Surgical Decision Making [6th Edition] 9780323567916

Table of contents :
00000000......Page 1
Surgical Decision Making......Page 2
Copyright Page......Page 4
Dedication......Page 5
Contributors......Page 6
Preface......Page 21
Preface......Page 22
1 Preoperative Laboratory Evaluation......Page 23
Keywords......Page 24
References......Page 25
2 Preoperative Cardiac Evaluation......Page 26
Keywords......Page 27
References......Page 28
3 Preoperative Pulmonary Evaluation......Page 29
Keywords......Page 30
References......Page 32
4 Bleeding Disorders in Surgical Patients......Page 33
Keywords......Page 34
References......Page 36
5 Hypercoagulable Patient......Page 37
Keywords......Page 38
References......Page 39
References......Page 40
Keywords......Page 41
7 Bridge Anticoagulation......Page 43
Keywords......Page 44
References......Page 46
8 Intraabdominal Infection......Page 47
Keywords......Page 48
References......Page 49
Preoperative Optimization......Page 50
Keywords......Page 51
References......Page 52
References......Page 53
Keywords......Page 54
Cardiovascular Implantable Electronic Device (CIED)......Page 56
Keywords......Page 57
Tachyarrhythmias......Page 58
Bradyarrhythmias......Page 59
References......Page 60
12 Perioperative Myocardial Ischemia and Infarction......Page 61
Keywords......Page 62
References......Page 64
Introduction......Page 65
Keywords......Page 66
References......Page 68
14 Goal-Directed Resuscitation......Page 69
Keywords......Page 70
References......Page 72
References......Page 73
Keywords......Page 74
16 Ventilator- Associated Pneumonia......Page 76
Keywords......Page 77
References......Page 78
17 Nutritional Support......Page 79
Keywords......Page 80
References......Page 82
Acute Respiratory Distress Syndrome......Page 83
Keywords......Page 84
High-PEEP Open Lung Strategy......Page 85
References......Page 86
References......Page 89
Keywords......Page 90
21 Acid–Base Disorders......Page 95
Keywords......Page 96
References......Page 97
Introduction......Page 98
Keywords......Page 99
References......Page 101
Hypokalemia......Page 102
Keywords......Page 103
References......Page 104
24 Calcium Disorders......Page 105
Keywords......Page 106
References......Page 107
References......Page 108
Keywords......Page 109
26 Neck Mass......Page 111
Keywords......Page 112
References......Page 114
27 Nonmelanoma Skin Cancer of the Face......Page 115
Keywords......Page 116
References......Page 118
Sentinel Node Negative......Page 119
Keywords......Page 120
References......Page 121
29 Lung Nodule......Page 122
Keywords......Page 123
References......Page 126
Introduction......Page 127
Keywords......Page 128
References......Page 130
References......Page 131
Keywords......Page 132
References......Page 134
Keywords......Page 135
33 Esophageal Motility Disorders (Other Than Achalasia)......Page 137
Keywords......Page 138
References......Page 139
34 Esophageal Perforation......Page 140
Keywords......Page 141
References......Page 143
References......Page 144
Keywords......Page 145
36 Gastroesophageal Reflux Disease......Page 147
Keywords......Page 148
References......Page 150
37 Barrett’s Esophagus......Page 151
Keywords......Page 152
References......Page 154
38 Esophageal Diverticulum......Page 155
Keywords......Page 156
References......Page 157
SURGICAL MANAGEMENT......Page 158
Keywords......Page 159
References......Page 161
40 Gastric Ulcer......Page 162
Keywords......Page 163
References......Page 164
41 Duodenal Ulcer......Page 165
Keywords......Page 166
References......Page 168
42 Morbid Obesity......Page 169
Keywords......Page 170
References......Page 172
43 Upper GI Bleeding......Page 173
Keywords......Page 174
References......Page 175
44 Bleeding Esophageal Varices......Page 176
Keywords......Page 177
References......Page 178
45 Jaundice......Page 179
Keywords......Page 180
References......Page 181
46 Obstructive Jaundice......Page 182
Keywords......Page 183
References......Page 184
47 Cholelithiasis......Page 185
Keywords......Page 186
References......Page 187
48 Choledocholithiasis......Page 188
Keywords......Page 189
References......Page 190
49 Hepatic Abscess......Page 191
Keywords......Page 192
References......Page 194
References......Page 195
Keywords......Page 196
51 Solid Liver Lesion......Page 198
Keywords......Page 199
References......Page 201
52 Acute Pancreatitis......Page 202
Keywords......Page 203
References......Page 204
53 Chronic Pancreatitis......Page 205
Keywords......Page 206
References......Page 208
54 Pancreatic Pseudocysts......Page 209
Keywords......Page 210
References......Page 211
Classifications......Page 212
Keywords......Page 213
Severe Acute Pancreatitis and Abdominal Pain......Page 214
Minor Duct Sphincteroplasty......Page 215
References......Page 216
Introduction......Page 217
Keywords......Page 218
References......Page 220
57 Acute Mesenteric Vascular Occlusion......Page 221
Keywords......Page 222
References......Page 224
58 Short Bowel Syndrome......Page 225
Keywords......Page 226
References......Page 227
References......Page 228
Keywords......Page 229
60 Crohn’s Disease of the Small Bowel......Page 231
Keywords......Page 232
References......Page 233
61 Right Lower Quadrant Pain......Page 234
Keywords......Page 235
References......Page 236
62 Volvulus......Page 237
Keywords......Page 238
References......Page 239
63 Diverticulitis......Page 240
Keyword......Page 241
References......Page 242
References......Page 243
Keywords......Page 244
References......Page 246
Keywords......Page 247
Introduction......Page 249
Keyword......Page 250
References......Page 251
67 Toxic Megacolon......Page 252
Keywords......Page 253
References......Page 254
References......Page 255
Keywords......Page 256
69 Large Bowel Obstruction......Page 258
Keywords......Page 259
References......Page 261
70 Rectal Prolapse......Page 262
Keywords......Page 263
References......Page 264
Introduction......Page 265
Keywords......Page 266
References......Page 268
References......Page 269
Keywords......Page 270
73 Anorectal Abscess and Fistula-in-Ano......Page 272
Keywords......Page 273
References......Page 275
74 Hemorrhoids......Page 276
Keywords......Page 277
References......Page 279
75 Pilonidal Disease......Page 280
Keywords......Page 281
References......Page 283
76 Anal Fissure......Page 284
Keywords......Page 285
References......Page 286
77 Groin Hernia......Page 287
Keywords......Page 288
References......Page 290
78 Ventral Hernia......Page 291
Keywords......Page 292
References......Page 293
79 Cancer of Unknown Primary......Page 294
Keywords......Page 295
References......Page 296
80 Esophageal Cancer......Page 297
Keywords......Page 298
References......Page 300
81 Gastric Cancer......Page 301
Keywords......Page 302
References......Page 303
82 Cholangiocarcinoma......Page 304
Keywords......Page 305
References......Page 308
83 Hepatocellular Carcinoma......Page 310
Keywords......Page 311
References......Page 314
84 Gallbladder Carcinoma......Page 315
Keywords......Page 316
References......Page 319
85 Gastrointestinal Stromal Tumors (GISTs)......Page 320
Keywords......Page 321
References......Page 323
86 Pancreatic Neuroendocrine Tumors......Page 324
Keywords......Page 325
References......Page 327
87 Periampullary Carcinoma......Page 328
Keywords......Page 329
References......Page 330
88 Pancreatic Cystic Neoplasms......Page 331
Keywords......Page 332
References......Page 333
89 Pancreatic Mass......Page 334
Keywords......Page 335
References......Page 336
90 Retroperitoneal Mass......Page 337
Keywords......Page 338
References......Page 340
Introduction......Page 341
Keywords......Page 342
References......Page 343
92 Colon Polyp......Page 344
Keywords......Page 345
References......Page 348
93 Colon Cancer......Page 349
Keywords......Page 350
References......Page 351
94 Rectal Cancer......Page 353
Keywords......Page 354
References......Page 356
95 Anal Cancer......Page 357
Keywords......Page 358
References......Page 360
96 Metastatic Colorectal Carcinoma......Page 361
Keywords......Page 362
References......Page 364
References......Page 365
Keywords......Page 366
References......Page 368
Keywords......Page 369
99 Palpable Breast Mass......Page 371
Keywords......Page 372
References......Page 374
100 Nonpalpable Breast Lesions......Page 375
Keywords......Page 376
References......Page 377
101 Early Breast Cancer......Page 378
Keywords......Page 379
References......Page 381
102 Advanced Breast Cancer......Page 382
Keywords......Page 383
References......Page 384
103 Recurrent Breast Carcinoma......Page 385
Keywords......Page 386
References......Page 388
References......Page 389
Keywords......Page 390
105 Breast Reconstruction......Page 392
Keywords......Page 393
References......Page 395
High-Risk Anatomy......Page 396
Keywords......Page 397
High-Risk Biology......Page 398
References......Page 399
107 Cutaneous Melanoma......Page 400
Keywords......Page 401
References......Page 402
References......Page 403
Keywords......Page 404
109 Thyrotoxicosis......Page 406
Keywords......Page 407
References......Page 408
Introduction......Page 409
Keywords......Page 410
References......Page 411
111 Well- Differentiated Thyroid Cancer......Page 412
Keywords......Page 413
References......Page 414
112 Medullary Thyroid Carcinoma......Page 415
Keyword......Page 416
References......Page 417
113 Hypercalcemia and Hyperparathyroidism......Page 418
Keywords......Page 419
References......Page 421
114 Hypoglycemia and Insulinoma......Page 422
Keywords......Page 423
References......Page 425
115 Zollinger-Ellison Syndrome......Page 426
Keywords......Page 427
References......Page 429
116 Adrenal Incidentaloma......Page 431
Keyword......Page 432
References......Page 434
117 Pheochromocytoma......Page 435
Keywords......Page 436
References......Page 437
118 Cushing’s Syndrome......Page 438
Keywords......Page 439
References......Page 441
119 Primary Aldosteronism......Page 442
Keywords......Page 443
References......Page 444
Correct Metabolic Derangements......Page 445
Keywords......Page 446
References......Page 447
121 Airway Management......Page 448
Keywords......Page 449
References......Page 450
References......Page 451
Keywords......Page 452
123 Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA)......Page 454
Keywords......Page 455
References......Page 456
124 Emergency Department Thoracotomy......Page 457
Keywords......Page 458
References......Page 459
125 Penetrating Neck Trauma......Page 460
Keywords......Page 461
References......Page 462
References......Page 463
Keywords......Page 464
127 Rib Fractures......Page 466
Keywords......Page 467
References......Page 468
128 Hemo- Pneumothorax......Page 469
Keywords......Page 470
References......Page 471
Emergency TEVAR for Grade IV Injuries......Page 472
Keyword......Page 473
References......Page 475
References......Page 476
Keywords......Page 477
131 Annotations to Thoracoabdominal Trauma......Page 479
Keywords......Page 480
References......Page 481
132 Blunt Abdominal Trauma......Page 482
Keywords......Page 483
References......Page 485
References......Page 486
Keywords......Page 487
134 Blunt Splenic Injury......Page 489
Keywords......Page 490
References......Page 491
135 Liver Injury......Page 492
Keywords......Page 493
References......Page 494
136 Abdominal Vascular Injuries......Page 495
Keywords......Page 496
References......Page 499
137 Pancreatic Injury......Page 500
Keywords......Page 501
References......Page 502
138 Duodenal Injury......Page 503
Keywords......Page 504
References......Page 505
139 Penetrating Injury of the Colon......Page 506
Keywords......Page 507
References......Page 508
140 Penetrating Rectal Injury......Page 509
Keywords......Page 510
References......Page 511
141 Damage-Control Laparotomy......Page 512
Keywords......Page 513
References......Page 515
142 Abdominal Compartment Syndrome......Page 516
Keywords......Page 517
References......Page 519
References......Page 520
Keywords......Page 521
144 Renal Injury......Page 523
Keywords......Page 524
References......Page 525
145 Ureteral Injuries......Page 526
Keywords......Page 527
References......Page 529
References......Page 530
Keywords......Page 531
147 Pelvic Fractures......Page 533
Keywords......Page 534
References......Page 535
148 Closed Head Injury......Page 536
Keywords......Page 537
References......Page 539
Neurologic Status......Page 540
Keywords......Page 541
Disposition......Page 542
References......Page 543
Introduction......Page 544
Keywords......Page 545
Conclusion......Page 548
References......Page 549
References......Page 550
Keywords......Page 551
152 Burns......Page 553
Keywords......Page 554
References......Page 556
Rapid External Rewarming......Page 557
Keywords......Page 558
Contraindications to the Thrombolytic Protocol......Page 559
References......Page 560
154 Electrical Burn Injury......Page 561
Keywords......Page 562
References......Page 563
3-s2.0-B9780323525244000209.pdf......Page 0
Introduction......Page 92
Keywords......Page 93
References......Page 94

