chronicity, severity, and precise location of the injury. Adding to the variability in practice, the volume of injectate used for therapy has varied from study to study and likely also varies from physician to physician during treatment, although how much this influences outcome is unclear. In spite of these problems, increasing excitement about the potential therapeutic benefits of PRP has pushed its application into a wide variety of musculoskeletal pathologies. Public interest has also grown rapidly, spurred by increased media coverage that tends to portray the treatment as a routine and effective part of care for athletes [46]. While positive evidence is mounting for PRP in a variety of applications, findings are still contradictory at times and high-quality evidence is lacking. A large Cochrane review done in 2013, for example, found no evidence for efficacy among the highest quality trials available at that time with the exception of a small effect on short-term pain for treatment of soft tissue injuries [47]. One area of intense research is the application of PRP to tendon and ligament pathology. A systematic review and meta-analysis performed by Chen et al. [48] examined 11 RCTs comparing PRP to a variety of different interventions for ligaments and tendon pathology. They found largely superior results to other modalities in the short- (6.5 months) months. PRP use for injury of the patellar tendon, Achilles tendon, rotator cuff tendons, ulnar collateral ligaments, and plantar fasciitis has been trialed, but the studies are uncontrolled or small with much of the positive data coming from case studies or case series [44, 48–50]. Evidence is also emerging for PRP use as a therapeutic agent in cases of osteoarthritis (OA). PRP injection has provided symptomatic and functional improvement for those with knee OA, both alone and in comparison to steroid and hyaluronic acid [51–54]. It’s important to note that almost all studies involved multiple PRP injections, often a series of three injections [51]. Research on hip and ankle OA has also been performed, but is currently limited [49]. Interest also exists about the possible regenerative effect of PRP on articular cartilage, but data demonstrating consistent, in vivo evidence of cartilage regeneration is lacking [55].

Mesenchymal Stem Cells Mesenchymal stem cells (MSCs) are a heterogenous class of stromal cells with regenerative properties found in a variety of adult tissues. They are united by their ability to differentiate into multiple lineages (bone, muscle, cartilage, and fat), their

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ability to modulate the immune system through paracrine effects, their cell surface receptors, and their rapid colony formation in vitro [56]. They are relatively easy to harvest from bone marrow, synovium, periosteum, adipose, blood, and umbilical cord tissues and give rise to a variety of cells in the musculoskeletal system [56]. As with the prior therapies discussed, the mechanism of action for MSCs is unknown. Initially, it was hoped that placing these cells in damaged areas would foster direct tissue regeneration [56]. However, subsequent research has shown this not to be the case. Instead, MSCs may act through immunomodulation, suppression of inflammation, and paracrine modulation [56]. Methods for MSC derivation and delivery are variable. Commercial systems and labs often use unique methods of extraction from donor tissue, many of which are proprietary. MSCs have been put to use with varying degrees of success and these differences in preparation may be partly responsible for the variable results. OA has been a prime target, but even the best studies on the topic are small, uncontrolled, and highly varied in their means of MSC preparation and delivery [57, 58]. Promising results have been found in knee osteoarthritis with improved function, decreased pain, and possible regeneration of articular tissues as measured through MRI evaluation of thickness and arthroscopic examination [58]. MSCs have also been applied to meniscus, tendon, ligament, muscle, nonunion fractures, and femoral head necrosis, but this data is too limited for recommendations to be made about their use [59, 60].

Conclusion All of these therapies are still considered experimental, and the FDA has yet to approve any injectable versions of these medications for intra-articular, tendinous, or ligamentous applications. As noted for all applications, the data is mixed, with some good evidence for certain diagnoses and limited evidence for others. Further research will help expand our understanding of how these therapeutics work and which diagnoses may respond the best to their use.

Technological Applications for the Athlete Introduction In this section of the chapter, we will discuss innovation in athletic training and performance. Specifically, we will discuss technological advancement in motion capture and wearable devices. As sports medicine clinicians, it is important to understand how technology can best serve athlete patients regarding injury prevention and optimizing their performance.

Motion Capture Human motion capture has become recognizable as a mainstream application for both the entertainment and video game industries. However, there has been steady

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innovation in its use for biomechanical analysis in athletes with improvements in both two-dimensional (2D) video capture and three-dimensional (3D) motion capture technology. Motion capture should be viewed distinct from motion analysis. Motion capture is the process of acquiring a representative and accurate sequence of motion, whereas motion analysis takes data from that sequence for the purpose of quantifying various aspects of a specific movement. For the purpose of discussing the current evidence using motion capture in sports, it is helpful to become familiar with three general principles: structure, tracking, and recognition [61]. Structure can be represented utilizing simple stick figures or model-based volumetric representations of body parts such as an elliptical cylinder or surface-based sensor projecting the subject shape. Model-based systems will show a representation of the human body in either 2D or 3D. Tracking involves a single-camera or multi-camera setup with markers or computer-defined features that can be demonstrated in a sequence of images. Included in both the principles of structure and tracking is the ability to mark specific parts of the body. Joints can be marked with physical moving light displays (MLDs) or reflective markers that establish joint position and angles [61, 62]. Recognition is the process of using computer vision and algorithms to generate the full motion sequence from the tracking of the structure and markers. Specific programs can be used to match body templates, 2D meshes, or state-space approaches [61]. The interplay of the chosen body structure, tracking system, and recognition design can take place in a variety of motion capture systems available in the academic and private sector. Human motion capture systems can take several forms depending on how data is acquired based on one or more of the previously described principles. Four basic forms include the following: electromagnetic, image processing systems, optic motion capture, and inertial measurement units (IMUs) [62]. Electromagnetic systems involve using transponders attached to subjects that transmit electromagnetic waves, such as radio waves, back to a base recording unit to mark the time and distance away from the base unit. It has been found to be most useful for outdoor and indoor team sports because it does not require a predefined area for capture; however, the further away from the local receiver the subject gets, the more disruption occurs in the data acquisition process [62]. This system emphasizes the principle of tracking and is often coupled with a global positioning satellite (GPS) to overcome this limitation. An interesting application of this type of system has been seen in performance analysis in surfing [63]. Image processing systems utilize computer vision-based systems and algorithms to allow for both marker-based and marker-less tracking. Marker-based approaches have been found to be more accurate, while marker-less approaches are more convenient. This system demonstrates the principle of image recognition. For example, the Microsoft Kinect™ is a gaming system that uses a high-quality camera with infrared to create a 3D motion capture. Due to the relative public availability and affordability, there have been studies that have sought to validate the Kinect™ as a viable motion capture system for sport-specific movements [64, 65]. A notable attempt to validate a marker-less system for the extreme outdoor sport of motocross was conducted for start gate mechanics utilizing GoPro™ cameras and demonstrated high intra-tester reliability [66]. Optic motion capture systems are often regarded as the gold standard in motion capture. It often involves a fixed array of cameras at predefined distances and angles

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to capture motion in a restricted area often organized in a grid. This allows for a high level of control and accuracy. Optic motion capture systems are usually used indoors and are best for capturing the movements of individual subjects rather than large groups [62]. Maximizing the number of cameras will allow for more data points. However, this can be costly as each camera is usually highly specialized. This system also uses markers in either an active or passive manner where active markers have a source of light for the sensors, i.e., MLDs, and passive markers simply reflect light back, i.e., reflective markers. Many of the industry-leading and commercially available motion capture systems are optic based. International examples include Qualisys in Sweden, Vicon in the United Kingdom, Xsens in the Netherlands, and Phoenix Technologies in Canada. Domestic examples in the United States include Motion Analysis, OptiTrack, myoMotion, and DARI Motion. At the time of publication, the most versatile motion capture device is the inertial measurement unit (IMU). IMU is defined as a device that has the combined input of an accelerometer, gyroscope, and magnetometer. Specifically, the accelerometer gives acceleration relative to gravity, the gyroscope provides rotational velocity with orientation, and the magnetometer defines magnetic north. Think of IMUs as highly mobile forms of motion capture measurement. They are also more capable of detecting rapid movements compared to the other systems [62]. IMUs are useful because of the large amount of data that is collected simultaneously from a small, noninvasive device. IMUs have been shown to provide the best real-time measurements when combined with optic capture systems to analyze the motion of multiple segments [67]. These principles are central to motion capture in sport and can be used to understand the kinematics (such as velocity, time, and displacement) and the kinetics (such as force and acceleration) of a specific athletic movement. Kinematic and kinetic motion analyses are important when addressing neuromuscular control, which is the relationship between proprioception and muscular control. Motion analysis may serve as an important tool for sports clinicians in the setting of neuromuscular training during the recovery and functional stages of rehabilitation. For instance, when applied to the contact sport of rugby, marker-­based motion analysis systems demonstrated significant kinematic differences in tackling styles in rugby athletes that impacted both tackling performance and risk of injury such as shoulder dislocation [68, 69]. In soccer, marker-based optic systems have been applied to adolescent athletes with low back pain and demonstrated altered kicking dynamics that could impact lumbar spine stress during kicking rotation [70]. With regard to optimizing performance, IMUs have been used for speed skating by capturing the angle of the skate on straightaway sprints, allowing skaters to have reliable feedback on technique [71]. In the sport of taekwondo, a study was performed using Vicon as a motion capture system and provided biomechanical feedback on ways to raise the impact velocity of a jumping front-leg axe-kick [72]. Kinematic information can be readily available in a sequence of motion capture, but lacks force information needed to understand kinetic information. In order to acquire kinetic information, many systems use force platforms or plates to measure ground reaction force (GRF) and force moments. Force platforms are often combined with other systems to generate kinetic data in the appropriate context.

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Understanding the biomechanics of the jump shot in basketball is an example of how optic motion capture and force plates can be used, especially when trying to quantify the impact of the force of landing [73]. Force platforms can present a limitation since they confine motion analysis to an indoor setting. A recent study was able to demonstrate the feasibility to accurately predict ground reaction forces and moments based on motion capture alone, without relying on force platforms [74]. While the newest applications emphasize 3D motion capture and analysis, 2D video analysis remains a relatively lower cost and greater accessibility due to the ability to use standard digital video cameras and recording on mobile and tablet devices. In studies of young baseball players, 2D video analysis was seen as technology that would be more available to both players and coaches for the purpose of understanding pitching biomechanics [75, 76]. Commercial indoor 3D motion capture systems are very costly and pricing can depend on the space used, number of cameras, and technical and data collection fees”. This can add up to thousands of dollars per day depending on one’s needs. In addition to commercial or private settings, 3D motion capture technology is seen in laboratories at universities where access is often limited to research or evaluation of elite athletes. This highlights the need for something more accessible to athletes in both professional and recreational sports, as well as the general, physically active population in recent years, wearable devices have emerged as a possible solution to this growing need.

Wearable Devices As technology continues to advance in the area of motion capture and analysis, wearable devices to track performance in sports are also experiencing advancements. As a market, wearable devices are estimated to be valued at 27 billion dollars by 2022 [77]. Popular brands include Fitbit, Apple, Garmin, Samsung, and Polar with many smart watch companies now including this technology. The reduced size and improved comfort of these devices combined with the multidimensional data capture of sensors provides athletes with real-­time data capture and performance monitoring. Although many of these wearable devices are also used by non-performance-driven individuals, it is important not to underestimate the significance of these devices in capturing and providing data in evaluating athletic performance and improvement measurements. Wearable performance devices make use of sensors to capture inertial measurements such as acceleration, orientation in time/space, and direction [78]. These sensors capture movements and physiologic measurements, which allows the individual to balance performance improvements with effort expended. Considering many of these devices now are waterproof, the devices have been incoporated into the training programs of athletes participating in indoor, outdoor, and even water sports such as swimming and crew. The most common example of a movement sensor requiring limited technology for data capture is a pedometer, which records a “step” defined as a measured

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instance of vertical acceleration. Although a starting point for measuring improvements in physical activity in the general population, pedometers have very limited use for elite athletes because of their inability to measure energy expenditure and changes in direction. On the other hand, accelerometers and gyroscopes have provided a means for athletes to measure variances in movement and physiological measurement following altered exercise programs. Remember that IMUs are a small form of motion capture technology that track acceleration, rotational velocity, and orientation, so they are often employed in wearable devices given their compact size. With the advancement of microelectromechanical systems (MEMS), sensors on accelerometers and gyroscopes can capture movement in multiple dimensions [78]. Moreover, accelerometers can track energy expenditure which is an important physiological measurement in assessing the intensity of a training program. Wearable GPS provides an alternative to accelerometers and gyroscopes in measuring speed and positional data of athletes [78]. Physiologic sensors integrated into wearable devices capture heart rate and temperature. Heart rate fluctuations during athletic performance provide key data to quantify exercise intensity and energy expenditure. For this reason, heart rate monitors have become a method for measuring physiologic response and metabolic demand during competition in sports like basketball, rugby, and soccer [79]. Temperature monitors in arm bands measure heat flux through the skin but generally have poor correlation to core body temperature, especially during high-intensity exercise. A method was subsequently developed in which a capsule is ingested and data is transmitted to an external log [80]. Lastly, integrated sensor systems combine the components listed above to simultaneous collection of movement and physiologic data. Because of the wide variety of available wearable devices on the market, research studies are usually limited to testing one or a few different devices in a given study. Most of the research focuses on the use of wearable devices on elite and sub-elite athletes [79]. Research in wearable devices has been growing for many years, especially regarding validity in specific performance situations such as high-speed running [81]. Combining different physiologic parameters into one system is also of research interest given the growing demand for consolidating more sensors into one integrated device. An example of this is in the design of wireless systems that combine heart rate and the agility index through specific filter-based algorithms [82]. While the arm and wrist are the most commonly used body regions for placement of wearable devices, accelerometers can be placed in other locations such as on the trunk, shoulder, elbow, hip, knee, and ankle. Football players wore a trunkmounted accelerometer to assess validity and reliability of the system in different players. The results were highly dependent on the players’ locomotion mechanics and velocity [83]. An additional example can be found in elite runners where sensors placed on the feet allow for real-time feedback on foot biomechanics allowing the athlete, coach, and physician to make real-time decisions on performance [84]. Monitoring of movement and physiologic parameters has become an important part of assessing fatigue and recovery in athletes. Emphasis on training load through physiologic measurements can be applied on an individualized level, which is valuable for both players and coaches [85].

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Conclusion By integrating the principles of sports ultrasound, regenerative medicine, motion analysis software, and wearable devices, the field of sports medicine is changing in a dynamic and impactful way for active individuals and athletes of all skill levels. To assist our patients as athletes, we need to understand them as individuals with both a desire to perform at the highest level and to explore newer interventions and technologies that aid them in that endeavor. Applying the latest research and technology will better position us to support our patients, prevent injuries, and help them achieve their goals.

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do?product=WOS&search_mode=GeneralSearch&qid=1&SID=5ABj7MiFTlmpvkQiDSE& page=1&doc=1. 35. McAlindon TE, LaValley MP, Harvey WF, Price LL, Driban JB, Zhang M, et  al. Effect of intra-articular triamcinolone vs saline on knee cartilage volume and pain in patients with knee osteoarthritis: a randomized clinical trial. JAMA. 2017;317(19):1967–75. 36. Martin SD, Conaway WK, Lei P. Use of intra-articular corticosteroids in orthopaedics. J Bone Joint Surg Am. 2018;100(10):885–91. 37. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials. Lancet. 2010;376(9754):1751–67. 38. Dean BJF, Lostis E, Oakley T, Rombach I, Morrey ME, Carr AJ. The risks and benefits of glucocorticoid treatment for tendinopathy: a systematic review of the effects of local glucocorticoid on tendon. Semin Arthritis Rheum. 2014;43(4):570–6. 39. Malanga G, Abdelshahed D, Jayaram P. Orthobiologic interventions using ultrasound guidance. Phys Med Rehabil Clin N Am. 2016;27(3):717–31. 40. Distel LM, Best TM. Prolotherapy: a clinical review of its role in treating chronic musculoskeletal pain. PM R. 2011;3(6 Suppl 1):S78–81. 41. Reeves KD, Sit RWS, Rabago DP.  Dextrose prolotherapy: a narrative review of basic science, clinical research, and best treatment recommendations. Phys Med Rehabil Clin N Am. 2016;27(4):783–823. 42. Reeves KD, Hassanein KM. Long-term effects of dextrose prolotherapy for anterior cruciate ligament laxity. Altern Ther Health Med. 2003;9(3):58–62. 43. Jensen KT, Rabago DP, Best TM, Patterson JJ, Vanderby R Jr. Response of knee ligaments to prolotherapy in a rat injury model. Am J Sports Med. 2008;36(7):1347–57. 44. Kia C, Baldino J, Bell R, Ramji A, Uyeki C, Mazzocca A.  Platelet-rich plasma: review of current literature on its use for tendon and ligament pathology. Curr Rev Musculoskelet Med. 2018;11(4):566–72. 45. Mautner K, Malanga GA, Smith J, Shiple B, Ibrahim V, Sampson S, et al. A call for a standard classification system for future biologic research: the rationale for new PRP nomenclature. PM R. 2015;7(4 Suppl):S53–9. 46. Rachul C, Rasko JEJ, Caulfield T. Implicit hype? Representations of platelet rich plasma in the news media. PLoS One. 2017;12(8):e0182496. 47. Moraes VY, Lenza M, Tamaoki MJ, Faloppa F, Belloti JC. Platelet-rich therapies for musculoskeletal soft tissue injuries. Cochrane Database Syst Rev. 2013;(12):CD010071. 48. Chen X, Jones IA, Park C, Vangsness CT Jr. The efficacy of platelet-rich plasma on tendon and ligament healing: a systematic review and meta-analysis with bias assessment. Am J Sports Med. 2018;46(8):2020–32. 49. Le ADK, Enweze L, DeBaun MR, Dragoo JL.  Platelet-rich plasma. Clin Sports Med. 2019;38(1):17–44. 50. Wu PI-K, Diaz R, Borg-Stein J.  Platelet-rich plasma. Phys Med Rehabil Clin N Am. 2016;27(4):825–53. 51. Lai LP, Stitik TP, Foye PM, Georgy JS, Patibanda V, Chen B. Use of platelet-rich plasma in intra-articular knee injections for osteoarthritis: a systematic review. PM R. 2015;7(6):637–48. 52. Meheux CJ, McCulloch PC, Lintner DM, Varner KE, Harris JD.  Efficacy of intra-articular platelet-rich plasma injections in knee osteoarthritis: a systematic review. Arthroscopy. 2016;32(3):495–505. 53. Piuzzi NS, Chughtai M, Khlopas A, Harwin SF, Miniaci A, Mont MA, et  al. Platelet-rich plasma for the treatment of knee osteoarthritis: a review. J Knee Surg. 2017;30(7):627–33. 54. Di Y, Han C, Zhao L, Ren Y. Is local platelet-rich plasma injection clinically superior to hyaluronic acid for treatment of knee osteoarthritis? A systematic review of randomized controlled trials. Arthritis Res Ther. 2018;20(1):128. 55. Fice MP, Miller JC, Christian R, Hannon CP, Smyth N, Murawski CD, et  al. The role of platelet-rich plasma in cartilage pathology: an updated systematic review of the basic science evidence. Arthroscopy. 2019;35(3):961–76.e3.

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78. Li RT, Kling SR, Salata MJ, Cupp SA, Sheehan J, Voos JE. Wearable performance devices in sports medicine. Sports Health. 2016;8(1):74–8. 79. Camomilla V, Bergamini E, Fantozzi S, Vannozzi G.  Trends supporting the in-field use of wearable inertial sensors for sport performance evaluation: a systematic review. Sensors [Internet]. 2018;18(3). https://doi.org/10.3390/s18030873. 80. Domitrovich JW, Cuddy JS, Ruby BC. Core-temperature sensor ingestion timing and measurement variability. J Athl Train. 2010;45(6):594–600. 81. Alexander JP, Hopkinson TL, Wundersitz DWT, Serpell BG, Mara JK, Ball NB. Validity of a wearable accelerometer device to measure average acceleration values during high-speed running. J Strength Cond Res. 2016;30(11):3007–13. 82. Li M, Kim YT. Design of a wireless sensor system with the algorithms of heart rate and agility index for athlete evaluation. Sensors [Internet]. 2017;17(10). https://doi.org/10.3390/ s17102373. 83. Barreira P, Robinson MA, Drust B, Nedergaard N, Raja Azidin RMF, Vanrenterghem J. Mechanical Player Load™ using trunk-mounted accelerometry in football: is it a reliable, task- and player-specific observation? J Sports Sci. 2017;35(17):1674–81. 84. Muniz-Pardos B, Sutehall S, Gellaerts J, Falbriard M, Mariani B, Bosch A, et al. Integration of wearable sensors into the evaluation of running economy and foot mechanics in elite runners. Curr Sports Med Rep. 2018;17(12):480–8. 85. Halson SL.  Monitoring training load to understand fatigue in athletes. Sports Med. 2014;44(Suppl 2):S139–47.

3

Exercise Prescription Walter Alomar-Jiménez, Adam Fry, and Gerardo Miranda-Comas

Introduction In the USA, an estimated $117 billion in annual healthcare costs and about 10% of premature mortality are associated with inadequate physical activity [1]. Despite the widely accepted health benefits of physical activity and exercise, only 26% of men, 19% of women, and 20% of adolescents report performing sufficient activity in the USA [1]. Accordingly, physical inactivity is considered the biggest public health problem of this century leading to an increase prevalence of lifestyle diseases including heart disease and diabetes [2]. The promotion of physical activity for patient health and well-being should therefore be a priority for clinicians throughout the healthcare system. This chapter will focus on the concept of exercise as medicine and its role in health promotion, rather than athletic performance, addressing the bigger public health issue.

W. Alomar-Jiménez (*) Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA A. Fry · G. Miranda-Comas Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_3

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Physical Activity and Exercise Physical activity is defined as any body movement that requires energy expenditure [1, 3, 4]. This can be divided in different domains: occupational, transportation, household, and leisure-time [3]. Exercise is a type of leisure-time physical activity. It is planned, repetitive, and structured, and its purpose is to improve or maintain physical fitness [1, 3, 4]. The scientific evidence showing the numerous benefits of physical activity and exercise is abundant. The cardiovascular health benefits of physical activity have been extensively studied since Morris and Crawford in 1958 [5] identified a lower incidence of coronary heart disease in London double-decker bus ticket collectors compared to the bus drivers who were less physically active in their occupation. A physically active lifestyle has been associated with better quality of life and multiple health-related benefits in the pediatric and adult population (see Table 3.1). Given the extensive benefits of physical activity to all manner of physical and psychological conditions, the informed promotion of physical activity should be considered the responsibility of clinicians of all specialties. The goal with an Table 3.1  Physical activity-related health benefits [1, 3, 4] Pediatric (school-age children and adolescents)   ↑ bone health (ages 3–17 years)   ↑ weight control (ages 3–17 years)   ↑ cardiorespiratory fitness (ages 6–17 years)   ↑ cardiometabolic health (ages 6–17 years)   ↑ cognitive function (ages 6–13 years)   ↓ risk of depression (ages 6–13 years) Adults   ↓ risk of all-cause mortality   ↓ risk of cardiovascular disease mortality   ↓ cardiovascular disease (including heart disease and stroke)   ↓ risk of hypertension   ↓ risk of type 2 diabetes   ↓ risk of hyperlipidemia   ↓ risk of cancers of the bladder, breast, colon, endometrium, esophagus, kidney, lung, and stomach   ↑ cognitive function   ↓ risk of dementia (including Alzheimer disease)   ↓ anxiety   ↑ quality of life   ↓ risk of depression   ↑ sleep   ↓ weight gain   ↑ weight loss, particularly when combined with reduced calorie intake   ↑ bone health   ↑ physical function   ↓ risk of falls (older adults)

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exercise prescription is an increase in physical activity and a reduction in sedentary periods such as watching television and computer use because they can be detrimental for health [6].

Physical Activity Recommendations General physical activity recommendations have been proposed by several agencies, including the American College of Sports Medicine (ACSM) and the US Department of Health and Human Services [1, 3, 4]. They recommend adults do at least 150–300 min per week of moderate-intensity, or 75–150 min per week of vigorous-intensity, aerobic physical activity, or an equivalent combination of both. The guidelines also state that some physical activity is better than none, and additional health benefits can be obtained by engaging in more than 300 min of aerobic physical activity. In addition to aerobic activity, adults should engage in muscle strengthening and flexibility activities involving all major muscle groups on 2 or more days per week. The new physical activity guidelines include high-intensity interval training (HIIT) as an exercise modality that may include aerobic (cardio) exercises, resistance training (power training), or a combination of both as a possible replacement to the traditional moderate-intensity continuous training (MICT) regimen. HIIT programs have become popular due to their comparable health benefits to MICT, fitness improvement, and decrease training time [3]. The exercise prescription is analogous to any other medical prescription in terms of format. It requires frequency, intensity, time, type, total volume, pattern, and progression (FITT-VPP) [1, 3, 4]. The exercise program should target different areas such as aerobic exercise, muscular strength, flexibility, and neuromotor exercise. Before beginning an exercise program, especially vigorous-intensity exercise, one should consider exercise testing to assess cardiorespiratory fitness in a subset of individuals. Testing should be performed in high-risk occupations like pilots, firefighters, law enforcement officers, and mass transit operators; men over 40 years of age (y) and women over 50 years who have a sedentary lifestyle and plan to start a vigorous-intensity exercise regimen; and individuals with new or changing symptoms of cardiovascular disease (CVD); two or more risk factors for CVD [age ≥45 years in men and ≥55 years in women, family history of CAD or death age 10-year history of DM-2 or >15-year history of DM-1, HLD, smoking, peripheral artery disease (PAD), autonomic neuropathy]; end-stage renal disease; and pulmonary diseases like cystic fibrosis, asthma, interstitial lung disease, and COPD [7]. Nevertheless, start of a moderate-intensity exercise program should not be delayed by pending exercise testing [7]. During the exercise training session, the heart rate (HR) and/or the rate of perceived exertion (RPE) is commonly used to measure intensity (see Table 3.2) [4].

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Table 3.2  Training intensity reference for aerobic and resistance exercise [4] Training intensity Very light Light Moderate Vigorous Near max to max

Aerobic exercise intensity %HRmax RPE (scale 6–20) 25% osseous defect of the glenoid or humeral head [14].

Return to Play An athlete can return to play when there is relatively symmetric pain free shoulder range of motion, symmetric strength, including sport specific functional strength, and no anterior apprehension on physical exam. For an in-season athlete, this

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Fig. 10.11 Stimson technique for anterior GHJ dislocation

usually takes 1–3 weeks [10, 14]. Motion limiting braces that restrict abduction and external rotation can be considered during sport for non-overhead athletes. Braces improve the subjective sense of shoulder stability, but have not been shown to reduce recurrent dislocation [10]. Risk of recurrent GHJ dislocations is extremely high for athletes less than 20 years old and those in contact sports [10]. Return to play in the postoperative shoulder is guided by the surgeon but generally involves 6 weeks of shoulder immobilization with 6–9 months of rehabilitation thereafter.

Clavicle Fracture Mechanism of Injury/Pathophysiology Clavicle fractures occur in contact sports from direct shoulder trauma more commonly than falls on an outstretched arm. Fractures are broadly categorized by location. Middle 1/3 clavicle shaft fractures are the most common fracture site. Distal 1/3 clavicle fractures occur less commonly. Medial 1/3 fractures are rare [15]. Further sub classification systems based on fracture characteristics exist. Clinical Presentation Clavicle fractures present as a deformity of the anterior shoulder with tenderness over the fracture site. Tenting of the skin from fracture displacement can occur with middle and medial 1/3 fractures. Midclavicular shaft fractures typically cause inferior displacement of the lateral fragment with superior displacement of the medial fragment due to pull of the sternocleidomastoid [15]. High velocity injuries may have associated injuries, such as brachial plexopathy, pneumothorax, or rib fractures. Diagnosis Clavicle radiographs with AP clavicle, Zanca, and axillary should be obtained to confirm clinical suspicion and evaluate fracture characteristics. Advanced imaging

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with CT provides detail about clavicle shortening and articular fracture extension when surgery is being considered.

Treatment Nondisplaced midclavicular shaft fractures are treated with sling immobilization for 2–4  weeks until there is bony healing on radiographs and clinical healing with improved pain [16, 17]. Thereafter, range of motion and use of arm for daily activities can begin, with progression at 6  weeks to a shoulder strengthening program [16]. Figure-of-eight bandages have fallen out of favor due to potential complications, like upper limb thrombosis [15]. Displaced midshaft clavicle fractures are now treated commonly with surgical fixation to reduce risk of nonunion, particularly in adults where surgery has been shown to significantly reduce the nonunion rate, shorten time to union, and correlate to better functional outcomes [18]. Management of displaced midshaft clavicle fractures in children and adolescents is controversial, as this population has a very low rate of nonunion and surgery has not been clearly shown to have better functional outcomes; however, surgery can be considered particularly if faster return to play is desired [16, 17]. Absolute indications for surgical management include open fractures and displaced fractures with neurovascular compromise. Postoperative management is guided by the surgeon but typically involves some period of shoulder immobilization. Return to Play In the nonoperative setting, return to play is typically 10 weeks or more post injury [17]. Postoperative return to play is guided by the surgeon, but may be as soon as 6 weeks postoperatively [17].

Overuse Injuries Rotator Cuff Tendinopathy Mechanism of Injury/Pathophysiology Rotator cuff (RC) tendinopathy is remarkably common, particularly in the adult athlete population. The term tendinopathy is preferred over tendonitis, as inflammatory processes are rarely a prominent feature of chronic tendinopathy. Tendinopathy refers to chronic degenerative tendon changes, usually related to overuse, poor biomechanics and/or aging. The histopathological changes of tendinopathy include increased mucoid ground substance, neovascularization, and disorganized cellular proliferation [19]. Partial thickness tendon tears can occur with rotator cuff tendinopathy. While the underlying cause of RC tendinopathy is chronic overuse and microtrauma, the terms internal impingement and external impingement may be used to describe specific patterns of pathology. Internal impingement refers to repetitive stress to the posterior-superior RC from compression between the greater tuberosity

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and posterior glenoid in a shoulder abducted externally rotated position [3]. This is a multifocal issue with elements of scapular dyskinesis, posterior capsular tightening, and physiologic shoulder remodeling usually contributing to the RC tendinopathy [3]. Throwing athletes, particularly baseball pitchers, are at risk for internal impingement. External impingement refers to impingement of the RC, typically the supraspinatus tendon, in the subacromial space. This is often due to dynamic abnormalities from scapular dyskinesis, scapular malposition, and RC weakness. Static abnormalities, such as hooked acromion morphology or osteophyte formation, may predispose to external impingement [20]. Bursal-sided tendon pathology may occur in external impingement since the superficial aspect of the tendon is being impinged.

Clinical Presentation RC tendinopathy related to internal impingement typically presents as posteriorly located shoulder pain in abducted externally rotated shoulder positions. Throwing athletes may describe shoulder stiffness and deterioration in throwing performance [3]. Associated pathologies seen with internal impingement include labral tears, ossification of posterior glenoid rim, and anterior GHJ instability [3]. On exam, there may be posterior GHJ tenderness, decreased total arc of motion on the affected side with loss of internal rotation due to posterior capsule tightness, scapular dyskinesis, and positive posterior impingement sign [3]. The posterior impingement sign is posterior shoulder pain reproduced with placement of the shoulder in 90° abduction, slight extension, and maximal external rotation (positioning is similar to Fig. 10.7). RC tendinopathy related to external impingement presents as insidious onset anterolateral shoulder pain that may radiate down the lateral shoulder, pain worse with overhead activities (due to this position further narrowing the subacromial space), and pain with side lying at night. On exam, there may be tenderness to palpation about the subacromial space, a painful arc of active shoulder abduction from 60° to 120°, and pain with impingement maneuvers that attempt to compress the RC within the subacromial space. Neer impingement test is performed by the examiner stabilizing the patient’s scapula posteriorly and passively flexing the shoulder in an internally rotated arm position (Fig.  10.12) [8]. Hawkins impingement test is Fig. 10.12 Neer impingement test

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Fig. 10.13 Hawkins impingement test

performed by the examiner applying a passive internal rotation force to the patient’s supported arm in a position of 90° shoulder flexion and 90° elbow flexion (Fig. 10.13) [8]. Strength testing of the rotator cuff is important to rule out a significant RC tear. Supraspinatus strength testing with the full can test is performed by applying downward resistance to the patient’s extended arms in 90° shoulder flexion, 30° horizontal abduction (arm in the scapular plane), and neutral rotation with thumbs pointing upward (Fig. 10.14). Subscapularis strength can be tested with the belly press or bear hug tests. Belly press test is performed with the patient pressing the palm against the abdomen, while maintaining the elbows in a forward position; weakness presents as asymmetry in elbow positioning with the weak side having a more posteriorly directed elbow (Fig. 10.15). Bear hug test evaluates strength by the patient resisting an anterior directed force to the patient’s palm with the palm placed against the contralateral anterior shoulder (Fig. 10.16). Hornblower’s test evaluates infraspinatus and teres minor strength and is performed by applying a shoulder internal rotation force to the patient’s forearm in a position of 90° shoulder flexion with the elbow flexed (Fig. 10.17).

Diagnosis RC tendinopathy diagnosis can be made with history and physical alone. Shoulder radiographs (minimum AP-internal rotation, AP-external rotation, and axillary) can be helpful as an initial imaging evaluation. Shoulder radiographs may show secondary signs of chronic RC stress, such as sclerosis or subchondral cysts about the greater tuberosity, calcifications within the distal tendons, or a narrowed acromiohumeral interval with humeral subluxation in chronic high grade supraspinatus tears. Shoulder MRI (with or without intra-articular gadolinium) and US are the best advanced imaging modalities to directly visualize and assess RC tendon pathology. MRI allows evaluation of intra-articular structures to identify co-existing pathology of the labrum or GHJ and may be preferred in the preoperative setting, but is more expensive than US. US allows for dynamic evaluation and the potential

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Fig. 10.14 Full-can supraspinatus strength testing

Fig. 10.15  Belly press subscapularis strength testing

for guided therapeutic injections at the same time as tendon evaluation; however, it is operator dependent and the intra-articular evaluation is incomplete.

Treatment Management is primarily nonoperative, with relative rest from pain provoking activities and a progressive rehabilitation program. Key rehab elements include strengthening of the scapular stabilizers and RC musculature, stretching of the anterior shoulder and chest, improving thoracic spine extension, and postural optimization. If pain limits therapy tolerance or impacts the athletes daily function, pain control with icing, NSAID trial, or steroid injections can be considered. Subacromial-­subdeltoid bursal steroid injections are generally the best initial injectate target, but intra-articular GHJ injections can be considered for articular-sided tendon pathology. Ultrasound guidance for injections increases accuracy. In the setting of calcific RC tendinopathy, ultrasound guided lavage and aspiration with a subsequent rehabilitation program can be considered.

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Fig. 10.16  Bear hug subscapularis strength testing

Fig. 10.17 Hornblower infraspinatus strength testing

In the setting of internal impingement, the athlete should undergo several weeks relative rest from overhead throwing activities, stretching of the posterior shoulder capsule, and strengthening of the shoulder girdle with focus on improving scapular dyskinesis [3]. When the athlete is pain free, evaluation and optimization of overhead throwing mechanics can be performed. If a standard nonoperative approach fails after several months, alternative ultrasound guided tendon procedures, such as prolotherapy or platelet-rich plasma injections with or without needle fenestration/tenotomy, can be considered [21]. Surgery should be considered for acute massive RC tears or failed nonoperative management of chronic RC tendinopathy with associated tears involving 50% more of the tendon [3].

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Bicipital Tendinopathy Mechanism of Injury/Pathophysiology Long head of the biceps tendon (LHBT) tendinopathy refers to chronic degenerative tendon changes that occur from overuse and recurrent impingement at the anterior-­ superior GHJ in certain positions. The winding course of the proximal LHBT as it traverses the intertubercular groove and turns to attach to the superior labrum predisposes it to microtrauma injury with repetitive activities. Overhead athletes are particularly at risk for LHBT pathology. Partial LHBT tendon tears and tenosynovitis may occur in conjunction with LHBT tendinopathy. Clinical Presentation Athletes present with anterior to anterolateral shoulder pain that may radiate down the anterior arm and is worse with overhead activities, such as throwing and lifting. Exam may reveal tenderness to palpation around the intertubercular groove at the proximal anterior shoulder and pain reproduction with special tests like Speed and Yergason tests. Speed test is performed by the patient resisting a downward force applied to their arm in a position of 90° shoulder flexion, elbow extension, and forearm supination (Fig. 10.18) [8]. Yergason test is performed with the patient at 90° elbow flexion with the arm adducted at the side, while externally rotating the shoulder and supinating against examiner resistance at the wrist (Fig.  10.19) [8]. This may provoke pain at the bicipital groove or the examiner may palpate tendon subluxation. Associated pathology seen with LHBT tendinopathy include LHBT instability, superior labral anterior-posterior (SLAP) tears, RC tendinopathy and RC tears [22, 23]. Fig. 10.18  Speed test for LHBT

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Fig. 10.19  Yergason Test for LHBT

Diagnosis Shoulder radiographs can be obtained to rule out bony pathology. Shoulder MRI or US are the best advanced imaging modalities to directly visualize the LHBT. MRI will be able to evaluate the entire intra-articular extent of the LHBT and identify the presence of concomitant labral or GHJ pathology. US cannot fully visualize the intra-­articular portion of the LHBT or concomitant intra-articular pathology, but does allow for dynamic evaluation to identify LHBT instability as well as an opportunity for guided LHBT injections, if desired. Treatment Management is usually nonoperative and involves relative rest from painful activities and a comprehensive rehabilitation program, focusing on correction of any underlying biomechanical causes for LHBT irritation. In general, a rehab program should include optimization of shoulder range of motion and improvement of scapular dyskinesis with a progressive strengthening of the scapular stabilizers and rotator cuff working towards sport specific strengthening activities. Limited use of NSAIDs (oral or topical) or corticosteroid injections can be considered. A biceps tendon sheath injection is frequently the initial injectate target. Intra-articular GHJ injections can be considered as the biceps sheath does communicate with the joint space, and this allows for management of potential co-existing intra-articular and extra-articular pathology. US guidance for injections is recommended to increase accuracy [23]. Other management options to supplement a rehabilitation program include topical nitroglycerin, iontophoresis, and extracorporeal shock wave therapy [23]. Additionally, alternative tendon procedures, such as ultrasound guided prolotherapy or platelet-rich plasma with or without needle fenestration/tenotomy can be considered [23].

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Surgery for isolated LHBT pathology is rare, but typically involves LHBT tenodesis. In acute LHBT rupture, tenodesis can be considered if there is noticeable loss of strength in high demand athletes or associated recurrent painful muscle spasm.

GHJ Instability Mechanism of Injury/Pathophysiology Shoulder instability is pathologic translation of the humeral head in the glenoid fossa, causing pain and functional impairment. In the athlete, shoulder instability can develop following an acute traumatic GHJ dislocation, from repetitive microtrauma or from atraumatic causes [24]. Instability in the post traumatic GHJ dislocation setting, in particular anterior instability following anterior GHJ dislocation, is the most common type of shoulder instability [25]. Instability is caused by damage to the static GHJ stabilizers (glenohumeral ligament, glenoid labrum, and/or bony containment) from the initial dislocation. Associated injuries that occur during a GHJ dislocation that may lead to recurrent anterior instability include Bankart lesions, damage to the inferior glenohumeral ligament, SLAP tears, humeral avulsion of the glenohumeral ligaments (HAGL), anterior labroligamentous periosteal sleeve avulsion (ALPSA) , and engaging Hill-Sachs lesion [24]. The mnemonic “TUBS” describes the patient with a traumatic shoulder injury on history, unilateral instability on exam, associated Bankart lesion on imaging, and surgical management generally being the best management. Instability from repetitive microtrauma can occur. In athletes, this is usually posterior instability from repetitive loading of the posterior shoulder with the arm flexed in front of the body. This occurs in football lineman, swimmers, and weightlifters [24, 26]. In contrast to unilateral instability, an athlete may present with atraumatic instability related to multidirectional instability (MDI). While MDI can develop pathologically following trauma or be seen in the setting of connective tissue disorders like Marfan syndrome or Ehlers-Danlos syndrome, MDI in athletes is usually related to underlying generalized capsular hyperlaxity in the setting of atraumatic repetitive overuse with sports. In high level athletes, where hyperlaxity confers a competitive advantage, such as swimming or gymnastics, advanced neuromuscular control usually co-exists to counter the hyperlaxity. However, when this neuromuscular control breaks down from acute or chronic deterioration of the dynamic stabilizers, this baseline hyperlaxity can become symptomatic MDI [24]. The mnemonic “AMBRI” describes the patient with an atraumatic shoulder pain history, multidirectional instability on exam, bilateral laxity on exam, rehabilitation being preferred management, and inferior capsular shift being a potential surgical management in recalcitrant cases. The TUBS-AMBRI classification is a very simplified view of shoulder instability. The FEDS classification of shoulder instability is a more descriptive system that incorporates frequency of instability episodes per year (solitary episode, occasional

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2–5 episodes, or frequent >5 episodes), etiology of instability (traumatic or atraumatic), direction (anterior, posterior, inferior), and severity (subluxation or dislocation) [24, 25].

Clinical Presentation The athlete with shoulder instability may have a history of GHJ dislocation and present with episodic pain or apprehension related to instability episodes during shoulder movement. In the patient with anterior instability, symptoms usually occur in end range abduction-external rotation, while in posterior instability, symptoms typically occur in end range adduction-internal rotation. On exam, special tests can help discern the direction of instability. Anterior apprehension test (Fig. 10.7), relocation test (Fig. 10.8), and anterior load and shift will be positive in the setting of anterior instability. Anterior load and shift test (Fig. 10.20) is performed with the patient sitting with the arm relaxed at the side, and the examiner grasps the humeral head to impart an anterior force while stabilizing the scapula. The anterior load and shift test is abnormal if there is increased humeral head translation compared to the contralateral side, or the examiner feels the humeral head begin to ride up to or over the glenoid rim. The posterior apprehension test and posterior load and shift test are used to detect posterior instability. The posterior apprehension test (Fig. 10.21) is performed with the patient supine in a position of 90° shoulder flexion, shoulder internal rotation, and elbow flexion, while the examiner applies a posteriorly directed force to the olecranon process [8]. During the maneuver, the examiner’s hand is positioned over the posterior GHJ. A positive test is reproduction of pain, sense of instability, or increased posterior translation of the humeral head as noted by the examiner’s hand. The posterior load and shift test (Fig. 10.22) is similar to the anterior version, but involves assessment for increased posterior humeral head translation when a posteriorly directed force is applied to the humeral head in a seated, arm-relaxed position. MDI may have increased translation with both anterior and posterior load and shift tests as well as Fig. 10.20  Anterior load and shift test for GHJ instability

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Fig. 10.21 Posterior apprehension test for GHJ instability

Fig. 10.22  Posterior load & shift test for GHJ instability

a sulcus sign. The sulcus sign is elicited with the patient seated in a shoulder relaxed neutral position, while the examiner grasps around the humeral supracondylar region to provide an inferiorly directed force (Fig. 10.23) [8]. Development of a gap or “sulcus” at the lateral acromiohumeral interval suggests inferior instability. The Beighton scale can diagnose hyperlaxity, with a score of 2 or more being associated with a higher risk of instability episodes [27].

Diagnosis Shoulder instability in an athlete is largely diagnosed by history and physical exam. Shoulder radiographs can be obtained to rule out bony pathology. Shoulder MRI with intra-articular gadolinium can evaluate the integrity of the glenohumeral ligaments, glenoid labrum, and associated glenohumeral changes that may lead to recurrent instability events. As mentioned above, common findings in anterior instability include Bankart lesions, Hill-Sachs lesions, damage to the inferior

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Fig. 10.23  Sulcus sign for GHJ instability

glenohumeral ligament, HAGL deformity, ALPSA deformity, and SLAP tears. In posterior instability, MRI may show reverse Bankart lesions (tear of the posteroinferior glenoid labrum), posterior glenoid bony defects, and reverse Hill-Sachs lesions (impaction fracture of anterior humeral head medial to the lesser tuberosity) [24]. CT may be obtained in the preoperative setting for more detailed bony morphology evaluation.

Treatment Athletes with recurrent shoulder instability related to previous history of trauma generally require surgical intervention for best long-term management of the instability [11]. Conservative management with a progressive rehabilitation program emphasizing shoulder girdle strengthening and normalization of scapular dyskinesis can be trialed, particularly for the in-season athlete. Motion limiting braces that restrict abduction and external rotation can be considered during sport for non-­ overhead athletes. Braces improve the subjective sense of shoulder stability but have not been shown to reduce recurrent dislocation [10]. MDI, particularly related to generalized ligamentous capsular laxity, is best managed with a comprehensive rehabilitation program emphasizing strengthening of the glenohumeral and scapular stabilizers. In the setting of recalcitrant symptomatic MDI that fails 6+ months of appropriate physical therapy, surgical consultation can be considered [27].

Glenoid Labrum Tears Mechanism of Injury/Pathophysiology The labrum is a fibrocartilaginous rim attached to the outer glenoid that serves to increase contact and stability of the GHJ and serves as the attachment for glenohumeral ligaments and the origin of the LHBT. Tears can occur anywhere along the

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labrum. SLAP tears are located near the LHBT origin and may occur in the setting of overuse injuries in the overhead athlete from increased shear forces and LHBT traction forces acting on the shoulder during throwing. Posterior labral tears may occur from repetitive microtrauma to the posterior GHJ-labral complex, and often seen in athletes such as football lineman. Labral tears can also result from traumatic falls or direct shoulder trauma.

Clinical Presentation Glenoid labral tears will present as shoulder pain with motion and may have associated mechanical symptoms of painful popping or clicking with motion. On physical exam deep GHJ tenderness to palpation may be present. O’Brien’s test and dynamic labral shear test are special tests for labral pathology. O’Brien’s test is deep GHJ pain reproduced with resistance of an inferiorly directed force to the patient’s arm in a shoulder position of 90° flexion, 15°adduction, and internal rotation (Fig. 10.24) with subsequent improvement of pain when the force is applied to the arm in the same position except in external rotation (Fig. 10.25) [8]. The dynamic labral shear test is performed with the examiner stabilizing the scapular posteriorly; supporting the olecranon in a position of 90° shoulder abduction, end range external rotation, and 90° elbow flexion; and then applying an axial compressive and shear force through an arc of shoulder abduction (Fig. 10.26) [28]. A positive response is deep GHJ pain reproduction or a painful click sensation. Athletes with labral tears commonly have a history of shoulder dislocation, concomitant shoulder instability, and/or LHBT pathology. The differential diagnosis for shoulder pain with mechanical symptoms includes LHBT instability, GHJ loose body, and GHJ osteoarthritis. Diagnosis Shoulder radiographs can be obtained to rule out bony pathology. Shoulder MRI is best to directly visualize labral tears. MRI with intra-articular gadolinium is Fig. 10.24  O’Brien’s test for labral tear

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Fig. 10.25  O’Brien’s test for labral tear part 2

Fig. 10.26 Dynamic labral shear test for labral tear

generally preferred as this increases the sensitivity to detect small labral tears. Labral tears, however, are quite common and can be seen on MRI evaluation in the majority of the asymptomatic middle-age population; thus having a corresponding history, exam, imaging, and potentially response to diagnostic or therapeutic injections may be needed for accurate diagnosis [29].

Treatment Nonoperative management should be trialed first in most situations. For SLAP lesions, particularly in throwers, rehabilitation should focus on stretching of the posterior shoulder and strengthening of the scapular stabilizers to optimize scapular position and improve scapular dyskinesis [29]. In the setting of a painful labral tear without instability, an ultrasound guided intra-articular GHJ steroid injection can be considered for further pain control.

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Surgery for labral tears can be considered in the setting of failed nonoperative management. Surgical outcomes, particularly in the setting of SLAP tears, have better outcomes in younger athletic population [27, 29]. Multiple different surgical techniques exist, depending on the specific co-existing pathologies and underlying anatomy, but, in general, will include either arthroscopic debridement or labral repair. Return to play is guided by pain and restoration of shoulder range of motion, strength, and functional sport specific activity.

References 1. Robinson CM, Shur N, Sharpe T, Ray A, Murray IR. Injuries associated with traumatic anterior glenohumeral dislocations. J Bone Joint Surg. 2012;94(1):18–26. 2. Piasecki DP, Romeo AA, Bach BR Jr, Nicholson GP. Suprascapular neuropathy. J Am Acad Orthop Surg. 2009;17(11):665–76. 3. Corpus KT, Campl CL, Dines DM, Altchek DW, Dines JS. Evaluation and treatment of internal impingement of the shoulder in overhead athletes. World J Orthop. 2016;7(12):776–84. 4. Kibler WB, Kuhn JE, Wilk K, et al. The disabled throwing shoulder: spectrum of pathology-­10-­ year update. Arthroscopy. 2012;29(1):141–161 e26. 5. Li X, Ma R, Bedi A, Dines DM, Altchek DW, Dines JS. Management of acromioclavicular joint injuries. J Bone Joint Surg. 2014;96(1):73–84. 6. Simovitch R, Sanders B, Ozbaydar M, Lavery K, Warner JJ. Acromioclavicular joint injuries: diagnosis and management. J Am Acad Orthop Surg. 2009;17(4):207–19. 7. Pallis M, Cameron KL, Svoboda SJ. Epidemiology of acromioclavicular joint injury in young athletes. Am J Sports Med. 2012;40(9):2072–7. 8. Bowen JE, Malanga GA, Pappoe T, McFarland E. Physical examination of the shoulder. In: Malanga GA, Nadler SF, editors. Musculoskeletal physical examination: an evidenced based approach. Philadelphia: Elsevier; 2006. 9. Zacchilli MA, Owens BD.  Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg. 2010;92(3):542–9. 10. Owens BD, Dickens JF, Kilcoyne KG, Rue JP. Management of mid-season traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518–26. 11. Dickens JF, Rue JP, Cameron KL, et al. Successful return to sport after arthroscopic shoulder stabilization versus nonoperative management in contact athletes with anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2017;45(1):2540–6. 12. Ufberg JW, Vilke GM, Chan TC, Harrigan RA.  Anterior shoulder dislocations: beyond traction-­countertraction. J Emerg Med. 2004;27(3):301–6. 13. Hendey GW. Managing anterior shoulder dislocation. Ann Emerg Med. 2016;67(1):76–80. 14. Watson S, Allen B, Grant JA. A clinical review of return-to-play considerations after anterior shoulder dislocation. Sports Health. 2016;8(4):336–41. 15. Khan LA, Bradnock TJ, Scott C, Robinson CM. Fractures of the clavicle. J Bone Joint Surg. 2009;91(2):447–60. 16. Yang S, Andras L.  Clavicle shaft fractures in adolescents. Orthop Clin North Am. 2017;48(1):47–58. 17. Robertson GA, Wood AM. Return to sport following clavicle fractures: a systematic review. Br Med Bull. 2016;119(1):111–28. 18. Guerra E, Previtali D, Tamorini S, Filardo G, Zaffagnini S, Candrian C.  Midshaft clavicle fractures: surgery provides better results as compared with nonoperative treatment: a meta-­ analysis. Am J Sports Med. 2019;47(14):3541–51. 19. Khan KM, Cook JL, Bonar F, Harcourt P, Astrom M. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med. 1999;27(6):393–408.

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20. Tagg CE, Campbell AS, McNally EG. Shoulder impingement. Semin Musculoskelet Radiol. 2013;17(1):3–11. 21. Weiss LJ, Wang D, Hendel M, Buzzerio P, Rodeo SA. Management of rotator cuff injuries in the elite athlete. Curr Rev Musculoskelet Med. 2018;11(1):102–12. 22. Chalmers PN, Verma NN.  Proximal biceps in overhead athletes. Clin Sports Med. 2016;35(1):163–79. 23. Schickendantz M, King D.  Nonoperative management (including ultrasound-guided injections) of proximal biceps disorders. Clin Sports Med. 2016;35(1):57–73. 24. Murray IR, Goudie EB, Petrigliano FA, Robinson CM. Functional anatomy and biomechanics of shoulder stability in the athlete. Clin Sports Med. 2013;32(4):607–24. 25. Hettrich CM, Cronin KJ, Raynor MB, et  al. Epidemiology of the Frequency, Etiology, Direction, and Severity (FEDS) system for classifying glenohumeral instability. J Shoulder Elb Surg. 2019;28(1):95–101. 26. Brelin A, Dickens JF.  Posterior shoulder instability. Sports Med Arthrosc Rev. 2017;25(3):136–43. 27. Van Blarcum GS, Svoboda SJ.  Glenohumeral instability related to special conditions: SLAP tears, pan-labral tears, and multidirectional instability. Sports Med Arthrosc Rev. 2017;25(3):e12–7. 28. Kibler WB, O’Driscoll S. Dynamic labral shear test in diagnosis of SLAP lesions: letter to the editor. Am J Sports Med. 2013;41(7):NP36–7. 29. Mathew CJ, Lintner DM. Superior labral anterior to posterior tear management in athletes. Open Orthop J. 2018;12:303–13.

Elbow and Forearm Injuries

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Jonathan Ramin, Jasmin Harounian, and Gerardo Miranda-Comas

Introduction Elbow and forearm injuries are very common in athletes, especially those that practice overhead sports. They can be divided into acute and overuse or chronic injuries. Acute injuries typically occur in contact sports, whereas overuse injuries to the elbow and forearm are usually the result of repetitive stress at the elbow. This chapter will cover region-specific anatomy, elbow biomechanics, as well as common elbow and forearm pathologies seen in athletes.

Anatomy and Biomechanics [1] Bones and Ligaments The elbow is a synovial hinge joint comprised of three articulations between the humerus, ulna, and radius bones. The humeroulnar joint is formed by the trochlea of the humerus and the proximal ulna, allowing for flexion and extension at the elbow. Lateral to the trochlea is the capitellum, which articulates with the radial head to form the humeroradial or radiocapitellar joint. The articulation between the proximal radius and ulna forms the radioulnar joint. Both the radiocapitellar and radioulnar joints allow for pronation and supination at the elbow. The elbow joint is surrounded by a fibrous capsule which forms the lateral or radial collateral ligament (RCL) and the medial or ulnar collateral ligament (UCL). The RCL provides varus support, while the more injury-susceptible UCL provides valgus support.

J. Ramin (*) · J. Harounian · G. Miranda-Comas Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_11

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Muscles Several muscles pass through the elbow joint that allow for elbow flexion and extension and forearm pronation and supination. Anteriorly, the biceps and brachioradialis muscles function as the primary flexors of the elbow. The biceps also assists the supinator muscle in forearm supination. The short head of the biceps originates from the coracoid process, while the long head originates at the supraglenoid tubercle and both insert at the radial tuberosity and fascia of the forearm. The brachioradialis originates from the supracondylar ridge of the humerus and inserts at the lateral distal radius. Most of the anterior elbow joint is covered by the brachialis, which is another elbow flexor. It originates from the distal anterior half of the humerus and inserts at the ulnar tuberosity. Posteriorly, the triceps functions as the primary elbow extensor. The long head of the triceps originates from the scapula, while the medial and lateral heads originate from the posterior surface of the humerus. The three heads of the muscle join to insert at the olecranon process and fascia of the forearm. The anconeus muscle also aids in elbow extension, originating from the posterolateral epicondyle and inserting at the posterior-proximal ulna. The pronator teres and pronator quadratus are the primary pronators of the forearm. The musculature of the anterior forearm is comprised of the flexor carpi radialis, flexor carpi ulnaris, flexor digitorum superficialis and profundus, pronator teres, and palmaris longus. The pronator teres has two heads which originate from the ulnar coronoid process and humeral medial epicondyle and insert in the middle one-third of the lateral radius. It also contributes to elbow flexion. Of note, the pronator quadratus aids in pronation distally. It originates from the medial distal ulna and inserts at the anterior distal radius. The common flexor tendon serves as the proximal attachment site for the anterior forearm muscles. The musculature of the posterior forearm is comprised of the extensor carpi radialis longus and brevis, extensor carpi ulnaris, extensor digitorum, and extensor digiti minimi. The common extensor tendon serves as the proximal attachment site for the posterior forearm muscles. The anterior and posterior forearm musculature are primarily responsible for flexion and extension at the level of the wrist and fingers, as well as forearm supination and pronation.

Nerves Three nerves primarily traverse through the elbow musculature: the median, radial, and ulnar nerves. The median nerve travels anteriorly under the bicipital aponeurosis, passing through the two heads of the pronator teres and into the flexor compartment of the forearm, where it branches into the anterior interosseous nerve (AIN) and the continuation of the median nerve. The ulnar nerve travels from the posterior aspect of the medial epicondyle through the cubital tunnel, emerging anteriorly and continuing along the ulnar aspect of the forearm. The radial nerve travels laterally along the spiral groove of the humerus to the lateral epicondyle, where it crosses the elbow anteriorly between the brachialis and the brachioradialis. It then branches into the posterior interosseous nerve (PIN) and the superficial radial nerve.

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Biomechanics The primary function of the elbow is to stabilize and position the distal forearm and hand. Positioning is achieved through coordinated combinations of elbow flexion/ extension and forearm pronation/supination. The average range of motion in elbow flexion and extension is 0–150 degrees; however, only approximately 30–130 degrees is required for functional use. The average range of forearm pronation and supination is nearly 180 degrees about the longitudinal axis. Forearm supination accounts for up to 85 degrees, whereas pronation accounts for 75 degrees. The previously discussed bones, joints, and ligaments work in conjunction to provide passive stabilization, while the muscles serve to actively stabilize the elbow joint.

Acute Elbow Injuries Fractures and Dislocations [2] Pathophysiology Fractures and dislocations of the elbow often occur in conjunction but can be an isolated injury. Elbow fractures fall into four categories: [1] radial head fractures, [2] supracondylar fractures, [3] olecranon fractures, and [4] radioulnar fractures. Elbow dislocations can be characterized as either simple or complex, most often occurring in athletes competing in football, wrestling, or gymnastics. The joint can dislocate in multiple directions, the most common of which is posteriorly. An elbow dislocation without an associated fracture is considered simple, while an elbow dislocation with an associated fracture or nerve damage is considered complex. Clinical Presentation Patients often report a history of high-velocity impact or falling on an outstretched hand (FOOSH) as the primary mode of injury leading to severe pain in the elbow. Numbness (i.e., medial, radial, and ulnar nerve damage) and weakness can be seen in more severe cases. Diagnosis Although history (mechanism of injury) and physical exam are sufficient to diagnose dislocation, plain radiographic studies are essential to evaluate for an associated fracture. When fracture is suspected, anteroposterior (AP) view in full extension and lateral view in 90-degree flexion should be obtained. Smaller fractures may not be visible on x-ray initially but may become more evident 3 weeks post-injury. In children, oblique views may be more helpful when fractures are not evident, and the fat pad is displaced. Supracondylar fractures, which are most common in children, can often be confused with a dislocation. More complex fractures may require CT imaging to visualize bony fragments. Further classifications of fracture and dislocation types can be seen in Tables 11.1, 11.2, 11.3, and 11.4 [3]. If neurovascular injury is suspected, athletes must be evaluated for acute compartment syndrome.

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Table 11.1  Classifications for radial head fractures [3] Mason’s classification for radial head fractures Type I Non-displaced or minimally displaced (2 mm) or angulated II Type Comminuted fracture III Type Radial head fracture with associated IV elbow dislocation

Treatment Hinged elbow splinting with early ROM Open reduction and internal fixation (ORIF) or surgical excision of fragments Excision of the radial head Reduction of dislocation Treat fracture based on type I–III classification

Table 11.2  Classifications for supracondylar fractures [3] Classification for supracondylar fractures Type I Non-displaced fracture Type II Type III

Displaced fracture with intact posterior cortex Displaced fracture with no cortical contact, unstable

Treatment Long-arm cast or splinting Reduction and fixation Reduction and fixation

Table 11.3  Classifications for olecranon fractures [3] Classification for olecranon fractures Type I Non-displaced or minimally displaced (2 mm), minimal-moderate comminution, II elbow stable Type Fracture with moderate-severe comminution, III dislocation, elbow unstable

Treatment Long-arm cast or ORIF ORIF Open reduction and stabilization of olecranon

The increased intracompartmental pressure within the arm or forearm can lead to weakness, paresthesia, pulselessness, pallor, and pain with passive digit extension in the affected arm. Compartment pressures can be measured to confirm diagnosis.

Treatment Any fracture or dislocation at the elbow should be monitored closely for neurovascular compromise, especially with supracondylar or midshaft radioulnar fractures. Compartment syndrome can lead to neurovascular compromise; therefore, surgical intervention with emergent fasciotomy is indicated to relieve pressure and prevent tissue necrosis. For simple dislocations, reduction can be performed on the field or in the office setting. Physical therapy emphasizing ROM is important after the immediate acute phase. Splinting for >3 weeks may lead to adverse outcomes [4]. When there is any suspicion of a dislocation, pre- and post-reduction films are essential to evaluate the fracture and ensure proper alignment. For most non-­displaced elbow fractures, immobilization is the primary treatment. Displaced fractures often require surgical intervention (i.e., ORIF) (Tables 11.1, 11.2, 11.3, and 11.4) [3].

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Table 11.4  Bado classification for Monteggia fracture-dislocations [3] Bado classification for Monteggia fracture-dislocations Type I Fracture of the proximal or middle third of the ulna with anterior dislocation of the radial head Type Fracture of the proximal or middle third of the ulna with posterior II dislocation of the radial head Type Fracture of the ulnar metaphysis (distal to coronoid process) with III lateral dislocation of the radial head Type Fracture of the proximal or middle third of the ulna and radius with IV dislocation of the radial head in any direction

Treatment Reduction and fixation

Return to Sport Athletes with neurovascular injuries or post-compartment syndrome fasciotomies can return to play when symptoms improve and the surgical site has completely healed. Such athletes should continue to be monitored regularly. If no residual instability is noted with full range of motion after a simple dislocation, most athletes can return to play after 6  weeks, with reintroduction of varus or valgus loading at 12  weeks. Prior elbow dislocation does not predispose athletes to repeat injury. Compliance with a comprehensive rehabilitation program is essential to recovery. In complex dislocations and elbow fractures, return to sport is often not recommended until after 6 months following the injury. Athletes with such injuries require a more extensive rehabilitation program with emphasis on range of motion to avoid contractures. A valgus overload hinged elbow brace is also recommended during rigorous play to avoid valgus stress on the elbow.

Olecranon Bursopathy (Bursitis) [5] Pathophysiology Olecranon bursitis is an inflammation of the bursa overlying the olecranon process at the proximal aspect of the ulna. Bursal inflammation occurs by a variety of mechanisms, including acute or repetitive trauma. An acute hemorrhagic bursitis is often seen after direct trauma to the posterior elbow. Repetitive trauma to the posterior elbow will often lead to a nonhemorrhagic effusion. Less commonly, the inflammation may be due to infection. Clinical Presentation When the bursitis is secondary to an acute trauma, patients generally present with pain and focal swelling at the posterior elbow. Pain tends to be exacerbated with pressure on the area. However, when the bursitis develops after repetitive irritation of the bursa, the patient will present with focal swelling and minimal pain. Diagnosis The most classic physical finding is swelling over the olecranon process. If the area is red or warm, infection should be considered. Elbow ROM is usually normal

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because the bursa is extra-articular, but movement may occasionally be limited by pain. Radiographs of the elbow should be performed to assess for possible olecranon fracture if significant trauma occurred or an avulsed osteophyte is suspected. Given the risk associated with infection, bursa aspiration should be considered in most patients, as physical exam cannot alone distinguish septic from aseptic bursitis. Definitive diagnosis occurs with laboratory evaluation of cell count, gram stain, and crystal analysis.

Treatment In the absence of infection, most patients respond very well to a series of one to two aspirations, since recurrence rate is high. This is often combined with NSAIDs, rest, ice, compression, and protection of the elbow with an elbow pad. In a subacute or chronic presentation, aspiration and corticosteroid injection into the bursa may be considered, although the effectiveness of the corticosteroids is questionable. Return to Sport The athlete is able to return to sport without restriction when symptoms and physical examination findings resolve. A good measure for return to play is the ability to perform sport-specific drills. If there is no recurrence of symptoms or physical exam findings, the athlete may be cleared for activity.

Triceps Rupture Pathophysiology Avulsion of the triceps tendon often occurs in the setting of a deceleration stress superimposed on a contracted triceps muscle. Rupture of the tendon can occur at three places: the tendon attachment to bone, the musculotendinous junction, or in the muscle body itself. Clinical Presentation Triceps rupture can be seen in athletes participating in competitive weight lifting and bodybuilding, associated with anabolic steroid use. They most commonly present with posterior elbow pain and weakness. The classic presentation is weakness of elbow extension and a palpable gap in the muscle body. In the setting of acute trauma, ecchymosis or localized tenderness can be appreciated. Diagnosis History and physical exam are the primary tools of diagnosis. Ultrasound and MRI are also excellent diagnostic tools for visualizing and differentiating between partial and complete triceps tendon tears [6, 7]. Treatment For partial tears involving less than 50% of the tendon as well as proximal tears localized to the muscle belly, nonsurgical treatment initially consists of analgesics

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and splint immobilization at 30 degrees of elbow flexion for 4 weeks. This is followed by physical therapy with emphasis on ROM exercises after 4  weeks and strengthening exercises after 8 weeks. Complete tendon ruptures are surgically repaired if the athlete presents within 3 weeks of injury [2]. Moreover, in chronic triceps tendon ruptures, surgical reconstruction should be considered. This is followed by a similar immobilization protocol for 2 weeks with progression to active-assisted range of motion in 2–6 weeks and eventual strengthening exercises with weight restrictions beginning after 6 weeks.

Return to Sports Almost all triceps tendon ruptures require a comprehensive rehabilitation program. Once completed, return to play in nonoperative cases is recommended when athletes have regained full ROM and are no longer symptomatic. In postoperative cases, return to play is not recommended until at least 4–6 months after surgery.

Distal Biceps Tendon Rupture Pathophysiology Distal biceps tendon ruptures are rare and account for approximately 3–10% of all biceps ruptures. Generally, athletes are predisposed to this injury when they have already incurred progressive degeneration of the tendon. When forceful extension is applied to a flexed elbow, this already weakened structure can rupture. Clinical Presentation Distal biceps tendon rupture is characterized by sudden pain over the anterior aspect of the elbow after a forceful effort against resistance. Athletes often report an audible snap at the time of injury, followed by swelling and bruising. A visible or palpable mass may also develop in the upper arm. Diagnosis The history and physical exam findings are often suggestive of diagnosis. Swelling and ecchymosis along with gross deformity and tenderness to palpation are often noted at the antecubital fossa. Provocative maneuvers include the hook test, in which the examiner attempts to hook their finger under the distal biceps tendon at the antecubital fossa with the forearm supinated and the elbow flexed at 90 degrees. Plain radiographs may reveal hypertrophic spurring or bony irregularities that increase the likelihood of rupture and support a clinical suspicion of this diagnosis. Anteroposterior and axillary films are the most useful views for ruling out fractures in this setting. Ultrasound and MRI may also be performed to confirm the diagnosis. Treatment Generally accepted clinical guidelines advocate surgical reattachment in athletes within 3 weeks of injury before development of tendon contracture [8]. Cosmetic

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concerns may also prompt a surgical approach. ROM exercises begin 3 weeks postoperatively, followed by strength training at roughly 8 weeks after surgical intervention. Conservative management is considered appropriate for elderly individuals. This approach involves rest, followed closely by ROM and strengthening exercises for the shoulder and elbow. When conservative management is chosen, there is often a significant reduction in power of elbow flexion and supination.

Return to Sport Return to sport is often recommended after a comprehensive rehabilitation program is completed and the athlete is 4–5-month postsurgical intervention. Athletes competing in high-impact sports may require the full 5 months to prevent re-rupture.

Overuse Elbow Injuries Lateral Epicondylopathy [2, 9, 10] Pathophysiology Commonly referred to as tennis elbow, lateral epicondylitis or epicondylalgia or epicondylopathy is the most common overuse injury of the elbow. It is an injury to the extensor tendons, most commonly the extensor carpi radialis brevis, and generally arises from repetitive microtrauma and overload. The tendinous insertion is flooded with neovascularization and fibroblasts termed angiofibroblastic proliferation. Clinical Presentation Athletes commonly present with aching pain over the lateral elbow, which is worsened with activation of the wrist extensors and alleviated by rest. In more chronic cases, the pain may be persistent and associated with forearm weakness. Diagnosis Diagnosis is based primarily on physical exam and history. Pain is elicited on palpation of the lateral epicondyle and is aggravated by wrist extension and radial deviation. In Cozen’s test (Fig. 11.1), the examiner palpates the lateral epicondyle while providing resistance against wrist extension. A positive exam will reproduce the painful symptoms. In more severe cases, decreased grip strength may be noted. MRI or ultrasound can be used for diagnosis but is usually reserved for patients who fail conservative therapy. Treatment Initial treatment includes NSAIDs, RICE, and activity modification. In tennis players, activity modification involves evaluation and adjustment of the racquet, training regimen, and technique. Inappropriate grip size, higher string tensions in the racquet, and poor stroke mechanics can all contribute.

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Fig. 11.1  Cozen’s test

Long-term treatment should focus on ROM exercises. Although bracing is a common treatment, continuous immobilization may be harmful as studies have suggested that tendons need stress to heal. If the above conservative management is not sufficient, injections with corticosteroids, platelet-rich plasma, or prolotherapy have also shown to provide relief of symptoms [11, 12]. Surgery is reserved for those with significant decrease in arm strength and may often only restore 90% of the tensile strength.

Return to Sport Play can be resumed when an athlete has full strength and is able to complete all necessary movements with minimal pain. A brace may be used temporarily, but athletes must continue to participate in a therapy program while recovering.

Medial Epicondylopathy Pathophysiology Often referred to as golfer’s elbow, medial epicondylitis or epicondylalgia or epicondylopathy is an injury to the common flexor tendons, most commonly involving the flexor carpi radialis tendon. This injury is far less common than lateral epicondylitis. Medial epicondylitis results from repetitive eccentric loading of the wrist flexors and forearm pronators causing excess valgus stress on the medial epicondyle. Clinical Presentation Athletes typically present with pain and tenderness over the medial elbow radiating to the proximal forearm. Symptoms are often exacerbated with activation of the wrist flexors. In more chronic cases, weakness can be reported in the forearm and wrist.

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Fig. 11.2  Resisted wrist flexion with medial epicondyle palpation

Diagnosis Diagnosis is based primarily on physical exam and history. Palpation of the medial epicondyle often elicits pain. Provocative testing with resisted wrist flexion with palpation of the medial epicondyle may reproduce symptoms (Fig.  11.2). Ulnar neuropathy may be associated with numbness, weakness, or a positive Tinel test at the elbow. Imaging studies are often unnecessary, but may show calcification adjacent to the medial epicondyle in 7% of affected patients [7, 13]. Treatment Initial treatment includes NSAIDs, RICE, and activity modification as poor stroke biomechanics in golf and excessive topspin in racquet sports can contribute. Physical therapy emphasizing ROM and strengthening is an important strategy. Counterforce bracing and taping can be useful when return to play is a pressing priority. If the above conservative management is not sufficient, injections with corticosteroids, platelet-rich plasma, or prolotherapy have also shown to provide relief of symptoms. Surgery is reserved for cases that fail conservative treatment, but these athletes often have a longer recovery time of 4–6 months. Return to Sport Athletes may ideally return to sport when pain has resolved with activity. Since many athletes are unwilling to wait, bracing and activity modification may be used to reduce aggravation of symptoms.

Triceps Tendinopathy Pathophysiology Most commonly seen in weight lifters, triceps tendinopathy is due to repetitive overuse and subsequent degeneration of the triceps tendon insertion at the olecranon.

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Clinical Presentation Athletes present with posterior elbow pain that is worsened with resisted elbow extension. Chronic cases can present with decreased ROM and a palpable depression along the olecranon process. Diagnosis History and physical are the primary tools of diagnosis. Plain films may show calcification outlining the tendon. If triceps tendon rupture is suspected, imaging with ultrasound may be sufficient for detection. However, if ultrasound findings are equivocal but a high clinical suspicion remains, MRI should be considered [13]. Treatment The primary treatment is RICE and NSAIDs. Physical therapy emphasizing triceps strengthening and activity modification to improve weight lifting technique is important in long-term treatment. Intratendinous steroid injection should be avoided due to the risk of tendon rupture. Although relatively novel, orthobiologics such as platelet-rich plasma may be considered if primary treatment methods are unsuccessful [9, 12]. Return to Sport Return to sport is acceptable when symptoms are tolerable, activity modification is addressed, and strength is at least 90% of baseline.

Ulnar Neuropathy at the Elbow (UNE) Pathophysiology Also referred to as cubital tunnel syndrome, UNE is the second most common nerve compression disorder after carpal tunnel syndrome. The pathway of the ulnar nerve predisposes it to compressive, traction, and friction forces. The cubital tunnel is found deep to the arcuate ligament of Osborne, which connects the ulnar and humeral heads of the flexor carpi ulnaris (FCU) muscle. Repeat elbow flexion and repetitive throwing motions can cause irritation of the ulnar nerve through this tunnel and lead to nerve irritation and dysfunction. Clinical Presentation Athletes present with complaints of numbness and tingling in the elbow and lateral hand, especially the fifth digit. Muscle weakness can be noted in more chronic or severe cases. Diagnosis History and physical are the primary tools of diagnosis. Provocative maneuvers, such as the elbow flexion test which involves forearm supination, wrist extension, and full elbow flexion, often reproduce symptoms when the position is held over 1 minute. Tinel test at the medial elbow can also reproduce symptoms (Fig. 11.3). A

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Fig. 11.3  Ulnar nerve palpation at the elbow

thorough neurological and muscular examination should assess for severity of the neuropathy and to rule out other pathologies. Equivocal physical exam findings with continued suspicion for ulnar nerve entrapment at the elbow may warrant further evaluation with electrodiagnostics, including nerve conduction studies (NCS) and electromyography (EMG). Imaging modalities such as dynamic ultrasound can help in visualizing possible areas of structural compression through full range of motion at the elbow [7].

Treatment Treatment varies depending on etiology. Physical therapy, including strengthening and stretching, along with NSAIDs should be considered. Nighttime splinting of the elbow in extension to avoid further injury may also be helpful. Steroid injections are often avoided as they do not effectively improve symptoms. Recent studies suggest there may be a role for hydrodissection of the cubital tunnel to decompress the ulnar nerve [14]. Surgical decompression of the ulnar nerve or submuscular transposition may be considered if there is persistent weakness or if conservative therapy fails.

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Return to Sport Recovery and return to play vary depending on therapy and response time. When athletes are asymptomatic with full ROM, they may resume play with continued therapy and movement modification. For postoperative cases, return to sport is generally recommended at 1–3 months.

Pronator Syndrome Pathophysiology The most common site of median nerve entrapment in the forearm is between the two heads of a hypertrophied pronator muscle teres. Other sites of median nerve entrapment in pronator syndrome include the ligament of Struthers, the lacertus fibrosus in the antecubital fossa, or under the flexor digitorum superficialis. Clinical Presentation Athletes often complain of pain or paresthesias in the median nerve distribution with prominent complaints in the anterior proximal forearm. A patient may note that the throwing motion or swinging a racquet aggravates the pain. Diagnosis Median nerve symptoms with negative Tinel and Phalen tests at the wrist should raise suspicion for pronator syndrome. Compression of bilateral pronator teres muscles at the proximal forearm with pain reproduced only on the symptomatic limb (positive Gainor test) is consistent with this diagnosis. Athletes with pronator syndrome also have difficulty making an OK sign due to weakness of the median nerve-­ innervated flexor pollicis longus and flexor digitorum profundus. Key features that distinguish pronator syndrome from carpal tunnel syndrome are decreased sensation over the thenar eminence and the lack of nocturnal symptoms. Decreased sensation of the thenar eminence is only seen in pronator syndrome, as this area is innervated by the palmar cutaneous sensory branch of the median nerve, which does not pass through the carpal tunnel. Electrodiagnostic testing can provide further evidence for the diagnosis of pronator syndrome. Treatment Treatment of pronator syndrome involves rest, activity modification, NSAIDS, and elbow splinting. After pain subsides, the athlete can begin simple hand exercises (ball squeeze). This can progress to light wrist flexion and extension, followed by pronation and supination exercises. If this treatment fails after 4–6 weeks, surgical exploration for anatomical nerve decompression can be considered. Postoperative mobilization should take place within 1 week with therapy directed at nerve gliding and strengthening.

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Return to Sport Return to play is usually appropriate when pain is resolved and the cause for compression is addressed through either biomechanical or anatomical changes. Strength should be equal to that of the unaffected side at the time of return to activity. Postoperative return to sport is typically seen at 6–8  weeks but can take up to 6 months.

Anterior Interosseous Nerve Syndrome (Kiloh-Nevin Syndrome) Pathophysiology Anterior interosseous nerve (AIN) syndrome involves the median nerve as it divides approximately 5 cm below the lateral epicondyle of the elbow. The AIN innervates the flexor pollicis longus, the radial half of the flexor digitorum profundus, and the pronator quadratus. Entrapment of the AIN usually occurs under the flexor digitorum profundus arch, although more commonly the cause is idiopathic. Clinical Presentation Athletes more prone to this injury are those who do repetitive forceful gripping or repetitive pronation. They generally experience weakness in the thumb and index finger without any associated sensory deficits. The athlete may also note a loss of coordination of the fingers. Diagnosis Since the AIN is purely a motor nerve, clinical weakness in its distribution is diagnostic. Patients are classically unable to form the “OK” sign with the thumb and index finger. Their “OK” sign attempt will reveal inability to flex the distal interphalangeal joint (DIP) of the index finger and hyperextension of the interphalangeal joint (IP) joint of the thumb. There may also be a compensatory increase in flexion of the proximal interphalangeal joint (PIP) joint of the finger. This pinch is characteristic of anterior interosseous syndrome. Electrodiagnostic studies (EDX) can provide further evidence to confirm the clinically suspected diagnosis, and if there is concern for a possible space-occupying lesion, an ultrasound or MRI may be warranted [6]. Treatment Conservative treatment is the initial intervention of choice. This includes relative rest, ice, and pain control. If there is evidence of axonal loss on the EDX study or no improvement is seen in 3–6 months of conservative management, surgical exploration is indicated. Return to Sport Return to play is usually appropriate when the pain has resolved and the nerve compression has been addressed either through biomechanical or anatomical

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changes. This generally takes 6 weeks, but may often take 6–12 months for full motor recovery.

Valgus Extension Overload Pathophysiology Commonly a result of the valgus stress during repetitive throwing movements, valgus extension overload is an injury resulting from impingement of the tip of the posteromedial olecranon and the olecranon fossa. In the young athlete, not only synovitis and traction apophysitis can occur, but also this microtrauma may result in osteophyte formation, which can cause fractures and loose bodies. Delayed diagnosis and treatment can lead to growth plate disruption and permanent deformity. Clinical Presentation Although athletes most often present with medial elbow pain, lateral and posterior pain can be provoked with palpation. Pain is most commonly elicited during the cocking and/or accelerating phase of throwing, but has also been reported in the deceleration phase as well. Diagnosis History and physical are the primary tools of diagnosis. The posteromedial tip of the olecranon is especially painful to palpation and is often a distinguishing characteristic of valgus extension overload. There can also be concomitant injury to the medial ulnar collateral ligament as it is also stressed with valgus loading. Radiographic studies can be helpful when the diagnosis is unclear or when other pathology, such as fracture, is suspected. Treatment Treatment is determined by the chronicity of disease. In the acute phase, RICE and physical therapy are important. Oral NSAIDs may be used for pain control, and therapy should emphasize correction of the kinetic chain deficits and biomechanical alterations. There is no evidence to suggest that steroid injections are helpful. In more severe and chronic conditions, casting or surgery may be required in addition to physical therapy. Return to Sport Most athletes can return to sport within 4–6 weeks or after the completion of a rehabilitation program. Throwing should be prohibited during the rehabilitation process, and therapy should focus on shoulder girdle strengthening as well as eccentric exercises involving elbow flexion. Gradual return to throwing with proper technique should be emphasized in conjunction with a throwing program.