Citation preview

Surgical Decision Making Sixth Edition

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Surgical Decision Making Sixth Edition Robert C. McIntyre, Jr., MD, FACS Professor and Chief Division of GI, Trauma, and Endocrine Surgery Vice Chair of Finance Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Richard D. Schulick, MD, MBA, FACS Professor & Chair of the University of Colorado Department of Surgery Director of the University of Colorado Cancer Center The Aragón/Gonzalez-Gíustí Chair University of Colorado School of Medicine Aurora, Colorado

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1600 John F. Kennedy Blvd. Ste. 1800 Philadelphia, PA 19103-2899

SURGICAL DECISION MAKING, SIXTH EDITION

ISBN: 978-0-323-52524-4

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

Notices Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. ISBN: 978-0-323-52524-4

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Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

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This book would not have been possible without the hard work and dedication of our editorial assistant, Shelly Lange, who always “improves every life.” Robert C. McIntyre, Jr. Richard Schulick

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Contributors  ix

Contributors Jad Abou-Khalil, MD, CM, MSc(Epid), FRCSC

Minerva A. Romero Arenas, MD, MPH

Associate Professor of Surgery Hepato-Biliary and Pancreatic Surgery Unit Department of Surgery University of Ottawa Ottawa, Ontario

Assistant Professor of General and Endocrine Surgery Department of Surgery The University of Texas Rio Grande Valley School of Medicine Edinburg, Texas

Brett D. Arnoldo, MD Anosheh Afghahi, MD, MPH Assistant Professor Division of Medical Oncology Department of Medicine University of Colorado School of Medicine Aurora, Colorado

Gretchen Ahrendt, MD Director, Diane O’Connor Thompson Breast Center University of Colorado Hospital Professor Division of Surgical Oncology Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Nita Ahuja, MD, MBA, FACS Surgeon-in-Chief, Yale New Haven Hospital William H. Carmalt Professor and Chair of Surgery and Oncology Department of Surgery Yale School of Medicine New Haven, Connecticut

Maria B. Albuja-Cruz, MD, FACS Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Yewande Alimi, MD, MHS Department of Surgery MedStar Georgetown University Hospital Washington, DC

Peter J. Allen, MD Chief, Division of Surgical Oncology Department of Surgery Duke Cancer Institute Duke University School of Medicine Durham, North Carolina

Professor and Interim Chief General and Acute Care Surgery University of Texas Southwestern Medical Center Dallas, Texas

Juan A. Asensio, MD Director of Trauma Center and Trauma Program Creighton University Medical Center Professor and Vice-Chairman of Surgery Chief, Division of Trauma Surgery and Surgical Critical Care Department of Surgery Creighton University School of Medicine Omaha, Nebraska

Chady Atallah, MD Assistant Professor of Surgery Department of Surgery Johns Hopkins University School of Medicine Baltimore, Maryland

Lori Baird, MD, MBA Chief, Trauma, Surgical Critical Care, and Acute Care Surgery Department of Surgery University of Miami Miami, Florida

Charles M. Balch, MD Founding Editor-in-Chief Emeritus, Annals of Surgical Oncology Professor of Surgery Department of Surgical Oncology University of Texas MD Anderson Cancer Center Houston, Texas

Carlton C. Barnett, Jr., MD, FACS Chief, Surgical Oncology Rocky Mountain Regional Veteran’s Affairs Medical Center Professor Division of Surgical Oncology Department of Surgery University of Colorado School of Medicine Aurora, Colorado

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x Contributors

Rachel E. Beard, MD

Brooke C. Bredbeck, MD

Assistant Professor Rhode Island Hospital and the Lifespan Cancer Institute Division of Hepatobiliary Surgery Department of Surgery Alpert Medical School of Brown University Providence, Rhode Island

Department of Surgery University of Michigan Ann Arbor, Michigan

Daine Bennett, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Walter L. Biffl, MD Director, Trauma and Acute Care Surgery N. Paul Whittier Chair of Trauma Scripps Memorial Hospital La Jolla La Jolla, California

James H. Black, III, MD, FACS Associate Professor and Chief of Vascular Surgery and Endovascular Therapy The Johns Hopkins University School of Medicine Baltimore, Maryland

Virginia Borges, MD, MMSc Professor Division of Medical Oncology Department of Medicine University of Colorado School of Medicine Aurora, Colorado

Robert E. Breeze, MD Professor and Vice Chair Department of Neurosurgery University of Colorado School of Medicine Aurora, Colorado

Murray F. Brennan, GNZM, MD Benno C. Schmidt Chair in Clinical Oncology Department of Surgery Memorial Sloan Kettering Cancer Center New York, New York

L.D. Britt, MD, MPH, DSc (Hon), FACS, FCCM Henry Ford Professor and Edward J. Brickhouse Chairman Department of Surgery Eastern Virginia Medical School Norfolk, Virginia

Clay Cothren Burlew, MD Director, Surgical Intensive Care Unit Denver Health Medical Center Denver, Colorado Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Gregory M. Borst, MD Trauma Acute Care Surgery University of Colorado Health–Memorial Hospital Colorado Springs, Colorado

Judy C. Boughey, MD Professor of Surgery Department of Surgery Mayo Clinic College of Medicine Rochester, Minnesota

Jason C. Brainard, MD Associate Professor Department of Anesthesiology University of Colorado School of Medicine Aurora, Colorado

John L. Cameron, MD Alfred Blalock Distinguished Professor of Surgery Department of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Eric M. Campion, MD Assistant Professor Denver Health Medical Center Denver, Colorado Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

DuyKhanh Pham. Ceppa, MD Karen J. Brasel, MD, MPH Professor and Program Director Division of Trauma, Critical Care, and Acute Care Surgery Department of Surgery Oregon Health and Science University Portland, Oregon

Assistant Professor of Surgery Division of Cardiothoracic Surgery Department of Surgery Indiana School of Medicine Indianapolis, Indiana

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Contributors  xi

Brandon C. Chapman, MD

Mitchell J. Cohen, MD

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

The Bruce M Rockwell Distinguished Chair in Trauma Surgery Denver Health Medical Center Denver, Colorado Professor and Vice Chair of Surgery Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Akshay Pratap Chauhan, MBBS, MCh Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Mary Condron, MD Tae Chong, MD Associate Professor Division of Plastic and Reconstructive Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Paul H. Chung, MD Assistant Professor Department of Urology Jefferson University Hospitals Philadelphia, Pennsylvania

David J. Ciesla, MD Chief Trauma Acute Care Surgery Tampa General Hospital Professor and Division Chief Division of Trauma & Acute Care Surgery Department of Surgery Morsani College of Medicine University of South Florida Tampa, Florida

Trauma and Acute Care Surgeon Saint Charles Medical Center Bend, Oregon

Michelle L. Cowan, MD Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Daniel Craig, MD Department of Neurosurgery University of Colorado School of Medicine Aurora, Colorado

Chasen A. Croft, MD Associate Professor of Surgery Department of Surgery University of Florida Health Science Center Gainesville, Florida

Juliane Y. Cruz, MD Audra T. Clark, MD Department of Surgery University of Texas Southwestern Medical Center Dallas, Texas

Department of Surgery Huntington Hospital Pasadena, California

Alan P. B. Dackiw, MD, PhD, MBA Joseph C. Cleveland, Jr., MD Fred and Carol Grover Endowed Chair and Professor of Surgery Division of Cardiothoracic Surgery Vice Chair of Faculty Affairs Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Kathryn E. Coan, MD Assistant Professor Department of General Surgery Creighton Medical School Phoenix, Arizona

Professor of Surgery Department of Surgery University of Texas Southwestern Medical Center Dallas, Texas

Thomas A. D’Amico, MD Professor Division of Cardiovascular and Thoracic Surgery Vice Chair Department of Surgery Duke University Medical Center Durham, North Carolina