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Ulnar Collateral Ligament Injuries Pathophysiology Repetitive strain during activities like throwing in baseball causes repetitive stress on the ulnar collateral ligament (UCL), resulting in eventual laxity and possible tearing of the ligament. Clinical Presentation Athletes most commonly present with insidious onset medial elbow pain and swelling. The onset of symptoms may correlate with a change in training regimen and possible decline in performance. Valgus stress at 25% elbow flexion can help localize the pain, which is generally located slightly posterior and distal to the olecranon at the UCL’s point of insertion. Diagnosis History and physical along with MRI or diagnostic ultrasound can be used for a definitive diagnosis. Plain films may be obtained to rule out fracture initially. Diagnostic ultrasound can also be used for a definitive diagnosis. A neurological assessment should be done to rule out an associated ulnar nerve injury. Treatment Conservative management includes activity modification or rest, bracing, and physical therapy with an emphasis on strengthening, joint stability, and stretching. Orthobiologics, specifically platelet-rich plasma, have recently been shown to be effective treatment options in partial UCL tears [15]. Surgical intervention should be considered for all throwing athletes and athletes who fail conservative therapy. A brace to prevent valgus stress should be used in the postoperative period. Return to Sport Most athletes will require a period of 3–6  months after conservative therapy. Postoperatively, return to sport is often recommended at 9–12 months after surgical intervention and an extensive rehabilitation program.

Conclusion From the infrequent acute fractures and dislocations to the more common repetitive stress injuries of tendons and ligaments, athletes can present with a variety of upper limb complaints. Elbow and forearm injuries are particularly common in athletes with repetitive strenuous forces through the joint (i.e., throwing, racquet sports, etc.). It is important for sports physicians to be familiar with the most common sports-related injuries involving the elbow and forearm as summarized in this chapter.

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References 1. Martin S, Sanchez E. Anatomy and biomechanics of the elbow joint. Semin Musculoskelet Radiol. 2013;17(5):429–36. 2. Nocerino EA, Cucchi D, Arrigoni P, Brioschi M, Fusi C, Genovese EA, et al. Acute and overuse elbow trauma: radio-orthopaedics overview. Acta Biomed. 2018;89(Suppl 1):124–37. 3. Court-Brown C, Heckman J, McQueen M, Ricci W, Tornetta P, McKee M.  Rockwood and Green’s fractures in adults. 8th ed. Philadelphia: Lippincott Williams & Wilkins/Wolters Kluwer Health; 2015. 4. McGuire DT, Bain GI. Management of dislocations of the elbow in the athlete. Sports Med Arthrosc Rev. 2014;22:188–93. 5. Reilly D, Kamineni S. Olecranon bursitis. J Shoulder Elb Surg. 2016;25(1):158–67. 6. Read PJ, Morrison WB. Imaging injuries in throwing sports beyond the typical shoulder and elbow pathologies. Radiol Clin N Am. 2016;54(5):857–64. 7. Lin A, Gasbarro G, Sakr M.  Clinical applications of ultrasonography in the shoulder and elbow. J Am Acad Orthop Surg. 2018;26(9):303–12. 8. Sarda P, Qaddori A, Nauschutz F, Boulton L, Nanda R, Bayliss N. Distal biceps tendon rupture: current concepts. Injury. 2013;44(4):417–20. 9. Taylor SA, Hannafin JA. Evaluation and management of elbow tendinopathy. Sports Health. 2012;4(5):384–93. 10. Kancherla VK, Caggiano NM, Matullo KS. Elbow injuries in the throwing athlete. Orthop Clin North Am. 2014;45(4):571–85. 11. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet-rich plasma. Am J Sports Med. 2006;34(11):1774–8. 12. Kwapisz A, Prabhakar S, Compagnoni R, Sibilska A, Randelli P.  Platelet-rich plasma for elbow pathologies: a descriptive review of current literature. Curr Rev Musculoskelet Med. 2018;11(4):598–606. 13. Bucknor MD, Stevens KJ, Steinbach LS.  Elbow imaging in sport: sports imaging series. Radiology. 2016;279(1):12–28. 14. Guo D, Kliot M, McCool L, Senk A, Tonkin B, Guo D. Percutaneous cubital tunnel release with a dissection thread: a cadaveric study. J Hand Surg Eur Vol. 2019;44(9):920–4. 15. Podesta L, Crow SA, Volkmer D, Bert T, Yocum LA. Treatment of partial ulnar collateral ligament tears in the elbow with platelet-rich plasma. Am J Sports Med. 2013;41(7):1689–94.

Hand and Wrist Injuries

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Introduction Wrist and hand injuries are common in sports that require upper limb weight-­ bearing activities such as gymnastics, and extensive wrist and hand forces like climbing. It is important to identify and diagnose these injuries early since late intervention can lead to significant disability. Acute wrist injuries are common after falls on outstretched hands, while the hand is susceptible via direct contact with an object. Repetitive stress in the wrist can cause injury to the joint, tendons, and nerves. Treatment will depend on the specific injuries with some injuries requiring early surgical intervention to improve functional outcomes long term.

Anatomy of the Hand and Wrist [1] Bones and Ligaments The wrist is formed by the articulation of the radius, ulna, and eight carpal bones. The radiocarpal joint is formed by the distal radius, scaphoid, and lunate. The ulna does not articulate directly with the carpal bones; instead, a fibrocartilage triangle sits between the distal ulna and triquetrum. The scaphoid bone links the proximal carpal bones (lunate and triquetrum) and the distal carpal bones (trapezium, trapezoid, capitate, and hamate). The distal row of carpal bones articulates with the metacarpal bones to form the carpometacarpal joints.

C. Schepker (*) Department of Physical Medicine and Rehabilitation, New York-Presbyterian Hospital of Columbia and Cornell, New York, NY, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_12

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The hand has five metacarpal bones. From proximal to distal, they are each comprised of a base, shaft, and head. Distal to the metacarpal head is the metacarpophalangeal joint, which represents the link between the phalanx and the metacarpal. MCP joints can flex, extend, abduct, and adduct. Using a combination of these movements, they can move in restricted circumduction. These joints are supported by strong palmar and collateral ligaments. Additionally, the deep transverse metacarpal ligaments connect the medial four joints to each other. The hand also has 14 phalanges. Each digit contains three phalanges; the thumb contains two. More distally, the proximal and distal interphalangeal joints function as simple hinge joints. Palmar and collateral ligaments support these joints in flexion and extension.

Muscles Wrist motion is described in three planes: flexion/extension, pronation/supination, and radial/ulnar deviation. Pronation and supination largely occur proximal to the wrist joint proper, and involve the elbow and forearm. Wrist flexion is accomplished primarily by the flexor carpi radialis and ulnaris. Wrist extension is driven primarily by extensor carpi radialis and ulnaris. Rotators of the wrist include the pronator teres, pronator quadratus, and the supinator. Radial deviation, also known as abduction of the wrist, is usually combined with flexion or extension, and is driven primarily by flexor carpi radialis and extensor carpi radialis longus. Ulnar deviation, also known as adduction of the wrist, is also frequently combined with some degree of wrist flexion or extension. The muscles involved in ulnar deviation are extensor carpi ulnaris and flexor carpi ulnaris. The superficial forearm contains a large number of muscles that are divided into dorsal and ventral compartments. Wrist and finger extensors reside in the dorsal compartment, and attach to a common extensor origin on the lateral epicondyle of the humerus. Ventrally, the superficial flexors have a common origin on the medial epicondyle of the humerus. The muscles in the ventral flexor compartment also include extrinsic hand muscles. Their force is transmitted to the hand through long tendons. The deeper flexor digitorum profundus attaches more distally on the fingers than the superficial flexor digitorum superficialis, which means that the FDS tendon has to split to allow the FDP pass through it. The intrinsic muscles of the hand include the lumbricals, interossei, hypothenar, and thenar groups. The lumbricals are muscles that attach proximally to the tendons of the flexor digitorum profundus, and distally to the extensor expansions. They flex the MCP joint and extend the IP joint. The interosseous muscles are located in the intervals between the metacarpal bones. The interossei consist of both dorsal and palmar muscles. The interossei act to abduct (palmar) and adduct (dorsal) the MCP joints of the finger. Four small muscles of the thumb are found on the thenar side of the hand: abductor pollicis brevis, flexor pollicis brevis, opponenspollicis, and adductor pollicis. The first three of these muscles constitute the thenar eminence. The thenar muscles originate from the flexor retinaculum and carpal bones, and insert onto the base of the thumb or onto the side of the first metacarpal bone. The median nerve innervates the thenar muscles, except for the adductor pollicis, which

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is supplied by the deep branch of the ulnar nerve. In addition to the thenar muscles, the abductor pollicis longus inserts onto the base of the thumb, but originates at the posterior surfaces of the ulna and radius. It acts to abduct the thumb and extend the carpometacarpal joint. Three small muscles of the fifth digit are found on the hypothenar side of the hand, and are innervated by the ulnar nerve. These muscles include the abductor digiti minimi, flexor digitiminimi, and opponensdigitiminimi. The hypothenar muscles originate from the flexor retinaculum and carpal bones. The hypothenar muscles insert onto the base of the fifth metacarpal.

Nerves All of the nerves that travel to the hand cross the wrist. The three main nerves include the radial nerve, the median nerve, and the ulnar nerve. All three originate from the brachial plexus at the level of the shoulder. These nerves carry signals from the brain to the muscles that move the arm, hand, fingers, and thumb. The radial nerve provides sensory innervation to the dorsum of the hand, thumb, index, middle, and part of the ring finger. The median nerve enters the hand through the carpal tunnel and provides motor and sensory innervation to much of the hand. Specifically, the median nerve supplies the thenar muscles and the two radial lumbrical muscles. Sensory innervation is provided to the palmar surface of the thumb, index, middle, and part of the ring finger. The ulnar nerve innervates the hypothenar muscles, the ulnar two lumbrical muscles, and the interosseous muscles. It also provides sensory innervation to the fifth digit and part of the ring finger. Biomechanics The radiocarpal joint provides the majority of wrist flexion, extension, ulnar deviation, and radial deviation. When all motions are taken in combination, the wrist can be circumducted. Flexion occurs primarily at the midcarpal joint, and extension at the radiocarpal joint. Radial and ulnar collateral ligaments as well as palmar and dorsal radiocarpal ligaments provide stability to the joint. The primary movers of the wrist have dual action. The flexor carpi radialis (FCR) produces both wrist flexion and radial deviation, the flexor carpi ulnaris (FCU) produces both flexion and ulnar deviation, the extensor carpi radialis (ECR) produces both extension and radial deviation, and the extensor carpi ulnaris (ECU) produces both extension and ulnar deviation. To produce pure flexion, extension, radial deviation, or ulnar deviation requires coactivation of at least two muscles whose actions will balance one another. For example, the two flexors produce pure flexion, because the associated radial and ulnar movements negate one another. The primary role of the hand is grasping and manipulation. These fine movements are controlled by intrinsic hand muscles. The superficial palmar ventral group includes the thenar and hypothenar eminences, which move the thumb and fifth digit, respectively. The thumb is rotated 90 degrees in relation to the digits, such that flexion of the thumb moves it medially across the palm of the hand, abduction moves it anteriorly, extension moves it laterally, and adduction moves it posteriorly. The special movement of opposition stems from combined flexion and adduction of the thumb, which brings the palmar surface of the tip of the first digit toward the palmar surface of the tips of any of the other four digits.

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The tendon arrangement around the fingers is complex. The flexor digitorum profundus (FDP) tendon pierces the FDS tendon to attach to the base of the distal phalanx, and the lumbricals attach to the FDP tendons and the extensor digitorum communis (EDC). The EDC tendon connects to the lumbricals, the dorsal interossei, and all three phalanges. This is known as the extensor expansion. This arrangement allows for complex movements, such as unscrewing a pen top while holding it in the same hand.

Acute Hand and Wrist Injuries [2] Distal Radius Fracture [3] Fracture of the distal radius is the most common forearm fracture. The mechanism of injury classically involves a fall onto an outstretched hand, although different subsets of this fracture group may have slightly different etiologies. Classification of distal radius fractures is based on angulation, displacement, intra- or extra-­ articular injury, and ulnar or carpal bone involvement. Distal radial fractures go by many names depending on radiographic presentation and anatomic involvement. These include: Colles’ fracture, Smith’s fracture, Barton’s fracture, and Chaffeur’s fracture. The Colles’ fracture is reported to be the most common distal radius fracture. Specifically, it refers to a radial fracture in the distal 2 cm of the bone, along with dorsal displacement. An ulnar styloid fracture may or may not be present.

Clinical Presentation The most common history provided with regard to this injury is a fall on an outstretched hand with considerable force. The patient usually notes tenderness and swelling at the wrist. Diagnosis Deformity, swelling, tenderness, and loss of wrist range of motion are classic physical exam findings when a distal radius fracture is present. Median nerve function should be assessed at the time of presentation, as well as before and after closed reduction if it is required. Postero-anterior (PA), lateral, and oblique radiographs of the injured forearm should be obtained. Oblique views may reveal intra-articular involvement which may not be apparent on the other views. The examiner should note the direction of displacement, angulation, degree of comminution, presence of intra-articular involvement, and radial length or variance as compared with the unaffected side. Universal Classification of Distal Radius Fracture 1. Nonarticular, nondisplaced 2. Nonarticular displaced: (a) Reducible, stable (b); reducible, unstable (c); irreducible 3. Articular, nondisplaced 4. Articular, displaced: (a) Reducible, stable (b); reducible, unstable (c); irreducible (d) Complex

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Treatment Management of a distal radius fracture involves anesthetizing the affected area and placing the arm in traction to unlock any fragments. The deformity is then reduced with a closed reduction and casted. X-ray is used to ensure that the reduction was successful. It should be noted that maintaining good position in adults is particularly difficult and serial imaging is required. X-rays should be taken weekly for the first few weeks to ensure proper reduction and alignment. If callus is seen on x-ray at 3 weeks, the cast can be replaced with a removable splint. A continued use of a splint with activities for up to 5 months post-injury is often advised. Many orthopedic surgeons favor a more extended period of 6 weeks in a cast, even in the presence of callus formation. After cast removal, a period of rehabilitation is required to allow for recovery of strength and range of motion. Failure of casting is common, and has a large risk of adverse outcomes. Studies have shown that the fracture often re-displaces to its original position in a cast. Long term, this increases the risk of joint stiffness and development of osteoarthritis, leading to chronic wrist pain and loss of function. Given these findings, surgical interventions such as open reduction internal fixation (ORIF), external fixation, or percutaneous pinning are often pursued. Return to Sport Prognosis and return to play correlate with severity of injury, with a nondisplaced extra-articular fracture having a better prognosis than an unstable, displaced intra-­ articular fracture. If managed with a cast, time course to return of play is largely dependent upon healing. Those with nondisplaced fractures may be able to return to play within 8 weeks of the injury, with a continued use of a protective splint. In order to be a candidate for return to play, the patient should exhibit early signs of healing on imaging, and pain should have resided completely. Additional precautions should be taken for those participating in contact sports; and deferment of play for at least a few weeks following the resolution of pain is advisable. After ORIF, athletes may return to play with protection in as little as 3  weeks. This time is increased to 6 weeks if the fracture was displaced. A patient should never return to play if strength and function are not adequate to prevent reinjury.

Wrist Sprain Humans instinctually use an outstretched hand to break a fall when losing balance. Because of this, the wrist is at high risk for injury. A wrist sprain occurs as a result of sudden forceful action at the wrist that transmits forces through supporting ligaments that is beyond their maximal capacity. It is generally a diagnosis of exclusion. A sprain should be distinguished from a fracture or a strain, which involves injury to bone, muscle, or tendon. Wrist sprains are graded on a three-point scale according to severity of injury. Grade I is described as mild; Grade III is severe (see following list). Given the risk inherent to certain activities, protective splints are utilized as a preventive measure in higher-risk sports such as rollerblading, street

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hockey, and snowboarding. It is also generally recommended to avoid using a pole secured to the wrist while skiing.

Clinical Presentation Common complaints when presenting to a physician are pain with the movement of the wrist, swelling around the joint, and bruising. Typically there is a history of acute trauma, such as a fall onto an outstretched hand. Diagnosis The diagnosis of wrist sprain is made based on history and physical exam. X-ray can be used to rule out fracture and is likely appropriate in most cases, given that mechanisms involved in wrist sprain and fracture are often identical. Grading of Wrist Sprain • Grade I: Mild injury, the ligaments are stretched but not torn. • Grade II: Moderate injuries, partial tear of ligaments. • Grade III: Severe injury, ligaments are completely torn with resultant joint instability.

Treatment Treatment of a wrist sprain in the absence of instability is initially with the conservative RICE method (rest, ice, compression, and elevation). The first 24–48 hours are a critical treatment period of relative rest, during which all activities that involve wrist motion should be avoided. This relative rest can be facilitated with the use of a soft but firm neutral wrist splint or Ace wrap. The bandage should be wrapped from the base of the fingers to the top of the forearm; for severe sprains, immobilization at the elbow to limit pronation and supination may be pursued. If the fingers become cold, numb, or tingle, the wrap is too tight and should be adjusted. Activity should be gradually reintroduced after this initial rest period, as tolerated by pain. After the initial period of treatment, the patient advances to rehabilitation exercises aimed at restoring function. Return to Sport The amount of rehabilitation and the time needed for recovery depend on the severity of injury and an individual’s rate of healing. A mild sprain may take as little as 3–6 weeks to recover, while a more severe sprain can take up to 8–12 months. In general, sport can be performed as tolerated after the initial days of healing. If the sport carries increased risk, protective gear is recommended until there is full healing of the injury.

Scapholunate Ligament Disruption [4] Often misdiagnosed as a “wrist sprain,” disruption of the scapholunate ligament is a potentially disabling injury if left untreated. Mechanism of injury is similar

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to that for wrist fractures and sprains, such as a fall onto an outstretched hand with the wrist extended. If left untreated, the injury will progress down a degenerative cascade, resulting in scapholunate advanced collapse (SLAC). This begins with early radial styloid and scaphoid arthritis (as a result of edge-loading), progresses to proximal capitate migration, and eventually leads to pancarpal arthritis.

Clinical Presentation Disruption of the scapholunate ligament will result in carpal instability, generalized wrist pain, and eventual loss of range of motion and degenerative arthritis at the scapholunate articulation. On physical exam, a positive Watson’s test results in a palpable clunk while applying dorsal pressure to the volar scaphoid tubercle while the wrist is passively being moved from ulnar to radial deviation. Diagnosis Standard x-rays of the hand may reveal static instability in the form of abnormal carpal alignment. Stress radiographs may be necessary to demonstrate dynamic instability, also manifesting as abnormal carpal alignment. The deformity appreciated is known as dorsal intercalated segmental instability (DISI), which presents with scaphoid hyperflexion and lunate hyperextension. This is most apparent on lateral x-rays, which may show a scapholunate angle greater than 70 degrees (normal is around 47 degrees). AP radiographs may show a widened scapholunate interval (>3 mm). Comparison of bilateral clenched-fist stress views may be compared to appreciate a diastasis at the scapholunate articulation. MRI is more sensitive than radiographs to detect the ligamentous injury. Arthroscopy is considered the gold standard for diagnosis. Treatment Treatment is contingent upon the severity of the injury. If there is only partial disruption to the ligament, arthroscopic debridement followed by postoperative immobilization may be all that is necessary. Complete scapholunate ligament rupture requires primary open repair with pinning of the scapholunate interval. Other repair techniques include tenodesis, bone-ligament-bone autograft reconstruction, and intercarpal fusion. In cases of chronic instability that have resulted in SLAC, operative options range from radial styloidectomy to total wrist fusion. Postoperative rehabilitation and immobilization is contingent upon the severity of injury and extent of surgical intervention required. In general, for scapholunate ligament repairs, the wrist will subsequently be immobilized in neutral with an above-elbow thumb spica cast for 8 weeks. Following this period of immobility, a passive range of motion exercises are permitted, along with the use of a short arm cast for an additional 4–6  weeks. The focus of the range of motion exercises should be centered around regaining functional movement, with the avoidance of reaching end-range in any plane. Progression to concentric grip and intrinsic hand strengthening follows.

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Return to Sport Even after successful surgical repair, scapholunate ligament injuries may result in long-term deficits in grip strength and range of motion, particularly with wrist flexion and radial deviation. Limited wrist flexion is the most common deficit observed, and patients are often advised against attempting to regain the last 10–20 degrees of wrist flexion as it may put them at risk for weakening surgical reconstruction. Athletes are permitted to return to sports once there is clinical evidence of complete healing and stabilization of the unstable joints affected, which may take up to 6 months following surgery.

Triangular Fibrocartilage Complex (TFCC) Injury At the distal end of the ulna exists a meniscus homologue, which stabilizes the distal radioulnar joint (DRUJ). This meniscus is known as the triangular fibrocartilage complex (TFCC). It is anchored to the ulnar styloid via dorsal and volar radioulnar ligaments. As a load-bearing cushion, the TFCC may bear up to 20% of the load across the wrist in individuals with neutral ulnar variance. Those with a propensity toward positive ulnar variance will ultimately place relatively more stress through the TFCC, which can result in central thinning of the central articular disc component. Additional degenerative injury to the TFCC may manifest as small chronic degenerative tears and eventual chondromalacia of the lunate. A tendency toward positive ulnar variance may be idiopathic or acquired, from prior malunion or growth arrest. Additionally, TFCC injuries can be traumatic, following an acute rotatory injury, such as a fall onto an extended wrist with forearm pronation, resulting in a tear. Traumatic TFCC tears are classified according to tear location. About 10–40% of the periphery of the TFCC is well-vascularized; however, the central portion is avascular and prone to poor healing.

Clinical Presentation Patients will present with ulnar-sided wrist pain following an acute rotatory injury, or following repetitive force-loading through the wrist, particularly in individuals with positive ulnar variance at baseline. The individual may complain of pain with rotatory activities, such as attempting to turn a door key. A peripheral tear at the base of the ulnar styloid may present with DRUJ instability. Diagnosis Physical exam may reveal a positive “fovea sign,” which is tenderness at the region of soft tissue between the ulnar styloid and the flexor carpi ulnaris tendon between the volar surface of the ulnar head and the pisiform. The fovea sign is 95% sensitive and 87% specific for disruption of the TFCC or ulnotriquetral ligament injuries. Patients may also present with pain with either active or passive ulnar deviation (TFCC compression), as well as radial deviation (TFCC tension). X-rays of the wrist are usually unrevealing. A zero-rotation PA view may be used to evaluate for

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positive ulnar variance. MRI may be used to confirm the diagnosis, and may reveal a tear at the ulnar portion of the lunate, indicative of ulnocarpal impaction. The sensitivity of MRI is between 75% and 100%. Arthroscopy remains the gold standard for diagnosis, but is reserved for patients who continue to be symptomatic despite months of conservative care. TFCC injuries are divided into two classes: Class 1 (traumatic) and Class 2 (degenerative). Each of these is further subdivided: • Class 1 – Traumatic TFCC injuries –– 1A: Central perforation or tear –– 1B: Ulnar avulsion (without ulnar styloid fracture) –– 1C: Distal avulsion (at the origin of the ulnolunate and ulnotriquetral ligaments) –– 1D: Radial avulsion • Class 2 – Degenerative TFCC injuries –– 2A: TFCC wear and thinning –– 2B: Lunate and/or ulnar chondromalacia + TFCC wear and thinning –– 2C: TFCC perforation + lunate and/or ulnar chondromalacia + TFCC wear and thinning –– 2D: Ligament disruption + TFCC perforation + lunate and/or ulnar chondromalacia + TFCC wear and thinning –– 2E: Ulnocarpal and DRUJ arthritis + ligament disruption + TFCC perforation + lunate and/or ulnar chondromalacia + TFCC wear and thinning

Treatment Initial management is almost always nonoperative, unless DRUJ instability is appreciated on exam, in which case surgery is likely to be pursued. Conservative care consists of immobilization in a neutral wrist splint, nonsteroidal anti-­ inflammatories, and steroid injections for cases of refractory pain. Gradual return to activity is permitted based on symptoms. Isometric wrist strengthening and attention to biomechanics and ergonomics at the wrist are key components of successful rehabilitation. Any DRUJ instability requires arthroscopic repair of a likely peripheral tear, and associated ulnar styloid fracture must be ruled out. Taken together, these conditions are amenable to internal fixation and surgical TFCC repair. In individuals with chronic positive ulnar variance, ulnocarpal impaction may be addressed surgically via an open ulnar shortening osteotomy or a wafer procedure, wherein a burr is used to remove the distal 1–4 mm of the ulnar through an associated central TFCC tear. Following simple surgical debridement, a short period of immobilization can be followed soon thereafter with a simple range of motion exercises. Following surgical repair, patients may be placed in a sugar-tong splint for 2 weeks, followed by a short arm or Munster cast for an additional 4 weeks. This is followed by range of motion, and strengthening at 10 weeks post-surgery.

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Return to Sport Acute TFCC tears that are surgically repaired within 3 months of onset regain about 80% of strength and range of motion. Poor functional outcomes are associated with continued ulnar positive variance, loss of grip strength, and reduced range of motion. Athletes are typically cleared to return to sport within 6–12 weeks of initial injury.

Scaphoid Fracture [5] Scaphoid fractures are the most common carpal bone fracture, and are typically associated with a fall on an outstretched arm while the wrist is in forced hyperextension and radial deviation. Since pain may improve soon after the fall, a patient may not present to a clinician until late after the injury. This late presentation puts the patient at risk for avascular necrosis. Only one small artery enters the bone, at the end that is closest to the thumb. If the fracture tears the artery, the blood supply is lost and avascular necrosis is the ultimate result.

Clinical Presentation If a patient presents early, the key examination finding is tenderness in the anatomical snuffbox. This may be accompanied by swelling and loss of grip strength. More specific clinical tests for acute scaphoid fracture include (1) pain on axial compression of the thumb toward the radius or (2) pain on direct pressure on the scaphoid tuberosity with radial deviation of the wrist. Diagnosis Given high risk for avascular necrosis, tenderness in the anatomical snuffbox necessitates further workup to rule out scaphoid fracture. Patients may also have point tenderness to the scaphoid tubercle on the volar aspect of the palm. Plain x-ray with scaphoid views may demonstrate the fracture; however, normal x-ray does not exclude the diagnosis of a fracture. Standard wrist trauma x-ray series (PA, lateral, oblique, and scaphoid [30 degrees of wrist extension with 20 degrees of ulnar deviation]) will not yield a diagnosis in over 30% of cases. In cases in which imaging is negative but clinical suspicion is high, MRI or bone scan can be pursued and may reveal a fracture not visualized on x-ray. If an MRI or bone scan is not available, the wrist should be immobilized for 2–3 weeks in a thumb spica cast in order to give the fracture time to present on x-ray. A subsequent x-ray may show a radiolucent line, representing bone resorption at the fracture site. In patients presenting months after injury, avascular necrosis can be visible on x-ray. Treatment Most literature suggests that suspicion for a scaphoid fracture warrants immediate placement in a thumb spica splint or cast until radiographic confirmation can be obtained. If a nondisplaced distal fracture is diagnosed, treatment entails a short arm thumb spica cast in slight extension with the thumb IP joint left free. A distal pole fracture should be immobilized for 4–6 weeks, a waist fracture for 10–12 weeks,

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and a proximal pole fracture for 12–20 weeks. These are guidelines, and as a rule, immobilization should be continued until union is documented on serial radiographs. Following the immobilization of a scaphoid fracture, the patient usually develops stiffness and loss of mobility at the wrist joint, as well as wasting and atrophy of the thenar muscles. Mobilization of the joint should begin immediately after plaster removal. For a fracture displaced >1  mm and/or presence of altered scapholunate angle or documented nonunion (humpback deformity), immediate orthopedic evaluation is warranted as ORIF may be indicated.

Return to Sport Nondisplaced fractures that are treated with a short arm thumb spica cast can participate in sport after initial healing is documented. After the removal of the cast, the wrist should be protected by a rigid splint for an additional 2 months or until the strength in the affected wrist is at least 80% of the uninjured side. Return to sport can be achieved after an open reduction and internal fixation surgery. After ORIF, patients are immobilized in a long arm thumb spica cast for about 6 weeks, followed by a short arm thumb spica cast. Active rehabilitation is usually delayed until the evidence of union is appreciated on x-ray or CT.

Hook of the Hamate Fracture Fracture of the hamate can occur while swinging a golf club, tennis racquet, or baseball bat. There is often a history of blunt trauma to the palm. The fracture is especially likely to happen if the golf club strikes the ground instead of the ball, forcing the top of the handle of the club against the hook of the hamate. This mechanism may also compress the terminal branches of the ulnar nerve, producing sensory and motor changes.

Clinical Presentation Patients usually present with reduced grip strength, numbness and tingling in the distribution of the ulnar nerve, and ulnar-sided wrist pain after an acute, high-energy trauma to the palmar aspect of the hand in the region overlying the hamate. Diagnosis Early examination reveals tenderness over the hook of the hamate. Swelling may or may not be prominent. Plain x-rays of the wrist do not image the fracture; instead, carpal tunnel views with the wrist in dorsiflexion or an ulnar oblique view must be obtained to fully evaluate the involved anatomy. Hamate fractures may go undiagnosed until there is rupture of the long flexor tendon of the small finger. Treatment The hook of the hamate serves as the point of attachment for hypothenar muscles, and when fractured through the base, there is predisposition toward nonunion due to unopposed muscle activity at the bony fragment. As a result, this fracture rarely

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heals with immobilization. Surgical removal of the fractured hook followed by 3  weeks of wrist immobilization is usually required. After this, a comprehensive rehabilitation program is undergone to restore full mobility and function.

Return to Sport Assuming no complications and proper healing, sport can be resumed 6 weeks after surgery.

 CL Tear/First Metacarpophalangeal Instability (Gamekeeper’s U Thumb, Skier’s Thumb) [6] Injury to the thumb ligament is one of the most common skiing injuries, ranking second only to knee sprains. Skier’s thumb is a strain or tear to the thumb’s major stabilizing ligament—the ulnar collateral ligament of the MCP joint of the thumb. The ulnar collateral ligament assists with grasping, pinching, and stabilizing items in the hand. “Skier’s Thumb” usually refers to an acute sprain or tear injury to the UCL, while “Gamekeeper’s Thumb” references a chronic and repetitive stress to the ligament, which renders it lax and nonfunctional.

Clinical Presentation Forced hyperextension and abduction of the thumb may result in sprain or disruption of the ulnar collateral ligament. Injury to the thumb while skiing usually results from a fall on an outstretched hand that continues to hold the ski pole. At impact, the thumb is driven directly into the snow and is bent back or to the side, away from the palm and index finger, resulting in a sprain or complete disruption of the ligament. When injured, the ulnar collateral ligament cannot support the thumb, making grasping or pinching with the thumb difficult. Patients often will complain of pain and swelling along the ulnar aspect of the MCP joint. This initial complaint of pain may progress to weakness or instability. Diagnosis Valgus stress determines the laxity of the ulnar collateral ligament. An incomplete rupture is characterized by 5 degrees than the uninjured thumb. X-rays should be performed to rule out avulsion. In the absence of avulsion, x-rays are negative. MRI can be performed to determine the relationship of the torn ligament to its surrounding muscles. This may be useful if surgery is required. A Stener lesion is present in 80% of complete tears, and consists of interposition of the adductor pollicis aponeurosis between the avulsed UCL and its insertion site on the base of the proximal phalanx. This prevents healing of the UCL tear and requires surgical ligamentous repair. On ultrasound evaluation, the normal ulnar collateral ligament will appear hypoechoic, and situated on the ulnar aspect of the joint between the head of the metacarpal and the proximal phalanx. If a sprain is present, there will be relative hypoechogenicity

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of the injured segment, but no loss of continuity. With partial tears, there may be incomplete loss of continuity with an associated hematoma or joint effusion (anechoic); full tears will show full-thickness loss of continuity. Avulsed bone fragments may appear as small hyperechoic formations attached to the ligament.

Treatment Referral to an orthopedist or hand surgeon is indicated when x-ray shows an avulsed fragment >11 mm displaced from its origin. Referral is also appropriate for those with complete ligament tears determined by physical exam and/or ultrasound. For nonsurgical candidates, ice should be immediately applied to the affected area. A dorsal hood or thumb spica splint is used to immobilize the joint for at least 4–6 weeks. As a preventive measure to avoid injury, skiers can use strapless poles. An additional protective measure is to advise skiers to discard poles when they fall, which will ultimately prevent radial deviation of the thumb upon impact. For a previously injured thumb, athletes can utilize a glove with a built-in splint. Return to Sport After an incomplete injury, the thumb must remain completely protected for 4 weeks, after which a removable splint is used for an additional 2 weeks fulltime, followed by activities for up to 3 months. A gentle range of motion exercises can begin within 4–6  weeks; however abduction of the thumb should be avoided for a minimum of 12 weeks. In most cases, full return to sports can be resumed by 1 month in mild non-operative cases, and 4 months in more severe cases requiring surgery.

Metacarpal Shaft/Neck Fracture Injury to the metacarpals is caused by many different etiologies. Typically, fractures are classified according to bony pathology (transverse, oblique, or spiral). The fracture pattern tends to correlate with injury mechanism. Direct or axial injury results in a transverse or oblique fracture, whereas torsional force tends to cause a spiral fracture. Fractures of the fifth metacarpal neck are among the most common hand fractures, and are most often associated with striking a solid object with a closed fist. Although these fractures have been nicknamed “boxer’s fractures,” they rarely occur during boxing. A skilled fighter is more likely to fracture the index metacarpal, given that this is along the greatest line of force when throwing a punch with correct form.

Clinical Presentation Fracture of the metacarpal is usually a result of force applied to a clenched fist or a direct blow to the hand. A patient will usually provide a history consistent with such an injury. Pain and swelling are typical complaints. Asymmetry of the knuckles may also be apparent.

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Diagnosis Metacarpal fractures are easily diagnosed by localized tenderness and swelling on physical exam. In addition, there is loss of the normal contour of the dorsum of the finger. Ecchymosis on the palmar surface is highly suggestive of fracture. X-ray can be used to confirm what is clinically suspected. Treatment Treatment of metacarpal fractures focuses on reduction when necessary and splinting. Splints should be forearm-based and allow motion at the IP joint. They should extend over the dorsal and palmar aspect of the entire affected metacarpal. Generally, the wrist should be placed in 20–30 degrees of extension and the MCP joint immobilized in 70–90 degrees of flexion. Buddy taping the fingers can aid in maintaining some degree of rotational control. After a short period of immobilization, patients should be encouraged to use the affected finger. With regard to metacarpal shaft fractures, only small amounts of angulation are acceptable. The exact degree is dependent on the digit involved. The more proximal the fracture, the more pronounced the deformity and the less angulation that is acceptable. All malrotation must be addressed surgically. Metacarpal neck fractures can tolerate a larger degree of angulation (50–60 degrees). Rarely does a neck fracture require surgery. Open fractures always require operative debridement and irrigation followed by stable internal or external fixation. The patient should be monitored throughout the healing process with serial imaging to ensure proper positioning. Return to Sport Immobilization does not usually extend beyond 4 weeks. At this time, there is usually evidence of healing on imaging. After this period of initial immobilization, an orthotic should be used for additional 4–6 weeks when participating in sports.

Digital Extensor Tendon Injury (Mallet Finger) [7] “Mallet finger,” also known as “baseball finger,” is caused by sudden passive flexion of the extended DIP joint, causing rupture of the extensor tendon. It is also known as baseball finger because it can occur when a finger is “jammed” while catching a ball. The digital extensor tendon can be disrupted in various zones; mallet finger is caused by disruption of zone 1, the terminal extensor tendon at or distal to the DIP joint from a sudden forced flexion of an extended fingertip.

Clinical Presentation Clinically, the DIP joint presents as flexed, and cannot be actively extended. The patient may give a history of a ball “jamming” the finger. Diagnosis Mallet finger is diagnosed by physical examination. On exam, the patient is asked to actively extend the fingertip. If the most distal joint cannot be straightened

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actively, then a diagnosis of mallet finger is most likely. Other physical exam findings suggestive of mallet finger include swelling and tenderness around the fingertip. An x-ray may be indicated to rule out avulsion if clinically suspected. Chronic mallet finger may result in prolonged DIP flexion and resultant swan-neck deformity. The underlying anatomical correlates include attenuation of the transverse retinacular ligaments at the PIP joint, dorsal subluxation of the lateral bands, and PIP hyperextension.

Treatment Conservative treatment involves splinting of the DIP in extension for 6–8  weeks with a stack splint. Position should be checked weekly to prevent contracture formation. For the 2 weeks following initial splinting, gentle active flexion and nightly splinting should be performed. If healing is poor, or there is an avulsed fragment, then surgical treatment may be indicated. Surgical repair typically involves direct repair of the tendon, but may also involve percutaneous pinning through the DIP joint if there is volar subluxation of the distal phalanx. Return to Sport If the splint is worn as indicated, activity can be resumed immediately. Certain sports are more risky than others with regard to re-injury, and a decision to return to play must be made on a case-by-case basis. Not seeking medical attention immediately after injury and failing to allow complete healing can lead to permanent injury or deformity of the hand. In complex cases with multiple associated injuries and surgical repair, athletes may not be cleared to return to play until full postoperative healing has occurred, which typically requires 3–4 months.

 lexor Digitorum Profundus Tendon Avulsion Injury F (Jersey Finger) [8] Jersey finger refers to an injury to the flexor digitorum profundus tendon resulting in an inability to bend the fingertip. The common action in all injuries is extension of the finger against resistance, more specifically, a forced extension of the DIP during grasp. This is most often noted in athletes who grab one another’s jerseys. Strain, rupture, or avulsion occurs when the jersey is pulled from the athlete’s finger. The fourth digit is the most commonly involved digit because of its limited independent extensibility (75% of cases).

Clinical Presentation Patients usually complain of pain when moving the injured finger and an inability to bend the last joint. A “pop” or “ripping” sensation may have been felt in the finger at the time of injury. The patient will be unable to flex the distal phalanx with the PIP joint held in extension.

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Diagnosis Diagnosis is based largely on history and physical exam. The finger can be passively, but not actively flexed, and a nodule may be felt in the palm or finger, representing retracted or swollen tendon. There may be tenderness along the course of the FDP. After 48 hours, ecchymosis is common. X-rays may be used to rule out an associated fracture. Treatment The initial phase of rest, ice, and elevation is usually followed by surgery. Surgery consists of open inspection of the FDP and pulley system to determine extent of disruption, followed by reattachment of the tendon to the distal phalanx. Rehabilitation protocols begin with protected range of motion early on to increase tendon excursion and decrease adhesion formation. After 6–8 weeks, blocking exercises and passive range of motion in extension can begin. Between 8 and 14 weeks, tendon gliding may begin, with progression to full active and passive range of motion. Return to Sport Return to sports is usually not recommended for at least 3 months after surgery.

Finger Dislocations Traumatic dislocations are not uncommon in the hand, and are most common at the PIP and DIP joints. Additionally, dislocations may also occur at the MCP joints and thumb CMC. Both PIP and DIP joints act as hinge joints, protected against radial and ulnar deviation by proper and accessory ligaments. PIP joint dislocations may occur in the volar, dorsal, or lateral planes. Dorsal PIP dislocations result from PIP joint hyperextension with longitudinal compression, such as with a ball striking a fingertip. DIP joint dislocations are often associated with nail bed injuries and fracture of the distal phalanx. They are typically dorsal or lateral and often associated with avulsion of the volar lip and associated FDP. MCP dislocations are typically dorsal dislocations that result from a fall onto the hand with hyperextension of the MCP joint. The index finger is the most commonly involved digit, and up to 50% of cases have a concomitant fracture of the base of the proximal phalanx or metacarpal head. CMC dislocation is typically associated with very high-energy trauma, with axial force placed on a flexed thumb, which results in dorsal dislocation.

Clinical Presentation In all dislocations, patients often present with pain and deformity at the affected digit. There may be puckering of the overlying skin, indicating interposition of soft tissues within the joint. Dorsal PIP dislocations will present with a swan-neck deformity, while volar PIP dislocations will present with a boutonniere deformity.

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CMC dislocations will present with pain, bruising, and swelling over the thenar eminence, and inability to form a fist.

Diagnosis Clear deformity is usually apparent visually and palpably on physical exam. AP, lateral, and oblique x-rays of the hand should be pursued to evaluate for joint alignment and, at the very least, should be performed post-reduction to ensure proper joint repositioning. They are not often required prior to reduction unless crush injury or complex fractures are also suspected. X-rays performed prior to reduction may show joint space widening. In the case of MCP dislocation, entrapment of a sesamoid within the MCP joint is indicative of a complex dislocation, which requires open (surgical) reduction. MRI is reserved for persistent and recurrent instability after reduction, and is used to guide surgical ligamentous reconstruction. Treatment Treatment for PIP and DIP dislocations is closed reduction and splinting, followed by buddy-taping or splinting for 3–6 weeks for a dorsal dislocation and 6–8 weeks for a volar dislocation. If volar plate entrapment blocks reduction, or a concurrent fracture results in joint instability, open reduction and internal fixation may be required. In MCP dislocations, reduction is followed by immobilization in a dorsal blocking splint (30 degrees of flexion) for 2  weeks, which is followed by active range of motion in the dorsal blocking splint. Following CMC reduction, the joint is immobilized in extension and pronation for 6–8 weeks, followed by gradual return to range-of-motion activities.

Overuse Wrist and Hand Injuries [9] De Quervain’s Tenosynovitis De Quervain’s tenosynovitis is a painful inflammation of the sheath of the extensor pollicis brevis (EPB) and abductor pollicis longus (APL) tendons, and is caused by either repetitive overuse or direct trauma to the thumb tendons as they pass over the distal radial styloid. If left untreated, inflammation may result in fibrosis, with a resultant loss in flexibility and mobility of the thumb. This condition is known as stenosing tenosynovitis.

Clinical Presentation Common complaints are pain and tenderness on the radial side of the wrist, loss of grip strength, and localized swelling over the radial styloid. Diagnosis Diagnosis is made largely on history and physical exam. Imaging is generally not necessary, except to rule out other pathology, such as in the case of trauma and if fracture or soft tissue disruption is suspected. Musculoskeletal ultrasound may

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reveal fluid within the tendon sheath, irregularity in the expected fibrillar structure of the tendon itself, and/or hyperemia on Doppler. In chronic disease, there may be little to no fluid in the tendon sheath. Physical signs include localized swelling and tenderness and pain with passive ulnar deviation of the wrist toward end-range, which places tension on the affected tendons. Global loss of thumb and/or wrist active range of motion may be present. Physical exam assesses the area of tenderness, thumb range of motion, and provocative maneuvers. Finkelstein’s test is a classic special test, which attempts to elicit pain by passively stretching the thumb tendons over the radial styloid while the thumb is flexed. Diagnosis can be confirmed by an anesthetic block over the radial styloid.

Treatment Noninvasive methods of treatment include frequent application of ice at the radial styloid to reduce local inflammation and the use of a dorsal hood splint or thumb spica splint to allow for relative rest. The available evidence shows that steroid injection is the most effective treatment, with about 70% of patients responding to the maximum of two injections. Injections should be spaced at least 6 weeks apart. Surgical intervention is generally not considered until failure of 1 year of conservative management. Physical therapy does not play a prominent role in treatment of De Quervain’s tenosynovitis. It does, however, play a role in preventing recurrence. Stretching the extensor and abductor tendons into the palm can be performed in sets of 20 with each stretch being held for 5 seconds. Return to Sport After injection, gripping, grasping, and direct pressure over the styloid should be avoided for 3  days. The wrist should be protected for 3–4  weeks with a thumb spica splint.

Carpal Tunnel Syndrome Carpal tunnel syndrome (CTS) is a compression neuropathy of the median nerve. Although compression of the median nerve can occur at multiple levels, CTS refers to compression at the wrist by the transverse carpal ligament. The floor of the carpal tunnel consists of the carpal bones and the roof is formed by the flexor retinaculum. Proximally, the walls of the tunnel are formed by the pisiform on the ulnar side, and the scaphoid bone on the radial side; distally, the walls are formed by the hook of the hamate on the ulnar side, and the tubercle of the trapezium on the radial side. Nine flexor tendons and one nerve, the median nerve, pass through the carpal tunnel. CTS is the most common compression mononeuropathy. It frequently affects racquet sport athletes, cyclists, and wheelchair athletes. The primary overuse-­ associated risk factor is repetitive wrist flexion. Other associated risk factors include female sex, obesity, pregnancy, hypothyroidism, and diabetes. Rarely, CTS can result from a direct trauma to the volar wrist, such as with a high-energy trauma resulting in a distal radius fracture and fracture-dislocation of the radiocarpal joint.

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Clinical Presentation The degree of symptoms depends on the chronicity and degree of compression. Symptoms can progress from purely sensory to include motor loss with associated thenar atrophy. Sensory loss occurs at the tips of the first three fingers and may travel to the palmar forearm and wrist. Grip weakness may occur in more severe and advanced cases. Patients typically state that symptoms are worst at night, when the wrists are often held in pronounced flexion posture, or after participating in a repetitive activity that requires finger and/or wrist flexion. Symptoms are classically experienced in the palmar aspect of the radial 3 ½ digits. Large sensory fibers (light touch and vibration) are affected before small fibers (pain and temperature). Chronic compression resulting in demyelination, fibrosis, and axonal loss will result in motor weakness in median distribution distal to the carpal tunnel. Diagnosis History and physical exam are highly suggestive of the diagnosis of CTS. Sensation should be tested in the median nerve distribution, as should the strength of thumb opposition. Provocative tests include Tinel’s sign and Phalen’s sign. Tinel’s sign involves tapping over the transverse carpal ligament with the wrist held in extension. Phalen’s sign involves holding both wrists in extreme volar flexion for 30–60 seconds. The most sensitive provocative test is the carpal compression test, also known as Durkin’s test, which involves application of pressure over the volar wrist at the level of the carpal tunnel while the arm is held in a supinated position. A positive test results in numbness and tingling in the median nerve distribution within 30 seconds of continued compression. Electromyography (EMG) and nerve conduction studies (NCS) can be performed to confirm clinical suspicion. NCS testing is positive in approximately 70% of cases. It should be noted that a negative NCS does not exclude the possibility of median nerve compression. If symptoms are intermittent and mild, NCS/EMG may be normal. In these cases, a median nerve block can be used to confirm the diagnosis. Musculoskeletal ultrasound findings in carpal tunnel syndrome include median nerve enlargement, hypoechogenicity of the nerve, and loss of normal fascicular appearance. The flexor retinaculum may be enlarged, hypoechoic, and show volar bulging. These findings tend to occur later in the course of the disease, and mild CTS may show a normal-appearing nerve and retinaculum under ultrasound. Doppler may demonstrate hypervascularity within the nerve. Additionally, fluid within the flexor tendon sheaths may be visible on ultrasound, indicating simultaneous flexor tenosynovitis. Musculoskeletal ultrasound can also be used to evaluate the cross-sectional area of the median nerve. The cross-sectional area should be evaluated and measured at both the level of the carpal tunnel and more proximally, at the level of the pronator quadratus muscle. A difference in cross-sectional area of greater than or equal to 2 mm^2 is strongly associated with symptomatic CTS. Treatment Mild-to-moderate CTS can be managed conservatively, whereas advanced CTS requires surgical release to prevent further neurological injury. Conservative

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management includes activity modification in order to minimize provocative factors. This may require reduced gripping, grasping, or repetitive wrist motion. A soft but firm neutral wrist splint with a metal stay to allow for relative rest is also recommended. At the least, the splint should be used at night. When indicated, a steroid injection can assist with symptom management. Corticosteroid injection is advanced just through the transverse carpal tunnel ligament to bathe the nerve and relieve inflammation. Steroid injections result in temporary relief in up to 80% of patients; however only 22% remain symptom-free at 12 months. At 1 year, 40% are symptom-­ free only if their symptoms were present for less than 1 year prior and they demonstrate normal two-point discrimination, no thenar atrophy, and no denervation potentials on EMG. No response to steroid injection is associated with poor outcomes even if and when surgical intervention is pursued. Surgical intervention is reserved for refractory cases, and/or cases with significant associated motor or sensory loss as evidenced on NCS/EMG. Surgery involves the release of the transverse carpal ligament on the ulnar side of the median nerve; it can be performed open or endoscopically. If surgery is pursued, post-operative rehabilitation consists of immobilization in a neutral wrist splint for only 3–4 days, after which point patients are encouraged to move their wrist, hand, and fingers as soon as possible.

Return to Sport Those suffering from CTS can participate in sport as tolerated. Splints as described in the treatment section may assist with avoiding aggravating factors. If surgery has been pursued, patients are encouraged to return to activities of daily living as soon as possible, with gradual reintroduction to sporting activities and resistance exercises over 6–8 weeks post-operative.

Ulnar Nerve Palsy Ulnar nerve palsy at the wrist (Handlebar palsy) is a common problem for competitive and recreational cyclists. Compression is the result of direct pressure on the ulnar nerve as the cyclist grips the handlebars and in some cases, depending on body mechanics, places weight and force through the hypothenar region of the palm. Additionally, the nerve may be stretched or hyperextended when a drop-down handlebar is held in the lower position. Due to the change of riding position and shape of handlebars (horn handle) in recent years, a single bicycle ride may be sufficient to cause disruption of the ulnar branch. This is especially relevant in downhill riding when a large proportion of bodyweight is supported by the hand on the corner of the handlebar, leading to a high load at Guyon’s canal. Guyon’s canal is bordered by the volar carpal ligament (roof), the transverse carpal ligament (floor), the hook of the hamate (radial), and the pisiform and abductor digiti minimi muscle belly (ulnar); it is about 4 cm long and divided into three zones: (1) proximal to the bifurcation of the nerve; (2) surrounding the deep motor branch; and (3) surrounding the superficial sensory branch. The most common cause of ulnar nerve palsy is not direct trauma, but rather a ganglion cyst compressing the nerve within or on either side of

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the canal (80% of nontraumatic cases). Other potential causes include nonunion of the hook of the hamate, ulnar artery thrombosis, hypertrophy of the palmaris brevis, or an anomalous muscle.

Clinical Presentation The ulnar nerve controls sensation in the fourth and fifth digits, and controls most of the muscular function of the hand (hand intrinsics). The pressure placed on the ulnar nerve results in numbness and tingling in the ring and little finger, intrinsic muscle weakness, or a combination of both. Symptoms may be purely motor, purely sensory, or a combination based on the zone that is being compromised. Diagnosis Diagnosis is made largely on the basis of history and physical exam. Localization can be confirmed by performing EMG/NCS studies. CT can be used to rule out a fracture of the hook of the hamate, and MRI may be useful to rule out a ganglion cyst or other space-occupying lesion. Musculoskeletal ultrasound may also reveal a ganglion as a well-defined, poorly-compressible anechoic mass within or surrounding the pisohamate tunnel. Doppler can be used to evaluate for the evidence of thrombosis. With large, macroscopic nerve lesions, changes in normal ulnar nerve fibrillar appearance can be appreciated. Anomalous muscles may also be seen on ultrasound. Treatment Symptoms can take several days to months to resolve, but surgical treatment is rarely necessary. Rest, stretching exercises, and anti-inflammatory medications usually help relieve symptoms. Activity and biomechanical modification centered around applying less pressure or weight to the handlebars and avoiding hyperextension can help to prevent a recurrence. Other advisable changes include padded gloves, wrist splints, and adjusting the position of the hands on the handlebar. Operative treatment consists of decompression of the canal via a transverse carpal ligament release; this can also address concomitant carpal tunnel syndrome. Return to Sport Those suffering from ulnar neuropathy can participate in sport as tolerated. However, adjustments should be made to reduce the risk of reinjury.

Flexor Tenosynovitis (Trigger Finger) Trigger finger refers to an inflammation of the flexor tendon sheath of the finger. The flexor tendons for each digit course through a sheath located between the metacarpal and distal interphalangeal joint. Specifically, the flexor digitorum superficialis attaches to the middle phalanges and the flexor digitorum profundus attaches to the distal phalanges. Repetitive trauma can cause inflammation of the flexor tendon and sheaths at the metacarpophalangeal joint. The resultant abnormal gliding

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impairs the flexion pulley system, and ultimately forms a nodule in the tendon. As the digit flexes, the nodule passes under the pulley system and will become caught on the annular sheath, typically at the A1 pulley, locking the finger into a flexed position. The primary repetitive overuse risk factor is repeated grasping activities. Other associated risk factors include female sex, diabetes, and rheumatoid arthritis.

Clinical Presentation Patients often report pain and more commonly, popping, snapping or locking when they flex and/or extend the affected digit. They often complain of a locking of the finger into a flexed position. There may be pain and tenderness in the distal palm near the location of the A1 pulley. Diagnosis Diagnosis is based on history and physical exam. On exam, there is tenderness at the base of the finger. Clicking or locking with flexion may be noted. In addition, a nodule may be felt at the base of the finger. A local anesthetic block can be used to confirm diagnosis but is rarely necessary. Musculoskeletal ultrasound can be used to visualize associated A1 pulley thickening, which presents as marked hypoechogenicity of the A1 pulley. There may be concomitant tenosynovitis of the involved tendon, which manifests as fluid within the tendon sheath. A clinical classification scheme developed by Green is divided into four stages: • • • •

Stage 1: pain and tenderness at the A1 pulley Stage 2: catching of the digit with flexion and/or extension Stage 3: clear locking of the digit, which is passively correctable Stage 4: locked digit that is fixed in place

Treatment Conservative treatment involves the use of NSAIDs and steroid injections, as well as physical therapy. All of these interventions reduce swelling of the tendon, allowing it to glide freely in and out of the sheath. A single injection is all that is needed in 50% of cases. A further 25% will respond to a second injection (i.e., three fourths of patients can be successfully treated in this way). Injection is generally well tolerated without side effects, but occasionally the skin around the injection site can become thinned by the steroid; therefore, two injections are generally considered to be the maximum. Surgery may be indicated if steroid injections are unhelpful. Surgical intervention involves a small procedure under local anesthetic. The A1 pulley is released via a longitudinal incision at the level of the distal palmar crease. The digit is then passively flexed and extended to ensure that triggering has ceased. Return to Sport After injection, the finger should be allowed relative rest for 3 days. Following this initial period of rest, the fingers can be used but in a protected manger (buddy taped) for the next 3–4 weeks. Repetitive grasping, gripping, and vibration should be avoided, with gradual reintroduction of range of motion followed by activities of daily living.

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Intersection Syndrome (Oarsman’s Wrist) Intersection Syndrome, also known as “Oarsman’s Wrist,” is used to describe a tenosynovitis at the intersection of the first (APL, EPB) and second (ECRL, ECRB) dorsal compartments. Proximal to their insertions, the ECRL and ECRB tendons pass beneath the tendons of the APL and EPB. With repetitive wrist extension, friction at the crossover point can result in intersection syndrome, affecting the long abductor and short extensor of the thumb, and the short radial extensors of the wrist. It commonly presents in rowers and golfers, as well as those who perform repetitive wrist extension.

Clinical Presentation Patients often complain of dorsal forearm and wrist pain proximal to the radioulnar joint. They may describe a history of crepitance or “creaking” about 5 cm proximal to Lister’s tubercle, a bony prominence located at the distal end of the dorsal radius. Diagnosis Physical exam may reveal tenderness and crepitus at palpation about 5 cm proximal to the wrist joint on the dorsal side. This is especially marked with resisted wrist extension and simultaneous thumb extension. Imaging is generally not required. X-rays of the wrist will be unrevealing. MRI may be pursued if the differential is otherwise large and to confirm a diagnosis. In fluid-sensitive sequences, the most likely MRI finding is peritendinous edema or fluid surrounding the first and second extensor compartments. Tendinosis, muscle edema, tendon thickening, and loss of the normal “comma shape” of the tendon may also be seen. Bedside musculoskeletal ultrasound will show fluid within the tendon sheaths, most commonly involving the ECRL and ECRB tendons. Rarely, a small effusion can be appreciated in the tendon sheath of the first dorsal compartment, or a serous bursa with bursitis can be seen located between the two tendon groups. Treatment Intersection syndrome rarely requires surgery is often amenable to conservative treatment with activity modification, relative rest, nonsteroidal anti-inflammatories, and if needed, injections and splinting. Steroid injection is aimed into the second dorsal compartment, which contains the ECRL and ECRB tendons. Surgical intervention is only indicated in those who have failed an extensive and concerted course of conservative care. Surgical intervention may involve surgical release of the second compartment with debridement of the bursa at the intersection of the two compartments. Following surgery, the wrist may be splinted in 10 degrees of extension for 2 weeks, followed by early gentle hand, wrist, and finger range of motion exercises. This is progressed to tendon glides and strengthening exercises as tolerated. Return to Sport Patients who follow a conservative plan of care may return to sporting activities as dictated by pain symptoms, in as early as 3–4 weeks. Patients who have undergone

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surgical compartment release may return to basic activities of daily living within 1 month, but will require a more gradual return to resistive activities, returning to sport in 3–4 months. Following reduction, it is important to clinically assess for stability of the joint. Lateral stress should be applied with the joint in full extension and 30 degrees of flexion. Injury to the collateral ligaments can be divided into three grades: (1) pain with no laxity; (2) laxity with a firm endpoint and stable arc of motion; and (3) gross instability with no endpoint. Additionally, neurovascular testing should be performed, with special attention to perfusion and sensation distal to the dislocation, as well as in the adjacent digits. It is not uncommon for patients with digit dislocations to experience traction neuropraxia from stretch injury to adjacent digital nerves. Complications include PIP flexion contracture (pseudoboutonniere), swan neck deformity, mallet finger deformity, and joint stiffness with progression to early osteoarthritis. In children, dislocations may result in premature physeal closure.

Return to Play Patients can typically return to play within 6–8  weeks with continued splint or buddy tape use while in play to protect against reinjury. Continued splint use may be discontinued by 3–4 months if there is no evidence of laxity or ongoing pain.

Suggested Readings 1. Slaby FJ, McCune SK, Summers RW.  Gross anatomy in the practice of medicine. 1st ed. Baltimore: Lippincott Williams & Wilkins; 1994. 2. Rettig AC. Athletic injuries of the wrist and hand. Part I: traumatic injuries of the wrist. Am J Sports Med. 2003;31(6):1038–48. 3. Scneppndahl J, Windolf J, Kaufmann RA. Distal radius fractures: current concepts. J Hand Surg. 2012;37:1718–25. 4. Lewis DM, Lee Osterman A.  Scapholunate instability in athletes. Clin Sports Med. 2001;20:131–40. 5. Meals C, Meals R. Hand fractures: a current review of treatment strategies. J Hand Surg Am. 2013;38:1021–31. 6. Brunton LM, Graham TJ, Atkinson RE. Hand injuries. In: Miller M, Thompson SR, DeLee J, Drez D, editors. DeLee & Drez’s orthopedic sports medicine principles and practice. Philadelphia: Saunders; 2015. p. 884–907. 7. Lin JD, Strauch RJ. Closed soft tissue extensor mechanism injuries (mallet, boutonniere, and sagittal band). J Hand Surg Am. 2014;39:1005–11. 8. Netscher DT, Badal JJ. Closed flexor tendon ruptures. J Hand Surg Am. 2014;39:2315–23. 9. Rettig a C. Athletic injuries of the wrist and hand: part II: overuse injuries of the wrist and traumatic injuries to the hand. Am J Sports Med. 2004;32(6):262–73. 10. Miller MD, Chhabra B, Konin J, Mistry D, Mistry D. Sports medicine conditions: return to play, recognition, treatment, planning: Wolters Kluwer Health; 2013. 11. Mesplie G.  Hand and wrist rehabilitation: theoretical aspects and practical consequences. Switzerland: Springer; 2015.

Chest Trauma and Thoracic Spine Injuries

13

Ilya Aylyarov, Kevin Kuo, and Amie Kim

Introduction With increasing participation in high-contact sports, providers should be familiar with a wide range of trauma to the torso. Most chest injuries are benign and self-­ limiting, but more critical injuries to the chest can be rare and catastrophic. Sideline providers should be well versed in several, immediately life-saving procedures. Proper diagnosis and management ensure safe participation, while prompt interventions can prove life-saving.

Anatomy Bones The skeletal thoracic cage protects the viscera of the chest and the upper abdomen. It includes the sternum, 12 pairs of ribs, and 12 thoracic vertebrae in the spinal column. The first seven ribs are the true ribs because they attach directly to the sternum through costal cartilage. Ribs 8–10 are the false ribs because they have an indirect connection to the sternum by a shared cartilage of the adjacent rib. Ribs 11 and 12 I. Aylyarov (*) Department of Emergency Medicine, NYU Medical Center/Bellevue Hospital, New York, NY, USA e-mail: [email protected] K. Kuo Emergency Department, Mount Sinai St. Luke’s and West, New York, NY, USA A. Kim Emergency Department, Physical Medicine & Rehabilitation, Mount Sinai Beth Israel Medical Center, New York, NY, USA © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_13

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Clavicle

Manubrium Sternal angle

True ribs (1-7)

Body

Sternum

Xiphoid process

False ribs (8-10) Floating ribs (11,12)

Fig. 13.1 Thoracic bony cage, anterior. (Printed with permission from © Mount Sinai Health System)

are the floating ribs, because they terminate in the posterior abdominal muscles and do not meet the sternum. The sternum is divided into the manubrium, body, and xiphoid process [7] (see Figs. 13.1 and 13.2).

Nerves The ribs and their costal cartilages are separated by the intercostal spaces. Each space is innervated by an intercostal nerve and supplied by an intercostal artery and vein. The intercostal nerves form from the ventral rami of the thoracic spinal nerves T1 to T11. Together, this forms the neurovascular bundle that travels inferiorly along each rib margin and deep to each intercostal muscle group.

Muscles and Ligaments On the bony thoracic cage are the primary thoracic muscles (see Figs. 13.3 and 13.4). At the anterior chest, the pectoralis major medially rotates, adducts, and flexes the humerus. The pectoralis minor depresses the shoulder and protracts the scapula. The subclavius is a glenohumeral joint stabilizer through clavicle adduction and shoulder depression. At the posterior chest, the ribs provide bony attachment to musculature of the neck and back. The serratus anterior at the lateral thorax rotates the scapula and pulls it against the thoracic wall. The serratus posterior attaches at the vertebrae and the ribs to assist with inspiration [7].

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Scapula True ribs (1-7)

False ribs (8-10)

Floating ribs (11,12)

Fig. 13.2 Thoracic bony cage, posterior. (Printed with permission from © Mount Sinai Health System)

Clavicle

Sternocleidomastoid Subclavius

Pectoralis major Pectoralis minor Sternum

Fig. 13.3  Anterior thoracic wall muscles, superficial and deep. (Printed with permission from © Mount Sinai Health System)

Deep to the muscles of the anterior and posterior chest wall, the intercostal spaces include the external and internal intercostal muscles. They are continuous with the external and internal obliques, respectively, and facilitate respiratory inspiration and expiration, respectively. The innermost intercostal muscles lie deep to the intercostal nerves and vessels.

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Trapezius Rhomboid minor Deltoid Rhomboid major

Erector spinae Serratus anterior Latissumus dorsi

Serratus posterior External oblique Internal oblique

Fig. 13.4  Posterior thoracic wall muscles, superficial and deep. (Printed with permission from © Mount Sinai Health System)

Lungs The lungs facilitate the uptake of oxygen and removal of carbon dioxide. Each lung is covered by pleural membrane. The visceral pleura lines the lung surface, while the parietal pleura lines the chest wall. The pleural cavity is the potential space between the two pleurae and can pathologically accumulate air (pneumothorax) or blood (hemothorax) (see Fig. 13.5). Lung alveoli are the terminal branches of the respiratory bronchioles and the primary interface for gas exchange with pulmonary vasculature. This network is particularly vulnerable to trauma with subsequent respiratory collapse [36].

Heart The heart is responsible for delivering oxygen and nutrients while removing metabolic waste and by-products. The contractility of the heart is driven by its electrical conduction system. The sinoatrial node generates an electrical P wave through both atria. The impulse passes through the atrioventricular node, bundle of His, and

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Fig. 13.5  Thoracic cavity. Right demonstrates large pneumothorax with chest drainage inserted through chest wall. Left demonstrates normal pulmonary space. (Printed with permission from © Mount Sinai Health System)

Fig. 13.6 Normal electrocardiogram. (Adapted from “ECG Interpretation from pathophysiology to clinical application” by F. Kusumoto (2009), New York: Springer. Springer Publications Copyright)

P wave

T wave QRS

Purkinje network, terminating in the ventricles to generate the QRS complex. The ventricles generate a T wave during repolarization. Disturbances to this conduction can lead to fatal dysrhythmias (see Fig. 13.6).

Acute Injuries Pulmonary Contusion Mechanism of Injury/Pathophysiology Pulmonary contusion occurs with significant trauma to the chest wall and leads to alveolar hemorrhage, increased permeability, and decreased lung compliance. Mediated by inflammatory cytokines, the injury can develop into acute respiratory distress syndrome (ARDS) and respiratory failure [8]. Clinical Presentation Athletes present with pleuritic chest pain, dyspnea, and tachypnea. They may be hypoxic and hypercarbic due to ventilation perfusion mismatch from alveolar injury.

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Fig. 13.7  Chest x-ray demonstrates left-sided pulmonary contusion. (Adapted from “Chest radiography diagnosis of pulmonary contusion is associated with increased morbidity and mortality” by Cobanoglu [7], Indian Journal of Thoracic and Cardiovascular Surgery. Springer Publications Copyright)

Physical exam reveals tenderness to palpation along the chest wall, chest wall ecchymosis, and rales on lung auscultation.

Diagnosis Diagnosis should be clinically suspected. Chest x-ray can range from patchy opacification to consolidation, though initial radiographs can be normal (see Fig. 13.7). With further suspicion for injury, Chest CT with contrast is superior in visualizing contusion pattern and will typically demonstrate peripheral parenchymal opacification. Point-of-care ultrasound is helpful in immediate assessment [45]. The linear probe is placed over the suspected site of injury. An area of B lines over the injured lung can be characteristic of a pulmonary contusion (see Fig. 13.8). Treatment Athletes are likely to be hypoxic; therefore supplemental oxygen through nasal cannula or non-rebreather should be initiated. Adequate pain control is vital to prevent splinting, a decreased inspiration due to pain. If victims exhibit respiratory distress or are persistently hypoxic, the clinician should consider advanced airway strategies such as bag-valve mask ventilation or rapid sequence intubation. The goal is to re-­ expand the injured lung by forcing air into the damaged alveoli through positive end expiratory pressure (PEEP). By maintaining a set of alveolar pressure at the end of expiration, PEEP can recruit collapsed alveoli and push pulmonary edema out of the alveoli.

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Fig. 13.8  Sonographic findings of normal lung vs injured lung. Left: “A lines,” horizontal lines caused by pleural reverberation artifacts, reflect normal physiology. Right: “B lines” over injured lung segment, hyperechoic artifactual vertical lines originating from the pleura, reflect pulmonary edema. A positive study must contain at least three “B lines” and travel a minimum depth of 18 cm. (Reproduced from The POCUS Atlas)

Any athlete suspected of pulmonary contusion should be referred to the nearest emergency department for definitive imaging and airway management if needed. A subset of moderate to severe pulmonary contusions can develop pneumonia or ARDS within 24–48 hours [52]. The majority of athletes with pulmonary contusions will ultimately be managed supportively [8].

Return to Play Mild pulmonary contusion typically resolves without further intervention over 7–10 days. Athletes may return to regular activity once asymptomatic. Those with additional injuries such as pneumothorax or flail chest should expect a significantly prolonged recovery time. Depending on the severity of the chest trauma, pulmonary contusions can lead to decreased pulmonary function, namely, decreased functional residual capacity following injury, which can persist months to years [24].

Rib Fractures Mechanism of Injury/Pathophysiology Acute rib fractures occur with a traumatic force to any of the 12 rib segments of the thoracic cavity. Simple rib fractures are benign and self-resolve. The middle ribs are

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commonly injured, and displaced fracture segment risks injury to underlying viscera. The clinician should have a high suspicion for additional injuries at their respective pulmonary or abdominal levels. The first rib is in a protected position posterior to the clavicle, but fracture risks neurovascular injury to the brachial plexus and subclavian vessels.

Clinical Presentation In the setting of recent thoracic trauma, athletes can present with pain at the site of injury and compromised inspiratory effort. Physical exam may reveal bruising and bony tenderness to palpation. It is important to note any vital sign abnormalities such as tachypnea and hypoxia. The most severe complication is flail chest, three or more consecutive rib fractures at two points. This creates a floating rib that causes a flail segment of the chest wall to move paradoxically with the rest of the chest wall by moving inward during inspiration and outward during expiration. Flail chest is associated with a significant mortality rate between 10% and 15% [39].

Diagnosis Most rib fractures are diagnosed clinically. Isolated rib fractures can result from relatively minor trauma and are self-limiting. Anteroposterior and lateral chest x-ray is evaluated, and dedicated rib films are usually not mandatory (see Fig. 13.9). Chest x-ray however will only identify about 50% of all rib fractures. Confirmatory imaging is typically not required unless there is suspicion for multiple rib fractures or underlying injuries. Ultrasonography can reliably detect rib fractures although can be somewhat uncomfortable for the athlete due to the pressure exerted by the probe [18, 46] (see Fig. 13.10).

Treatment For simple rib fractures, adequate pain control, rest, and ice are typically sufficient through resolution. An incentive spirometer is used to prevent pulmonary atelectasis. Intercostal nerve block can aid in pain control [19]. Rib taping is no longer recommended as it can impede inspiratory effort. Multiple rib fractures or flail chest should be referred to the emergency department as they may require supplemental oxygen or advanced airway management.

13  Chest Trauma and Thoracic Spine Injuries Fig. 13.9  Chest x-ray of rib fractures. Acute traumatic posterior fractures of ribs 5 through 8. (No photo cred needed)

Fig. 13.10 Sonographic appearance of displaced rib fracture. Ultrasound demonstrates hyperechoic density with step-off in the middle revealing a displaced rib fracture seen with the linear probe. (Reproduced from The POCUS Atlas. Submitter: Dr. Stephen Alerhand)

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Return to Play Return to play depends on the athlete’s level of pain and functionality following the injury. Typically rib fractures require 4–6 weeks to heal, though the pain and discomfort can persist for months [34]. Athletes can return to contact activity if they exhibit painless and full chest excursion without analgesia. Although most rib fractures selfresolve, serial imaging may be obtained to assess for callus formation and alignment [33]. Rarely, a small percentage of rib fractures will exhibit nonunion, and surgical referral may be indicated if pain persists beyond the expected recovery time [6].

Sternal Fractures Mechanism of Injury/Pathophysiology Sternal fractures typically occur with trauma to the chest wall such as with football helmet or other sporting equipment [42]. They are high-energy injuries, and athletes should be evaluated for associated injuries to the lung, heart, and bony skeleton.

Clinical Presentation Injured athletes will complain of chest pain or shortness of breath with inspiration. Physical exam shows tenderness to palpation along the sternum, ecchymosis, swelling, or visible deformity which suggests a displaced fracture. A detailed examination should include assessment of the neurovasculature of the upper extremities as well.

Diagnosis An anteroposterior and lateral chest x-ray should be obtained to rule out concomitant intrathoracic injuries. Lateral and oblique views can evaluate fracture displacement or dislocation [50] (see Fig.  13.11). CT scan remains the gold standard modality and can detect nondisplaced sternal fractures more reliably than x-ray (see Fig. 13.12). Similar to rib fractures, point-of-care ultrasonography can aid in diagnosing long bone injury [37].

Treatment In athletes with isolated sternal fractures, adequate pain control and outpatient follow-­up are appropriate [25]. With any suspicion for fracture displacement, dislocation, or concomitant injuries, referral to the nearest emergency department for surgical stabilization should be obtained due to high risk of mediastinal injury [22].

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Fig. 13.11 Lateral radiograph demonstrates sternal fracture of anterior cortex (arrow). (Adapted from “Isolated sternal fracture – a swing-related injury in two children” by Defriend et al. [10], Pediatric Radiology, Springer Publications Copyright)

a

b

Fig. 13.12  Computed tomography of the chest demonstrates subacute transverse fracture through sternal body (arrow). (Adapted from “Sternal Injuries in Sport: A Review of the Literature” by Alent et al. [1], Sports Medicine, Springer Publications Copyright)

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Return to Play Athletes suffering isolated sternal fractures have a great prognosis with a 10-week mean recovery time [11]. Nonunion is rare, and athletes may return to sport once the fracture has radiographically healed and pain is no longer limiting.

Pneumothorax Mechanism of Injury/Pathophysiology A pneumothorax is the collection of air in the pleural cavity between the chest wall and the lung. This can either be spontaneous or traumatic. Traumatic pneumothorax occurs when air enters the pleural space through direct penetration from the external chest wall or rupture of the lung and alveoli. They are classified into three types: 1. Simple  – air enters the pleural cavity without communication with the atmospheric air. In blunt trauma, this is due to fractured rib causing pleural laceration or traumatic alveoli rupture. 2. Communicating – air enters the pleural cavity from direct communication with atmospheric air. This typically occurs in penetrating trauma and is termed as a “sucking chest wound.” Air escapes in and out of the defect due to paradoxical motion of the chest wall during inspiration and expiration. 3. Tension – wound acts like a one-way valve leading to a rapid accumulation of air within the pleural space. This produces a mass effect and compressive shifting of the mediastinal structures into the opposite hemithorax.

Clinical Presentation Victims complain of shortness of breath, chest pain, and dyspnea upon exertion. Physical exam findings may include hypoxia, a deviated trachea, distended neck veins, hyperresonance on percussion, and decreased lung sounds. An athlete with a pneumothorax exhibiting tension physiology will look acutely ill, with hemodynamic instability due to compression of surrounding cardiopulmonary structures.

Diagnosis Ultrasonography can more rapidly and accurately detect a pneumothorax than conventional chest x-ray and is part of the initial extended FAST (focused assessment with sonography for trauma) exam [2, 49] (see Fig. 13.13). If ultrasound is unavailable, an anteroposterior and lateral chest x-ray should be rapidly obtained. Tension pneumothorax must be recognized clinically given the risk of rapid decompensation. Absent or diminished unilateral breath sounds, distended neck veins, mediastinal shift, or obstructive shock should prompt immediate intervention.

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Treatment Treatment of a simple pneumothorax in symptomatic athletes includes administration of high flow oxygen to assist with air resorption within the pleural cavity [12, 17]. Small pneumothoraces (15–30%) should be admitted to the hospital for further monitoring and serial chest x-rays, while larger pneumothoraces require insertion of a chest tube and surgical management. In individuals with a communicating wound, the wound should be immediately covered with a partially occlusive dressing to convert the open pneumothorax into a closed pneumothorax. Due to the possibility of converting into a tension pneumothorax, these individuals need monitoring for decompensation (see Fig. 13.14).

Fig. 13.13  Sonographic findings of normal lung vs pneumothorax. Left: “Seashore” sign with normal lung sliding. Right: “Barcode” sign with absent lung sliding. Sonographic “lung point” displays normal lung sliding adjacent to an area without lung sliding. It is pathognomonic for pneumothorax. (Reproduced from The POCUS Atlas. Submitter: Dr. Eric Roseman)

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Fig. 13.14 Open pneumothorax dressing. Three-way occlusive dressing applied over open pneumothorax defect. This allows air to escape through the open end during expiration while preventing air from entering during inspiration. (No photo cred needed)

If tension physiology is suspected, immediate needle decompression is mandated. Large-bore catheter or IV cannula is inserted into the second intercostal space in the midclavicular line or fifth intercostal space in the anterior axillary line. A large hiss of air is heard upon release of the trapped air within the pleural cavity [44].

Return to Play There are no clear guidelines for return to play, but activities should not resume until about 1 month after resolution of pneumothorax [43]. Spontaneous pneumothorax has a high rate of recurrence, but no data suggest a recurrence pattern in traumatic pneumothorax. Athletes can progressively increase their physical activity if they remain asymptomatic and pain-free.

Commotio Cordis Mechanism of Injury/Pathophysiology Commotio cordis, translated from Latin “agitation of the heart,” is among the most common causes of sudden cardiac death in young healthy athletes [3]. It

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refers to a fatal ventricular fibrillation caused by a precisely timed chest wall impact. In early ventricular repolarization, the vulnerable window is 10–30 milliseconds before the peak of the T wave, where a force against the chest wall causes ventricular depolarization and subsequent electrical deterioration [29]. Small spherical objects carry a higher commotio cordis risk than large nonspherical objects [21].

Clinical Presentation The typical presentation will be a blunt traumatic injury to the anterior chest wall leading to sudden collapse and cardiac arrest. An immediate electrocardiogram or defibrillator will reveal ventricular fibrillation.

Diagnosis Commotio cordis is diagnosed clinically in the setting of directed blunt trauma and cardiac collapse.

Treatment Cardiopulmonary resuscitation is immediately initiated. Automated external defibrillators should be readily available to initiate early defibrillation. Once defibrillated, victims should experience a return of spontaneous circulation otherwise continue cardiopulmonary resuscitation efforts.

Return to Play Commotio cordis is commonly fatal, especially if defibrillation is delayed, with a 25–35% survival rate. Surviving victims should be taken to the nearest emergency department [30]. Additional cardiac injury or structural abnormality should be evaluated, with a minimum observation period on telemetry for the next 12  hours. Before return to play, survivors must clear a complete cardiac workup including echocardiography, stress tests, magnetic resonance imaging, and other pharmacologic testing for Brugada and long QT syndrome [26]. An interdisciplinary preventative approach including coaching, blocking techniques, and sporting equipment design should be implemented to reduce the rate of commotio cordis. Chest protective equipment have showed variable success in preventing commotio cordis [31].

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Pectoralis Major Tear Mechanism of Injury/Pathophysiology Pectoralis major tear has become increasingly more common with popularity in recreational strength training. The most common mechanism of injury is during the “bench press” when the arm is abducted and externally rotated and the muscle undergoes maximal eccentric contraction [40]. This results in tendinous ruptures or tears at or near the humeral insertion site of the muscle [3]. In contrast, direct blunt force trauma to the athlete such as a punch or helmet to the chest wall causes ruptures of the muscle belly itself.

Clinical Presentation Athletes may report a history of excessive tension or impact to the pectoral region. Sometimes an audible pop may be heard, along with a sharp tearing pain and weakness along the chest and shoulder girdle. Physical exam can reveal swelling or ecchymosis of the affected side, with tenderness to palpation and pain with movement. A more specific sign of pectoralis major tear is the loss of the anterior axillary fold compared to the unaffected side [5]. A bulging mass may also be appreciated (see Fig. 13.15).

Diagnosis Pectoralis major tear is typically a clinical diagnosis. Radiographic imaging can aid if bony avulsion injury is suspected. Ultrasound can evaluate the extent and location

Fig. 13.15  Diagnosis of acute tendon tears of the pectoralis major muscle. Loss of anterior axillary fold (white arrows and solid circle) on affected side relative to unaffected side (dashed circle). (Adapted from “Clinical results of a surgical technique using endobuttons for complete tendon tear of pectoralis major muscle: report of five cases” by Uchiyama et  al. [47], Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology. Springer Publications Copyright)

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of the myotendinous rupture [41]. MRI of the pectoralis major remains the gold standard for presurgical evaluation and planning.

Treatment Initial management consists of rest, ice, analgesia, and sling immobilization with the shoulder adducted and internally rotated. Expedited surgical repair of pectoralis major tears should be considered in all operative candidates [16]. Nonoperative management is typically reserved for partial tears or minor muscle belly rupture. Physical therapy begins with gentle range of motion.

Return to Play Surgical management of pectoralis major tears usually results in excellent return of function and pre-injury level of activity within 6–12 months of repair. In general, conservative management leads to poorer outcomes in pain, function, and strength [9, 23].