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xii Contributors

David R. Farley, MD

Jonathan E. Efron, MD

Professor of Surgery Department of Surgery Mayo Clinic College of Medicine Rochester, New York

Associate Professor of Surgery and Urology Department of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Stephanie Davis, MD

Bryan A. Ehlert, MD

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

Assistant Professor Division of Vascular Surgery Department of Surgery East Carolina University Greenville, North Carolina

Frederic W.-B. Deleyiannis, MD, MPhil, MPH Professor Division of Plastic and Reconstructive Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Oliver Fackelmayer, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Ronald P. DeMatteo, MD, FACS

Josefina C. Farra, MD

Vice Chair Department of Surgery Memorial Sloan Kettering Cancer Center New York, New York

Assistant Professor of Surgery Department of Surgery University of Miami Miami, Florida

Rodrigo Donalisio de Silva, MD

Carlos A. Fernandez, MD, FACS

Assistant Professor Denver Health Medical Center Denver, Colorado Division of Urology Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Assistant Professor Division of Trauma Surgery & Surgical Critical Care Department of Surgery Creighton University School of Medicine Omaha, Nebraska

Therese M. Duane, MD, MBA, CPE Professor Department of Surgery John Peter Smith Health Network Fort Worth, Texas

Lisa Ferrigno, MD, MPH Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Christina A. Finlayson, MD Linda A. Dultz, MD, MPH Assistant Professor Department of Surgery University of Texas Southwestern Dallas, Texas

Professor Division of Surgical Oncology Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Barish H. Edil, MD

Yuman Fong, MD

Professor and Chair John A. Schilling Chair in Surgery Department of Surgery University of Oklahoma College of Medicine Oklahoma City, Oklahoma

Chairman Department of Surgery City of Hope Medical Center Duarte, California

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Contributors  xiii

Zhi Ven Fong, MD, MPH

Fiona Gaunay, MD

Department of Surgery Massachusetts General Hospital Boston, Massachusetts

Colon and Rectal Surgeon Penn Medicine Lancaster General Health University of Pennsylvania Health System Philadelphia, Pennsylvania

Charles J. Fox, MD Chief of Vascular Surgery Denver Health Medical Center Denver, Colorado Associate Professor of Surgery Division of Vascular Surgery and Endovascular Therapy Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Richard Frazee, MD Professor Department of Surgery Baylor Scott & White Healthcare Texas A&M Health Science Center Temple, Texas

David A. Fullerton, MD John T. M. Wright Endowed Chair in Heart Valve Surgery Professor and Head Division of Cardiothoracic Surgery Vice Chair of Research Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Csaba Gajdos, MD, FACS Clinical Associate Professor Buffalo Veterans Affairs Medical Center Department of Surgery University of Buffalo Jacobs School of Medicine and Biomedical Sciences Buffalo, New York

Maxx Gallegos, MD Clinical Instructor Department of Urology Michigan State University Detroit, Michigan

O. James Garden, CBE, BSc, MB ChB, MD, FRCSEd, FRCPEd, FRSE, FRCSCan(hon), FRACS(hon), FACS(hon), FRCS(hon), FCSHK(hon), FRCSI(hon) Regius Professor of Clinical Surgery Department of Clinical Surgery University of Edinburgh Royal Infirmary Edinburgh, Great Britain

Susan L. Gearhart, MD Associate Professor of Surgery Department of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

David A. Geller, MD, FACS Richard L. Simmons Professor of Surgery Chief, Division of Hepatobiliary and Pancreatic Surgery Department of Surgery University of Pittsburgh Pittsburgh, Pennsylvania

Nicholas H. George Department of Emergency Medicine University of Maryland School of Medicine Baltimore, Maryland

Jean-Francois H. Geschwind, MD PreScience Labs LLC

Sepideh Gholami, MD Assistant Professor Division of Surgical Oncology Department of Surgery University of California, Davis Sacramento, California

Alicia A. Heelan Gladden, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Ana Gleisner, MD, PhD Assistant Professor Division of Surgical Oncology Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Rene Gonzalez, MD Professor Division of Medical Oncology Department of Medicine University of Colorado School of Medicine Aurora, Colorado

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xiv Contributors

Karyn A. Goodman, MD

Scott Helton, MD, FACS

Professor Department of Radiation Oncology University of Colorado School of Medicine Aurora, Colorado

Director Liver, Biliary, and Pancreas Surgery Center of Excellence Digestive Disease Institute Virginia Mason Medical Center Seattle, Washington

Melissa A. Gorman, MD Assistant Professor Department of Orthopedics University of Colorado School of Medicine Aurora, Colorado

Patrick T. Hangge, MD Department of Surgery Mayo Clinic College of Medicine Scottsdale, Arizona

Laura A. Harmon, MD Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Taryn Hassinger, MD Department of Surgery University of Virginia Charlottesville, Virginia

Thomas J. Herron, MD Assistant Professor Division of Trauma & Acute Care Surgery Department of Surgery Morsani College of Medicine University of South Florida Tampa, Florida

Vanessa P. Ho, MD, MPH Assistant Professor of Surgery Department of Surgery Case Western Reserve University Cleveland, Ohio

Maggie McQueen Hodges, MD, MPH Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Jordan R. H. Hoffman, MPH, MD

Madigan Army Medical Center Tacoma, Washington

Fellow in Cardiothoracic Surgery Division of Cardiothoracic Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Bryan R. Haugen, MD

Courtenay M. Holscher, MD

Mary Rossick Kern and Jerome H. Kern Chair in Endocrine Neoplasms Research Professor and Head Division of Endocrinology, Metabolism, and Diabetes Department of Medicine University of Colorado School of Medicine Aurora, Colorado

Department of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Quinton M. Hatch, MD

Jin He, MD, PhD Assistant Professor Division of Surgical Oncology Department of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Tracy L. Hull, MD Professor of Surgery Department of Colon and Rectal Surgery The Cleveland Clinic Foundation Cleveland, Ohio

Jonathan B. Imran, MD Department of Surgery University of Texas Southwestern Medical Center Dallas, Texas

Alexandra Heerdt, MD, MPH

Kenji Inaba, MD

Attending Surgeon, Breast Service Department of Surgery Memorial Sloan Kettering Cancer Center Associate Professor of Surgery Weill Cornell Medical School New York, New York

Associate Professor of Surgery, Anesthesia, and Emergency Medicine Department of Surgery University of Southern California Los Angeles, California

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Contributors  xv

William R. Jarnagin, MD

Amir Y. Kamel, PharmD, BCNSP

Chief, Hepatopancreatobiliary Service Benno C. Schmidt Professor of Surgical Oncology Memorial Sloan Kettering Cancer Center Professor of Surgery Weill Cornell Medical College New York, New York

Clinical Specialist in Nutrition Support and Critical Care University of Florida Health Shands Hospital Clinical Assistant Professor University of Florida College of Pharmacy Gainesville, Florida

Farah Karipineni, MD, MPH Eric K. Johnson, MD, FACS, FASCRS Associate Professor of Surgery MultiCare Colorectal Surgery Uniformed Services University of the Health Sciences Tacoma, Washington

Endocrine Surgery Fellow Division of Surgical Oncology Department of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Bobby L. Johnson III, MD

Howard S. Kaufman, MD, MBA

Instructor Department of Surgery University of Cincinnati College of Medicine Cincinnati, OH

Chairman, Department of Surgery Huntington Hospital Medical Director, Huntington Hospital Cancer Center Director of Colorectal Research Program, Huntington Medical Research Institutes Pasadena, California

Edward L. Jones, MD, FACS Assistant Professor Rocky Mountain Regional Veteran’s Affairs Medical Center Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Teresa S. Jones, MD, FACS Assistant Professor Rocky Mountain Regional Veteran’s Affairs Medical Center Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Electron Kebebew, MD, FACS Professor of Surgery Chief, Division of General Surgery Harry A. Oberhelman, Jr. And Mark L. Welton Professor Program Leader, Endocrine Oncology Program Department of Surgery and Stanford Cancer Institute School of Medicine, Stanford University Stanford, California

Abid D. Khan, MD Trauma and Acute Care Surgeon Department of Surgery University of Colorado Health–Memorial Hospital Colorado Springs, Colorado

Bellal A. Joseph, MD, FACS Associate Professor of Surgery Department of Surgery Banner University Medical Center Tucson, Arizona

Stephanie Joyce, MD Surgical Critical Care Fellow Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Kyle J. Kalkwarf, MD Assistant Professor Division of Trauma and Acute Care Surgery Department of Surgery University of Arkansas for Medical Sciences Little Rock, Arkansas

David Khechoyan, MD Assistant Professor Division of Plastic and Reconstructive Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Fernando J. Kim, MD, MBA, FACS Chief of Urology Denver Health Medical Center Denver, Colorado Associate Professor Division of Urology University of Colorado School of Medicine Aurora, Colorado

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xvi Contributors

Teresa S. Kim, MD

Ryan A. Lawless, MD

Assistant Professor Division of General Surgery, Section of Surgical Oncology Department of Surgery University of Washington Seattle, Washington

Assistant Professor Denver Health Medical Center Denver, Colorado Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

V. Suzanne Klimberg, MD, FACS Professor and Director of Breast Cancer Program Department of Surgery Winthrop P. Rockefeller Cancer Institute University of Arkansas Little Rock, Arkansas

Patrick D. Kohtz, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Rosemary A. Kozar, MD, PhD Director of Translational Research Associate Director of Shock Trauma Anesthesia Research Center R. Adams Cowley Shock Trauma Center University of Maryland School of Medicine Baltimore, Maryland

Rachel Kruer, PharmD Clinical Pharmacist, ICU The Johns Hopkins University School of Medicine Baltimore, Maryland

John I. Lew, MD Professor and Vice Chair of Surgery, Chief of Endocrine Surgery DeWitt Daughtry Department of Surgery University of Miami Miller School of Medicine Miami, Florida

Aaron Lewis, MD Assistant Clinical Professor Division of Surgical Oncology, Department of Surgery City of Hope National Medical Center Duarte, California

Anne O. Lidor, MD, MPH, FACS Professor Department of Surgery University of Wisconsin School of Medicine and Public Health Madison, Wisconsin

Keith D. Lillemoe, MD

Assistant Professor of Surgery University of Pittsburg Medical Center Seneca, Pennsylvania

Surgeon in Chief Massachusetts General Hospital HMS W. Gerald Austen Professor of Surgery Harvard Medical School Boston, Massachusetts

Sepehr Lalezari, MD

Gary Linkov, MD

Medical Staff Department of Surgery Good Samaritan Hospital Los Angeles, California

Instructor Otolaryngology—Head and Neck Surgery Lewis Katz School of Medicine Temple University Hospital Philadelphia, Pennsylvania

Mustapha El Lakis, MD

Lung W. Lau, MD Department of Surgery Case Western Reserve University Cleveland, OH

Harish Lavu, MD, FACS Associate Professor Chief, Section of Hepatopancreatobiliary Surgery Department of Surgery Thomas Jefferson University Philadelphia, Pennsylvania

Pamela A. Lipsett, MD, MHPE, MCCM Warfield M. Firor Endowed Professorship in Surgery Program Director, Residency in General Surgery and Fellowship in Surgical Critical Care Co-Director, Surgical Intensive Care Units Assistant Dean of Assessment and Evaluation The Johns Hopkins University School of Medicine Baltimore, Maryland

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Contributors  xvii

Tarik D. Madni, MD

Robert A. Meguid, MD, MPH/MSPH

Department of Surgery University of Texas Southwestern Medical Center Dallas, Texas

Associate Professor Division of Cardiothoracic Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Gregory A. Magee, MD, MSc Assistant Professor Department of Surgery University of Southern California Los Angeles, California

David Mann, MD Department of Neurosurgery University of Colorado School of Medicine Aurora, Colorado

David Mathes, MD Professor and Chief Division of Plastic and Reconstructive Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Sarah Mayson, MD Assistant Professor Division of Endocrinology, Metabolism, and Diabetes Department of Medicine University of Colorado School of Medicine Aurora, Colorado

Martin D. McCarter, MD Professor Division of Surgical Oncology Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Ashley K. McCusker, MD, MSc Trauma and Acute Care Surgery University of Colorado Health–Memorial Hospital Colorado Springs, Colorado

Robert C. McIntyre, Jr., MD, FACS Professor and Chief Division of GI, Trauma, and Endocrine Surgery Vice Chair of Finance Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Travis J. McKenzie, MD Division of Breast, Endocrine Metabolic and GI Surgery Department of Surgery Mayo Clinic College of Medicine Rochester, Minnesota

Caleb Mentzer, DO Department of Surgery Ryder Trauma Center Jackson Memorial Hospital Miller School of Medicine of the University of Miami Miami, Florida

Benjamin D. Medina, MD Research Fellow Department of Surgery Memorial Sloan Kettering Cancer Center New York, New York

John C. Messenger, MD Professor Division of Cardiology Department of Medicine University of Colorado School of Medicine Aurora, Colorado

Bria Meyer, MD Department of Surgery University of Nebraska Medical Center Omaha, Nebraska

Jordan D. Miller, DO Assistant Professor Division of Cardiothoracic Surgery Department of Surgery University of Kentucky Lexington, Kentucky

John D. Mitchell, MD Chief, General Thoracic Surgery University of Colorado Hospital Professor Division of Cardiothoracic Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Damian James Mole, BMedSc, MBChB, PhD, FRCS Honorary Consultant Surgeon Department of Surgery Senior Clinical Lecturer MRC Centre for Inflammation Research University of Edinburgh Edinburgh, Great Britain

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xviii Contributors

Paul Nobert Montero, MD, FACS

Benedetto Mungo, MD

Associate Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

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

Ernest E. Moore, MD Director, Surgical Research Denver Health Medical Center Denver, Colorado Professor Division of GI, Trauma, and Endocrine Surgery Vice Chair for Research Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Kenric M. Murayama, MD Chair Department of Surgery John A. Burns School of Medicine University of Hawaii at Manoa Honolulu, Hawaii

Alexander P. Nagle, MD Assistant Professor Department of Surgery Northwestern University Feinberg School of Medicine Chicago, Illinois

Frederick A. Moore, MD

Attila Nakeeb, MD

Professor and Chief Division of Acute Care Surgery Department of Surgery University of Florida School of Medicine Gainesville, Florida

Professor Department of Surgery Indiana University of School of Medicine Indianapolis, Indiana

Hunter Burroughs Moore, MD, PhD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

John T. Moore, MD Associate Chief of Staff for Education Rocky Mountain Regional Veteran’s Affairs Medical Center Volunteer Clinical Faculty Division of GI, Trauma, and Endocrine Surgery Department of Surgery Aurora, Colorado

Laura J. Moore, MD, FACS Medical Director, Shock Trauma Intensive Care Unit Texas Trauma Institute Memorial Hermann Hospital Texas Medical Center Associate Professor Chief of Surgical Critical Care University of Texas Health Science Center Houston, Texas

Eliza E. Moskowitz, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Nicholas Namias, MD, MBA, FACS, FCCM Medical Director Ryder Trauma Center Jackson Memorial Hospital Chief, Division of Trauma and Acute Care Surgery University of Miami Miller School of Medicine Miami, Florida

Lena M. Napolitano, MD Director, Trauma and Surgical Critical Care Professor and Division Chief Acute Care Surgery Associate Chair Department of Surgery University of Michigan Health System Ann Arbor, Michigan

Erinn Ogburn, MD Department of Surgery University of Kentucky Lexington, Kentucky

Dmitry Oleynikov, MD, FACS Chief of Gastrointestinal Minimally Invasive Surgery Department of Surgery University of Nebraska Medical Center Omaha, Nebraska

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Contributors  xix

Douglas M. Overbey, MD

Frederic Pieracci, MD, MPH

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

Associate Professor Denver Health Medical Center Denver, Colorado Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Alessandro Paniccia, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Amit Prabhakar, MD Ian M. Paquette, MD Associate Professor of Surgery Department of Surgery University of Cincinnati Cincinnati, Ohio

Fellow Anesthesiology and Critical Care Fellow The Johns Hopkins University School of Medicine Baltimore, Maryland

Sanjeev Puri, MD Bruce C. Paton, MD Director, The Given Institute Aspen, Colorado Emeritus Clinical Professor of Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Marco G. Patti, MD Professor of Medicine and Surgery Department of Medicine and Surgery Center for Esophageal Diseases and Swallowing University of North Carolina at Chapel Hill Chapel Hill, North Carolina

Michael Patz, MD Department of Anesthesiology Mercy Regional Medical Center Durango, Colorado

Erik Peltz, DO Assistant Director, Trauma and Acute Care Surgery University of Colorado Hospital Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

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

Jennifer M. Racz, MD Assistant Professor of Surgery Department of Surgery Mayo Clinic College of Medicine Rochester, Minnesota

Michael Radomski, MD Trauma and Acute Care Surgery Fellow Department of Surgery Denver Health Medical Center Denver, Colorado University of Colorado School of Medicine Aurora, Colorado

Christopher D. Raeburn, MD Associate Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Judi Ann Ramiscal, MD Department of Surgery University of Hawaii at Manoa Honolulu, Hawaii

Nancy Dugal Perrier, MD, FACS Walter and Ruth Sterling Endowed Professor of Surgery Surgical Oncology University of Texas MD Anderson Cancer Center Houston, Texas

Bradley N. Reames, MD Assistant Professor Division of Surgical Oncology Department of Surgery University of Nebraska Medical Center Omaha, Nebraska

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xx Contributors

T. Brett Reece, MD

Hai Nguyen Salfity, MD

Director, Thoracic Aortic Program University of Colorado Hospital Professor Division of Cardiothoracic Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Department of Surgery Indiana University School of Medicine Indianapolis, Indiana

Jason M. Samuels, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

John A. Ridge, MD, PhD, FACS Chief, Head and Neck Surgery Professor and Vice-Chair, Department of Surgical Oncology Louis Della Penna Family Chair in Head and Neck Oncology Fox Chase Cancer Center Temple Health Philadelphia, Pennsylvania

David Rivadeneira, MD, MBA, FACS, FASCRS Director of Colorectal Surgery and Surgical Services Huntington Hospital Huntington, New York Professor of Surgery Hofstra University School of Medicine Hempstead, New York

Amy Rivere, MD Breast Surgical Oncologist Ochsner Medical Center New Orleans, Los Angeles

Tyler P. Robin, MD, PhD Department of Radiation Oncology University of Colorado Hospital Aurora, Colorado

Thomas N. Robinson, MD, FACS Chief of Surgery Rocky Mountain Regional Veteran’s Affairs Medical Center Professor Division of GI, Trauma, Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Richard A. Santucci, MD Specialist-in-Chief Department of Urology The Detroit Medical Center Clinical Professor Surgical Specialties Michigan State College of Osteopathic Medicine Detroit, Michigan

Robert G. Sawyer, MD Professor and Chair Department of Surgery Western Michigan University Homer Stryker MD School of Medicine Kalamazoo, Michigan

Morgan Schellenberg, MD, MPH Trauma/Critical Care Fellow Trauma and Surgical Critical Care Los Angeles USC Medical Center Los Angeles, California

Todd R. Schlachter, MD Assistant Professor Department of Radiology and Biomedical Imaging Yale University School of Medicine New Haven, Connecticut

Francisco Schlottmann, MD, MPH Department of Surgery University of North Carolina Chapel Hill, New Jersey

Stanley James Rogers, MD, FACS, FRCS

Jonathan A. Schoen, MD

Professor Department of Surgery University of California, San Francisco San Francisco, California

Associate Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Martin D. Rosenthal, MD Assistant Professor Department of Surgery University of Florida Gainesville, Florida

Thomas J. Schroeppel, MD Trauma Medical Director Trauma and Acute Care Surgery University of Colorado Health–Memorial Hospital Colorado Springs, Colorado

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Contributors  xxi

Michael Schweitzer, MD

Jason W. Stoneback, MD

Director, Johns Hopkins Center for Bariatric Surgery Associate Professor of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Chief, Orthopedic Trauma and Fracture Surgery University of Colorado Hospital Assistant Professor Department of Orthopedics University of Colorado School of Medicine Aurora, Colorado

Luke V. Selby Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Paulesh K. Shah, MD Assistant Professor of Surgery Department of Surgery University of Maryland School of Medicine Baltimore, Maryland

Eduardo Smith Singares, MD, FACS Director SICU University of Illinois Hospital and Health Sciences System Chief, Division of Surgical Critical Care Department of Surgery University of Illinois College of Medicine at Chicago Chicago, Illinois