Stress Fracture: Ribs Overuse Injuries Mechanism of Injury/ Pathophysiology Ribs are nonweight-bearing bones but subject to significant traction forces from inserting muscle attachments. Athletes who perform repetitive tasks of the upper extremities or increased loading of the ribs are at risk for stress fractures, and atraumatic rib pain should be carefully evaluated. Athletes in rowing, throwing, golf, weight lifting, and swimming are at particular risk. Repetitive upper extremity activity generates opposing tensile and compressive forces that stress the bony rib cage. Stress insertions include the serratus anterior, middle, and lower fibers of the trapezius, the external obliques, and the rectus abdominis [32, 35].

Clinical Presentation Patients endorse a recent increase in activity load, but the mechanism will be atraumatic. Pain is typically gradual in onset, exacerbated by activity, especially rib cage torque or upper extremity rotation. Exam may show point tenderness at the affected site or increased pain with deep inspiration and position change. Active range of motion at the glenohumeral joint, resisted flexion and extension of the trunk, and protraction and retraction of the scapula can reproduce symptoms [13, 32].

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Fig. 13.16  Bone scintigraphy scan with radioisotope uptake (circled) at the right anterolateral sixth rib demonstrates fracture. (Adapted from “Rib stress fractures among rowers: definition, epidemiology, mechanisms, risk factors, and effectiveness of injury prevention strategies” by McDonnell et al. [32], Sports Medicine. Springer Publications Copyright)

Diagnosis A radiographic rib series is the initial test of choice, but findings can be delayed by 2–12 weeks, particularly in non-displaced fracture [32]. Callus formation may be the only indication of a prior stress fracture on serial imaging. Bone scintigraphy has high sensitivity and can diagnose multiple bony stress injuries simultaneously. It can identify injuries earlier than plain radiographs but also lags behind symptom resolution (see Fig.  13.16). MRI carries similar sensitivity and higher specificity than bone scans in detecting stress injury and can delineate associated injuries. Ultrasonography has also been demonstrated to aid in diagnosis [13, 32, 35].

Treatment Initial treatment involves activity restriction, including upper limb activities, for 1–2 weeks until symptoms improve. Nearly all athletes have complete resolution of symptoms with 6–8 weeks of progressive return to activity, although injury may lag radiographically. Most rib stress fractures resolve without complication, but athletes who continue provocative activity risk fracture malunion or displacement.

Return to Play Rehabilitation should focus on scapular and shoulder stabilization exercises, core muscle strengthening, and correction of forward head posture [27]. Conditioning should be

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addressed, as muscle fatigue with sustained exercise load alters mechanics and force distribution [13, 32]. Athletes should be pain-free with truncal twisting movements and resisted upper extremity motion before return to play. Abdominal exercises in particular should be avoided and are the last exercises to resume.

Stress Fracture: Sternum Mechanism of Injury/ Pathophysiology Stress fractures of the sternum are associated with extreme upper body stress such as in golf, weight-lifting, or hyperflexion of the torso in wrestling. Sternal muscle attachments generate repetitive and opposing forces on the sternum and costal cartilage that eventually exceed bony tensile strength. These muscles include the sternocleidomastoid at the manubrium, sternocostal head of the pectoralis major anteriorly, the sternohyoid and sternothyroid posteriorly, and the rectus abdominis distally [4, 15].

Clinical Presentation Athletes endorse increased intensity in chest or abdominal training. They will describe anterior chest pain ranging from dull to progressively sharp in the context of sustained exercise. The pain may be worse with movement or deep inspiration. On exam, there may be swelling and tenderness with peri-sternal palpation.

Diagnosis The initial diagnostic of choice is anteroposterior and lateral chest x-ray. Lateral and oblique sternal views can also be included. Findings can be subtle, particularly in non-displaced fracture, with MRI for definitive evaluation (see Fig. 13.17) [4, 15].

Treatment Sternal stress fracture is a low-risk fracture. Initial management is conservative; rest from the causative activity and pain management for weeks to months will resolve symptoms. Unlike traumatic sternal fractures, they are generally not accompanied by intrathoracic trauma and do not require cardiopulmonary monitoring [4, 15].

Return to Play When athletes are symptom-free, a progressive strengthening program is indicated before return to play. Refer to “Stress Fracture: Rib,” for return-to-play guidelines [4, 15].

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Fig. 13.17  MRI of a weight-lifter demonstrating left lateral sagittally oriented fracture of the manubrium (arrows in a and b) with surrounding bone marrow and periosteal edema: (a) axial T2-weighted images, (b) coronal STIR images, and (c) coronal T1-weighted images. (Adapted from “Manubrial stress fractures diagnosed on MRI: report of two cases and review of the literature” by Baker and Demertzis [4], Skeletal Radiology. Springer Publications Copyright)

Slipping Rib Syndrome This injury is also known as Tietze’s syndrome, rib-tip syndrome, clicking or snapping rib, and traumatic intercostal neuritis.

Mechanism of Injury/Pathophysiology Slipping rib syndrome is attributed to hypermobility of the false ribs that are not directly connected to the sternum but through shared cartilage of the adjacent rib. A weakness or separation at the anterior costal cartilage or the costochondral, sternocostal, and costovertebral ligaments can cause subsequent overriding of adjacent ribs and intercostal nerve impingement [14, 15, 28]. Seen in contact sports like football, wrestling, or hockey, it can be caused by rib cage compression or injury to the articulation site when the arm is forcefully abducted from neutral.

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Clinical Presentation Athletes may describe insidious onset or a pop at the time of injury followed by a sharp pain at the costal cartilage site. Pain is exacerbated by deep inspiration or trunk movement, and a clicking sensation may be felt as the cartilage overrides the bone with palpable deformity [14, 28]. Pain may be reproduced by “hooking maneuver,” which involves hooking the fingers under the costochondral junction and pulling the rib cage anteriorly and superiorly. Referred pain due to shared spinal cord roots of visceral sympathetic nerves and intercostal nerves, particularly over the eighth and ninth ribs, results in pain that can mimic appendicitis, biliary or renal colic [14].

Diagnosis Slipping rib syndrome is primarily a clinical diagnosis. Chest x-ray or radiographic rib series are generally unremarkable but can rule out concomitant injury. Local anesthetic injection can be used as a diagnostic maneuver. Dynamic ultrasound has been described for evaluating ribs 6–10. Cine clip images are obtained in a supine patient. In the short axis, beginning at the ossified portion of the lateral rib and scanning medially to the cartilaginous tip, hooked or dysmorphic appearance of the rib tips can be seen. Abdominal crunch maneuver or rib push maneuver (ultrasonographer uses graded pressure in a deep and cranial motion just below the rib tip of interest) can evaluate dynamic laxity or displacement. Valsalva maneuver has also been studied but found to be insensitive (see Fig. 13.18) [14, 28, 48].

Treatment Conservative management includes activity modification. Long-acting anesthetic injection with or without corticosteroid is considered. Rib strapping has been described, with caution for reduced inspiratory effort. Surgical resection of the costochondral junction with sparing of the intercostal nerve or repair of cartilage may be indicated for failed conservative management [14, 15, 28].

Return to Play This injury is slow to resolve, and 9–12 weeks of restricted activity may be required. Athletes may return to play when asymptomatic, but complete healing is rare. These athletes are prone to reinjury and may benefit from extra padding such as a rib protector in contact sports [28].

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Fig. 13.18 Sagittal ultrasound images of the eighth and ninth ribs (a) at rest (b) during the crunch maneuver demonstrating the ninth rib moving deep to and abutting the adjacent eighth rib. (Adapted from “Dynamic ultrasound in the evaluation of patients with suspected slipping rib syndrome” by Van Tassel et al. [49], Digital Skeletal Radiology. Springer Publications Copyright)

Scapulothoracic Bursitis Mechanism of Injury/Pathophysiology Also known as snapping scapula syndrome or scapulothoracic crepitus, inflammation occurs at the interface between the scapula and the thoracic wall. The articulation site is without joint capsule or synovial lining but is instead lined with bursae that allow for smooth, gliding movement [20, 38, 51]. The four potential bursal sites of injury include the scapulothoracic (infraserratus) bursae at the superomedial angle and at the inferior angle of the scapula, the scaphotrapezial (trapezoid) bursa, and the subscapularis (supraserratus) bursa (see Fig. 13.19). Repetitive overhead activities of the upper extremity, such as baseball pitching or freestyle swimming, cause bursal inflammation. Structural lesions that cause abnormal gliding at the scapulothoracic articulation can be a mechanical cause for this injury. These include a normal variant of anterior bending of the upper scapula toward the thoracic wall, bony prominence of the superomedial angle of the scapula known as Luschka’s tubercle, or osteochondromas of the ribs or scapula [20, 38, 51].

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Fig. 13.19  Illustrations of the scapula and scapular bursae seen on (a) posterior and (b) axial views. (Adapted from “Scapulothoracic pathology: review of anatomy, pathophysiology, imaging findings, and an approach to management” by Osias et  al. [38], Skeletal Radiology. Springer Publications Copyright)

Clinical Presentation Athletes will report a history of shoulder overuse or a single event of injury and nonspecific pain under the scapula. Periscapular fullness and scapular winging may be seen [20]. Crepitus may be palpated at the scapulothoracic articulation with shoulder motion. Athletes with kyphotic postural abnormalities may be prone to injury.

Diagnosis Scapulothoracic bursitis is typically a clinical diagnosis. Plain radiographs may identify osseous lesions that contribute to bursitis. Ultrasonography with color flow Doppler can detect bursal inflammation (see Fig.  13.20). Rarely, scapulothoracic bursitis may be visualized as well circumscribed lesions on MRI sequences. Diagnostic injection of local anesthetic into the bursa may relieve pain and confirm diagnosis [20, 38, 51].

Treatment A trial of conservative therapy with biomechanical evaluation with postural training and resistance training of scapular stabilizers is recommended. Ultrasound-guided aspiration or corticosteroid injection has been used, with a risk of iatrogenic pneumothorax cautioned. If nonoperative treatment fails or space-occupying lesions are identified, surgical resection of the symptomatic scapulothoracic bursa may be indicated [20, 38, 51].

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Fig. 13.20  Scapulothoracic bursitis as seen on (a) longitudinal ultrasound image with septated anechoic fluid (white arrows) superficial to the thoracic wall and deep to the surface musculature, (b) axial T2 FSE, and (c) axial T1 images with hyperintense fluid (long arrow) deep to the serratus anterior (short arrow) and superficial to the thoracic wall (arrowheads). (Adapted from “Scapulothoracic pathology: review of anatomy, pathophysiology, imaging findings, and an approach to management” by Osias et al. [38], Skeletal Radiology. Springer Publications Copyright)

Return to Play Athletes should avoid repetitive activities that reproduce pain including upper extremity overhead motions. Improvement is typically seen within 3–4 months, and return-to-play protocol can be initiated with painless resisted shoulder and scapular maneuvers.

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Thoracic Spine Injuries Injuries to the vertebral column cluster at junctional areas where a rigid spinal segment articulates with a relatively flexible segment. These include the craniocervical (occiput to C2), cervicothoracic (C7 to T1), and thoracolumbar (T11 to L2) junction. The notable stiffness of the thoracic spine is due to the constraining effects of the bony rib cage and relatively thinner intervertebral discs. Refer to “Cervical Spine” and “Lumbar Spine” chapters for shared acute and overuse injury patterns.

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Vandana Sood and Jonathan S. Kirschner

Introduction Low back pain is one of the most common reasons for seeking medical care and is frequent in athletes and nonathletes alike. The lifetime prevalence is thought to be as high as 80–90% [1]. In 2013, 57 million patients presented to physicians with a complaint of back pain. This number does not capture those who are treated by chiropractors, physical therapists, or others involved in caring for back pain [2]. Despite extensive efforts, low back pain remains a leading cause of disability particularly in industrialized countries. In athletes, low back pain comprises 10–15% of all sports injuries and is the most common spine-related reason for missed playing time [3]. In one study of American collegiate football players, 30% lost playing time due to low back pain [4]. Lumbar spine pain is much more common than cervical or thoracic spine pain. The prevalence of low back pain in athletes ranges from 1% to 30% [3]. Rates are dependent on many factors including chosen sport and position, gender, training, frequency, and intensity [5–7]. A pilot study at the Sydney Olympics demonstrated that elite athletes have more low back pain and degenerative disc disease than their peers [8]. Despite the prevalence of symptoms, low back pain in athletes generally tends to be self-limited.

V. Sood NewYork-Presbyterian Hospital, New York, NY, USA Weill Cornell Medicine, New York, NY, USA e-mail: [email protected] J. S. Kirschner (*) Weill Cornell Medicine, New York, NY, USA Hospital for Special Surgery, New York, NY, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_14

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Evaluation There are a number of common sources of lumbar spine pain in athletes, and their frequency varies based on age. A study comparing 100 adolescent athletes with low back pain to adult athletes with low back pain found that nearly half of the adolescents had pain related to spondylolysis or bone stress fracture, whereas this accounted for symptoms in only 5% of the adult patients. Conversely, disc-mediated pain was the source of low back pain in 48% of the adults but only 11% of the adolescents. Pain related to degenerative changes in the spine became more of a contributor in older athletes [9]. In adolescent athletes, the skeletal system is immature, and repetitive stress can result in overuse injuries such as spondylolysis. When comparing adolescent athletes to their nonathletic peers with low back pain, the prevalence of spondylolysis increases from 2% to 32% [10]. Young athletes are less likely to present with muscle strains than adults. In the adult athletes, the bone is skeletally mature, and changing forces across the body result in an increased presentation of discogenic pain related to herniation. In the senior athlete, degenerative conditions such as lumbar stenosis and facet arthrosis are more likely to be the pain generators [6, 9, 11]. Medical causes of LBP such as infection and neoplasm are less common but must not be forgotten particularly in the very old and very young where they tend to be relatively more common. When evaluating the lumbar spine, an anatomic review is helpful in identifying potential pain generators.

Bone The bony complex of the lumbar spine involves the vertebral bodies, spinous and transverse processes, pars interarticularis, superior and inferior articular processes, pedicles, and the sacrum (Fig. 14.1). Fig. 14.1  Lumbar spine anatomy. (Springer Image) Lumbar vertebra

L4

Facet joint Spinous process

Disc

Foramen for spinal nerve

L5 Lumbar vertebra

Sacrum

Spinal nerve

S1

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Spinal Variants In the lumbar spine, there are typically five vertebral bodies between the rib cage and the sacrum. Variants exist where there are four or six lumbar vertebral bodies. This occurs due to the sacralization of the L5 vertebra or the lumbarization of the S1 vertebra, known as a transitional segment. The presence of either of these variants may affect the biomechanical forces around the hip and spine. Another common spinal variant is the enlargement of the transverse processes of L5 which can then either articulate or fuse with the sacrum on one or both sides. When this becomes symptomatic, it is called Bertolotti’s syndrome. This leads to decreased motion at the L5-S1 segment and can result in excessive stress and early degenerative changes at the L4-L5 level.

Scoliosis The pre-participation physical is an opportunity to perform a routine wellness exam and evaluate for scoliosis. In adolescents, curvature between 20 and 40 degrees requires close monitoring as curvature can increase during periods of rapid growth. However, unless the spinal curvature is severe enough to impact pulmonary function, it should not impair sports performance.

Scheuermann’s Disease Etiology and Clinical Presentation Scheuermann’s disease or juvenile osteochondrosis of the spine is a condition where three consecutive vertebrae in the thoracic spine are wedged >5 degrees resulting in thoracic kyphosis. It is a common cause of back pain in adolescents, occurring in boys and girls equally, with a prevalence of 4–8% in the general population [12]. It is thought to be due to weakening of the cartilaginous vertebral body end plates secondary to repetitive microtrauma and fatigue failure. There is often a genetic predisposition to this condition [13]. Clinically, the athlete will present with a kyphotic curve that is more abrupt than one that is typically observed with postural round back. It is also not correctable with position change. The Adam’s test is helpful in assessing the degree of curvature. The kyphosis is often accompanied by hyperlordosis of the cervical and lumbar spine and can also be associated with scoliosis. An atypical lumbar variant also exists in which the affected vertebrae are between T10 and L4 [14].

Work-Up Classic signs on imaging include disc space narrowing, irregularities of the vertebral end plates and Schmorl’s nodes [15]. Disc herniation with resulting compression of the thecal sac may also be seen.

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Treatment First-line treatment includes physical therapy and bracing, which is most effective when initiated prior to skeletal maturity. Juvenile kyphosis that is asymptomatic does not preclude athletic participation. Bracing protocols generally allow for removal of the brace if needed during athletic participation. If an athlete is having pain related to the abnormal vertebral architecture, rest is indicated [16]. Symptoms generally resolve when the athlete reaches skeletal maturity, but secondary disc herniation can result in symptoms later in life, particularly in the lumbar variant of the disease. Surgical treatment is rarely indicated but may be considered for severe curvature or neurologic deficit [17].

Acute Traumatic Injuries Acute traumatic injuries to the spine where fracture is suspected can be broken down into minor and major injuries. Minor injuries include fractures of the transverse and spinous processes, facet joint complex, or pars interarticularis. Major injuries can be divided into compression fractures, burst fractures, seat belt-type injuries, and fractures with dislocations [18]. When evaluating the spine for stability, it is useful to use the three-column model. The anterior column is composed of the anterior longitudinal ligament and the anterior 2/3 of the vertebral body. The middle column contains the posterior 1/3 of the vertebral body and the posterior longitudinal ligament. The posterior column begins at the posterior longitudinal ligament and extends to the supraspinous ligament. The spine is considered to be unstable if two or more contiguous columns are injured [18, 19].

Vertebral Fractures Etiology and Clinical Presentation Vertebral compression and burst fractures are more common in the elderly but can also be a result of traumatic injury in athletes of all ages. In athletic activities that involve repetitive flexion and extension, avulsion fractures can result from injury to the ring apophysis. Avulsion fractures of the anterior portion of the vertebral ring seem to be most common in wrestlers and female gymnasts [20]. The mechanism of injury is typically axial compression with transition from flexion to extension such as with bending to lift heavy weights. Compression fractures are a result of failure of the anterior column of the spine, whereas burst fractures require compromise of both the anterior and middle columns of the spine. In burst fractures retropulsion of osseous fragments into the spinal canal can result in neurologic injury [21]. Vertebral fractures are generally more common in women. This is thought to be due to smaller vertebral cross section which results in higher forces for any given

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axial load [22]. Low bone mineral density, the most significant risk factor for vertebral fracture, is also more common in women [23, 24]. It is important to screen athletes for the female athlete triad (disordered eating, amenorrhea, osteoporosis) if they present with a fracture. Other risk factors for fracture include low body weight, calcium or vitamin D deficiency, advanced age, and alcohol, tobacco, or corticosteroid use. Compression fractures commonly occur at the thoracolumbar junction at the transition from the restricted thoracic spine to the more mobile lumbar spine. Having one compression fracture greatly increases the risk of developing a second fracture, and this is commonly found to occur at the superiorly adjacent vertebrae [25, 26]. Patients present with localized pain at the level of injury. Pain can radiate locally but is generally not radicular in nature. Symptoms are reproducible with palpation or percussion, as well as flexion or weight-bearing, and classically resolve with lying supine. Severe, wedge-shaped compression fractures can result in a kyphotic deformity.

Work-Up Radiographs may show a wedge-shaped anterior compression of the vertebral body. Burst fractures result in loss of vertebral height at the affected level and may show misalignment and disruption of the posterior elements of the spine. An apophyseal avulsion fracture can be identified on lateral lumbar radiographs as an ossified fragment. CT and bone scans are useful if radiographs are negative, but clinical suspicion remains high to identify fractures or displaced fragments that may not be detected on MRI. In burst fractures, MRI of CT imaging is useful to evaluate the integrity of the posterior elements.

Treatment Nonoperative management for vertebral fractures includes activity modification and topical or oral anti-inflammatory medication when needed. Intranasal calcitonin is also thought to be very effective in addressing bone pain after fracture [27]. Bracing with a TLSO may be considered for compression and burst fractures without neurologic compromise; however there is insufficient evidence to determine if it improves physical function or quality of life [28]. Extension-based physical therapy with a focus on core strengthening and ROM is thought to be helpful in those who can tolerate upright positioning, but it does not reduce the rate of fracture. Burst fractures can similarly be managed conservatively if there are no neurologic deficits and the PLL remains intact [21]. Interventional procedures for vertebral fractures include vertebroplasty, the injection of cement into the vertebral defect for stabilization, and kyphoplasty, the injection of cement after the use of an inflated balloon to re-expand the vertebral height. Vertebroplasty has not been shown to improve clinical outcomes compared to placebo in patients with painful vertebral fractures [28]. The evidence in support

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of kyphoplasty for improving pain, disability, and quality of life has been mixed, and the effects seem to diminish with time [28]. Surgery may be considered if there are neurologic deficits, spinal canal compromise, significant kyphotic deformity, or refractory pain despite nonoperative care.

Spinous Process and Transverse Process Fractures Etiology and Clinical Presentation Fractures of the spinous or transverse process can result from trauma to the posterior spine or in the case of the transverse process, from sudden forced contraction of the psoas muscle. This violent flexion and extension force can occur in many sports, particularly football, rodeo events, skate boarding, or Broadway-type dancing. Neurologic injury is uncommon, but concomitant visceral injury needs to be ruled out. Patients usually present with well-localized pain over the area of injury.

Work-Up Radiographs are first-line imaging but may not identify the fracture, particularly if bowel gas is present. A CT scan is useful for its increased sensitivity in detecting fracture and is also helpful in evaluating for abdominal or visceral injury such as laceration to the liver, kidney, or spleen or a retroperitoneal bleed [29].

Treatment The mainstay of treatment is activity modification. Oral or topical anti-­inflammatory medications can be used to address acute pain. Physical therapy focusing on core strength and lumbar alignment can be initiated if tolerated. There is no indication for surgical intervention in isolated fractures of the posterior column. The indication for return to play for an athlete is pain-free range of motion.

Spondylolysis Etiology and Clinical Presentation Spondylolysis (Fig. 14.2) is a posterior defect resulting from a bone stress reaction or fracture to the pars interarticularis, a bony structure which connects the zygapophysial joints in the spine with the pedicle and lamina [30]. It can result from acute trauma but is more common in athletes as a result of repetitive overuse. It is frequent in active adolescents particularly in those who are involved in organized sports. Child and adolescent athletics have become more competitive in recent

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Fig. 14.2 Spondylolysis. (Springer Image)

years, and many young athletes play year-round which increases their risk for overuse injury. Repetitive extension and rotation motion such as in gymnastics, karate, rowing, lacrosse, or football result in increased load and stress on the bone which can lead to a fracture. Bilateral involvement is common, with one study observing that occurs 65% of the time [31]. When bilateral fractures develop, vertebral translation or spondylolisthesis can occur. The athletes will typically present with pain and stiffness in the lower lumbar spine that is worse with activity and improves with rest. Reaching overhead and lying prone can aggravate symptoms by loading the pars defect. Symptoms are generally restricted to the lumbar spine, without associated numbness, tingling, or weakness in the legs.

Pedicle Stress Reaction While spondylolysis is the most common injury to the neural arch, unilateral spondylolysis has been shown to increase stress on the contralateral pedicle, predisposing to additional stress fracture of the pedicle [32, 33]. This is common in young athletes who are involved in sports that apply a torsional force to the spine such as

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dancing. The pedicle can generally resist greater shear force than the pars and is usually less likely to fracture. Despite this, there have been case reports of isolated pedicle stress fractures in young athletes presenting with back pain [34, 35].

Work-Up Radiographic imaging is first line for the detection of pars or pedicle fractures, but may be not be sensitive enough to detect early fractures or stress reactions. CT is more sensitive, but care should be taken in an adolescent population to use low dose and focused exams whenever possible. An MRI can be helpful for further assessment of stress reaction without gross fracture and surrounding soft tissues; however the sensitivity for detecting pars defects depends on the sequences and slice thickness of the MRI scan. A bone scan would detect increased cellular activity in the injured bone and is helpful in differentiating symptomatic acute injury from chronic findings but exposes the athlete to significant radiation [36].

Treatment There is limited research on the treatment of spondylolysis or pedicle fractures. Most treatment approaches for symptomatic pars defects focus on relative rest, with cessation of the offending sporting activity and heavy lifting until pain-free. The role for bracing is controversial but is helpful in restricting motion or an overzealous athlete. Physical therapy to strengthen core musculature and increase flexibility in the legs is indicated when pain subsides. Anti-inflammatory medications can be used for pain control if needed. Surgical intervention is typically not indicated except in the rare occasion that nerve root compression develops and requires laminectomy for decompression, or if the fractured segment of bone becomes loose or unstable. Most patients with symptomatic pars defects do well with a conservative approach, even if complete osseous healing is not achieved [37]. Return to play is indicated when the athlete has regained full painless lumbar range of motion. Treatment and recovery generally take at least 3 months but can continue for longer.

Spondylolisthesis Etiology and Clinical Presentation Spondylolisthesis is a translation of the one vertebral body on the one below it [30, 38]. This requires either a fracture, elongation of the pars, or incompetence of the facet joints. It can occur in all ages and is prevalent in young athletes who are exposed to repetitive microtrauma [39]. Evaluated in the sagittal plane, the translation is classified as either anterior (anterolisthesis) or posterior (retrolisthesis). The Wiltse classification of spondylolisthesis defines five different types [40]:

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• Type 1 or dysplastic spondylolisthesis is due to congenital dysplasia of the sacrum. • Type 2 is called Isthmic spondylolisthesis and has three subtypes A–C. Type 2A or lytic spondylolisthesis is due to an overuse fatigue fracture of the pars. In Type 2B the pars remains intact but is anatomically elongated. Type 2C is defined as an acute fracture of the pars. Type 2A is the most prevalent in athletes, most commonly occurring at the L5 level. There is a risk of slippage when bilateral spondylolysis is present, but progression of the slip is rare after adolescence [41]. • Type 3 is the result of a degenerative process related to intersegmental instability and degeneration of the posterior elements resulting in elongation and slippage [42]. This subtype tends to occur more frequently in females and is the most common subtype in adults. It occurs most commonly at the L4–L5 junction. • Type 4 is classified as traumatic spondylolisthesis and is the result of traumatic injury of the bony complex other than the pars, usually from a flexion/extension mechanism. This leads to gradual forward slippage of the superincumbent vertebral body. • Type 5 is pathologic spondylolisthesis and is due to underlying bone disease where the bone being unable to support the weight of the overlying vertebral body. Translation of the vertebral body can result in stenosis of the spinal canal or neural foramina resulting in nerve root impingement. Isthmic listhesis typically affects the L5 nerve by causing foraminal stenosis, whereas degenerative listhesis typically affects the L5 nerve in the subarticular zone and lateral recess. The clinical presentation often begins with low back pain with possible radicular pain, often into the buttocks. The athlete will likely report pain that is worse with motion, particularly in extension. Leaning forward or sitting may offload neural compression and provide relief. On exam there may be tenderness along the spinous processes and paraspinal musculature at the affected level. There may also be a palpable step-off deformity at the level of translation, but typically not unless the slippage is more than 25%. A thorough neurological exam is imperative to rule out neurological compromise (progressive neurologic deficit, cauda equina syndrome) that would necessitate surgical intervention.

Work-Up Radiographs are indicated to measure translation, with flexion-extension views used to evaluate for segmental motion. Advanced imaging with MRI or CT can help with evaluating adjacent structures including any associated stenosis.

Treatment The treatment for spondylolisthesis is grade dependent. The Meyerding grading system classifies translation based on percentage of slippage of the superincumbent

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vertebral body on the level below. Grade 1 40  years old) in endurance and ultra-endurance (>6  h) events. The number of athletes older than 50  years in the New  York City marathon increased 119% from 1983 to 1999, with significant improvement in completion times as compared with younger age groups. Male master runners represent now more than 50% of total male finishers, while female master athletes represented 40% of total female finishers, respectively [7]. This finding corroborates previous observations for 100- and 161-km ultra-marathon running where master runners represent the greatest part of the finishers, up to 73% for 100 km [8]. Similar trends have been observed for multiple discipline events such as triathlons (swimming, cycling, running). For example, master triathletes represent now more than 55% of the total field for males and more than 45% of the total field for females at the Ironman World Championship triathlon in Hawaii [9]. In addition, there have been master athletes in their 90s competing and even centenarians competing in endurance sports, jumps, and sprints in official master athletics events. Fauja Singh became the first centenarian to finish a marathon in 2011. French cyclist Robert Marchand when he was 102  years old set the hour record in track cycling in 2014. Japanese Swimmer, Mieko Nagaoka, set several swimming world records in the 100–104 age group. These are a few of the examples of centenarian master athletes that are flooding the world. It is interesting to see the phenomenon of increasing master athletes not only in the centenarian division but also in all of the divisions leading up to the centenarian, beginning with those individuals 35 years and older. In addition, the ages of elite athletes are increasing; the current age of elite marathoners is around 30 years for both males and females [10]. Globally, three countries have the largest proportion of older adults out of their total population; Japan with 26.3% of its population being older than 65 years old, Italy at 22.4%, and Greece with 21.4%. Currently, this aging population is 15% in the USA, and by 2060 the 65 and older population will rise to nearly 24%. According to recent census data provided by the US Census Bureau, in 2050, the population aged 65 and over is projected to be 83.7 million, almost double its estimated population of 43.1 million in 2012. This increase is largely attributed to the “baby boom” generation born between 1946 and 1964 who began to turn age 65 in the year 2011. Similarly, the European Innovation Partnership on Active and Healthy Ageing predicts an increase in the number of people aged 65+ in the European Union (EU) from 85 million in 2008 to 151 million in 2060. Because the >65-year-old population is the fastest growing in the world, the main increase in the population of master athletes noted in the >65-year-old group is thought be a reflection of this change in global population. Master athletes play an important role in public health domain extending beyond athletics. Public report has shown that sedentary older individuals are the least active demographic group with few older adults meeting the recommended physical activity guidelines. Master athletes have a superior functional capacity compared to their sedentary peers from “chronic” structured exercise training throughout lifespan. Master athletes, therefore, serve as a unique non-pharmacological model of healthy aging and can potentially help researchers distinguish the contribution of primary and secondary aging to the decline in health, function, and performance

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[11, 12]. There is an extensive literature about master athletes’ relatively preservation of aerobic and strength capacity. Recent meta-analysis reported that master endurance athletes did not show decline in maximal oxygen consumption (VO2 max) observed in aged-matched untrained group and maintaining values similar to those observed in young untrained individuals [12]. Master strength athletes have greater strength compared to young untrained individuals and lower body fat similar to the young. These findings highlight that regardless of exercise modality, chronic exercise training delays the canonical age-related deterioration in physical function and body composition.

Injury Rate in Master Athletes The injury rate in master athletes varies depending on the type of sports events and level of athletes. In elite master athletes, it has been reported to be comparable or lower than their youthful cohorts. Ganse et al. reported the prevalence of injuries in master athletes compared to more youthful cohorts competing in the 2012 European Masters Athletics Championships. The results of the study showed only 2.4% (76 individuals registered injuries) out of 3154 older participants with an average of 53.2 years which is markedly lower than 13.5% of the youthful cohorts in previous years [13]. On the other hand, a retrospective study of 32 marathon runners older than 60 years of age reported 46.9% of injury rate which was comparable to the expected injury rate of a theoretical younger population [14]. There is also a report of higher injury rate in master athletes compared to younger athletes in running [15]. In general, the master athletes sustain overuse-type injuries rather than acute injuries [16]. Much of the location and types of injuries seen in master athletes depends on the type of sport they are involved in. As athlete ages, the risk of injury may increase at an individual level due to a loss of bone mass, muscle mass and flexibility, and increasing fatigue with exercise [17]. It has been estimated that 89% of master athletes experience one sports-related injury since turning 50  years; of these injuries, 68% are due to repetitive overuse [18]. As long as these athletes practice injury prevention, it has been reported that experienced master athletes may remain to be at a low risk of injury with age [13].

 ge-Related Changes Relevant to Maintaining a High Level A of Performance at Older Age Physiologic changes associated with aging described in the literature have been based on the observational studies of relatively sedentary older adults. Clinicians should be aware of physiological changes related to aging, yet noting that most of these findings were demonstrated in sedentary aging individuals and master athletes may be seen with a different lens than their sedentary counterparts.

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Musculoskeletal System Sarcopenia may result from age-related atrophy of individual muscle fibers and a decrease in the number of muscle fibers. These age-related changes have been attributed to a decrease in anabolic agents such as testosterone and growth hormone, confounding the incorporation of amino acids into skeletal muscle, while an increase in catabolic factors such as interleukin-6 enhances muscle wasting [1]. Despite this process, there is an evidence that specific resistance training, regardless of age, dampens sarcopenia [1]. In fact, research has shown that the loss in muscle mass is primarily due to sedentary lifestyle rather than aging [19]. According to Tanaka and Seals, 70% of decline in muscle strength and mass is due to deconditioning [4]. Master athletes who intensely train 4–5 times per week did not demonstrate the same loss of total lean muscle mass as compared to age-matched sedentary individuals [20]. Given this information, it is imperative that master athletes continue resistance training as they age. Independent of the activity level, muscle mass still declines approximately 1.25% per year after age 35. Master athletes demonstrate the steepest rates of decline in strength-dependent sports events, whereas the least amount of decline with jumping and walking events [21]. Muscles of master athletes reach the same level of fatigue as those of younger athletes with a slower recovery time [22]. Muscle power, which reflects how fast muscle can generate strength, is increasingly recognized as an important parameter in minimizing decline in balance with aging [23]. Muscle strength and power training may not only improve athletic performance, but it may also enable them to minimize their susceptibility to falls [24]. The natural aging process affects the ability of connective tissues to adapt to high stress, which is due to low rate of metabolism, higher cross-linkage, progressively decreasing elasticity, and low tensile strength [25]. The older athlete’s tissue becomes stiffer and less able to tolerate a given workload. Flexibility can decline by 6% in every decade after age 50 [26]. Bone health is another area of concern in the older athlete especially the female athletes. Menopause can accelerate bone loss of 1.5–2% annually from menopause and several years post menopause [27]. Regular running up to 15–20 miles per week may maintain bone mineral density; on the other hand, more mileage than this may reduce the bone density [28]. It has also been demonstrated that resistance training has a positive effect on bone health in older women by maintaining or increasing bone mineral density [29, 30].

Cardiovascular System Age is the strongest predictor of cardiovascular risk in most risk estimates including Framingham Risk Score. This is likely due to changes in arterial health (more specifically arterial stiffness/compliance) which has been widely regarded as a barometer of biological or physiological aging. With advancing age, most individuals experience stiffening of large conduit arteries but at different rates [31].

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Maximal oxygen consumption (VO2 max) is commonly used parameter for cardiovascular fitness of an individual. In sedentary individuals, the VO2 max declines at a rate of 10% per decade after 30 years of age [4]. This finding of decline in VO2 max in sedentary population is reflective of a less efficient pumping heart, stiffness in the vascular system, and a drop in lung capacity. From the age of 20–70, the maximum lung capacity declines by 40%. Similar to muscular system, physical activity has been demonstrated to combat these effects associated with the sedentary aging. High-intensity exercise has been shown to minimize VO2 max decline by as much as 50% by mechanistically maintaining cardiac efficiency and lactate threshold [4]. Master athletes in their 70s can have a VO2 max similar to untrained 20-year-­ olds [4]. These findings are again emphasizing the point that generalizations about the aging are based on the sedentary individual; these broad generalizations are not to be applied to the individuals who maintain a high level of physical fitness including master athletes.

Gender Differences There is a relative stability of gender differences observed across the ages suggesting that the age-related declines in physiologic function did not differ between men and women. Gender differences in endurance performance for elite athletes are generally close to 10% [32]. Men have a greater VO2 max than women because they have larger hearts, greater hemoglobin concentration, less body fat, and greater muscle mass per unit of body weight [32] compared to women. Two parameters are often used to measure the effectiveness and efficiency of running (running economy, lactate threshold). Running economy is generally defined as the energy demand for a given velocity of submaximal running. Lactate threshold is defined as the maximal effort that can be maintained by an athlete with little or no increase in lactate in the blood. Running economy and the lactate threshold do not appear to differ between men and women [33]. For older master female athletes who are in their 50s–60s that experience menopause, hormonal changes can greatly affect the physiological changes. At times these hormonal and physiologic changes can require these athletes to make gender-specific training modifications to promote maximum athletic performance. For example, decreases in progesterone and estrogen can cause sleep disturbances. Also postmenopausal master women athletes use protein less effectively, and it is promoted for these athletes to take sufficient proteins before and post exercise.

 ositive Changes in Master Athletes Compared to Sedentary P Older Adults Maintaining physical fitness throughout one’s lifetime has been demonstrated to promote a more robust life and longevity when compared to sedentary counterparts [34, 35]. The following are the key changes noted in master athletes (Table 19.1).

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Table 19.1  Age-related changes in master athletes compared to sedentary adults Characteristic domain Telomere length Body mass index Brain volume Cognitive function Rate of sarcopenia Psychological domain

Master athletes Relatively increased (longer) than sedentary older adults Relatively lower than sedentary older adults Relatively higher volume of white and gray matter in subgyral, cuneus, and precuneus regions related to visuospatial function, motor control, and working memory than sedentary older adults Superior performance in verbal memory, reaction time Less decline in muscle mass and strength than sedentary adults Strong sense of self, control over their health, transferring confidence to other life domains (leadership, teamwork, respect others, contribution to community)

Increased Telomere Length Telomere length has been often considered as a valuable marker of aging at a molecular level. It had been understood that telomere length is shortened during aging. One study from the Universidade Católica de Brasília [36] looked at the telomere length of high-level master sprinters and nonathlete age-matched controls and analyzed the relationship of telomere length with performance and body fat. In this study, master sprinters had a longer telomere length, lower body fat and BMI, and better lipid profile than age-matched controls. This study suggested that elite master sprinters had longer telomeres than their untrained peers; this is associated not only with a greater overall health status but also sports longevity. Decreasing athletic performance was related to a decreasing telomere length [36]. This study is another point in the evidence that master athletes lead healthier lives with a higher level of performance than their untrained peers. Psychological Maturity A high proportion of older adults suffer from depression and social isolation. Master athletes have the advantage of having athletic experience and a strong sense of self. Master athletes demonstrated a confidence in having control over their health. Sports training and competition also give the master athletes a sense of commitment to their sport which solidifies their identity and sense of self. Compared to younger athletes, most master athletes adjust their training regimens to avoid injury [16]. Many master athletes cross-train and add varied activities to their regimen in an effort to maintain aerobic fitness but decrease the risk of overuse injuries. Self-­ awareness and adaptation to situations and training regimens demonstrate the psychological maturity that is one of the positive characteristics of master athletes. A qualitative study performed which looked at the personal psychological assets of master athletes by Dionigi in 2018 found that six key themes emerged psychological assets: competence and confidence, character, commitment, connection, cognition, and challenge [6]. Master athletes consistently linked their confidence to

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their competency in the master sport domain. They have self-recognition of a sense of accomplishment and pride in their capabilities and their confidence demonstrating transferability to other life domains. Finding ways to negotiate these sports-­ related challenges facilitates personal development. Furthermore, master athletes felt that their ability in sports includes leadership, teamwork, learning to work with and respect different personalities, and contributing to others in the community [6]. The participation of master athletes in their sports allows for them to develop more connections which ultimately facilitate expanded social networks and a sense of community [6]. Additionally, the continual training, learning, and refining of athletic skills provide opportunities to enhance cognition [6]. The personal challenges associated with injury, learning new skills, aging identities, and perceived boundaries of their capabilities that facilitate the physiological maturity and personal development are assets of master athletes. Decreased BMI Compared to Age-Matched Control Body mass index (BMI) can be an indirect predictor of health, due to the many of the negative health effects associated with obesity. A review of the literature performed by Walsh in 2018 demonstrated that master athletes compared to the general population/sedentary controls have significantly lower BMIs than the age-matched controls [37]. Overall, this review looked at 60 studies and found that in terms of BMI for the master athletes the mean was 23.8  kg/m2(± 1.1) with a range from 20.8 kg/m2(endurance runners) to 27.3 kg/m2 (soccer players); this was significantly lower (p 50 years of age and 15 μg/d for active adults >70 years of age; for calcium the adequate intake has been established at 1200 mg/d for men and women older than 50 years. There are no changes in recommendations made based on the activity level. For vitamin B6, folate, vitamin B12, thiamine, riboflavin, choline, and zinc, similarly to vitamin D and calcium, there are no recommendations specific to master athletes. For iron, on the other hand, there are athlete-specific recommendations; a conservative estimate is that athletes need 30% more iron than individuals who do not exercise. General recommendation for all athletes is 10.4 mg of iron a day [55].