Andrea M. Stroud, MD, MS Assistant Professor Department of Surgery Oregon Health & Science University Portland, Oregon

Joshua J. Sumislawski, MD Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Jon S. Thompson, MD Professor of Surgery Department of Surgery University of Nebraska Medical Center Omaha, Nebraska

Wayne Soong, MD, FCCP

Robert J. Torphy, MD

Department of Anesthesiology Rocky Mountain Regional Veteran’s Affairs Medical Center Aurora, Colorado

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

Philip F. Stahel, MD

Becky B. T. King, MD

Professor of Orthopedics and Neurosurgery Rocky Vista University College of Osteopathic Medicine Parker, Colorado

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

Gregory Stettler, MD

Jennifer F. Tseng, MD, MPH

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

Chief of Surgery Boston Medical Center Chair Department of Surgery Boston University School of Medicine Boston, Massachusetts

Lauren Steward, MD, MHSA, MPHS Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Gregory Van Stiegmann, MD John H. and Cynthia H. Schultz Endowed Chair and Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Anthony P. Tufaro, DDS, MD, FACS Associate Professor Department of Plastic and Reconstructive Surgery Associate Professor Department of Oncology The Johns Hopkins University School of Medicine Baltimore, Maryland

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xxii Contributors

John Twomey, MD

Michel Wagner, MD, FACS

Retired Director, Burn Center Department of Surgery Hennepin County Medical Center Minneapolis, Minnesota

Assistant Professor Division of Trauma Surgery and Surgical Critical Care Department of Surgery Creighton University Omaha, Nebraska

Todd F. VanderHeiden, MD Department of Orthopaedics Denver Health Medical Center Denver, CO Associate Professor University of Colorado School of Medicine Aurora, Colorado

George C. Velmahos, MD, PhD, MSEdpel Division Chief of Trauma, Emergency Surgery, and Surgical Critical Care Massachusetts General Hospital Boston, Massachusetts

Catherine Velopulos, MD, MHS Associate Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Neil Venardos, MD Division of Cardiothoracic Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Bryan B. Voelzke, MD, FACS Spokane Urology Spokane, Washington

Carrie D. Walsh, BA Thomas Jefferson University Philadelphia, Pennsylvania

Tracy S. Wang, MD, MPH Professor Chief, Section of Endocrine Surgery Department of Surgery Medical College of Wisconsin Milwaukee, Wisconsin

Michael Weyant, MD Professor Division of Cardiothoracic Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Elizabeth C. Wick, MD Associate Professor Department of Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland

Krzysztof Wikiel, MD Assistant Professor of Surgery Rocky Mountain Regional Veteran’s Affairs Medical Center Aurora, Colorado

Arek Wiktor, MD, FACS Jon D. Vogel, MD Director of Colorectal Surgery University of Colorado Hospital Associate Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Assistant Director of the Burn Center University of Colorado Hospital Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

David J. Winchester, MD Anne Lambert Wagner, MD, FACS Medical Director of the Burn Center University of Colorado Hospital Associate Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Senior Attending Department of Surgery NorthShore University HealthSystem Evanston, Illinois Clinical Professor Department of Surgery University of Chicago Chicago, Illinois

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Contributors  xxiii

Steven E. Wolf, MD, FACS

Martha Zeiger, MD

Chief of Staff Shriners Hospitals for Children - Galveston Professor and Chief JD and LH Jamail Distinguished Chair Division of Burn and Trauma Surgery Vice-Chairman, Finance Department of Surgery University of Texas Medical Branch, Galveston, Texas

S. Hurt Watts Professor and Chair Department of Surgery University of Virginia School of Medicine Charlottesville, Virginia

Frank Z. Zhao, MD Queen’s Medical Center John A. Burns School of Medicine University of Hawaii at Manoa Honolulu, Hawaii

Franklin L. Wright, MD Assistant Professor Division of GI, Trauma, and Endocrine Surgery Department of Surgery University of Colorado School of Medicine Aurora, Colorado

Brittany A. Zwischenberger, MD Assistant Professor Division of Cardiothoracic Surgery Department of Surgery Duke University Durham, North Carolina

Charles J. Yeo, MD, FACS Samuel D. Gross Professor and Chair Department of Surgery Sidney Kimmel Medical College at Thomas Jefferson University Philadelphia, Pennsylvania

Joseph B. Zwischenberger, MD Johnston-Wright Professor and Chair Department of Surgery University of Kentucky Lexington, Kentucky

Andrew J. Young, MD Department of General Surgery Naval Hospital Bremerton Bremerton, Washington

Tonia M. Young-Fadok, MD Professor of Surgery Department of Surgery Mayo Clinic College of Medicine Phoenix, Arizona

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Preface Ben Eiseman and colleagues first conceived of best-practice decision trees applied to prevalent surgical diagnoses and treatments in the late 1970s.i,ii At that time, care pathways, bundled care episodes, cost-effectiveness analysis for individual patients or patient cohorts, and the transition from analog to digital information flow were irrelevant. Or perhaps these ideas were aspirations for a few forward-thinking clinicians, for a few researchers interested in health policy and payment reform, and for elite informaticians dealing largely with complicated datasets not in the health-care universe. Six editions later, Surgical Decision Making algorithms could be viewed as having led the way, as a “forcing function” in coalescing default best practice in an ever-more-complex population of data. Surgical Decision Making has been and still is a practical attempt to optimize the everyday management of common surgical diseases. Many of the dilemmas apparent at the inception of the series are still present: • How to come to a consensus on best practice in diagnostic and therapeutic approaches • How to continuously update clinical expertise with an ever-expanding and dynamic basic and clinical research database • How to define and update intermediate- and long-term quality metrics • And most importantly, how to balance the art and the science of care without creating one of the popular false polarities in health care—cookbook medicine (one care template that fits all patients) versus “seat of the pants” individual

i Norton, L., Steele, G., Eiseman, B. 1978. Surgical Decision Making. W.B. Saunders Company, Philadelphia. ii Eiseman, B., Robinson, W., Steele, G. 1982. Follow-Up of the Cancer Patient. Thieme-Stratton, New York.

variation (“I do it my way because of what I was taught 35 years ago”) This sixth edition presupposes that surgeons will be the key managers of many prevalent medical problems. The present editors have added experts and expertise consistent with the immense new knowledge that contributes to better (i.e., more valuable) care for all of our patients. But these Surgical Decision Making algorithms do not substitute for judgment. The humility of Eiseman et al.’s preface to the third edition still stands: Clinicians understandably resist the idea of reducing multifactorial decisions, which are subject to variations of the patient and the provider, to simple line drawings. A cookbook approach to problem solving cannot possibly reflect the circumstances under which the surgeon exercises judgment. This book is not intended to prescribe behavior in every instance. It offers the reader an opportunity to follow the logic of an expert in selecting the best among many competing options of diagnosis and treatment. And I would argue that as the data and the complexities in diagnostics and therapeutics have expanded, the need for simplicity and default best-practice algorithms becomes even more critical as a starting point for determining a continued optimization of surgical care. As one of my former colleagues at Geisinger stated, “This is the stuff every surgical trainee should know if he or she is to pass the specialty board exams.”iii

iii

Casale, A., Paulus, R., Selna, M., Doll, M., Bothe, A., McKinley, K., Berry, S., Davis, D., Gilfillan, R., Hamory, B., Steele, G. 2007. “ProvenCareSM”: a provider-driven pay-for-performance program for acute episodic cardiac surgical care. Annals of Surgery 246 (4), 613–621.

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Preface Ben Eiseman and colleagues first conceived of best-practice decision trees applied to prevalent surgical diagnoses and treatments in the late 1970s.i,ii At that time, care pathways, bundled care episodes, cost-effectiveness analysis for individual patients or patient cohorts, and the transition from analog to digital information flow were irrelevant. Or perhaps these ideas were aspirations for a few forward-thinking clinicians, for a few researchers interested in health policy and payment reform, and for elite informaticians dealing largely with complicated datasets not in the health-care universe. Six editions later, Surgical Decision Making algorithms could be viewed as having led the way, as a “forcing function” in coalescing default best practice in an ever-more-complex population of data. Surgical Decision Making has been and still is a practical attempt to optimize the everyday management of common surgical diseases. Many of the dilemmas apparent at the inception of the series are still present: • How to come to a consensus on best practice in diagnostic and therapeutic approaches • How to continuously update clinical expertise with an ever-expanding and dynamic basic and clinical research database • How to define and update intermediate- and long-term quality metrics • And most importantly, how to balance the art and the science of care without creating one of the popular false polarities in health care—cookbook medicine (one care template that fits all patients) versus “seat of the pants” individual

i Norton, L., Steele, G., Eiseman, B. 1978. Surgical Decision Making. W.B. Saunders Company, Philadelphia. ii Eiseman, B., Robinson, W., Steele, G. 1982. Follow-Up of the Cancer Patient. Thieme-Stratton, New York.

variation (“I do it my way because of what I was taught 35 years ago”) This sixth edition presupposes that surgeons will be the key managers of many prevalent medical problems. The present editors have added experts and expertise consistent with the immense new knowledge that contributes to better (i.e., more valuable) care for all of our patients. But these Surgical Decision Making algorithms do not substitute for judgment. The humility of Eiseman et al.’s preface to the third edition still stands: Clinicians understandably resist the idea of reducing multifactorial decisions, which are subject to variations of the patient and the provider, to simple line drawings. A cookbook approach to problem solving cannot possibly reflect the circumstances under which the surgeon exercises judgment. This book is not intended to prescribe behavior in every instance. It offers the reader an opportunity to follow the logic of an expert in selecting the best among many competing options of diagnosis and treatment. And I would argue that as the data and the complexities in diagnostics and therapeutics have expanded, the need for simplicity and default best-practice algorithms becomes even more critical as a starting point for determining a continued optimization of surgical care. As one of my former colleagues at Geisinger stated, “This is the stuff every surgical trainee should know if he or she is to pass the specialty board exams.”iii

iii

Casale, A., Paulus, R., Selna, M., Doll, M., Bothe, A., McKinley, K., Berry, S., Davis, D., Gilfillan, R., Hamory, B., Steele, G. 2007. “ProvenCareSM”: a provider-driven pay-for-performance program for acute episodic cardiac surgical care. Annals of Surgery 246 (4), 613–621.