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Hydration Master athletes are at an increased risk of becoming dehydrated, due to the decreased physiologic changes to thirst sensation, sweating rates, renal adaptation to altered fluid and electrolyte status, and blood flow responses that can impair thermoregulation [55]. Aging athletes competing in hot and humid environments may sweat the same volumes as young competitors. However, in hot and dry environment, older athletes produce substantially less sweat than younger counterparts [56]. Assessing the athlete’s daily fluid intake and monitoring intake during training and competition can establish a baseline for developing a hydration strategy; generally the hydration strategies applied for younger athletes can be useful for master athletes, with the caveat due to the physiological changes that occur in master athletes.

Recovery Adequate recovery from training and following a race is critical, especially as an athlete ages. Factors that can help with recovery include days off from training, extra sleep, and adequate recovery nutrition [44]. Days off from workouts will provide time for muscles to rebuild and for connective tissue to recover from training stresses. A general rule of thumb is that 1 h of racing requires 3–5 days of recovery. One to 2 hours of extra sleep should be added after a taxing workout or race [44]. The importance of recovery nutrition is key and should be adjusted depending on the particular sport/athlete. As mentioned above, the timing of nutrition is key to recovery, within 30–60 minutes post exercise is recommended for all athletes.

Rehabilitation of Injury and Return to Sport After master athletes suffer an injury, the recovery and rehabilitation clinicians should work with the master athlete as a partner to discuss and execute the roadmap to recovery including rehabilitation plan and return to sport. Master athletes may suffer from two distinct types of injuries including those from current training and competitions and chronic injuries that occurred in their youth and nag them at later age. For the latter, setting expectations for athletes’ recovery is especially an important aspect of rehabilitation process. Rehabilitation for sports injuries is typically divided into acute, recovery, and functional phases. Each phase is correlated with the inflammatory, repair, and remodeling stages of tissue injury. The principle goal is to restore optimal function, and rehabilitation should begin immediately after the injury. Rehabilitation combines physical modalities, therapeutic exercises, assistive devices, and functional sports-specific training, which is applied to both young and older athletes. For older athletes, it is critical to minimize the detrimental effects of inactivity and facilitate the alternative form of training since older adults are prone to overall deconditioning from relative inactivity. During the acute phase of injury, the goal is to decrease pain and swelling, protect the injured structures, and allow the tissues to heal. In this phase different

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modalities are utilized to decrease secondary tissue damage, reduce muscle inhibition, as well as allow the initiation of therapeutic exercise. Orthotic equipment may be needed to protect the injured part. Once pain is under control with decreasing swelling and increasing tolerance of therapeutic exercise, athlete may move on to the recovery phase of rehabilitation. During recovery phase, athlete typically focuses on achieving full pain-free range of motion, improving flexibility, and regaining normal balance and muscle strength. Different modalities are utilized to decrease edema, increase circulation to the damaged and healing tissue, as well as improve collagen flexibility. Progression of functional training without recurrence of symptoms is required prior to advancing to the functional phase of rehabilitation. Lastly the functional phase aims to increase power and endurance, improve neuromuscular control in functional activities, and prepare the athlete to return to sports-specific training and competition. This phase addresses the specific kinetic chain that was involved in the injury as well as addressing biomechanical deficits and abnormal adaptations in sports-­ specific techniques. Return to play is considered after an athlete has completed all of the phases of rehabilitation. In general, when evaluating master athletes for return to sport, athletes need to return to a practice of their sport first. After full participation in a practice of their sport, master athletes can be evaluated for clearance of participation in competition of their sport. Decision of return to play is based on clinical evaluations, objective testing, and other psychological factors in discussion with athletes with transparency and ramification of decision.

Sports-Specific Considerations Running The demographics of the running population have shifted to relatively higher proportion of master athletes. In the USA, there has been a 300% increase in race finishers since 1990, with a 2–26% increase in participation in age brackets over 40  years of age. At the New  York marathon, male master runners represent now more 50% of total male finishers, while female master athletes represented 40% of total female finishers, respectively [7]. Master runners experience a steady decline in running performance including slower preferred and maximal running speeds especially after the age of 50. There is age-related muscle-tendon stiffness and reduced cardiopulmonary function including relatively higher heart rate response to progressively higher running speeds. Biomechanically, master runners showed greater internal knee rotation, lesser ground reaction forces, shorter stride length, longer stance time, and less angular displacement of lower body joints compared to the younger counterparts. These changes may be adaptive for master runners to be comfortable, reduce fatigue and potential injuries. Marathons and ultra-endurance events, however, are where the master athlete may have a competitive advantage over their more inexperience/youthful counter parts.

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Compared to younger runners, master runners have a higher musculoskeletal injury rate [15]. Prevention of injury is the key component of rehabilitation principles for longevity of running, and it is important to identify a modifiable risk factor for injuries. Running speed is one of the main modifiable risk factors for injuries since the loads on lower extremity joints and other musculoskeletal structures are higher with faster running speed. The most common injury seen in runners was Achilles tendinopathy with 0.0159 injuries per 1000  km running according to a study of runners in Germany. Mid-distance 1500–3000 m running, 5 km, and running on sand were associated with a significantly increased risk for Achilles tendinopathy [16]. Ultra-endurance events are events that exceed 6 hours in duration. In the past three decades, there has been an increase in the participation of master athletes in these ultra-endurance events. Ultra-endurance master athletes’ ability to maintain high exercise training has recently drawn attention of aging researchers. These master athletes represent an important insight into the ability of humans to maintain physical performance and physiological function with advancing age [57].

Swimming Swimming is relatively popular among older adults since the buoyancy of water is advantage in lower limb joints, and natural resistance from water allows older adults for strengthening combined with aerobic activities. In master swimming typically, the propelling efficiency decreases with increasing age; this is often attributed to the decreased amount of muscle tissue. Additional changes seen in master swimmers compared to their younger counterparts are changes in the cardiovascular (decreased maximal heart rate, decreased cardiac output), pulmonary (decreased total lung capacity, decreased maximal oxygen uptake), and musculoskeletal (decreased strength and bulk, decreased flexibility) system [58]. Because of these considerations it is key that the injuries of master swimmers be identified early to prevent progression. Rehabilitation and recovery from injuries in the master swimmer may need to be prolonged, with the ultimate goal of preventing the more rapid loss of flexibility, strength, and endurance than seen in younger athletes [58]. The physiology of the master swimmer is important to consider when compared to that of their youthful counterparts especially when treating and evaluating swimming specific injuries and concerns. The injuries that master athletes face are similar to those seen in younger swimmers. Acute injuries may occur due to trauma of striking the wall at the end of a sprint with the hand or feet during a flip turn. Common overuse injuries occur at shoulder and spine region. Shoulder pain is the most common musculoskeletal complaint among swimmers. The biomechanics during the swim stroke are crucial to preventing injuries. Poor biomechanics, especially when coupled with fatigue of the muscles of the rotator cuff and the scapular stabilizing muscles can lead to dynamic instability and impingement. Typically, the “swimmer’s shoulder,” a hypermobile glenohumeral joint combined with technique flaws or fatigue, can lead to

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impingement of the rotator cuff. Swimmers’ shoulder can be treated with rehabilitation and a proper strengthening routine as well as improvement in potential stroke flaws. Certain swimming styles and certain swim strokes can predispose master athletes to overuse injuries. For example, the overhead position of the backstroke can predispose athletes to acute shoulder subluxation. During breaststroke swimming, patellar subluxation can occur, and degenerative meniscus tears may be exacerbated due to valgus loads on the knee [58]. Master swimmers may experience back pain especially during breaststroke and butterfly-style swimming by the repetitive hyperextension causing spondylolysis or fatigue of the lumbar paraspinal muscles [58]. Careful history about training will enable the clinicians to link symptoms to different styles of swimming and guide to make rehabilitation plan for the athletes.

Golf Golf is popular with master athletes as a high level of performance is not limited by age. Although golf is a noncontact sport, serious musculoskeletal injury can occur without the proper mechanics, and prevention is the key in management. For example, warm-up routines greater than or equal to 10 minutes demonstrated a decreased injury rate. Overuse injuries are the most common type of injuries, and the most common sites for golfing injuries are the low back, elbow, shoulder, wrist, and knee [59]. The golf swing can be divided into five different phases: takeaway, forward swing, acceleration, early follow-through, and late follow-through. The overall incidence for rate of injury was 15.8 injuries per 100 golfers (range, 0.36–0.60 injuries per 1000 hours per person); 46.2% of injuries were reportedly sustained during the golf swing, and injury was most likely to occur at the point of ball impact (23.7%) [60]. Low back is the most common injury seen in master golfers. There are specific swing differences noted between the professional and novice golfers. Less-­ experienced master golfers attempt to generate more power and club speed using their upper extremity strength rather than their trunk rotation, which causes spinal torque and lateral bending forces on the lumbar spine, resulting in greater swing variability. The more experienced master golfers have greater trunk rotation on the downswing and larger angular velocities for the club shaft, trail elbow extension, and wrist extension. The golf swing can produce large loads in the spine and back musculature. The distribution of stress placed on the back during the golf swing is asymmetric. This is a result of the asymmetric trunk velocity during the takeaway phase, which is slower compared with the forward swing and follow-through phases. The trail side (the ipsilateral side as the dominant hand) of the back is more affected. Elbow and wrist injuries are commonly associated with the grip of the club, but trauma can also be caused when hitting the ball “fat” (when the club head hits the ground prior to hitting the ball) or when hitting the ball in thick high grass. Lateral epicondylitis and other tendinitis typically affect the lead arm. Shoulder injuries may occur at extremes of motion, such as at the top of the takeaway phase or the end of the follow-through phase. Knee injuries in golf are rare and only comprise 4–9%

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of golf-related injuries [59]. These injuries are thought to be attributed to internal and external rotation of the tibia on the femur, ligaments, and menisci resisting the force generated by golf swing.

Mountaineering Mountaineering includes traditional mountain sport activities such as mountain hiking, rock and ice climbing, as well as ski mountaineering. These sports occur at different altitudes which can be classified as low altitude, moderate altitude, high altitude, very high altitude, and extreme altitude. The environment plays a significant role in the athlete’s performance since it is often rugged terrain with cold temperature and hypoxia with increasing altitude. The energy consumption of uphill walking is much greater than standard-level walking. Oxygen consumption during level walking at 3  km/h is only 10  ml·min–1·kg–1; it rises to 25  ml·min–1·kg–1 when walking uphill at the same speed at a gradient of 15% [61]. These conditions may challenge the physical fitness of the master athlete. Mountaineering as with any other physical activity requires coordinated efforts of the lungs, heart, circulation, and musculoskeletal system. There are many physiological changes that can affect the master mountaineer: the aging cardiovascular system, the aging respiratory system, and the aging musculoskeletal system. In the cardiovascular system of the master mountaineer, there is both a decline in the VO2 max and the max heart rate. This is important to consider for the master mountaineer and the general energy consumption. Increase in heart rate and blood pressure (increase in cardiac work) during initial ascent to high altitude may induce angina and thus limit performance in people with coronary artery disease. In the hypoxic environments of mountaineering, ventilation has to be markedly increased at high altitude to counteract the low oxygen content of the air. This is easily achieved in young healthy mountaineers; however, it may become a limiting factor when lung function decreases with age or disease. In the musculoskeletal system of master mountaineers, prolonged high mechanical forces on the knee and hip joints during mountaineering cause excessive wear and tear of articular cartilages and promote the development of early degenerative changes. Knee and hip osteoarthritis are common problems in older mountaineers and often lead to termination of sports activities.

Triathlons Triathlons typically consist of three events such as swimming, cycling, and running. Triathlons are a natural cross-training sport, and they encompass a wide range of muscles and skill. Of the 2.9 million participants in triathlon in 2011, greater than 43% were in the 40 years and over-age division according to USA Triathlon. The largest growth was in the 35–39- and 40–44-year-old groups [44]. Master triathletes represent now more than 55% of the total field for males and more than 45% of the total field for females at the Ironman World Championship triathlon in Hawaii [9]. Age-related

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declines occur least in the cycling portion of the triathlons. Master triathletes are prone to overuse injuries due to endurance nature of the sport. However, when compared to master athletes who only compete in one sport (i.e., running), master triathletes have a significant decrease in the amount of overuse injuries [44]. Injury prevention in master triathletes should include an adequate warm-up and cooldown prior to and after training, strength training, and flexibility exercises. Master triathletes are unique in that they are essentially competing in three different types of exercise. Strategies should be made to master each of the individual techniques for running, cycling, and swimming. Within the swimming component, shoulder impingement/tendinopathy is the most common complaint [62]. The majority of the triathlon is spent on the bicycle, it is crucial to look at the comfort of master athletes on the bicycle and the pedaling biomechanics. The last portion of a triathlon, the running portion, is where most of the master athletes suffer their injuries. Seventy-one percent of the injuries reported by triathletes occur during the running component of training/racing and involve repetitive stress [18]. This is likely due to the fact that master athletes at this portion of the race are running on fatigued legs and the proper running form breaks down. Combined training for endurance and strength with sufficient recovery time may reduce the injury risk.

Summary and Key Points Master athletes are a unique population and have often been deemed as the successful model of aging. This population has continued to rise as the world population ages. There are a number of positive molecular, physiological, and morphologic changes noted in master athletes compared to sedentary counterpart: increased telomere length, psychological maturity, decreased BMI, relatively preserved brain, and muscle volumes. Master athletes demonstrate some of the physiologic changes of aging yet at markedly reduced rate compared to sedentary older adults. They also demonstrate lower incidence of cardiovascular and other chronic diseases when compared to sedentary older adults. Furthermore, master athletes are a non-­ pharmacological model of successful aging. Key principles of rehabilitation of master athletes lie in prevention which include pre-participation screening, especially from a cardiac aspect, pacing the training regimen, sufficient recovery time, and limiting inactive time by introducing alternative training to avoid deconditioning for sustained physical activity and athleticism throughout one’s life.

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52. St-Onge MP, Gallagher D. Body composition changes with aging: the cause or the result of alterations in metabolic rate and macronutrient oxidation? Nutrition. 2010;26(2):152–5. 53. van Pelt RE, Dinneno FA, Seals DR, Jones PP.  Age-related decline in RMR in physically active men: relation to exercise volume and energy intake. Am J Physiol Endocrinol Metab. 2001;281(3):E633–9. 54. Van Pelt RE, Jones PP, Davy KP, Desouza CA, Tanaka H, Davy BM, et al. Regular exercise and the age-related decline in resting metabolic rate in women. J Clin Endocrinol Metab. 1997;82(10):3208–12. 55. Rosenbloom CA, Dunaway A. Nutrition recommendations for masters athletes. Clin Sports Med. 2007;26(1):91–100. 56. Kenney WL, Anderson RK. Responses of older and younger women to exercise in dry and humid heat without fluid replacement. Med Sci Sports Exerc. 1988;20(2):155–60. 57. Lepers R, Stapley PJ.  Master athletes are extending the limits of human endurance. Front Physiol. 2016;7:613. 58. Khodaee M, Edelman GT, Spittler J, Wilber R, Krabak BJ, Solomon D, et al. Medical care for swimmers. Sports Med Open. 2015;2:27. 59. Gosheger G, Liem D, Ludwig K, Greshake O, Winkelmann W. Injuries and overuse syndromes in golf. Am J Sports Med. 2003;31(3):438–43. 60. McHardy A, Pollard H, Luo K. Golf injuries: a review of the literature. Sports Med (Auckland, NZ). 2006;36(2):171–87. 61. Khodaee M, Grothe HL, Seyfert JH, VanBaak K.  Athletes at high altitude. Sports Health. 2016;8(2):126–32. 62. Barbosa TM, Bragada JA, Reis VM, Marinho DA, Carvalho C, Silva AJ. Energetics and biomechanics as determining factors of swimming performance: updating the state of the art. J Sci Med Sport. 2010;13(2):262–9.

The Female Athlete

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Eliana Cardozo and Ariana Gluck

 he Female Athlete Triad and Relative Energy Deficiency T in Sport (REDs) The classic female athlete triad encompasses three components: 1. Low energy availability with or without disordered eating 2. Menstrual disturbances 3. Poor bone health The triad affects physically active girls and women and is thought of as a continuum. The athlete does not have to have all three components at the same time; having one or more (on any continuum) should raise a flag that the athlete is at risk. The key to management is prevention and early recognition as the syndrome can have serious health risks including the development of clinical eating disorders, amenorrhea, and osteoporosis [1]. The International Olympic Committee has also introduced a syndrome, relative energy deficiency in sport, which describes a state of impaired physiologic function which can affect both females and males [2, 3]. This describes a syndrome based on the International Olympic Committee consensus statement in which both female and male athletes are affected. There is an emphasis on changing the classic thought of the female athlete triad to a more comprehensive definition of a syndrome which is fundamentally caused by low energy availability. This syndrome causes impaired physiological function including, but not limited to, metabolic rate, menstrual function, bone health, immunity, protein synthesis, and cardiovascular health caused by relative energy deficiency [3]. The

E. Cardozo (*) · A. Gluck Icahn School of Medicine at Mount Sinai, New York, NY, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_20

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fundamental issue is low energy availability which leads to hormonal and metabolic imbalances and issues and can affect both female and male athletes. 1. Low Energy Availability With or Without Disordered Eating Energy availability is the calculation of energy intake (food) minus energy expenditure (calories expended by exertion and metabolic processes). A negative energy balance may occur from low caloric intake (intentional or not) and/or increased physical activity. Low energy availability is not easy to diagnose. Overt signs include a very low body mass index (40°) with compensatory excessive lumbar lordosis. Pain is present in the majority of cases. Management is aimed at limiting progression, physical therapy, and extension bracing with the consideration of surgery based on the degree of curvature and its progression as well as neurological compromise.

Hip Injuries Femoroacetabular impingement (FAI) is a common cause of hip pain in the young athlete defined as a non-spherical femoral head within a hemispheric acetabulum. Three subsets of FAI include Cam (bony overgrowth at the femoral head/neck junction), Pincer (overgrowth of the acetabular rim), and Mixed cam/pincer lesions. The Cam deformity is the most common. Patients commonly present with anterior groin pain worsened with activity, hip flexion, and rotation. Physical exam may show a decreased hip range of motion particularly in internal rotation and flexion. Plain radiographs (bilateral for comparison) allow for differentiation as well as measurement of the alpha angle and head-neck offset ratio. Management may include observation or surgical intervention [14]. Acetabular labral tears may be seen in young athletes with risk factors including bony disorders such as FAI, hip dysplasia, femoral retroversion, coxa valga, SCFE [14]. Traction apophysitis is described as chronic inflammation of the apophysis caused by repetitive trauma in a growing bone. This condition is common in the hip region due to the large number of musculotendinous attachments in the area. Common sites include the attachment of the sartorius to the anterior superior iliac spine, the rectus femoris to the anterior inferior iliac spine, the hamstring muscles to the ischial tuberosity, the iliopsoas to the lesser trochanter, and the gluteus medius to the greater trochanter. Management includes relative rest, activity modification, and strengthening. Legg-Calve-Perthes disease is described as idiopathic avascular necrosis of the proximal femoral epiphysis. This condition is most commonly seen affecting one

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hip in males aged 4–10 years old; presentation  6 with lateral pillar collapse of the femoral head over 50%. Return to sport is possible once asymptomatic and radiographs show some improvement. Sequelae may include femoral head or acetabular deformity, subluxation, premature physeal arrest, and OA [15]. Slipped capital femoral epiphysis (SCFE) is a condition in which there is slippage of the metaphysis relative to the epiphysis within the hypertrophic zone of the physis. It is typically seen in overweight adolescent boys (12–15 years old). The left hip is more common and approximately 20% of cases are bilateral. Patients present with a limp and knee pain usually insidious in onset. Physical exam reveals the leg held in external rotation and shortened with reduced internal rotation; the Drehmann sign is characteristic described as obligatory hip external rotation with hip flexion. Radiographs show widening and irregularity of the growth plate and cystic changes in the metaphysis; epiphyseal location medial to the Klein line on AP view is a sign of SCFE. Surgical management is favored due to the risk of subsequent avascular necrosis. Chronic pain may be seen in 5–10% of cases in addition to a high risk of osteoarthritis in the future with approximately 45% of patients requiring a total hip arthroplasty by 50 years after presentation [15]. Groin and lower abdominal pain is more prevalent in males and in sports with running, cutting, kicking, explosive turns/change in direction, and rapid acceleration/deceleration. Athletic Pubalgia results from an overuse injury to the muscular and/or fascial attachments near the anterior pubis although there is debate regarding the exact pathogenesis and anatomical disturbance. Pathogenesis includes involvement of the transversalis fascia at the posterior inguinal wall, the insertion of the distal rectus abdominis, the conjoint tendon at its distal attachment on the pubis, and/or the external oblique aponeurosis. Maneuvers including the resisted sit-up and valsalva may replicate the pain. Plain radiographs may reveal other pathologies (i.e., osteitis pubis, FAI, stress fractures) whereas MRI may demonstrate tears of the rectus musculature and bone marrow edema at the pubis. Diagnostic anesthetic injections may be considered to elucidate the pain-generator. Management includes rest (6–8  weeks) followed by physical therapy focused in core strengthening. Operative repair of the affected muscles has been described [16].

Knee Injuries Knee pain is a common concern for young athletes especially anterior knee conditions often secondary to overuse. Additionally, knee pain may also be referred to as

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pain from the hip or lumbar spine. Attention must be paid to rule out serious pathologies like septic arthritis involving the knee or hip which may cause pain, decreased range of motion of the affected joint as well as a limp. Osgood-Schlatter disease is a traction apophysitis or osteochondritis of the secondary ossification center at the tibial tubercle. The condition is more common in adolescent boys (12–15 years old) during rapid growth caused by repetitive stress on the knee extensor mechanism (quadriceps) seen in running and jumping sports. Girls present earlier between 11 and 13 years [17]. There is notable pain around the tibial tuberosity which is aggravated by activity or kneeling. Physical exam shows an enlarged tibial tubercle with associated tenderness to palpation and pain with resisted knee extension. Radiographs are not required but may show fragmentation of the tibial tubercle and possibly an ossicle in the patellar tendon. The condition is self-limited but does not resolve until skeletal maturity has been achieved. Management includes NSAIDs, ice, and activity modification to reduce pain although it does not accelerate the healing process; correction of biomechanical factors including excessive subtalar pronation, landing technique, lumbo-pelvic weakness is important. Ossicle excision may be indicated in skeletally mature patients with chronic pain [17]. Sinding-Larsen-Johansson disease is described as chronic apophysitis or minor avulsion injury of the inferior pole of the patella at the attachment of the patellar tendon due to repetitive traction. The condition is most commonly seen in 10–14-year-old children, especially children with cerebral palsy. Pain is described as insidious onset of intermittent pain aggravated by running and jumping. Radiographs show calcification and ossification at the patella-patellar tendon junction. Management is similar to Osgood-Schlatter disease. Osteochondritis dissecans involves delamination and localized necrosis of the subchondral bone, with or without the involvement of the overlying articular cartilage. The most common location is the lateral aspect of the medial femoral condyle (representing 75% of the lesions) commonly seen with repetitive high-impact landings. Male to female ratio is 4:1 and commonly presents with gradual onset of pain and swelling, occasionally an acute locked knee. Radiographs show a demarcated radiolucency seen on the tunnel view. Non-operative management includes restricted weight-bearing and braces for stable lesions in children with open physes. Orthopedic evaluation may be required for fixation of fragments or loose bodies [17]. Juvenile idiopathic arthritis affecting the knee may present as intermittent effusion, warmth and restricted range of motion. Work-up should include blood work including rheumatoid factor, ESR, CRP with the consideration of joint aspiration for symptoms relief and fluid analysis. Management includes activity modification with pain-free physical activity. Anterior cruciate ligament (ACL) injuries in the pediatric/adolescent population are most commonly non-contact injuries which occur by a pivoting mechanism with the knee partially flexed and foot planted, or landing on a hyperextended knee with a valgus/rotational force. ACL injuries make up a higher proportion of total injuries in women’s compared with men’s sports, specifically gymnastics, soccer, and basketball. There is commonly an audible “pop” with immediate knee swelling (hemarthrosis) and inability to bear weight. Over 70% of patients with a traumatic

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hemarthrosis are found to have an ACL tear. Radiographs are important to rule out traumatic fracture with subsequent MRI for definitive diagnosis and to determine the extent of injury. Non-operative treatment including PT and activity modification is considered for pediatric athletes with a partial tear, low demand, and compliant patient. Prior to surgical intervention for ACL surgical intervention (reconstruction or repair), a course of “pre-hab” is considered to ensure full range of motion and maintain quadriceps strength. Intra-articular surgical reconstruction includesphyseal sparing, partial transphyseal, and complete transphyseal methods. Extra-­ articular methods are also considered. The major risks of reconstruction include tunnel or graft failure, premature osteoarthritis, loss of range -of-motion, and infection. Primary repair during which the torn ends of the ACL are sutured together using the collagen- based BEAR (Bridge-enhanced ACL repair) scaffold developed at Boston Children’s Hospital has shown success in  vivo studies and currently undergoing clinical trials with promising results [18]. Similar to the adult population, patellar tendinopathy, popliteal (Baker’s) cysts, and referred hip pain are diagnostic considerations in the pediatric population. Less common causes of knee pain may include partial or complete discoid meniscus which may cause clunking or snapping of the knee and Blount’s disease described as osteochondritis of the proximal tibial growth plate [2].

 nkle and Foot Injuries A Acquired or congenital foot deformities may be a cause of foot pain in the pediatric athlete. Ankle injuries are the most common injuries sustained by high-school athletes. Lateral ankle sprains account for ~85% of all sprains with recurrent sprains more common in cheerleading, boys’ basketball, and girls’ gymnastics. Chronic ankle instability may result in decreased sport activity and early retirement. Sever’s disease is an overuse injury described as calcaneal apophysitis at the insertion of the Achilles tendon and a common cause of heel pain in the pediatric population. Additional risk factors include poorly fitting shoes and Achilles tendon contractures [19]. There is notable activity-related pain (especially with jumping) and associated tenderness and swelling surrounding the heel; children may relieve pain by walking on their toes. There may be associated gastrocnemius and soleus tightness and pain-limited ankle dorsiflexion. Radiographs may show sclerosis. Management includes activity modification, Achilles tendon flexibility exercises, and strengthening exercises of the ankle/foot muscles with consideration of a heel lift/cup or short leg cast immobilization. Sever’s disease is a self-limited disease and usually resolves over 6–12 months but may persist for 2 years or until closure of the apophysis; recurrence is common [19]. Congenital fusions of the bones of the foot may be undetected until sport activity has begun and presents with midfoot pain especially after repetitive running or jumping or after recurrent ankle sprains. The most common is a bony or cartilaginous bar between the calcaneus and navicular followed by the calcaneus and talus. Physical exam demonstrates restricted subtalar joint range of motion and a rigid pes planus deformity. Management includes the use of orthotics and consideration of surgical excision for refractory pain in symptomatic children.

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Osteochondrosis of the navicular bone is known as Kӧhler’s disease (Syndrome), commonly seen in boys age 4–10 and bilateral in up to 25% of cases. Although the etiology is unknown, the navicular bone may be vulnerable to mechanical compression injury due to its late ossification relative to the other tarsal bones. Patients present with a painful limp favoring the lateral aspect of the foot during ambulation and pain/tenderness over the medial aspect of the navicular bone worse with weight-­ bearing activities. Radiographs show increased sclerosis, fragmentation, and flattening of the navicular. Kӧhler disease is self-limited and generally resolves as the navicular bone reossifies (between 4 months to 4 years) without long-term sequela. Symptomatic patients may benefit from a short leg walking cast for 4–6 weeks [20]. Freiberg’s infarction (disease) is due to osteochondrosis of the metatarsal head most commonly the second, followed by the third, occurring in adolescents through their 20s, particularly ballet dancers. There is notable swelling, stiffness, and pain in the forefoot leading to a limp. Radiographs will show a widened MTP joint followed by collapse and sclerosis of the metatarsal head with growth plate fragmentation; however, MRI or bone scan may be indicated if radiographs are negative. Treatment includes activity modification (avoidance of high-impact running), metatarsal bar/pads, and the use of stiff-soled shoes. Recalcitrant cases may benefit from surgical intervention though there is a risk of early arthritis [19]. Apophysitis in the foot may be seen at the insertion of the tibialis posterior tendon on the navicular commonly seen with an accessory navicular or the peroneus brevis tendon attachment to the base of the 5th metatarsal.

Sport-Related Concussion Based on a comprehensive study which evaluated 3 national injury databases, it is estimated that in the United States as of 2016 there are 1.1–1.9 million SRRC (sports and recreation-related concussions) annually in children 18 years or younger. The recent increase in incidence and diagnosis is explained by an increased awareness and education of the public, coaches, and medical staff as well as increased media exposure and continued increased youth participation in sports. For boys, the highest risk of concussion is seen in American tackle football followed by lacrosse, ice hockey, and wrestling. For girls, soccer is the highest risk sport followed by lacrosse, field hockey, and basketball [21, 22]. Modified tools exist for pediatric concussions including the postconcussion symptoms scale and Sport Concussion Assessment Tool (Child SCAT-5 or SCAT-5) available for aged 5–12 years and older than 13 years. The King-Devick Test and vestibular/ocular motor screening may also be employed in addition to parental questionnaires. A prolonged rate of recovery (>28 days) is best predicted by a higher overall initial symptom burden, specifically of somatic symptoms. Girls tend to report a higher symptom burden compared with boys. The majority of pediatric and adolescent athletes with concussion will recover between 1 and 4 weeks [21, 22]. The acute management of an athlete with concussion involves education of the athlete and family and an individualized approach to each case. Once a concussion

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is suspected, the athlete should be removed from play and not be allowed to return the same day and recommended for physical rest described as subsymptom exercise while avoiding complete inactivity followed by the Graduated-Return-to-Sport Program. Conventional neuroimaging (CT or MRI) is typically normal and remains indicated in the presence of focal neurological deficit or if there is suspicion of a more severe intracranial injury or structural lesion. Cognitive rest will focus on limiting the use of electronics (cell phones, computers, TV and video-games) especially athletes reporting photophobia. Academic adjustments may be necessary when returning the athlete to school which may include partial school days, break times while at school, reduced workload or environmental triggers (visual or audible stimuli) which may exacerbate symptoms [21, 22]. Second-impact syndrome is a rare phenomenon believed to be the result of an individual sustaining a second head injury before fully recovering from the first with resultant cerebral vascular congestion, progressing to diffuse cerebral edema and death. Preventive interventions include equipment modifications like properly fitted, sport rule change, and education.

Nutrition and Hydration Considerations Relative energy deficiency in sport (RED-S) is defined by the IOC as a syndrome which refers to “impaired physiological functioning caused by relative energy deficiency and includes, but not limited to, impairments of metabolic rate, menstrual function, bone health, immunity, protein synthesis and cardiovascular health” [23]. The underlying issue is an inadequacy of energy to support the bodily functions for optimal health and performance. Although more common in females, male athletes may also experience low energy availability. The IOC consensus statement outlines the health consequences and potential performance effects as well as return-to-play decision making which involves the athlete, healthcare professionals, and sports organization [23]. Exertional heat illness is a spectrum of illnesses including muscle cramping, exhaustion, and exertional stroke which occur during exercise and sport during conditions of environmental heat stress (i.e., high temperature and humidity levels). Physiologic data suggests that in heat conditions, children and adults have similar rectal and skin temperature, cardiovascular response, and exercise tolerance. It has been noted that most heat injuries occur in August, during football practice that last more than 2 hours. Therefore, children are at increased risk of exertional heat illnesses because they are undergoing rigorous exercise during the summer and commonly ingesting insufficient fluid. Although often reported in the press, fatal exertional heat stroke is rare. Educating coaching and team members for early recognition and rapid cooling (ice water immersion), implementing heat acclimatization protocols, and modifying or cancelling practice and games are crucial to athlete safety [24].

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Exercise Prescription in School-Aged Children and Adolescents The school-aged children and adolescents are the population from 6 to 17 years old. This is a critical period to develop motor skills; moreover, establishing long-term habits about physical activity and exercise is essential. Parents and caregivers play an important role during this stage. Historically, there has been a debate regarding the safety in children and adolescent on resistance training. The guidelines and recommendations of the ACSM support youth strength training exercises when they are mature enough and able to follow instructions, generally at 7–8 age [25]. It is important that these exercises are supervised by qualified personnel for safety and to prevent injuries. The exercise recommendations for this population include 60 minutes of moderate to vigorous intensity aerobic exercise, resistance training, and bone strengthening on 3 more days a week.

Summary The participation of children in sporting activities provides physical, social, emotional, and psychological benefits. In order to foster these benefits, avoid overuse injuries and allow for continued participation, it is crucial to maintain the health and safety of young athletes. The sports medicine physician must be aware of the risk factors, unique pathologies, mechanism of injury, and treatment algorithms in order to successfully treat the pediatric athlete.

References 1. DiFiori JP, Benjamin HJ, Brenner JS, et al. Overuse injuries and burnout in youth sports: a position statement from the American Medical Society for Sports Medicine. Br J Sports Med. 2014;48(4):287–8. 2. Caine D.  Injury in pediatric and adolescent sports: epidemiology, treatment and prevention. 2015. 3. Hacquebord JH, Leopold SS. In brief: the Risser classification: a classic tool for the clinician treating adolescent idiopathic scoliosis. Clin Orthop Relat Res. 2012;470(8):2335–8. 4. Jones C, Wolf M, Herman M.  Acute and chronic growth plate injuries. Pediatr Rev. 2017;38(3):129–38. 5. Caine D. Physeal injuries in children’s and youth sports: reasons for concern? Br J Sports Med. 2016;40(9):749–60. 6. Cepela DJ, Tartaglione JP, Dooley TP, et al. Classifications in brief: Salter-Harris classification of pediatric physeal fractures. Clin Orthop Relat Res. 2016;474(11):2531–7. 7. Atanelov Z, Bentley T.  Greenstick fracture. In: StatPearls. Treasure Island: StatPearls Publishing; 2019. 8. Shelat N, El-Khoury G.  Pediatric stress fractures: a pictorial essay. Iowa Orthop J. 2016;36:138–46. 9. Feeley B, Schisel J, Agel J. Pitch counts in youth baseball and softball: a historical review. Clin J Sport Med. 2018;28(4):401–5.

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10. Maruyama M, Takahara M, Satake H. Diagnosis and treatment of osteochondritis dissecans of the humeral capitellum. J Orthop Sci. 2018;23(2):213–9. 11. Patel DR, Kinsella E. Evaluation and management of lower back pain in young athletes. Transl Pediatr. 2017;6(3):225–3. 12. Théroux J, Le May S, Fortin C, et al. Prevalence and management of back pain in adolescent idiopathic scoliosis patients: a retrospective study. Pain Res Manag. 2015;20(3):153–7. 13. Mansfield J, Bennett M.  Scheuermann disease. In: StatPearls. Treasure Island: StatPearls Publishing; 2019. 14. Frank JS, Gambacorta PL, Eisner EA.  Hip pathology in the adolescent athlete. J Am Acad Orthop Surg. 2013;21(11):665–74. 15. Karkenny AJ, Tauberg BM, Otsuka NY. Pediatric hip disorders: slipped capital femoral epiphysis and Legg-Calvé-Perthes disease. Pediatr Rev. 2018;39(9):454–63. 16. Elattar O, Choi H-R, Dills VD, Busconi B. Groin injuries (athletic Pubalgia) and return to play. Sports Health. 2016;8(4):313–2. 17. Patel DR, Villalobos A. Evaluation and management of knee pain in young athletes: overuse injuries of the knee. Transl Pediatr. 2017;6(3):190–8. 18. Perrone GS, Proffen BL, Kiapour AM, et al. Bench-to-bedside: bridge-enhanced anterior cruciate ligament repair. J Orthop Res. 2017;35(12):2606–12. 19. Jaimes C, Khwaja A, Chauvin N.  Ankle and foot injuries in the young athlete. Semin Musculoskelet Radiol. 2018;22(01):104–17. 20. Gillespie H. Osteochondroses and apophyseal injuries of the foot in the young athlete. Curr Sports Med Rep. 2010;9(5):265–8. 21. Halstead ME, Walter KD, Moffatt K. Sport-related concussion in children and adolescents. Pediatrics. 2018;142(6):e20183074. 22. Bryan MA, Rowhani-Rahbar A, Comstock RD, et al. Sports- and recreation-related concussions in US youth. Pediatrics. 2016;138(1):e20154635. 23. 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):491–7. 24. Nichols AW.  Heat-related illness in sports and exercise. Curr Rev Musculoskelet Med. 2014;7(4):355–6. 25. FaigenbaumAaM L.  Youth strength training. American College of Sports Medicine: Indianapolis; 2017.

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Matthew D. Maxwell, William Berrigan, and Roderick Geer

Adaptive Sports A Brief History To best set a foundation for understanding, it is first important to understand the origins of disabled rights within our society and how it has come to influence adaptive sports. A very thorough and insightful review of the relevant historical events, as well as more comprehensive clinical information, beyond the scope of this text can be found in the textbook Adaptive Sports Medicine [1]. Much of this brief review derives from that text. A growing recognition of the heathy but physically disabled population developed around the late 1700s, coinciding with advancements in surgical amputation and understanding of other functional impairments such as blindness and deafness, as well as neurological disorders such as cerebral palsy. The government of the newly formed United States of America recognized the need to promote the integration of injured veterans as productive members of society and instituted early programs to develop technology development and support for disabled veterans. Several decades later, the subsequent American Civil War brought these considerations into the wider public consciousness, as it resulted in an estimated 30,000 amputations in the Union Army, and many more in the opposing confederate army.

M. D. Maxwell (*) Georgetown School of Medicine, Washington, DC, USA MedStar National Rehabilitation Hospital, Division of Sports Medicine, Washington, DC, USA e-mail: [email protected] W. Berrigan · R. Geer Georgetown School of Medicine, Washington, DC, USA MedStar National Rehabilitation Hospital, Washington, DC, USA © Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4_22

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This precipitated the Great Civil War Benefaction program and its promotion of prosthetic development to help this injured population, essentially spawning the modern prosthetic industry as we know it today. This pattern of growing public recognition and ensuing funding progressed over the subsequent decades, with each major US military conflict serving as intermittent catalysts to the overall movement. As the growing recognition of physical disability proceeded into the era of the Second World War, the parallel civil rights movement was gaining momentum as well. The adversity encountered by the physically disabled, the racially segregated, and female populations shared many similarities, in that all faced prejudice which impeded full integration into working society. Not surprisingly, all groups shared in advocating for the gains we now recognize in modern American history teaching. It is less recognized in popular American history, however, the degree to which this era contributed to greater public accessibility for disabled populations. Additionally, this era ushered new legal progress against discrimination toward the physically disabled, as it relates to employment and opportunities within public institutions such as government and universities. Over subsequent decades, this progress culminated with the signing of national legislation called the Americans with Disabilities Act in 1990, providing federal protection against systemic discrimination. In parallel with the civil rights movements through the twentieth century, there were parallel developments in organized and competitive adaptive athletics throughout the world. Early developments in Europe around the turn of the century focused on populations with hearing impairment, evolving into the Deaflympics, now considered the longest running athletic event in adaptive sports [2]. Later, efforts by philanthropic groups and national organizations resulted in formal events for other impaired populations such as the Special Olympics for those with intellectual disabilities in the 1950s and 1960s, as well as the Cerebral Palsy International Sports and Recreation Association (CPISRA) which now serves on the International Paralympic Committee [1]. In concert with the growing attention to acquired disability due to trauma and illness, some advocated for the integration of formal athletics to improve the rehabilitation process. This idea spawned the Stoke Mandeville Games shortly after the end of Second World War. These “wheelchair games” evolved over time, gaining popularity and participation, morphing into what is now known as the Paralympic Games.