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Chapter

1 

PREOPERATIVE LABORATORY EVALUATION Stephanie Davis, MD, and Christopher D. Raeburn, MD

A The estimated cost of preoperative testing in the United States is between $3 billion and $18 billion each year. The majority of these tests are unnecessary and do not change perioperative morbidity or mortality or necessitate a change in management. Additional testing to evaluate borderline or falsely abnormal results further increases cost and, more important, can lead to iatrogenic injury. Thus routine preoperative testing should be avoided; instead, specific preoperative laboratory evaluation should be performed to confirm or rule out medical conditions that are likely to affect a patient’s perioperative course. Laboratory testing within 6 months of the operative date is acceptable if a patient’s medical history has not changed. A thorough history and physical alone are 96% accurate in predicting a patient’s fitness for surgery. B The magnitude and risk of the operative procedure should be considered when determining the extent of preoperative evaluation. Intracranial, thoracic, intraabdominal, and suprainguinal vascular operations are higher risk procedures. Multiple studies, including two large randomized controlled trials, have shown no difference in outcome between patients who underwent routine versus no preoperative testing before low-risk ambulatory surgery. C Asymptomatic patients without any comorbid disease who can perform 4 metabolic equivalents (METS; e.g., walking, golf, yard work) and are undergoing elective procedures need no preoperative laboratory evaluation regardless of age. Abnormal preoperative laboratory values in healthy, asymptomatic patients do not predict postoperative adverse outcomes. D A basic metabolic panel (BMP) including electrolytes, glucose, blood urea nitrogen, and creatinine is useful in patients with seizure disorders because electrolyte abnormalities may lower the seizure threshold during the perioperative period and complicate antiseizure therapy. A history of stroke may indicate a cardiac condition such as atrial fibrillation or simply be a marker of systemic atherosclerotic disease; thus a complete blood count (CBC), BMP, and electrocardiogram (ECG) should be considered in those undergoing a high-risk procedure. E Patients with a known history of coronary artery disease (CAD), and those with signs/symptoms or risk factors indicative of CAD, may require further preoperative cardiac evaluation (see Chapter 2, Preoperative Cardiac Evaluation). Patients with evidence of peripheral vascular disease should be

assumed to have CAD until proven otherwise. Routine preoperative laboratory testing is not indicated unless the patient’s cardiovascular comorbidities and/or the invasiveness of the operation indicate it. F In patients with pulmonary disease and a recent change in symptoms, preoperative chest x-ray is indicated to assess for the presence of acute or progressive disease. Patients with stable disease need not undergo chest x-ray. Pulmonary function tests (PFTs) and arterial blood gases (ABGs) may be warranted in patients with significant obstructive/reactive airway disease undergoing thoracic or upper abdominal surgery but should not be done in all patients. Spirometry may be helpful in a patient with chronic obstructive pulmonary disease or asthma if, after clinical assessment, it is uncertain whether the degree of airflow obstruction has been optimally reduced. A partial pressure of arterial carbon dioxide (PaCO2) greater than 45 mm Hg is a risk factor for pulmonary complications. Risk reduction can include cessation of smoking for 8 weeks before operation, airflow reduction with bronchodilators or steroids, elimination of infection, and instruction on lung-expansion maneuvers. G CBC, liver function tests (LFTs), prothrombin time (PT), international normalized ratio (INR), and partial thromboplastin time (PTT) are indicated in patients with a history of advanced liver disease because these patients are at increased risk for perioperative infections, hemorrhage, and wound complications. It remains controversial whether diabetes mellitus is an independent risk factor for perioperative complications, unless it is poorly controlled. Thus checking the HgbA1c is reasonable if the planned surgery would be delayed to optimize glycemic control. Although mild to moderate malnutrition does not affect perioperative complications, patients with severe malnutrition may have significant anemia, electrolyte disturbances, and coagulation defects. Severely malnourished patients undergoing elective surgery may benefit from preoperative nutritional support. Serum albumin level is a very reliable indicator of increased operative risk. H Renal dysfunction predisposes to electrolyte disturbances, which increase the risk for anesthetic complications and perioperative arrhythmias. Thus assessment and normalization of preoperative electrolyte abnormalities and anemia are indicated. I

A history of hematologic disorders such as anemia, thrombocytopenia, or bleeding tendency should be investigated. Malignancy affects perioperative morbidity and warrants a search for anemia, thrombocytopenia, and coagulation abnormalities if this has not previously been completed. J

A social history is important in identifying patients with a significant history of alcohol or tobacco abuse. Identification of liver disease in patients with a significant history of alcohol abuse may permit medical optimization before elective surgery. Cessation of smoking 4 weeks before surgery significantly reduces perioperative pulmonary complications. Concern that stopping smoking only a few weeks before surgery might worsen clinical outcomes has not been found in recent studies, which show no increase in complications. Routine preoperative laboratory testing in patients with a history of alcohol or smoking use is not recommended unless there is high suspicion of disease.

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Chapter 1  ◆  Preoperative Laboratory Evaluation  2.e1

Abstract

Keywords

A thorough history and physical alone are very accurate in predicting a patient’s fitness for surgery. The majority of preoperative tests are unnecessary and do not change perioperative morbidity or mortality or necessitate a change in management. Routine preoperative testing should be avoided; instead, specific preoperative laboratory evaluation should be performed to confirm or rule out medical conditions that are likely to affect a patient’s perioperative course.

preoperative risk laboratory surgery

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Chapter 1  ◆  Preoperative Laboratory Evaluation  3

C Healthy

Operation

Central nervous sytem

D

Seizure

BMP CBC, BMP, ECG

Stroke

A

Cardiovascular

E

CBC, BMP, ECG

History and physical examination Pulmonary

Preoperative patient

Systems assessment

B Operative procedure

F

Gastrointestinal G Liver disease Diabetes mellitus Malnutrition

Renal

CBC, BMP

Hematologic/oncologic

Medications K Anticoagulants Diuretics Urologic

L For specific urologic procedures, a preoperative urinalysis may be indicated. Alternatively, if a patient is complaining of signs/symptoms that may indicate a urinary tract infection (UTI), a urinalysis should be obtained. REFERENCES

CBC, LFT, PT, INR, PTT HgbA1c CBC, BMP, Albumin ± PT, INR, PTT

H

Social history J EtOH Smoking

K A careful review of medications is important because certain medications, such as anticoagulants and diuretics, may increase the risk for perioperative morbidity. There are increasing numbers of new oral anticoagulant (NOAC) medications available, most of which do not have an accurate laboratory test to assess the degree of anticoagulation effect. Thus it is important to understand the indications for and half-life of these medications to determine whether they should be held for surgery and if so, for how long. Testing of renal function is important in determining how long NOAC medication should be stopped before surgery.

CXR ± PFTS, ABG

L

I

CBC, PT, INR, PTT LFT, PT, INR, PTT if high suspicion CXR ± PFTS, ABG if high suspicion CBC, PT, INR, PTT BMP UA

Anesthesiologists task force on preanesthesia evaluation. Anesthesiology. 2012;116(3):522–538. Benarroch-Gampel J, Sheffield KM, Duncan CB, et al. Preoperative laboratory testing in patients undergoing elective, low-risk ambulatory surgery. Ann Surg. 2012;256(3):518–528. Chung F, Yuan H, Yin L, Vairavanathan S, Wong DT. Elimination of preoperative testing in ambulatory surgery. Anesth Analg. 2009;108(2): 467–475. Czoski-Murray C, Jones M, McCabe C, et al. What is the value of routinely testing full blood count, electrolytes and urea, and pulmonary function tests before elective surgery in patients with no apparent clinical indication and in subgroups of patients with common comorbidities: a systematic review of the clinical and cost-effective literature. Health Technol Assess. 2012;16(50):1–159. Matulis J, Liu S, Mecchella J, North F, Holmes A. Choosing wisely: a quality improvement initiative to decrease unnecessary preoperative testing. BMJ Qual Improv Rep. 2017;6(1). Schein OD, Katz J, Bass EB, et al. The value of routine preoperative medical testing before cataract surgery. Study of medical testing for cataract surgery. N Engl J Med. 2000;342(3):168–175.

Apfelbaum JL, Connis RT, Nickinovich DG, et al. Practice advisory for preanesthesia evaluation: an updated report by the American Society of

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Chapter

2 

PREOPERATIVE CARDIAC EVALUATION T. Brett Reece, MD, and Joseph C. Cleveland, Jr., MD

A A careful history and physical examination, and prudent evaluation of electrocardiograms and selected laboratory tests, should be able to screen the majority of patients at risk for noncardiac surgery. Important risk factors from the history include increasing age (≥55 years), coronary artery disease (prior myocardial infarction), history of prior cardiac revascularization— either percutaneous coronary intervention or coronary artery bypass grafting, history of heart failure, and prior stroke. B Numerous risk-prediction tools exist. The Revised Cardiac Risk Index (RCRI), the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) Myocardial Infarction and Cardiac Arrest (MICA) calculator, and the American College of Surgeons NSQIP Risk Calculator are three validated risk-prediction indices. Several caveats to the universal implementation of risk calculators exist. Patients with active major clinical predictors should be stabilized before surgery (including unstable coronary syndromes such as ST-elevation myocardial infarction [STEMI], non-ST-elevation myocardial infarction [NSTEMI] or unstable angina, decompensated congestive heart failure, significant arrhythmias, and severe valvular disease). In the vast majority of cases, preoperative cardiac evaluation should not delay or change plans for the primary presenting problem. Finally, “cleared by cardiology” should never substitute for good judgment and communication among surgeon, anesthesiologist, and other treating physicians or allied health providers. C Procedural risk has evolved into a combination of surgical and patient characteristics in the current version of risk modeling. This risk has also now become binary in definition, with the two labels being low risk and elevated risk. Previous versions of risk modeling had low-, intermediate-, and high-risk categories. This has been simplified to low risk, meaning the summative risk for the patient and the procedure predicts a risk for a major adverse cardiac event (MACE) of 10, Class IIa recommendation; METS 4–10, Class IIb recommendation). F Various noninvasive tests are now available for stress evaluation. Stress testing can be from exercise, usually on a treadmill with continuous electrocardiogram (ECG) monitoring, or pharmacologic, as seen with dobutamine, dipyridamole, and adenosine. Imaging studies, including echo and radionucleotide studies (thallium, sesta-MIBI), reveal not only exercise capacity but also the presence of previous MI and extent of reversible ischemia. The choice of stressor and imaging techniques should be determined in consultation with professionals who interpret these tests and or institutional experience. G Although most would consider any abnormality on stress imaging an indication for invasive testing, one may refer to the appropriate clinical practice guidelines regarding the appropriate indication for invasive testing. In general, revascularization strategies should be based on standard indications as outlined by the American College of Cardiology/American Heart Association clinical practice guidelines for coronary revascularization. Revascularization solely to reduce risk before noncardiac surgery should not be performed. H Antiplatelet therapy arises from powerful medications that reduce the risk for thrombosis in coronary stents. Although aspirin fits into this category, the currently used medications are much more effective in preventing thrombosis with the correlated magnified risk for bleeding from intervention. Antiplatelet therapy management perioperatively depends on various characteristics, such as the urgency of the procedure, the bleeding risk for the intervention, and the type of coronary stent. Most important, if surgical delay will adversely affect patient outcome, then operation must take precedence over stopping the antiplatelet therapy. If the bleeding risk, in terms of either amount of bleeding or adverse effects of bleeding, of the procedure is low, then there may be little need for cessation of antiplatelet therapy. Given the opportunity, the antiplatelet therapy should be continued for at least 30 days with bare-metal stents or 1 year for drugeluting stents. Some patients with drug-eluting stents at low risk for thrombosis may be able to hold antiplatelet therapy. I

The optimal delay for therapy depends on the specific medication. The length of delay should be explored specifically per the medication. The most commonly discussed is clopidogrel, which should be held for a week. Other forms of anticoagulation that should be considered to increased bleeding

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Chapter 2  ◆  Preoperative Cardiac Evaluation  4.e1

Abstract

Keywords

The preoperative cardiac evaluation seeks to match patient and procedural risks. In general, only patients with elevated risk and low functional capacity need additional noninvasive imaging prior to operation. All other patient risk and procedural risk categories can proceed directly to operation.

preop evaluation

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Chapter 2  ◆  Preoperative Cardiac Evaluation  5 History / physical exam / lab Ischemic heart disease A Cerebrovascular disease Congestive heart failure D Prior PCI Low risk Prior CABG Moderate or high functional capacity

B

E

Evaluate preoperative risk

Negative study Normal

F

C Procedural risk

Elevated risk/ low functional capacity

Noninvasive study Nuclear echo

G

Positive study

risk (time for hold before at-risk surgery) are the medications for treatment of atrial fibrillation, such as Coumadin (can be reversed with fresh frozen plasma [FFP] or vitamin K), and novel oral anticoagulants like rivaroxaban (Xarelto®, hold 1–3 days), apixaban (Eliquis®, hold 1–3 days), dabigatran (Pradaxa®, hold 2–4 days), and edoxaban (Savaysa®, submitted to the U.S. Food and Drug Administration [FDA]). All of these medications are at least partially cleared by the kidneys, prolonging their clearance in patients with renal insufficiency. Despite the short half-lives, the bleeding risk from these medications within their therapeutic windows can be considerable, which amplifies the significance of the lack of reversal agent for these medications.

Coronary angiogram

1, 2 vessel CAD Left main 3-vessel CAD

H

PCI

I

O p e r a t i o n

CABG

Cardiology/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2014;64:e77–e137. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/ SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2012;60:e44–e164. Wijeysundera DN, Duncan D, Nkonde-Price C, et al. Perioperative beta blockade in noncardiac surgery: a systematic review for the 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association task force on practice guidelines. Circulation. 2014;130:2246–2264.

REFERENCES Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of

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Chapter

3 

PREOPERATIVE PULMONARY EVALUATION Jordan R. H. Hoffman, MD, MPH, and Robert A. Meguid, MD, MPH, FACS Surgery and anesthesia involve the risk for postoperative pulmonary complications (POPCs). The risk for POPCs depends on patient, anesthetic, and surgical factors. The incidence is highly variable in different studies and ranges from 2% to 40%. These differences are likely due to variability in study design, definitions, and patient population. Attributable mortality also ranges from 10% to 25%. Patients with POPC have increased intensive care unit (ICU) admission, hospital length of stay, and hospital readmission. POPCs include atelectasis, pneumonia, bronchospasm, tracheobronchitis, pleural effusion, pulmonary collapse, acute lung injury, acute respiratory distress syndrome (ARDS), prolonged mechanical ventilation, postoperative reintubation, and respiratory failure. Annual costs attributable to POPCs are $3.4 billion, with an average of $72,333 per patient. The highest cost complication is respiratory failure with tracheostomy, which averages $120,579. A A thorough history and physical examination are indicated for all patients for whom operative intervention is being considered. In addition to standard preoperative questioning, respiratory symptoms should be addressed and further investigated. Signs of underlying pulmonary disease found on the physical examination should be well documented for future reference. In a systematic literature review, the American College of Physicians identified several patient-related risk factors for postoperative pulmonary complications. These risk factors include advanced age, American Society of Anesthesiologist physical status classification (ASA class), recent history of smoking, abnormal imaging, limitations in functional status, active or recent alcohol or tobacco use, presence of major comorbid medical conditions, active cardiopulmonary disease, malnutrition defined by acute fluctuations in weight, and the presence of impaired sensorium (excluding stable chronic psychiatric or neurologic conditions). B The risk for postoperative pulmonary complications is increased by several procedural-related risk factors. Studies indicate that the surgical site, type of operation, duration of surgery, type of anesthesia used, and the possibility of an emergent operation can all lead to increased risk for pulmonary complications. The risk for pulmonary complications is thought to be highest after operations near the diaphragm, such as during noncardiac thoracic surgery or upper gastrointestinal surgery. Similarly, aortic surgery, neurosurgery, and head and neck surgery also appear to increase the risk for postoperative pulmonary complications. Other procedural-related risk factors include

longer operations and operations involving general anesthesia rather than regional anesthesia. These factors increase the risk for development of postoperative pneumonia secondary to chest wall pain or the inability to reliably ambulate in the early postoperative period. C Because surgeons have special insight into the conduct of an operation, we are uniquely situated to evaluate a patient and identify concerns that could change the proposed surgical plan. Evidence supporting the use of perioperative medical consultation is inconsistent. Several studies have indicated that medical consultation may be associated with inferior patient outcomes and suboptimal resource utilization. Consequently, the surgeon should remain at the forefront of perioperative patient care. Well-validated pulmonary-specific risk assessment tools exist to help physicians determine which patients are at highest risk for developing postoperative respiratory complications. Preoperative risk stratification allows physicians to identify which patients may benefit from further preoperative testing, additional preoperative surgical optimization, and a more thorough discussion of postoperative expectations and management. The results of a preoperative history, physical examination, review of relevant studies, and risk stratification help surgeons identify patients who fall into the categories of low, moderate, or high risk for postoperative pulmonary complications. D A patient deemed to be at low risk should not need additional pulmonary-specific testing before an operation. Low-risk variables include young patient age, normal room air oxygen saturation, no history of recent respiratory infection, elective operation, short procedural duration, and location of surgical incision. E A patient who is considered moderate or high risk after risk stratification should undergo additional pulmonaryspecific testing before proceeding with operative intervention. F In addition to obtaining a thorough history and physical examination, preoperative pulmonary testing should include laboratory studies, such as a complete blood count, serum metabolic panel, serum albumin, and a posterior-anterior (PA) and lateral chest radiograph (CXR). Serum studies may help identify a pulmonary infection in a patient with concerning symptoms and signs on history and physical examination, anemia in a patient with unexplained shortness of breath, and the presence of an underlying chronic respiratory or metabolic acid–base disorder. Serum albumin may identify patients with malnutrition, a known risk factor for postoperative pulmonary complications. PA and lateral CXR will evaluate the lung fields, chest wall, and mediastinal contour in patients with concomitant medical conditions or a history of tobacco use. Additionally, radiographs may help to refine a diagnosis of preexisting infectious, inflammatory, neoplastic, and anatomic abnormalities. The results of routine preoperative assessment will further stratify a patient into moderate or high risk. G Adjunct testing should be reserved for preoperative patients with respiratory complaints when routine investigation is unrevealing. Arterial blood gas (ABG) may identify respiratory or metabolic acid–base disorders. Cross-sectional imaging, such

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Chapter 3  ◆  Preoperative Pulmonary Evaluation  6.e1

Abstract

Keywords

Postoperative pulmonary complications are associated with poor patient outcome, prolonged hospital stay and unplanned readmission. A thorough preoperative pulmonary work-up, including a history and physical exam, as well as serum laboratory markers, and dedicated chest imaging can help delineate which patients are at higher risk for pulmonary complications. Additional consideration should be made of the type, location and duration of the planned operation. Risk stratification may help guide preoperative optimization and decrease postoperative pulmonary complications. Additionally, postoperative strategies exist to decrease postoperative pulmonary complications.

preoperative pulmonary evaluation perioperative work-up lung risk stratification

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Chapter 3  ◆  Preoperative Pulmonary Evaluation  7 as a noncontrast or intravenous (IV) contrast chest computed tomography (CT) scan, will evaluate the pulmonary parenchyma and pulmonary vasculature and provide additional definition of the chest wall or muscles of respiration. Spirometry will detect restrictive or obstructive respiratory disorders and, with the addition of diffusion capacity, can help identify impairment in the transfer of gas across the pulmonary capillary-alveolar membrane. Pulmonary function testing (PFT) should not be considered a routine part of the preoperative pulmonary workup for nonthoracic surgery. PFTs should be used sparingly to answer very specific questions regarding a patient’s lung mechanics. As such, PFT results should not be used to exclude a patient from an operation but should be viewed as part of a patient’s total clinical picture. A ventilation–perfusion (V/Q) scan may be helpful in identifying pulmonary shunting or dead space. Results of these investigations may further help to risk-stratify patients. H Moderate-risk patients fall into one of three categories: (1) no abnormalities found on preoperative laboratory studies or imaging, (2) laboratory studies or imaging abnormalities indicative of disease processes that are unlikely to increase patient risk for postoperative complications, and (3) laboratory studies or imaging abnormalities indicative of disease processes that are modifiable with preoperative optimization. The first and second categories of patients may proceed to surgery without further pulmonary-specific testing. The third category of patients will benefit from further preoperative optimization, which may help minimize the risk for postoperative pulmonary complications. I

High-risk patients have abnormal, irreversible preoperative findings placing them at prohibitive surgical risk. In the event of emergency surgery, every attempt should be made to optimize preoperative pulmonary function. In addition, aggressive postoperative measures to minimize pulmonary morbidity should be instituted early. Consideration should be given to nonoperative management in patients deemed high risk.