Classification As with any clinical assessment of physical, mental, or psychological impairment, the evaluation and classification of the adaptive athlete derives from a detailed understanding and assessment of the underlying physical impairments and activity limitations which may influence participation in sport. As such, the formal framework on which adaptive sport classification is based stems from the International Classification of Functioning, Disability and Health (ICF), as proposed and formally approved by the World Health Organization in 2001 [3]. Over time, governing bodies such as the International Paralympic Committee (IPC) and subsidiary member organizations have adapted this framework to better address issues specific to athletic competition [4].

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A basic understanding of the ICF classification system is germane to adaptive sports specifically for the purposes of designating the appropriate classification status for safe, fair, and equitable athletic competition. Within this framework, impairments are separated into those of body function and those of body structure. Common examples of impaired body function include visual loss, mental function, and neuromuscular disease affecting motor strength or movement. Examples of impaired body structure include changes of anatomy such as those resulting from congenital limb deficiency or amputation. In total, there are eight types of physical impairment in the (IPC) Classification structure: 1. Impairments of function (a) Impaired strength (b) Impaired range of motion (c) Hypertonia (d) Ataxia (e) Athetosis 2. Impairments of structure (a) Limb deficiency (b) Leg length difference (c) Short stature In considering classification schema, one must also consider the activity in which the individual will engage, in this case the specific sport or athletic activity. Any particular impairment may have differing effects on the individual athlete depending on the area of competition. For instance, a trans-radial limb deficiency has profoundly different effects on participation in the biathlon as opposed to participation in cross-country skiing, although both activities would be affected by the impairment. Thus, the classification system for participation in sport accounts not only for the impairment of the athlete, but also for the ways in which that impairment specifically affects activity participation. The current methods for Paralympic classification have been most comprehensively developed by the IPC and its member federations. As such, most formal organizations follow a similar structure and it will serve as the basis for this introduction to classification as an overarching concept. The process of classification can be broken down into four stages [4]: 1. Assessment for health condition which may result in functional impairment. This step often requires submission of supporting medical records and other supporting information to document the underlying health condition which serves as the basis for participation. 2. Assess the presence of functional impairment.This step must be performed in person with a detailed assessment of the underlying health condition and its effects on the physical function of the athlete. 3. Assess the severity of the functional impairment. It must be formally determined that the observed functional impairment is severe enough to affect participation

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and competition in the designated sport. This step is, therefore, sport specific and is guided by sport-specific criteria which are developed by the respective governing organization. 4 . Designate class allocation. In this step, the individual athlete is assigned a class profile, or the level at which they are most appropriate to compete, such that it provides an equitable basis competition in the designated sport. The process through which one completes classification is sport-specific; however, there are several details and concepts which are common to all adaptive sports. First, there are many common assessment tools which are used in the assessment of health conditions and functional impairment which are common to all sports. Common assessment tools/techniques include: 1. 2. 3. 4.

Manual motor testing for strength Ashworth or modified Ashworth scale for spasticity Goniometry for range of motion Anthropometric techniques for measurement of limb deficiency, leg length discrepancy, or stature 5. Clinical coordination tasks such as finger-nose-finger, rapid alternating movements Secondly, common to all adaptive sport is the process through which one formally assesses the ways in which the individual’s impairment affects athletic participation and assigns a specific class allocation. Class allocation is effectively a function of five inputs for consideration [5, 6]: 1. 2. 3. 4.

Impairment assessment as detailed above Novel motor tasks which are unlikely to be practiced during athletic training Sport-specific motor tasks which are likely to be practiced during training Training history detailing the process through which the athlete has prepared for competition 5 . Personal and environmental factors contributing to the athlete’s readiness to compete After initial classification allocation has been determined, the athlete is then observed during competition to ensure that athletic performance is consistent with expected ability from the above criteria. Only after the classification panel has observed the athlete in competition can the final allocation be completed [5, 6]. It is important to note that many of the particulars of assessment and classification, while described well in IPC and other association guidance documents, have not been well-validated for the referenced purposes, nor have they been thoroughly evaluated in terms of their reliability and validity in the field of adaptive sports medicine. There are active and ongoing efforts to further develop an evidence-­ based, collective understanding of the ways in which we can ensure a more equitable competition among this unique group of athletes [4].

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Adaptive Sports Equipment Though the precise chronology of adaptive sports is not entirely known, the use of adaptive equipment in sports has expanded exponentially over the last century. In addition to improved medical care, public opinion and legislation began creating support structures for individuals with disabilities as detailed above. Thus, the room for “adapted physical activity,” or APA, grew rapidly with that growing public recognition. With the development of APA came the modification of adaptive equipment to better suit particular sports, as well the invention of innumerable new technologies and methodologies designed to support adaptive athletes.

Wheelchair Technology There are five basic components of sports wheelchairs: wheels, casters, footrests, backrest, and seat (Fig. 22.1). These technologies, and their modifications, lie at the heart of wheelchair sports and have enabled athletes with disabilities to compete in a variety of previously inaccessible ways. Wheelchair designs are generally customized for each individual sport and athlete. For example, if speed and agility are required, wheelchairs and seating systems must be modified to be more lightweight, form-fitting, responsive, and move with the least friction possible. In this way, wheelchairs are analogous to prosthetic limbs as they must “become one” with the athlete’s body [7]. A racing wheelchair, designed for speed, uses larger wheels, small hand rims, a forward-leaning bucket seat, and high-pressure tires. These are steered via handle bars, a compensator, or by performing a wheelie. Rugby wheelchairs, on the other hand, are built for stability in order to withstand impacts. While speed and maneuverability remain key components, the wheelchairs must also have bumpers, shields on the wheels, and casters for quick and stable turns. While sport wheelchairs are made from a variety of materials, the basic frame components are commonly made of highstrength steel, aluminum, titanium, or composite materials such as carbon fiber, Kevlar, or fiberglass. A combination of materials is perhaps the most common wheelchair composition. For example, wheel rims and hand rims may be constructed from aluminum, but the frame could be made of titanium and the axle steel [8]. Fig. 22.1  The basic components of sports wheelchairs include the wheels, casters, footrest, backrest, and seat. Note that this tennis chair has moderate seat dump, allowing for greater trunk stability, and moderate camber for lateral stability

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There are three primary aims of the seating system in a wheelchair: (1) to provide a stable base of support to maintain balance during sport-related activities; (2) to decrease the risk of skin breakdown and pressure-related tissue injury; and (3) to maintain a shape that fits the user snugly and is comfortable [7]. Seating Parameters  In terms of seat depth, the length should be designed such that there is about 2–3 inches between the front edge of the seat and the user’s popliteal fossae. Seat height, on the other hand, is related to the position of the upper extremity. The user should be positioned such that, with the upper arm in line with the trunk and the hands at the apex of the push rim, the elbow angle should be 90–120°. This is the ideal position for efficient propulsion. The seat dump, or seat angle, is commonly set at 5° of posterior tilt. Increasing the angle further would aid pelvic stability by holding the pelvis against the backrest; this is often done in cases of truncal instability. Too steep a tilt, however, will predispose to pressure-related tissue injury and affect the user’s center of gravity. It is important to note that seat fit is of the utmost importance, not just for maintaining the center of gravity and allowing for stability, but also for reducing the risk of pressure sore development. A snug and well-fitted seat will reduce shear forces and friction, which can be augmented with straps for additional support. Seats may even be custom-molded to the user for optimal fit. Lastly, the backrest is generally positioned at the lowest point possible to allow upper torso movement while maintaining a degree of lower back support that is appropriate for the user [8]. Sport-Specific Wheelchair Designs Basketball  Wheelchairs used in basketball commonly have a degree of camber (wheel tilt) that allows the user to perform quick, agile turns, protect the athlete’s hands, and allow for greater stability. Front and wheel casters are in place to prevent the wheelchair from tipping in cases of rapid direction change or contact (Fig. 22.2). Chairs may also be adjusted based on the athlete’s position. For example, forwards and centers may have a higher seat position for shots in the paint, while guards maintain lower seats for maneuverability and low center of gravity [9]. Fig. 22.2 Basketball wheelchair. These basketball wheelchairs have a greater degree of camber for increased lateral stability

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Fig. 22.3 Rugby wheelchair. Note that this particular chair design employs reinforced, solid wheels to prevent hooking and forward bumpers to absorb high-energy collisions

Rugby  Chairs used in wheelchair rugby are similar to those in basketball in that there is need for wheel camber and casters to prevent tipping (Fig. 22.3). However, in rugby, additional adaptations are needed to account for increased contact. These include a metal plate that covers wheel spokes to prevent “hooking” and wheel damage, as well as a forward bumper to capture and disrupt opposing players. For increased trunk control in athletes with tetraplegia, the backs to the chair are also often higher than those in basketball [9]. Racing  The frame, seat, wheels, and handrims of a racing wheelchair are modified specifically to promote speed. The wheelchair frame is often constructed using lighter weight materials, such as carbon fiber or aluminum. The seat allows the athlete to have a forward-leaning posture, and knees are commonly flexed greater than 90° to improve aerodynamics. Most racing wheelchairs will have three large wheels, two in the back and one in the front, with the front wheel smaller than the rear wheels. These will all be fitted with high-pressure tires. Note that larger wheels are associated with decreased rolling resistance. While a degree of camber is used, the angle is generally less than that used in rugby or basketball. The handrim size is

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related to both upper extremity motor strength and length. Smaller handrims require greater strength to push, while larger handrims require less force but greater hand speed. The rims are then coated with a surface, providing a high degree of friction. A proper propelling sequence initiates contact at about the two to three o’clock position, proceeds with extending the arms until the hands reach the seven o’clock position, and then releases to reset the motion. Note that the aforementioned modifications, apart from the handrims, can be used in the construction of a handcycle designed for racing. These may be upright, add-on, recumbent, or kneeling. Upright and add-on handcycles are used for transport, while recumbent and kneeling cycles are used for racing (Fig. 22.4).The recumbent position is better suited for athletes with poor trunk control. It decreases wind resistance but sacrifices speed in sprints or uphill terrain when compared to kneeling handcycles [8, 9].

 daptive Sports Prostheses A Standard general use prostheses are used to provide the athlete versatility in as many activities as possible. Most often, the initial goal is to fit an athlete with a prosthesis that will allow them to develop ambulatory skills and other activities of daily living. Once the individual commits to a specific sport, a new prosthesis or sport-specific prosthetic components may be required. If modifications are warranted, the athlete Fig. 22.4 Recumbent hand cycle used for racing and recreation

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may interchange distal components, such as prosthetic feet and knees. This can be more time- and cost-effective than possessing multiple individual prosthesis. Sport-Specific Prosthesis These often utilize various modifications to better suit the athlete to the sport in question. For example, the weight of the sport-specific prosthesis is often much lighter than their standard general use counterparts to avoid speed reduction. Alignment of the socket and shank of a lower limb prosthesis is another critical aspect affecting an athlete’s performance, as this may be different than prostheses used for activities of daily living. The liner, in turn, is often constructed from an elastomeric gel, which can help to mitigate the increased shear and pressure forces that occur with athletic activity [10]. The heels of prosthetic feet are designed to distribute and mitigate energy during loading. With the addition of running shoes to the prosthesis, this dissipated input energy can improve from 63% up to 73%. Shock-absorbing pylons can aid this process further. The addition of a prosthetic ankle component designed to absorb torque forces also allows for rotation between the socket and foot [11]. Running Prostheses  These require total direct contact in a form-fitted socket to maximize function. While thinner liners reduce motion in the socket, thicker liners provide more shock absorption. In terms of suspension, an airtight sleeve and expulsion valve provide the best limb stability in a transtibial prosthesis [12].The knee components in cases of transfemoral amputations are most commonly single axis, hydraulic, pneumatic, and computer microprocessor knee devices. The shank is generally fixed to the posterior aspect of the socket and has increased length to provide a longer lever arm, enhancing energy storage and release. Distally, an energy-­ storing, flexible keel best mimics the “push-off” of the foot that occurs with plantar flexion (Fig. 22.5). These can vary in flexibility and strength, thus allowing for a desired amount of kinetic energy storage. The shorter the keel and the greater the bend, the less the energy stored. Therefore, competitive athletes will often select longer, more linear keels. Running prostheses can be constructed without heel components, depending on the anticipated running speed of the athlete. For example, the heel is minimally used as speeds surpass 140  m/min; thus, faster or competitive runners commonly forgo heels, while joggers may require a heel in place [13]. Skiing and Snowboarding  Adaptive equipment in skiing varies, as athletes may ski in either the seated or standing position. Individuals with upper limb amputations may choose to ski without adaptive equipment. Alternatively, they can use a prosthesis designed to hold a ski pole or use “outriggers” which are essentially modified forearm (Lofstrand) crutches with a ski pole tip or additional ski. Individuals with lower limb amputations may also ski with or without a prosthesis, as a single ski may be coupled with outriggers. Alternatively, they can use a unilateral prosthesis and two skis; this is most common in unilateral transtibial amputations. For athletes with transfemoral amputations, several prosthetic knee components can be used. Single-axis knees are useful initial components, but they

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Fig. 22.5  Running blade with custom-made carbon fiber socket

can be exchanged for more dynamic knees over time as warranted. In terms of the construction, the center of gravity should be set in front of the ankle, with a shorter prosthesis length to form a flexed lower limb. The foot component is often dorsiflexed to maintain this position; the foot may even be attached directly to the ski bindings, thus eliminating the need for a boot. Alternatively, the skier may use any number of traditional foot components with a ski boot, commonly a solid ankle cushioned heel (SACH) or dynamic response foot. Seated skiing is generally reserved for those with bilateral lower limb amputations, spinal cord injuries, and other impairments affecting the lower extremities. The seat is mounted on a frame equipped with a shock absorber and suspension system (Fig. 22.6) [14]. For snowboarding, the current standard is to attach the terminal device of the prosthesis directly to the snowboard, with a coupler added to allow donning and doffing of the equipment. Specialized shock absorbers have been recently designed to support the knee in the flexed position required for snowboarding [15]. Sled Hockey  Athletes use custom sleds that fit the individual body shapes. Sled length ranges from about 0.6–1.2 m. The body of the sled is attached to two steel blades 3 mm in width, which must be tall enough to allow the puck to pass under the sled. The stick used in sled hockey has a blade on one end for shooting and a metal pick on the other. The pick allows the athlete to propel themselves on the ice (Fig. 22.7) [16].

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Fig. 22.6  Adaptive ski set-up with outriggers

Fig. 22.7 Sled hockey set-up

Assessment of the Athlete  re-participation Examinations (PPE) P All athletes may have medical conditions that prevent them from participating in sport. Therefore, it is important for adaptive athletes to have accurate and thorough pre-participation examinations with particular attention to medical conditions which may be associated with their underlying diagnoses and impairments, as well as any cardiorespiratory condition that could be detrimental to the athlete’s health. It may be even more important for the adaptive athlete, as the incidence of sports-specific abnormalities found on history and physical examination were reported to be up to 40% in the Special Olympics population versus 1–3% in able-bodied individuals [17]. In addition to the standard PPE for athletes, with guidelines placed by organizations such as the AAFP and other associated organizations such as the AMSSM, further considerations need to be taken for adaptive athletes [18, 19]. These include athletic goals, pre-disability health, present level of training, sports participation,

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medication/supplement use, presence of impairments, cardiopulmonary history, level of functional independence with activities of daily living, and need for adaptive equipment. The examination should be done with a multidisciplinary approach, as the assessment of equipment (wheelchair, prosthetics, orthotics, assistive devices) may be better accomplished by an orthotist, prosthetist, or other specialist. The PPE is recommended to be completed 6 weeks prior to competition to allow for adequate preparatory time. The quality of the information lies with the medical provider’s proper administration and a detailed consideration of relevant medical comorbidities.

 ports Injuries and Medical Complications in Wheelchair Athletes S The majority of athletes in wheelchairs will have spinal cord injuries. However, eligibility extends to those with multiple amputations, neurological disorders, spina bifida, and cerebral palsy [20]. Injuries to these athletes most often occur in the upper limbs, involving the wrist, hand, and shoulder. Not only are they susceptible to the same type of injuries as any other athlete, but wheelchair users are subject to the overuse phenomena associated with transfers, wheelchair pushing, and weight shifts. It is important to understand that, given the degree which wheelchair users rely on their upper extremities for mobility and activities of daily living, relative rest of the upper limbs after injury may not be possible. In both the London 2012 and Rio 2016 Summer Paralympic games, the highest incidence rate of injury (IR) per 1000 athlete days was to the shoulder at 2.1 and 1.8, respectively. Injuries to the wrist, hand, and finger complex were the next most common with an IR of 1.0. Injuries to the neck (0.7), spine (0.2–0.6), and lower limbs (0.2–0.9) were less common [21, 22]. In a survey of winter athletes, the shoulder remained the most common site of injury with an IR of 6.4. However, upper and lower limb injuries had a similar incidence rate at 8.5 and 8.4, respectively [23]. Upper Limb Injuries For wheelchair athletes, treatment planning can be complex given the dependence most athletes have on the use of the upper limb for basic daily mobility and performance of ADLs. Splinting, orthotics, inpatient rehab, home modifications, or additional outside assistance may be required. Wrist  Athletes are especially prone to mononeuropathies at the wrist. Carpal tunnel syndrome (CTS) is the most common mononeuropathy and is secondary to repetitive flexion/extension and palmar grip involved in propelling the wheelchair. Injury incidence ranges from 49–73% with significant correlation between time after injury and severity of CTS [24–26]. The second most common mononeuropathy is ulnar neuropathy at Guyon’s canal. This is often seen in marathon racers; one small study reported an incidence of 25% in this population [26]. Other chronic musculoskeletal injuries to consider are tendinopathies and De Quervain’s tenosynovitis. Treatment includes physical/occupational therapy, anti-inflammatories, and/or local injections.

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Elbow  The most common causes of elbow pain are lateral epicondylopathy (LE), osteoarthritis (OA), and olecranon bursitis. LE is often seen in wheelchair racquet sports secondary to incorrect backhand stroke or a late forehand hit behind the body. It may also be seen in wheelchair racers from excessive wheel grip forces and poor stroke technique. Proximally, mononeuropathies may also occur, including median and ulnar neuritis. Ulnar neuritis is most frequently seen in racquet sports. It may be prevented by proper stroke form and flexibility with a counterforce brace distal to the elbow for shock absorption [27]. Shoulder  The most common shoulder pathologies found include rotator cuff injury, subacromial bursitis, acromioclavicular joint abnormalities, coracoacromial ligament thickening, subacromial spurs, distal clavicle osteolysis, and impingement syndrome. The etiology of these disorders originates from the fact that wheelchair users are forced to use their upper limbs for wheelchair propulsion, transfers, and weight shifts, which are non-physiologic adaptations which can result in excessive biomechanical stress on these structures. Often, this overuse is exacerbated by muscle imbalance and fatigue related to athletic training and daily mobility requirements. During wheelchair propulsion, the deltoid and pectoral muscles are maximally active during the push phase. Athletes often will work to strengthen their deltoids, biceps, and triceps to increase propulsion speed. Their weaker rotator cuff muscles and shoulder adductors in comparison to deltoid abduction place athletes at risk for impingement and cuff pathology. Sports that require overhead movements such as shooting, basketball, weight training, and racquet sports amplify the wheelchair athlete’s risk factors due to these underlying imbalances. Prevention is the first step with athletes and should include strengthening the upper extremity adductors, internal rotators, and external rotators to counterbalance the pull of the humeral head by the deltoid. Posture training is also of benefit [27, 28]. Heterotopic Ossification  Athletes with traumatic brain injury, spinal cord injury, burns, or joint replacement can be affected by heterotopic ossification (HO). HO is the development of ectopic bone in soft tissues surrounding major joints. It most commonly affects the hip in spinal cord injury, but may also present in the knee, elbow, and shoulder. In amputees, HO can also present in the injured tissue of the residual limb. Athletes may present with an assortment of symptoms, including low-­ grade fever, effusion, localized erythema, warmth, soft tissue swelling, and decreased range of motion. Diagnosis can be made via bone scan or x-ray, but bone scan is more sensitive for early detection as HO takes 7–10 days to appear under x-ray. HO most commonly occurs 1–4 months after injury, but can present after the first 6 months. Treatment is to maintain range of motion, and pharmacological management may be considered with etidronate or NSAIDs. Severe cases require radiation or surgery [29]. Autonomic Dysreflexia (AD)  Autonomic dysreflexia is a potentially life-threatening syndrome affecting patients with spinal cord injury (SCI) at the level of T6 or above, yet has been reported as low as T10 [30]. It occurs when a noxious stimulus below the

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level of the lesion activates the spinal reflex pathways of the sympathetic chain from T1-L2. Given the spinal cord injury, the brain is unable to provide central inhibitory control of this reflex to the sympathetic chain below the level of neurological injury. This results in an uncontrolled release of epinephrine and norepinephrine. The carotid baroreceptors respond to acute hypertension by activating the parasympathetic nervous system which results in relative bradycardia with the acute hypertensive state. Systemically, the sympathetic response overwhelms the counter-response of the parasympathetic nervous system resulting in a potentially catastrophic hyperadrenergic state. Most commonly, AD is caused by over-distention of the bladder. Other causes include fecal impaction, pathology of the bladder and rectum, ingrown toenails, labor and delivery, orgasm, medical procedures, and other various conditions [30]. Athletes with AD will present with a diverse set of symptoms including headache, systolic and diastolic hypertension, profuse sweating and cutaneous vasodilation with flushing of the face, neck and shoulders, nasal congestion, pupillary dilatation, and bradycardia. This most often presents chronically 3–6 months after the injury. Hypertension can be so profound that it can cause myocardial ischemia, status epilepticus, intracerebral hemorrhage, and even death. If AD is suspected, the athlete should be removed from competitive play, sat upright, and have their clothes loosened. The clinician should then search for the noxious stimulus, most often the bladder. If medication management is needed, nitro paste applied above the level of injury or chewable nifedipine can be used. Transfer to an acute care facility should be considered. It is also important to note that athletes have been known to engage in the intentional induction of AD to enhance athletic performance commonly referred to as boosting. Boosting has shown to confer up to a 9.7% improvement in racing time [31]. Given the dangers to the athlete, the Paralympic Committee strictly bans this practice. Spasticity  Spasticity is a velocity-dependent increase in muscle tone that occurs after an upper motor neuron injury such as SCI, TBI, stroke, or other CNS degenerative diseases. It can significantly limit an athlete’s ability to play by restricting range of motion of the joint. A sudden change in spasticity not only will limit play, but also may be an indicator of a systemic or asymptomatic condition. This includes, but is not limited to, infections, intra-abdominal pathology, skin breakdown, or bladder distention. Treatment should focus on correcting the underlying pathology. Other treatments include physical therapy, specifically stretching, ROM, splinting, serial casting, and other modalities. Patients may be prescribed systemic medications such as baclofen, dantrolene, tizanidine, or benzodiazepines, or undergo local injections such as botulinum toxin. Severe cases may benefit from intrathecal pump administration of baclofen or surgical options such as tendon lengthening. Some ways to prevent spasticity are through education regarding daily stretching, avoidance of noxious stimuli, proper positioning, daily skin inspection, and adequate bowel and bladder programs [29]. Temperature Dysregulation  Following spinal cord injury, the neuro-pathway regulating temperature control is impaired. The normal pathway between the

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hypothalamus and its motor and sensory connections are lost. In higher SCI, most of the skin is insensate and the athlete may not detect hot or cold. In addition, the efferent sympathetic pathway is damaged, leading to impaired vasomotor control within the skin, in which case heat can neither be conserved nor lost. Sweating is ineffective below the level of injury as is shivering in response to cold stimuli. It has been shown that fluctuations in temperature affect paraplegics with lesions below the level of T6 less than those with lesions above T6 [32]. The discrepancy is even larger for tetraplegics. Prevention requires awareness by both the physician and the athlete to properly monitor for signs of hot or cold injury. It also requires the use of proper clothing and equipment, the availability of rehydration, and the avoidance of extremes of temperature when possible [21, 32]. Orthostatic Hypotension  Orthostatic hypotension is common in athletes with spinal cord injury. This is caused by a low level of efferent sympathetic nervous activity and loss of reflex vasoconstriction. There is also a peripheral dysregulation of the vasodilator, nitric oxide. A change in position in an individual with SCI results, therefore, in an excessive pooling of blood in the abdomen and lower extremities without appropriate compensation. This occurs more often in tetraplegics rather than paraplegics [33]. Prevention in this population should first be done with nonpharmacological methods. This includes appropriate fluid and salt intake, abdominal binders, compression stockings, and functional electrical stimulation. If these measures prove unsuccessful, medications such as Midodrine, Fludrocortisone and Ergotamine, Ephedrine, or L-DOPA are options, with the strongest level of evidence for Midodrine [34]. It is to be noted that Midodrine, Fludrocortisone, and Ephedrine are banned in competition by WADA and U.S. Anti-Doping Agency as performance enhancing drugs [21]. Skin Disorders  Many spinal cord injury athletes are insensate below the level of their lesion. This leads to skin breakdown and pressure ulcers, most commonly in the sacrum, coccyx, and ischial tuberosities. Prevention should focus on maintaining the skin clean and dry as well as on adequate pressure relief via routine positional change [35]. Wheelchair equipment should be fit properly to include cushioning, padding, and alignment as previously detailed. Athletic wheelchairs can often sacrifice pressure relief for higher performance. Therefore, the athlete and physician should practice increased vigilance in monitoring for signs of early skin breakdown. At the first sign of skin breakdown or pressure ulcer, activities should be modified or restricted to prevent further injury. Osteoporosis and Fractures  These are secondary to bone loss in athletes with SCI. This is attributed to decreased weight bearing and prolonged immobilization. All individuals with complete SCI develop osteoporosis and are twice as likely as healthy controls to experience fractures. The most common sites of these fractures are the metaphysis of the proximal tibia and distal femur. These fractures may be painless and, therefore, the examiner should pay close attention to erythema, fever, or limb deformity. Fractures may also first manifest as AD or an increase in

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spasticity, as opposed to pain. Prevention of osteoporosis can be done with vitamin D, calcium, and bisphosphonates. Therapeutically, functional electrical stimulation exercise is another option [21, 36].

 edical Injuries and Complications of Limb-Deficient Athletes M Athletes with total or partial absence of bones or joints, whether congenital or as a consequence of trauma or illness, are eligible to compete under the impairment classification of limb deficiency. These athletes may compete either sitting or standing. Depending on their underlying impairment and level of function, they may experience an assortment of medical complications. Skin Disorders  Amputees are subject to skin injury at the distal portion of the residual limb as it transitions to a weight-bearing surface. The most common skin disorders are ulcers, cysts, calluses, contact dermatitis, hyperhidrosis, verrucous hyperplasia, lichenification, and infection [27]. The etiology of these disorders is multifactorial, most often stemming from adjustments to the prosthesis or sudden changes in activity level. The socket itself fits tightly, not effectively circulating air, thereby trapping perspiration. Uneven loading of the socket can cause stress on the localized stump area leading to skin breakdown and tissue maceration. Specific pressure areas of breakdown for the transfemoral amputee include the adductor region of the thigh, the groin, and ischial tuberosity, all points of contact with the socket rim. For the transtibial amputee, pressure areas are the tibial crest, tubercle, and condyles, the fibular head, the distal tibia and fibula, the hamstring tendons, and the patella [37]. Any athlete found to have skin ulceration should be advised a period of relative rest with activity modification. In addition to treatment of the wound, adjustments should be made to the prosthesis to include proper socket fitting, silicone liners, padded sleeves, socks, and additional padding. Rashes may be allergic, bacterial, chemical, or fungal. In the case of allergy, the irritating agent should be identified and avoided. Treatment is with topical corticosteroids and symptomatic relief with cold compresses and bland anti-itch lotions. Bacterial infections such as folliculitis and furuncles may require oral or topical bacteriostatic or bactericidal agents and, in more severe cases, incision and drainage. Fungal infections such as tinea corporis can be treated locally or systemically with antifungals. Verrucus hyperplasia is a wart-like lesion that develops at the distal portion of the residual limb. It can be present chronically and is often associated with ulceration and edema. Treatment is often only temporary but includes external compression and adequate control of bacterial infections. Shrinker socks and socket modification may help prevent and resolve this problem. Cysts occur more often in the transfemoral amputee than the transtibial population. The condition is chronic and symptomatic relief can temporarily be provided through incision and drainage. It must be monitored for coinciding bacterial infection.

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Taken as a whole, when approaching skin disorders in the AWLD, the most effective treatment is prevention. This can be done through education, close monitoring of the prosthesis fit, strategic timing of donning a prosthesis, considerations of the time out of the prosthesis and liner and responding to environmental factors [21]. Neuromas  It can occur at the end of a stump in athletes with amputations. This may cause paresthesias, dysesthesias, and phantom radiating pain in the distribution of the transected nerve. Treatment includes activity modification and alteration of the prosthesis to unload the painful area. Medications such as acetaminophen, NSAIDs, anti-epileptics, and tricyclic antidepressants are used for primary management. If non-procedural measures fail, injection of local anesthetic and steroid or radiofrequency ablation may be tried. Surgical resection of the neuroma may be necessary [21].

Sport-Specific Considerations in the Adaptive Athlete Wheelchair Rugby Also known as “murder ball,” wheelchair rugby is a co-ed sport performed by athletes who have a disability affecting both their arms and legs. Most often, these athletes have a spinal cord injury, but play is eligible for those with cerebral palsy, muscular dystrophy, amputation, or other neurological conditions as well. Prior to participation, each player is assessed by a medical professional and given a classification range from 0.5 to 3.5. Classification is based on disability level with 0.5 having the lowest level of functionality and 3.5 having the highest level of functionality in regard to chair and ball handling. A team is comprised of four court players not to exceed a total classification value of eight. If a female athlete is present on the court, an extra 0.5 is allowed. The game is then played on a hardwood court measuring 28 m × 15 m with marked boundary lines, a center line, a center circle, and two key areas [38]. Wheelchair rugby is played with a regulation sized white volleyball. Manual wheelchair use is required for all athletes and specific regulations are put forth by the International Wheelchair Rugby Federation. Often, athletes use either an offensive or defensive wheelchair. Offensive chairs are set up for speed and mobility and contain a front bumper with wings to prevent other wheelchairs from hooking. These chairs are mostly used by athletes with functional level of 2.0 or greater. Defensive wheelchairs contain bumpers set up to hook and hold other players. These chairs are most often used with players whose functional level is less than 2.0. Other equipment includes gloves worn for grip and hand protection, and straps around waist, thigh, and feet for improved stability and performance. Wheelchair rugby involves aggressive contact, causing athletes to have a higher ratio of traumatic injury in comparison to other wheelchair sports. Upper extremity musculoskeletal injuries are most common, but acute trauma from contact with other wheelchairs, objects, and falls may lead to lower extremity injuries as well. This high level of impact increases the risk of head and neck trauma. Wheelchair

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athletes are also at risk for peripheral nerve entrapment, thermodysregulation, pressure ulcers, spasticity, HO, and autonomic dysreflexia as detailed previously [39].

Wheelchair Basketball The majority of athletes participating in wheelchair basketball have underlying spinal cord injury; however, other diagnoses include limb deficiency, amputation, or neurological disorders. Similar to rugby, each athlete is given a classification number based on functional ability and “volume of action.” The “volume of action” refers to the extremes to which the player’s trunk stability will allow them to reach without holding onto the wheelchair and before over-balancing. Classification range is from 1.0 to 4.5. Five players are on the court from each team at a given time, and the total classification points on the court cannot exceed 14 [40]. Wheelchairs are modified for sport. Increases in hand rim diameter and wheel axis height increase mobility. The camber is often widened to promote quicker mobility and prevention of contact, with the optimal angle being 18 degrees. Positioning of the footrest further underneath the seat is often performed to increase maneuverability. Castor wheels at the front of the chair provide stability with high velocity turns and rear castor wheels prevent tipping. Seat height can also be adjusted to allow for full elbow extension, maximizing the push angle of the athlete, with optimal position when the elbow angle is 100–130°. Neuromuscular injuries are the most common injuries in wheelchair basketball. Most often these are overuse syndromes affecting the upper extremity, the most frequent being shoulder impingement syndrome. Bicipital and rotator cuff tendinopathy and entrapment neuropathies are also common. As with all wheelchair sports, medical complications such as thermodysregulation, orthostatic hypotension, pressure ulcers, spasticity, HO, and autonomic dysreflexia should be taken into consideration upon athlete evaluation. Running Adaptive running includes three primary divisions: push-rim wheelchair and/or hand cycle, visually impaired, and mobility impaired. Specific equipment and adaptations include prosthetics (usually energy storing and returning carbon fiber polymer), racing chairs, and guide runners for help with visualization. Events include sprints, middle and long distance, the marathon, and the pentathlon. Athletes have also become more involved in major marathons as well with 28 wheelchair athletes and 48 hand-cycle athletes completing the 2018 Boston marathon. Depending on the event, participants must qualify for specific age and classification standards [41]. Considerations for medical coverage for adaptive racing are similar to any other athletic population. Concerns include hyponatremia, heat illness, exercise-induced asthma, and overuse injury. Skin conditions are also prominent. Wheelchair athletes have repeated contact with the wheelchair rim, tire, and locking mechanism; longer races also increase the likelihood of pressure ulcers if proper offloading techniques are not used. Limb-deficient athletes have significantly increased risk of skin disorders as detailed above.

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When looking at demographics, wheelchair athletes more commonly sustain upper extremity injuries. Amputee runners sustain injuries to the residual limb, contralateral limb, or spine. Knee and foot injuries are more common in athletes with cerebral palsy, and visually impaired athletes also have higher incidences of lower extremity injury. It is important to remember that any individual with a spinal cord injury should be monitored closely for impaired thermoregulation and AD.

Sled Hockey Ice sled hockey is a seated version of ice hockey designed for athletes with physical impairments that affect the ability to stand and skate. Because of the definition of eligibility, sled hockey players will exhibit a number of different impairments. As stated previously, the athletes sit in sleds supported by two blades. Two shortened hockey sticks are used, one with the hockey blade and the other with an ice pick for sled propulsion. Each team will have six players on the ice at a given time, including the goalie [42]. Sled hockey displayed the highest rate of injury based on data collected from the 2002 Salt Lake Paralympic Games [42]. Overuse injuries occur frequently in sled hockey, just as they do in ice hockey. However, as in adaptive skiing, sled hockey athletes tend to exhibit a larger number of upper extremity overuse injuries compared to their able-bodied counterparts, who tend toward lower extremity injuries. Specifically, sled hockey athletes commonly injure the shoulder, elbow, and wrist, due in part to the motions required for sled propulsion. Tendinopathy at the wrist, in particular, is one of the most frequently encountered overuse injuries in the sled hockey athlete due to wrist flexion during shooting. Shoulder ligament and tendon injures are likewise highly represented. The other major category of neuromusculoskeletal injuries affecting sled hockey athletes is acute traumatic injury, due primarily to the high impact potential (body checking) inherent in the sport. Therefore, concussions, contusions, and fractures are prevalent. In fact, it is suggested that concussions occur at an even higher rate in sled hockey due to upper body mechanics while checking [43]. Skiing and Snowboarding There are six categories of Paralympic alpine skiing as defined by the International Ski Federation. These include downhill (fast, steep terrain), slalom (most technical), giant slalom, super giant slalom, super combined, and snowboard. Runs are timed and performed individually [44]. In general, six major groups comprise the Paralympic skiing and snowboarding community. These are (1) amputee, (2) brain injury (stroke, cerebral palsy, traumatic brain injury), (3) visual impairment, (4) wheelchair users (includes spinal cord injury), (5) intellectual disability, and (6) Les Autres (a group for those who are not in the aforementioned categories). Because of the wide variety of diagnoses and levels of functional impairment, classification systems are extremely important to allow for appropriate competition. The three primary classification groups are: standing, sitting, and visually impaired. These are then subdivided further. For example, skiers who compete standing are classified from LW1 to LW9 (LW: Locomotor Winter), which relates to impairments in either upper or lower limbs. Skiers who compete sitting are classified as LW10 to LW12.

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Visually impaired athletes, on the other hand, are classified from B1 to B3 based on the level of visual impairment [15]. Medical conditions of the adaptive skier are typically similar to those encountered by able-bodied athletes. The medical provider must be aware of any preexisting medical history when caring for the athlete, including prior trauma and surgeries. In addition, the adaptive skier is at higher risk for medical conditions such as orthostatic hypotension, pressure sores, and neurogenic bowel or bladder, among others. Environmental factors must likewise be considered given that many adaptive skiers and snowboarders have impaired thermoregulation related to their underlying ailments. Acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), high-altitude cerebral edema (HACE), and frostbite injuries have occurred. Symptoms of AMS include headache, nausea, vomiting, dizziness, fatigue, dyspnea, and tachycardia. Severe cases can cause cyanosis, hemoptysis, and altered mental status. AMS can then progress to either HAPE or HACE. For standing alpine skiing, lower limb fractures and knee ligament injuries are the most common. Seated alpine skiing exhibits more frequent upper limb injuries overall, especially involving the shoulder and wrist. The three most common causes of shoulder injury in seated skiers are rotator cuff pathology, labral injury, and acromioclavicular joint separation. Lateral and medial epicondylopathy, ulnar nerve entrapment, carpal tunnel syndrome, and other peripheral nerve entrapments due to repetitive use are also very common in seated skiers due to propulsion mechanics and concomitant wheel chair use. Concussions and other head injuries are prevalent due to the high velocity impact potential inherent in the sport. It is also necessary to consider heterotopic ossification (HO), autonomic dysreflexia, and spasticity in these athletes. Individuals with traumatic brain injury, spinal cord injury, joint replacements, and amputations are at high risk for the development of HO in particular, which is compounded further by any trauma sustained while skiing.

Conclusion As summarized above, there are many special considerations to account for in caring for the adaptive athlete. The provider must not only be equipped with medical knowledge of related comorbidities related to underlying diagnoses, but also be cognizant of the complex interactions between functional impairments, equipment needs, sport participation, and unique patterns of injury. Additionally, these interactions have profound effects on the athlete throughout their athletic lives, as they affect training, qualification, classification, and ultimately competition.

References 1. Scholz J, Chen YT. History of adaptive and disabled rights within society, thus creating the fertile soil to grow, adaptive sports. In: AJ DL, editor. Adaptive sports medicine. Cham: Springer International Publishing; 2018. p. 3–20.

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Index

A Abductor pollicis longus (APL) tendons, 237 Acetabular labral tears, 427 Achilles tendinopathy, 372, 373 Achilles tendon, 19 Achilles tendon ruptures, 374, 375 ACJ joint injuries, 179–182 Active hamstring test, 299 Activity-induced medial tibial pain, 360 Acute cervical disc herniation, 158, 159 Acute compartment syndrome (ACS), 355, 356 Acute high-altitude illness, 103 Acute injuries, 5 Acute mountain sickness (AMS), 102, 103 Acute muscle and tendon injuries, 353–355 Acute respiratory distress syndrome (ARDS) and respiratory failure, 249 Acute traumatic injuries, 276 Acute wrist pain in children, 426 Adaptive equipment in skiing, 443 Adaptive running, 452, 453 Adaptive ski set-up with outriggers, 445 Adaptive skiers and snowboarders, 454 Adaptive sport athlete assessment tools/techniques, 438 class allocation, 438 classification, 437 evaluation and classification, 436 functional impairment, 437 ICF classification system, 437 Paralympic classification, 437 physical impairment in the (IPC) classification, 437 sport-specific classification, 438 Adaptive sports, 7, 435, 436 equipment, 439 prostheses, 442–445 Adductor muscle and tendon strains, 301, 302

Adolescent growth spurt, 422 Adolescent idiopathic scoliosis (AIS), 426 Aerobic activity, 35 Aerobic exercise, 35, 41 Aerobic physical activity, 33 Amenorrhea, 414 American College of Sports Medicine (ACSM), 9, 66 American Heart Association PPE Screening, 56 American Medical Society for Sports Medicine (AMSSM), 9, 57 Americans with Disabilities Act of 1990, 66 Anabolic agents (steroids), 88 Angiofibroblastic proliferation, 210 Ankle injuries diagnostic work-up, 370 treatment, RICE, 372 Ankle joint lateral collateral ligaments, 367 muscles, 368 Ankle ligamentous disruption, 347 Ankle mortise, 367 Ankle sprain grading, 370 Ankle sprains, 369 Ankle syndesmosis injury, 353, 354 Anterior apprehension test, 195 Anterior cruciate ligament (ACL) injury, 319–321 in pediatric/adolescent population, 429 Anterior drawer test, 370, 371 Anterior inferior iliac spine (AIIS), 295 Anterior interosseous nerve (AIN) syndrome, 216 Anterior load & shift test for GHJ instability, 195 Anterior load and shift test, 195 Anti-doping agencies, 8 Apophysitis, 286

© Springer Nature Switzerland AG 2021 G. Miranda-Comas et al. (eds.), Essential Sports Medicine, https://doi.org/10.1007/978-3-030-64316-4

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Index

458 Apophysitis in the foot, 431 Apprehension test for anterior GHJ instability, 183 Aquatic exercises, 40 Arrhythmogenic right ventricular cardiomyopathy, 51, 96 Athlete’s injury history, 50 Athletes with AD, 448 Athletes with impairments, 60–61 Athletes with lower limb deficiency, 61 Athletes with menstrual irregularities, 58 Athletes with neurovascular injuries or post-compartment syndrome fasciotomies, return to play, 207 Athletes with organ loss/impairment, 57 Athletes with respiratory tract infections, 100 Athletes with rheumatoid arthritis, 60 Athletes with spinal cord injuries, 60 Athletic pubalgia, 308, 309, 428 Athletic team physician, 4 Atlanto-occipital motion, 153 Atrial septal defects, 14 Automated external defibrillator (AED), 6 Autonomic dysreflexia (AD), 447 Autonomic dysreflexia for performance gains, 60 AWLD, 451 B B vitamins, 84 Bacterial pneumonia, 101 Balance error scoring system (BESS), 130 Bankart lesion on imaging, 194 Banned drugs/methods, 111, 113, 114 Banned supplements/ergogenic aids, 88 Barton’s fracture, 224 Baseball finger, 234 Baseball pitching, 179 Baseline concussion assessments, 8 Baseline testing, 136 Basketball wheelchair, 440 Bastrup’s disease, 285, 286 Bear hug subscapularis strength testing, 191 Bear hug test, 189 Beighton scale, 196 Belly press subscapularis strength testing, 190 BESS test, 130, 131 BESS, clinical balance assessment, 131 Biceps femoris, 295 Biceps tendon tendinopathy, 192–194 Bicuspid aortic valves, 14 Bilateral/double limb exercises, 36 Biomechanical/training load errors, 50

Biotin, 84 Blood doping, 56 Blunt cerebrovascular injuries, 165, 166 Blunt thoracoabdominal trauma, 15 Bone health, master athletes, 395 Bone stress injury/fracture, 359 Boosting, 448 Boxer’s fractures, 233 Brachioradialis, 204 Bronchitis, 101 Brugada syndrome, 95 Bruising, 349 C Caffeine, 88 Calcium, 85 Cancers, physical activity, 39, 40 Carbohydrates, 82 Cardiopulmonary disorders, 6 Cardiopulmonary resuscitation (CPR), 154 Cardiorespiratory fitness, 33 Cardiovascular contraindications to exercise, 39 Cardiovascular disease (CVD), insufficient physical activity, 38, 39 Cardiovascular portion of the past medical and family histories, 50 Cardiovascular screening, 93 Cardiovascular system, master athletes, 395–396 Carpal tunnel syndrome (CTS), 238–240, 446 Catastrophic cervical spine trauma, 163 Cerebral Palsy International Sports and Recreation Association (CPISRA), 436 Cervical cord neurapraxia with transient tetraplegia, 164, 165 Cervical disc herniation, acute, 158, 159 Cervical facet arthropathy, 167 Cervical facet mediated pain, 167 Cervical instability, 162 Cervical spine anterior longitudinal ligament, 153 atlas’ transverse ligaments and alar ligaments, 153 cervical nerve roots, 152 cervical zygapophyseal (facet) joints, 152 facet capsules, 153 interspinous ligaments, 153 interverbal discs, 152 intervertebral discs, 152, 153 lateral atlanto-axial joints, 153 ligamentum flavum, 153

Index neurologic assessment, 155 pathological neck mobility, 153 posterior longitudinal ligament, 153 range of motions, 152, 153 supraspinous ligament, 153 Cervical strains and sprains, 157 cervical paraspinal erector spinae, 157 diagnosis, 157 forced hyperflexion injury, 157 levator scapula, 157 return to play, 158 rhomboid muscles, 157 stretch injuries to musculotendinous junction, 157 trapezius, 157 treatment, 157 Chaffeur’s fracture, 224 Chest wall injuries, 245–269 Chilblains, 107 Chronic cervical radiculopathy, 168, 169 Chronic exertional compartment syndrome (CECS), 360–362 Chronic leg pain, differential diagnosis algorithm, 358 Chronic traumatic encephalopathy (CTE), 141, 142 staging systems, 142 Civil rights movements, 436 Clavicle fractures, 186, 187 Clicking/snapping rib, 264 Clinical test of sensory organization and balance (CTSIB), 131 Closed kinetic chain (CKC) exercises, 36, 325 CMC dislocation, 236 Cold related illnesses, 106, 107 Collagen- based BEAR (Bridge-enhanced ACL repair) scaffold, 430 Colles’ fracture, 224 Commotio cordis, 258, 259 Complementary training room clinic, 3 Comprehensive rehabilitation program, 207 Compressive garments during exercise, 60 Concussion in Sport Group (CISG), 120 Concussions, 52 Concussive convulsions, 121 Congenital coronary anomalies, 51 Congenital fusions of the bones of the foot, Pediatric Athlete, 430 Conjunctivitis, 101 Contact injuries, knee, 319 Continuing medical education (CME) credits, 9 Contusion, leg injuries, 349

459 Corticosteroid injection, 17 Coxa saltans, 309 Cozen’s test, 210, 211 Creatine, 87 Cubital tunnel syndrome, see Ulnar Neuropathy at the Elbow (UNE) Cunningham technique for anterior GHJ dislocation, 185 D Deep vein thrombosis (DVT), 96, 97 Deficiency of vitamin B12 or folate, anemia, 84 Degeneration and repetitive micro-trauma to the spine, 283 Degenerative TFCC Injuries, 229 Dehydration, 76 ADH, 77 cardiovascular strain, 77 consequences of, 76 heart rate, 77 risks for, 76 sufficient fluid, 77 Dehydroepiandrosterone (DHEA), 88 Depressed tibial plateau fracture, 346 De Quervain’s tenosynovitis, 237, 238 Dietary supplements, 87 Digital extensor tendon injury, 234, 235 Dilutional pseudoanemia, 86 Disc disruptions, 283 Disc herniation, 283 Disordered eating behaviors, 59 Disordered eating/eating disorders (DE/ED), 59 Displaced femoral stress fracture, 304 Distal biceps tendon ruptures, 209, 210 Distal radius fracture classification, 224 forearm fracture, 224 management, 225 physical exam findings, 224 rehabilitation period, 225 return to play, 225 Distal tibial fractures, 347, 348 Diuretic effect, 81 Doping, 8 Doping in sports, 111–114 Dorsal intercalated segmental instability (DISI), 227 Dynamic labral shear test for labral tear, 198, 199 Dysplastic spondylolisthesis, 281

460 E Early exercise, 139, 140 Early Screening for Cardiac Abnormalities with Preparticipation Echocardiography (ESCAPE) protocol, 15 Eating disorders in the diagnostic and statistical manual-V, 59 Ecchymosis, 322 Echocardiography, 14 Elastography, 16 Elbow and forearm injuries anterior interosseous nerve, 204 biceps and brachioradialis muscles, 204 biomechanics, 205 elbow, 203 extensor tendon, 204 forearm pronation and supination, 205 humeroulnar joint, 203 injury-susceptible UCL, 203 median nerve, 204 muscles, 204 musculature of anterior forearm, 204 musculature of posterior forearm, 204 nerves, 204 posterior interosseous nerve, 204 radial nerve, 204 superficial radial nerve, 204 ulnar nerve, 204 Elbow injuries, acute fractures and dislocations high-velocity impact or falling, 205 history (mechanism of injury) and physical exam, 205 neurovascular compromise, 206 olecranon fractures, 205 radial head fractures, 205 radioulnar fractures, 205 rehabilitation program, 207 supracondylar fractures, 205 surgical intervention, 206 tissue necrosis, 206 Electrolytes in water, 76 Electromagnetic systems, 21 Elite sports, 7 Emergency action plan (EAP), 4, 6 Endurance/cardio activity, 35 Energy availability, 414 Energy nutrients, in athletes, 81 Enhanced cardiovascular screening of all athletes using clinical tests, 52 Ephedrine containing medications, 100 Epidemiological surveys of SCD, 51 Epiphyseal growth plate injuries, 422 Epstein-Barr virus, 100

Index Euhydrated, 75 Euhydration, 76, 81 Evaporation of sweat, 75 Exercise-associated collapse (EAC), 98 Exercise-based cardiovascular rehabilitation programs, 39 Exercise induced asthma (EIA), 99 Exercise induced bronchospasm (EIB), 99 Exercise interventions, 39–40 Exercise intolerance, 139 Exercise prescription in school-aged children and adolescents, 433 Exercise program, 33 Exercise training session, 33 Exertional heat illnesses, 432 Exertional heat related illness (EHRI), 103, 105, 106 Exertional heatstroke, 78 Exertional rhabdomyolysis, 105 Extended FAST exam (eFAST), 15 Extensor digitorum communis (EDC), 224 Extensor pollicis brevis (EPB), 237 External impingement, 188 External rotation test, 370 Eye-Sync eye tracking headset, 7 F Family Educational Rights and Privacy Act (FERPA), 66 Fascial defect or muscle herniation, 352 Fat consumption, 83 Fatal dysrhythmias, 249 Fatigue, 6 Federation Internationale du Medicine du Sport (FIMS), 66 FEDS classification of shoulder instability, 194 Female athlete anatomic differences between men and women, 416 anterior cruciate ligament, 415 bone health issues, 414 labor and delivery of fetus, 419 low energy availability, 414 menstrual disturbances, 414 muscle recruitment, 416, 417 neuromuscular components, 416 nutritional requirement, 417 physiologic differences during pregnancy, 418 pre-pregnancy fitness level, 419 returning to sport after vaginal versus caesarean birth, 419 treatment, triad/REDs, 415

Index Female Athlete Triad (Triad), 59, 413–415 Female athlete, medical and musculoskeletal concerns, 57–60 Femoral neck stress fracture, 303, 304 Femoral neck version, 296 Femoroacetabular impingement (FAI), 304–306, 427 Fibula fractures in athletes, 348, 349 Fibular nerve injury, 351, 352 Fibular tendon injuries, 380, 381 Fibularis longus and brevis muscles, 380 Fibularis longus and brevis palsy, 352 Finkelstein’s test, 238 FITT-VPP principle during exercise prescription, 41 Flexibility exercises, 41 Flexibility/stretching program, 36, 37 Flexor carpi ulnaris (FCU) muscle, 213 Flexor digitorum profundus tendon avulsion injury, 224, 235, 236 Flexor hallucis longus (FHL) Tendinopathy/ Injury, 377, 378 Flexor tenosynovitis (Trigger Finger), 241, 242 Fluid intake after exercise, 81 Fluid intake before exercise, 78, 79 Fluid intake during exercise, 79 Focused Assessment with Sonography in Trauma (FAST), 15 Folate, 84 Food sources of the B Vitamins, 84 Foot and ankle joints, 369 Foot and ankle fractures, 386–387 Foot biomechanics, 24 Foot muscles, 368 Forced hyperextension and abduction of the thumb, 232 Fractures, ankle, 386–387 Freezing cold injuries (FCI), 107 Freiberg’s infarction (disease), 431 Full-can supraspinatus strength testing, 190 Fungal based skin infections, 101 G Gastrocnemius strain (“tennis leg”), 354, 355 Gender differences, master athletes, 396 GHJ dislocation, 182, 184–186 GHJ instability, 194–197 Glenoid labrum tears, 197–200 Glycogen measurement, 16 Golfer’s elbow, see Medial epicondylitis or epicondylalgia or epicondylopathy Graded symptom checklist (GSC), 131

461 Graduated-return-to-sport program, 432 Great Civil War Benefaction program, 436 Greater Trochanteric Pain Syndrome (GTPS), 306, 307 Groin and lower abdominal pain, 428 Ground reaction force (GRF) and force moments, 22 Gymnast wrist, 62 H Hamate fracture, 231, 232 Hamstring injuries, 297–299 Hamstring muscle strain injuries, 326–328 Hamstring muscles, 296 Hamstring strain, 298 Hand grasping and manipulation, 223 intrinsic muscles of the hand, 222 Handlebar palsy, 240, 241 Hawkins impingement test, 189 Headache management including behavior therapy, 126 Health care costs, 31 Health Insurance Portability and Accountability Act (HIPAA), 66 Heat cramps, 77, 105 Heat exhaustion, 77, 105 Heatstroke, 105 Heel fat pad contusion, 385 Hep B virus, 102 Heterotopic ossification, 447 High altitude cerebral edema (HACE), 102, 103 High altitude illness, 102, 103 High-altitude pulmonary edema (HAPE), 103 High heat stress, 104 HIIT programs, 33, 39 Hip adductors, 296 Hip joint biceps femoris, 294 biomechanics, 296 capsule, 295 muscles, 294 nerves, 294 Home exercise program, 169 Hook of the hamate fracture, 231, 232 Horacic cage lungs, 248 pectoralis major, 246 Hornblower infraspinatus strength testing, 191 Hornblower’s test, 189 Human motion capture, 20 Human motion capture systems, 21

462 Hydration, 76 participation in exercise, 75 Hydration program, 79 Hypertension, 94 Hypertrophic cardiomyopathy (HCM), 14, 94, 95 Hypohydrated, 75, 76 Hyponatremia, low blood sodium, 78 Hypothermia, 107 I Ice sled hockey, 453 Iliac crest contusions, 302, 303 Iliopsoas tendon-muscle complex, 295 Iliotibial band friction syndrome (ITBFS), 334–336 Image processing systems, 21 Immediate post-concussion assessment and cognitive test (ImPACT), 124 ImPACT assessment, 7 Indoor 3D motion capture systems, 23 Inertial measurement unit (IMU), 22 Infectious disease, 99, 100 Infectious mononucleosis, 100 Injury and sport participation history, 50 Internal impingement, 187 International Classification of Functioning, Disability and Health (ICF), 436 Intersection syndrome, 243, 244 Intervertebral disc complex, 282–284 Intra-nasal calcitonin, 277 Iron, 85 Iron supplementation, 86 Isolated nondisplaced fractures, 348 Isthmic listhesis, 281 Isthmic spondylolisthesis, 281 J Jersey finger, 235 Jumper’s knee, 62 Juvenile idiopathic arthritis, 429 K Karvonen method, 34 KilohNevin syndrome, 216 Kinematic and kinetic motion analysis, 22 Kinematic information, 22 King-Devick test, 7 Knee apophysitis (Osgood-Schlatter Disease and Sinding-Larsen-Johansson Disease), 332–334

Index Knee braces, 337 Knee injuries acute injuries, 315 arcuate popliteal ligament complex, 316 bone bruises, 320 bone-tendon-bone grafts, 321 bursae, 317 internal, external and capsular ligaments, 316 knee extensor muscles, or quadriceps femoris, 316 lever arms, 315 medial collateral ligament, 316 modifiable and nonmodifiable intrinsic and modifiable extrinsic risk factors, 319 multi-angle isometric contractions, 321 nonoperative rehabilitation, 321 patellofemoral joint, 317 posterior cruciate ligament, 316 Knee osteoarthritis (OA), 20, 336–338 acetaminophen, 337 intra-articular corticosteroid injections, 337 Knee pain, pediatric athlete, 428 Köhler disease, 431 L Lachman’s test, 320, 324 Lactate threshold, 396 Laryngoscopy, 16 Lateral collateral ligament (LCL) injury, 321, 322 Lateral epicondylitis/epicondylalgia/ epicondylopathy, 210, 211 Lateral epicondylopathy (LE), 447 Leg compartments, 342 cutaneous nerves, 344 dermatomes, 345 nerves, 343 Legg-Calve-Perthes disease, 427 Leukotriene receptor antagonist (LTRA), 99 Lift-and-slide technique, 156 Ligament effects, 18 Ligament sprains, 151 Ligamentous injury, 285 Limb deficient athletes, medical injuries and complications, 450–451 Little league elbow, 425 Log-roll technique with manual in-line cervical spine stabilization, 156 Long QT syndrome, 51 Low back pain, 273, 289

Index Low energy availability (LEA), 59 Lower leg injuries anterior compartment, 341 deep posterior compartment, 341 lateral compartment, 341 motor innervation, 343 myofascial compartments, 341 neurovascular structures, 341 sciatic nerve, 342 sensory innervation, 342–343 superficial posterior compartment, 341 tibia and the fibula, 343 Lumbar spine bony complex, 274 four or six lumbar vertebral bodies, 275 sources, 274 Lumbosacral plexus, 294 Lung alveoli, 248 Lytic spondylolisthesis, 281 M Macronutrient requirements carbohydrates, 82 fat, 83 protein intake, 83 protein requirement for athletes, 83 proteins, 82 Magnesium supplementation, 86 Magnetometry, 22 Maintenance of certification (MOC), 9 Mallet finger, 234 Marker-based motion analysis systems, 22 Marker-based optic systems, 22 Master athletes age related changes, 391, 397 body mass index, 398 carbohydrate requirements, 402 cardiovascular risk, 401 clearance of participation, 404 cognitive decline, 398 decreased rate of sarcopenia, 399 defined, 391, 392 dehydration, 403 golf, 406 injury prevention, 401 injury rate, 394 iron, 402 macronutrients, 402 master runners, 405 micronutrients, 402 mountaineering, 407 musculoskeletal injury, 401 participation of, 398

463 personal psychological assets, 397 physiologic changes, 394 pre-participation screening, 399–401 prevalence of traditional cardiac risk factors, 400 protein requirements, 402 public health domain, 393 recommended daily allowance (RDAs), 402 recovery from training, 403 recovery phase, 404 rehabilitation process, 403 resistance training, 401 resting metabolic rate, 401 running population, 404 self-awareness and adaptation, 397 strenuous exercise and intensity of training, 392 swimming, 405, 406 telomere length, 397 triathlon, 407, 408 ultra-endurance events, 405 Maximal oxygen consumption (VO2max), master athletes, 396 Maximum heart rate (HRmax), 34 MCP dislocations, 236 Medial and lateral menisci, 317 Medial collateral ligament (MCL) injuries, 323 Medial epicondylitis or epicondylalgia or epicondylopathy, 211, 212 Medial tibial stress syndrome (MTSS), 360, 361 Median nerve entrapment in the forearm, 215 Medical problems in athlete antihypertensives, 94 ARVC, 96 ARVD, 96 atraumatic collapse during exercise, 98 Brugada syndrome, 95 cardiovascular screening, 93 cold related illnesses, 106, 107 DVT, 97 EAC, 98 EHRI, 106 EIA, 99 EIB, 99 ERHI, 105 HCM, 94, 95 high altitude illness, 102, 103 hypertension, 94 infectious disease, 99–102 VTE, 96, 97

464 Meniscal injuries (lateral/medial meniscus), 325, 326 Menstrual dysfunction and BMD, 59 Mesenchymal stem cells (MSCs), 19 immunomodulation, 20 mechanism of action, 20 suppression of inflammation, 20 Metabolic energy expenditure (MET), 34 Metacarpal shaft/neck fracture, 233, 234 Metacarpophalangeal (MCP) instability, 232, 233 Metatarsalgia, 384 Microelectromechanical systems (MEMS), 24 Micronutrients B vitamins, 84 calcium, 84 hemoglobin synthesis, 83 iron, 84 magnesium, 84 muscle tissue during recovery from exercise, 83 vitamin D, 84 zinc, 84 Microtrauma, 187 Mild valvular abnormalities, 14 Mitral valve prolapse, 14 Model-based systems, 21 Moderate-intensity continuous training (MICT) regimen, 33 Molluscumcontagiosum, 102 Monteggia fracture-dislocations, Bado classifications, 207 Mood disorders, 124 Morton’s neuroma, 382, 383 Motion capture, 21 Movement sensor, 23 MSK disease, non-operative management, 18 Multidirectional instability (MDI), 194, 197 Multidisciplinary healthcare team, 5 Multidisciplinary sports medicine healthcare team, 8 Multi-joint movements, 36 Munich muscle classification, 327 Muscle power, master athletes, 395 Muscle strains, 151 Muscle strengthening and flexibility activities, 33 Muscle strengthening exercises, 35 Muscle-tendon junction, 284 Musculoskeletal injuries, 5 Musculoskeletal medicine, 3 Musculoskeletal pathologies and medical illnesses, 3 Musculoskeletal system, 395

Index Musculoskeletal system, master athletes, 395 Musculoskeletal ultrasound (MSK US) advantages, 13 lack of radiation, 13 osseous abnormalities beyond bony cortex, 14 patient cost, 13 patient satisfaction, 13 portability, 13 superb resolution, 13 use, 13 Myocarditis, 101 Myofascial pain syndrome, 166, 167 N National Coalition for Cancer Survivorship, 39 National Collegiate Athletic Association (NCAA), 8 National Federation of State High School Associations (NFHS), 67 National Football League (NFL), 122 Natural aging process, 395 Neer impingement test, 188 Neuroma, 451 Neuromotor exercises, 33, 37 Neuromuscular training, 41 Neuropathy of the deep fibular nerve, 352, 353 Neuropsychological (NP) testing, 131 Neurovascular compression syndrome, 169–172 Neurovascular Injury, 349–353 Niacin, 84 Noble’s ITB compression test, 335 Noncontact mechanism of injury, knee, 319 Nondisplaced and minimally displaced fractures, 346 Nondisplaced fractures, 231, 347 Nondisplaced midclavicular shaft fractures, 187 Nonfreezing cold injuries, 107 Non-scholastic sports, 121 Nutrition plan, 81 O O’Brien test for labral tear, 198, 199 Oarsman’s wrist, 243, 244 Ober’s test, 335 Obesity, physical activity, 40, 41 Office-based evaluations, 48 Olecranon bursitis, 207, 208, 447 Olecranon bursopathy (Bursitis), 207, 208 Olecranon fractures, classifications, 206

Index Omega-3 fatty acids (O3FA) in the rat model, 143 On-field cervical spine injury, preparation and management, 154 On-field management, 154, 155 Open kinetic chain (OKC), 36 Optic motion capture systems, 21 Optic nerve sheath diameter (ONSD), 15 Oral rehydration, 98 Organized scholastic sport, 121 Orthobiologics, 17, 18 Orthostatic hypotension, 449 Osgood-Schlatter and Jumper’s knee (or Sinding-Larsen-Johansson), 62 Osgood-Schlatter disease (OSD), 332–334, 429 Osteoarthritis(OA), 19, 447 physical activity, 41 Osteochondritis dissecans, 62, 429 Osteochondritis dissecans (localized avascular necrosis), 425 Osteochondrosis of navicular bone, 431 Osteoporosis and fractures, 449 Otitis media, 100 Ottawa ankle rules, 371 Outpatient clinical setting, 3 Outpatient healthcare team, 3 Overuse injuries, 61 Overuse upper extremity injuries, 60 P Pantothenic Acid, 84 Paper-and-pencil’ testing, 131 Paralympic alpine skiing, 453 Patellar dislocations, 318, 319 Patellar realignment, 332 Patellar tendinopathy, 328, 329 Patellar tendon, 19 Patellofemoral pain syndrome, 62 Patellofemoral syndrome, 330–332 Pathologic spondylolisthesis, 281 Pectoralis major tear, 260, 261 Pediatric athlete acquired or congenital foot deformities, 430 acute wrist pain, 426 anterior glenohumeral instability, 425 apophyseal (avulsion) fractures, 424 baseball pitchers, 425 bone structure during growth, 422 elbow injuries, 425 epiphyseal fractures, 423 etaphyseal fractures, 423

465 fractures in, 422 greenstick fracture, 423 growth and performance, 422 high risk stress fractures, 424 little league shoulder, 425 nonlinearity of growth and the unique response to skeletal injury, 421–422 overuse injuries, 424 patellar tendinopathy, 430 physeal stress injuries, 424 popliteal (Baker’s) cysts, 430 referred hip pain, 430 Salter-Harris classification, 423 scoliosis series, 426 shoulder and elbow injuries, 424 vertical plane compression of the spine in football and weight-lifting, 426 wrist flexor strengthening, 426 Pedicle stress reaction, 279, 280 Pelvic girdle, 293 Peptide hormones and growth factors, 88 Performance enhancement technique, 60 Peripheral nerve injuries, 177 Physical activity, 31 avoidance of, 34 benefits, 32 cancer treatment and prevention, 39, 40 cardiovascular health benefits, 32 definition, 32 dose-response relationship, 38 guideline levels, 38 household, 32 low-intensity physical activity, 38 obesity, 40, 41 occupational, 32 osteoarthritis, 41 physical and psychological conditions, 32 physiological responses, 40 recommendations, 33 time spent sedentary, 38 transportation, 32 Physical medicine and rehabilitation (PM&R), 9 Physiologic sensors, 24 Plantar aponeurosisis, 369 Plantar fasciitis, 19 Plantar fasciopathy, 376, 377 Platelet activation, 19 Platelet rich plasma (PRP), 18, 88 alpha granules within platelets, 18 applications, 19 clinical studies, 19 ligaments and tendon pathology, 19 therapeutic benefits, 19

Index

466 Pneumococcal pneumonia, 101 Pneumothorax, 256, 258 POLICE protocol (protection, optimal loading, ice, compression, and elevation), 298, 300 Popliteal artery entrapment, anatomic classification, 363 Popliteal artery entrapment syndrome (PAES), 362–364 Popliteus muscle injury, 356, 357 Post-concussion intervention, 140 Post-concussion symptom scale (PCSS), 131 Posterior apprehension test, 195, 196 Posterior cruciate ligament (PCL) ruptures, 323–325 Posterior load and shift test, 195, 196 Post-traumatic amnesia, 124 PPE Working Group, 48 Pregnancy, 417 Preparation variation, with host factors, 19 Pre-participation evaluation (PPE), 7, 14 adaptive sport athlete, 445–446 assessment of health status, 46 athletes clearance to play, 46 athletes with physical and mental disabilities, 60, 61 athletes, organ transplant/chronic organ enlargement, 57 cardiac abnormalities among athletes, 67 cardiac, and pulmonary screenings tests, 54 cardiovascular history, 50 categories of clearance, 65 children, sports specific injuries, 61 clearance level of an athlete, 65 clearing an athlete to play, 65 clinical examination, 45 clinical training of physicians, 48 community access to health care, 47 components of the medical history, 49 comprehensive assessment, 52 coronary artery disease, 63 ECG and/or echocardiogram, 56 enhanced cardiovascular screening, 52 federal regulation, 66 female athlete concussions, 58 diet/weight issues, 59 medical and musculoskeletal concerns, 57 menstrual irregularities, 58 pregnancy test, 58 risk factors, 58 stress fractures, 58 high yield history, 50, 51

history forms, 49 inherited arrhythmia syndromes, 51 injuries, children, 61, 62 injury and sport participation history, 50 institutional culture, 47 ion channel disorders, 51 local/regional regulations, 47 masters athletes, 62–65 medical and orthopedic conditions, 46 medical clearance, 47 medical comorbidities, 53 medical history, 45, 49 medical history gathering, 50 musculoskeletal abnormalities, 67 musculoskeletal/cardiopulmonary reasons, 48 neurologic conditions, 52 office-based format, 47 over specialization, 61 participation in sports, 45 physical and psychological repercussions of missed participation, 65 physical examination, 54–55 scope of, 46 screening protocols, 49 sensitivity and specificity, 67 sports and activity related history, 50 station-based format, 47 targeted physical examination, 49 urine testing, 56 Primary acute patellar dislocations, 318 Primary care sports medicine fellowships, 9 Prohibited substances in-competition, 114 in particular sports, 114 2019 WADA guidelines, 112, 113 Prolotherapy, 17, 18 Pronator syndrome, 215, 216 Proprioception and muscular control, 22 Protein and amino acid supplementation, 83 Protein intake for endurance and strength athletes, 82 Proteins, 82 Proximal rectus femoris, 299 Psychological skills training, 8 Pubic symphysis, 294 Pulmonary contusion, 249, 251 Pulmonary embolism (PE), 96 Q Quadriceps contusions, 299, 300 Quadriceps injuries, 299–301 Quadriceps muscle, 296 Quadriceps strain, 299, 326–328

Index R Racing, 441 Radial head fractures, classifications, 206 Rate of perceived exertion (RPE), 33 Recognition process, computer vision and algorithms, 21 Recumbent hand cycle used for racing and recreation, 442 RED-S clinical assessment tool (RED-S CAT), 59 Regenerative medicine, 10 Rehabilitation Act of 1973, 66 Relative Energy Deficiency in Sport (REDs), 59, 413–415, 432 Relocation test, 195 Relocation test for anterior GHJ instability, 183 Repetitive flexion and extension, 283 Repetitive microtrauma, 194 Repetitive strain during activities like throwing in baseball, 218 Resistance training exercises, 35, 36 Resisted wrist flexion with medial epicondyle palpation, 212 Retinal detachment, 15 Retrocalcaneal bursitis, 375, 376 Retrograde amnesia, 124 Return to play (RTP) protocol, 136–138 Return to play guidelines and consensus statements, 6 Return to play in postoperative shoulder, 186 Return to sport recommendations after injury to lumbar spine, 289 Rib fractures, 251, 252, 254 Riboflavin, 84 Ribs, stress fracture, 261, 262 Rib-tip syndrome, 264 Rockwood Classification scheme for ACJ injuries, 180 ROM exercises, 211 Romberg test, 131 Rotator cuff (RC) tendinopathy, 187–191 Rotator cuff tendons, 19 Rugby, 441 Rugby wheelchair, 441 Running blade with custom-made carbon fiber socket, 444 Running economy, 396 Running prostheses, 443 S Sacroiliac joint pain, 288 Sacroiliac joints, 294

467 Safety during exercise, 34 Salter-Harris classification system for physeal injuries, 423 Sarcopenia, 395 Scabies, 102 Scalene triangle, 170 Scaphoid fractures, 230, 231 Scapholunate Ligament Disruption, 226–228 Scapular dyskinesis, 178 Scapulothoracic bursitis, 266, 267 Scapulothoracic crepitus, 266, 268 Scarf test for ACJ injury, 181 SCAT5, 131 Scheuerman’s disease/juvenile osteochondrosis of spine, 275, 276 Scheuermann’s disease (Juvenile Kyphosis), 427 Scoliosis, 275 Seated alpine skiing, 454 Seating system in a wheelchair, 440 Seattle criteria, 93 Second impact syndrome” (SIS), 121 Self reduction technique for anterior GHJ dislocation, 184 Sensory organization test (SOT), 131 Serum creatine kinase, 105 Sever’s disease, pediatric athlete, 430 Shear wave elastography (SWE), 16 Shin splints, 360 Short acting beta 2 agonist (SABA), 99 Shoulder instability, 194 Shoulder pain and injuries, 175 acromioclavicular and coracoclavicularligaments, 178 bones, 175 brachial plexus, 175 glenohumeral and scapulothoracic motion, 178 glenohumeral ligaments, 177 musculature, 179 Shoulder pathologies, 447 Sickle cell trait testing, 54 Sinding-Larsen-Johansson Disease (SLJD), 332–334 Sinus tarsi syndrome, 383, 384 Sinusitis, 100 Skeletal thoracic cage, 245 Skier’s thumb, 232 Skiing and snowboarding, 443, 453 Skin disorders, 449 Skin infections, 101 Sled hockey, 444, 453 Sled hockey set-up, 445 Slipped capital femoral epiphysis (SCFE), 428

468 Slipping rib syndrome, 264, 265 Smith’s fracture, 224 Snapping hip syndrome, 309–311 Snapping scapula syndrome, 266, 267 Snowboarding, 444 Soft tissue contusions, 151 Spasticity, 448 Speed test, 192 Speed test for LHBT, 192 Spinal cord injury athletes, 449 Spinal stenosis, 288 Spinous/transverse process fractures, 278 Spinous process fractures, 161, 162 Spondylolisthesis, 280–282, 427 Spondylolysis, 274, 278, 279, 426 Sport Concussion Assessment Tool (SCAT5), 7, 431 Sport related concussion, classification systems, 52 Sports–related concussions (SRC) acceleration and deceleration forces, 127 advanced neuroimaging, 143 altered plasticity, 127 anxiety/mood subtype, 126 apolipoprotein E4 (APOE E4) genotype, 143 athlete’s personality or performance test, 129 axonal degeneration, 127 balance assessment, 131 baseline score, 130 BiodexBioSway, 136 biomarkers, 143 cervical subtype, 126 clinical presentation, 124 clinical subtypes, 126 cognitive-fatigue-related symptoms, 124 computer-based platforms, 131 concussive convulsions, 121 definition, 120 evaluation process, 130 fluid biomarkers and genetic testing, 143 football helmet design, 142 graded symptom checklists, 129 headache-migraine subtype, 126 incidence, 122 inflammatory cell activation, 127 intracranial pressure, 129 learning effect, 131 mechanism of action, 129 medical history, 129 motor control, 131 mouth guard use, 142 neurometabolic cascade, 127

Index neurometabolic cascade following traumatic injury, 128 non-scholastic sports, 121 oculomotor subtype, 125 office visit, 130 organized scholastic, 121 overlapping clinical profiles, 124 pathophysiology, 127 reaction time, 136 risk factors, 122, 123 risk of, 122 sensitivity, 131 sensor systems, 142 specificity, 131 subacute migraine headache, 123 subconcussive/non-concussive head impacts, 121 supplementation with O3FA, 143 symptoms, 123 test-retest reliability, 131 vestibular symptoms, 136 VOMS testing, 129 VOMS tool, 130 Sport-related eye injuries, 15 Sports Injuries and Medical Complications in Wheelchair Athletes, 446–450 Sports medicine healthcare teams, 10 Sports medicine organizations, 9 Sports medicine physicians, 3 Sports psychologists, 8 Sports, overhead movements, 447 Sport-specific agility testing, 323 Sport-specific prosthesis, 443 Sport-specific wheelchair designs, 440–442 Sports and recreation-related concussions (SRRC), 431 Sports-related injuries, 151 Sprain of the first metatarsophalangeal (MTP) joint, 381, 382 Squeeze test for ACJ injury, 181 Standardized assessment of concussion (SAC), 129 Station-based evaluation, 48 Stener lesion, 232 Sternal fractures, 254 Sternal stress fracture, 263 Stimson technique for anterior GHJ dislocation, 186 Strain elastography (SE), 16 Strength testing of the rotator cuff, 189 Stress fractures, 58 Subgluteusmedius bursa, 295 Subsymptom threshold exercise protocol, 139–141

Index Subsymptom threshold exercise protocol for prolonged symptoms, 139 Sudden cardiac death (SCD), 6, 51 Sulcus sign for GHJ instability, 197 Superficial fibular nerve (SFN), 352 Superficial forearm, 222 Supplements, dietary, 87 Supracondylar fractures, classifications, 206 Surface-based sensor, 21 T Talar tilt test, 370, 371 Talk test, 34 Tarsal tunnel syndrome (TTS), 349, 368 Temperature dysregulation, 448 Temperature monitors in arm bands, 24 Tendon stiffness, 16 Tennis elbow, 210, 211 Tension pneumothorax, 256 Tension-side stress fractures, 304 Tetanus prophylaxis, 107 Thawing process, analgesics, 107 Thiamin, 84 Thigh muscles, 295 Thoracic cage, muscles and ligaments, 246–247 Thoracic outlet syndrome (TOS), 169–172 Thoracic spine injuries, 245–269 3D motion capture, 21 3D motion capture and analysis, 23 Three-dimensional (3D) motion capture technology, 21 Thumb ligament injuries, 232 Tibial nerve injury, sports, 349–351 Tibial plateau fractures, 345, 346 Tibial stress fractures, 346, 347, 357–360 Tibialis anterior muscle, 378, 379 Tibialis posterior tendon injuries, 379, 380 Tibiofemoral modified hinge joint configuration, 317 Tietze’s syndrome, 264 Tinea pedis, 101 Tinel and Phalen tests at wrist, 215 Tissue trauma, 151 Torg ratio, 160 Traction apophysitis, 427 Transient brachial plexopathies and radiculopathies (Stingers/ Burners), 159–161 Transient tetraplegia, 164 Transient tetraplegia injury, 165 Trans-radial limb deficiency, 437 Transtibial prosthesis, 443

469 Traumatic finger dislocations, 236, 237 Traumatic intercostal neuritis, 264 Traumatic spondylolisthesis, 281 Traumatic TFCC Injuries, 229 Triangular fibrocartilage complex (TFCC), 228–230 classes, 229 Triceps tendinopathy, 212, 213 Triceps tendon rupture, 208, 209 Trigger finger, 241 Triple compression test, 350 Trunk-mounted accelerometry, 24 TUBS-AMBRI classification, 194 Two-dimensional (2D) video capture, 21 U UCL tear/first metacarpophalangeal instability, 232, 233 Ulnar collateral ligament (UCL), 19, 218 Ulnar nerve palsy at the wrist (Handlebar palsy), 240, 241 Ulnar neuropathy at elbow (UNE), 213–215 Ultrasound, types of bone injury, 16 Ultrasound tissue characterization (UTC), 16, 17 Uncoupling of energy availability with energy expenditure, 59 Unilateral transtibial amputations, 443 Unstable cervical fracture, 163, 164 Unstable cervical spine injuries, 162 US muscle glycogen content, 17 ocular evaluation, 15 office-based procedures, 14 U.S. Anti-Doping Agency (USADA), 8 V Valgus extension overload, 217 Valgus stress, 232 Valgus stress, knee, 322 Vegetarian diet, 85 Venous thromboembolism (VTE), 96, 97 Verrucus hyperplasia, 450 Vertebral compression and burst fractures, 276, 277 Vertebral fractures, 277 non-operative management, 277 Vestibular and oculomotor impairment and symptoms, 124 Vestibular/ocular-motor screening (VOMS), 7 Vigorous-intensity aerobic physical activity, 33

Index

470 Visually impaired athletes, 454 Vitamin B6, 84 Vitamin B12, 84 Vitamin D, 84, 85 Vocal cord dysfunction (VCD), 16 W Waste, 248 Water, temperature regulatory mechanism, 75 Wearable devices, 23, 24 Wearable performance devices, 23 Wheelchair athletes, treatment planning, 446 Wheelchair basketball, 452 Wheelchair designs, 439 Wheelchair games, 436 Wheelchair rugby, 451 Wheelchair technology, 439 pressure-related tissue injury, 440 seating parameters, 440 World Anti-Doping Agency (WADA), 8 Wrist and hand injuries carpal bones, 221 distal radius, 224, 225 extensor carpi radialis, 223 extensor carpi ulnaris, 223 flexion, 223

flexor carpi radialis, 223 flexor carpi ulnaris, 223 hypothenar muscles, 223 interosseous muscles, 222 metacarpal bones, 222 nerves, 223 palmar and collateral ligaments, 222 pronation and supination, 222 scaphoid bone, 221 sensory innervation, 223 thenar muscles, 222 Wrist motion, 222 Wrist sprain, 225, 226 grading, 226 Y Yergason test, 192 Yergason test for LHBT, 193 Z Zinc, 86 Zinc supplementation, 86 Z-plasty procedure, 310 Zyogapophyieal (facet) joints, 286, 287