J

Prevention of postoperative pulmonary complications begins before a patient entering the operating room. Preoperative smoking cessation has been shown to have dramatic effects on postoperative pulmonary recovery. Patients should be encouraged to abstain from smoking before an operation. Although data are conflicting regarding the optimal length of time between smoking cessation and surgery, most clinicians agree that there is benefit to even a short duration of cigarette abstinence, such as 2 weeks before an operation. If time permits, smoking cessation should be encouraged for at least 8 weeks before surgery. Patients with stable asthma or chronic obstructive pulmonary disease (COPD) should be medically optimized. Oral glucocorticoids should be weaned to an acceptable level. Patients should be evaluated and treated for obstructive sleep apnea (OSA) before elective operations. Enrolling patients in preoperative pulmonary rehabilitation programs should be considered when an operation can be safely delayed for several months. Consideration should be given to delaying an elective operation in patients with active, or recent, upper or lower respiratory tract infections. Active respiratory tract infections can cause difficulty oxygenating or ventilating, postoperative bronchospasm, postoperative tussis leading to increased intraabdominal pressure, inability to clear secretions, superimposed bacterial pneumonia, and ARDS. Because of this, most authors agree that an elective operation should be delayed during the acute phase of a respiratory tract infection, or at least 2 weeks. Some clinicians will postpone operative intervention for greater than 2 weeks depending on the likelihood of postoperative pulmonary complications after an operation. Last, patients should be given education on the importance of minimizing postoperative pulmonary complications. Smoking cessation, medication adherence, initiation or continuation of aerobic exercise programs, and breathing exercises should all be encouraged. K For patients proceeding to operative intervention, several intraoperative interventions have been demonstrated to

Preoperative Pulmonary Evaluation

A

Patient-related risks -Age -Pulmonary symptoms -Functional and general health status -Tobacco use history -Medical comorbidities

K

D

“Low” risk

J

C Perioperative risk assessment

E

B

“Moderate” or “high” risk

Procedural risks -Surgical site -Type of operation -Duration of surgery -Type of anesthesia -Emergent procedure

Perioperative optimization -Optimize medications -Preoperative incentive spirometer use -Smoking cessation -Evaluation and treatment of OSA -Preoperative pulmonary Normal (“moderate” risk) rehabilitation -Patient education -Delay operation

H

F

Pulmonary specific testing -PA and lateral CXR -Laboratory studies

G

Proceed to surgery -Anesthetic strategy -Minimally invasive approach -Avoid or reverse neuromuscular blockade -Minimize procedure duration

M

Postoperative considerations -Early mobilization & frequent ambulation -HOB > 30° -Aspiration precautions -Adequate pain control -Incentive spirometer/flutter Consider non-operative valve use -VTE prophylaxis management

L

I

Abnormal (“high” risk)

Adjunct testing -ABG -Cross-sectional imaging -Spirometry and diffusion capacity -Ventilation/perfusion (V/Q) scan

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8  Part I  ◆  Perioperative Care decrease the risk for postoperative pulmonary complications. Minimizing the duration of an operation by choosing a less aggressive surgical approach has been shown to reduce postoperative pneumonia in moderate- to high-risk patients. Conflicting data exist regarding the use of regional versus general anesthesia and its effect on postoperative pulmonary outcomes. When feasible, a spinal, epidural, or regional anesthetic strategy should be used for high-risk surgical patients. Similarly, minimally invasive surgical options should also be considered in high-risk patients. Last, neuromuscular blockade should be used sparingly and should be completely reversed before extubation. L Consideration should be given to nonoperative management in patients deemed at high risk for developing postoperative pulmonary complications. M The immediate postoperative period is characterized by an assault on the respiratory system. After major abdominal or thoracic surgery, patients typically experience a reduction in lung volumes for several weeks to months. Inadequate postoperative pain control can cause a restrictive pattern of breathing. Splinting, in conjunction with the possibility of diaphragm dysfunction, particularly after noncardiac thoracic surgery, increases patient risk for atelectasis, aspiration, and pneumonia. This risk is compounded by postoperative opioid use, which depresses respiratory drive. Strategies to increase patient lung volumes and respiratory drive will attenuate much of the possibility for postoperative pulmonary morbidity. Measures aimed at minimizing aspiration and pneumonia, including elevation of the head of the bed (HOB) to at least 30 degrees above horizontal, early mobilization and frequent ambulation, and avoidance of the use of nasogastric tubes, should be instituted. A routine and progressively more frequent ambulation schedule should be instituted and emphasized by everyone on the multidisciplinary care team. The benefit of incentive spirometer use in the postoperative period is debated. However, an incentive spirometer for deep breathing should be provided to all postoperative patients. Counseling on the importance of accurate use and frequency should be provided and reinforced daily. Adjuncts to narcotic pain control should be provided to minimize respiratory depression while maintaining an adequate level of pain control to prevent respiratory splinting. These adjuncts include scheduled nonopioid pain medications, placement of ice and local anesthetic–infused patches over the operative site, centrally acting gamma-aminobutyric acid (GABA) analogs, and liberal use of local anesthetic injection before, during, and after an operation. Last, early prophylactic subcutaneous anticoagulation in conjunction with intermittent lower-extremity compression minimizes the risk for venous thromboembolic (VTE) disease. Mounting

evidence suggests continuing prophylactic anticoagulation beyond the primary hospitalization for further VTE risk reduction in select populations.

CONCLUSIONS Successful care of the surgical patient is a rewarding endeavor and begins weeks to months before any operative intervention is undertaken. The surgeon is ideally suited to address all aspects of perioperative medical and surgical care. Given the nature of our long-term commitment to a patient considering an operation, surgeons will remain at the helm when a patient is being prepared for an operation. REFERENCES American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Obstructive Sleep Apnea. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: an updated report by the American Society of Anesthesiologists task force on perioperative management of patients with obstructive sleep apnea. Anesthesiology. 2014;120(2):268–286. Auerbach AD, et al. Opportunity missed: medical consultation, resource use, and quality of care of patients undergoing major surgery. Arch Intern Med. 2007;167(21):2338–2344. Bergqvist D, et al. Duration of prophylaxis against venous thromboembolism with enoxaparin after surgery for cancer. N Engl J Med. 2002;346(13): 975. Bilimoria KY, et al. Development and evaluation of the universal ACS NSQIP surgical risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surg. 2013;217:833–842. Brooks-Brunn JA. Predictors of postoperative pulmonary complications following abdominal surgery. Chest. 1997;111(3):564. Canet J, et al. Prediction of postoperative pulmonary complications in a population-based surgical cohort. Anesthesiology. 2010;113(6):1338–1350. Grosse-Sundrup M, et al. Intermediate acting non-depolarizing neuromuscular blocking agents and risk of postoperative respiratory complications: prospective propensity score matched cohort study. BMJ. 2012;345(6329). Hausman MS, et al. Regional versus general anesthesia in surgical patients with chronic obstructive pulmonary disease: does avoiding general anesthesia reduce the risk of postoperative complications? Anesth Analg. 2015;12(6):1405. Mastracci TM, et al. Effect of preoperative smoking cessation interventions on postoperative complications. J Am Coll Surg. 2011;212(6):1094. Meguid RA, et al. Surgical risk preoperative assessment system (SURPAS): III. Preoperative prediction of adverse outcomes with eight predictor variables. Annals Surg. 2016;264(1):23–31. Qaseem A, et al. Risk assessment for and strategies to reduce perioperative pulmonary complications for patients undergoing noncardiothoracic surgery: a guideline from the American College of Physicians. Ann Intern Med. 2006;144(8):575. Rodgers A, et al. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials. BMJ. 2000;321(7525):1493. Smetana GW, et al. Preoperative pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Intern Med. 2006;144(8):581. Wijeysundera DN, et al. Outcomes and processes of care related to preoperative medical consultation. Arch Intern Med. 2010;170(15):1365.

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Chapter

4 

BLEEDING DISORDERS IN SURGICAL PATIENTS Jason M. Samuels, MD, Hunter Burroughs Moore, MD, PhD, and Ernest E. Moore, MD

A The first step to identifying potential bleeding abnormalities is a thorough history and physical examination. Patients who report prior episodes of significant bleeding after surgical, endoscopic, or dental procedures are likely to have underlying coagulation abnormalities. A history of easy bruising, petechia, gingival bleeding, epistaxis, hemarthrosis, and heavy menstrual flow in women also suggests an underlying bleeding disorder. Similarly, patients with a family history of hospitalizations secondary to life-threatening bleeding should arouse concern. Chronic renal and liver disease, malnutrition, leukemia, and autoimmune disorders are risk factors for surgical bleeding. Finally, the patient’s prescribed medications, specifically, any oral anticoagulant or antiplatelet therapy, should be reviewed, and the most recent time of ingestion is critical. However, the most important step in a patient with a potential bleeding disorder is to determine if the patient is actively bleeding and needs an immediate intervention. Mechanical control of major bleeding is a priority, and waiting for coagulation results before taking the patient for definitive care will not benefit the patient. In this clinical scenario of a massive transfusion, the blood bank needs to be alerted, and early blood-based product resuscitation is needed. Conversely, preemptive transfusions in a hemodynamically stable patient with a presumed coagulation abnormality can be lethal. The decision to transfuse blood products into a patient in preparation for the operating room should be goal directed, with a laboratorybased assay with a defined threshold for each blood product administered that is coordinated with the timing of the operative intervention. B A complete blood count (CBC) provides a gross measurement of the patient’s circulating cellular components that contribute to coagulation. A normal CBC in a patient suspected to have ongoing bleeding does not rule out active bleeding and requires serial monitoring if there is a high clinical suspicion. The same is true for a low hemoglobin, which can suggest occult internal hemorrhage, chronic anemia resulting from an underlying disease, or potential bone marrow failure. Platelet counts provide a crude measurement of coagulation function. There is an increased risk for bleeding as platelet counts decrease below 100,000. However, it is not until patients reach a critical threshold of less than 20,000 that they are at risk for spontaneous bleeding. Also, a normal platelet count does not rule out platelet dysfunction. Conversely, in certain disease states, such as cirrhosis, an adaptive response to low platelet counts by the coagulation system develops, and the patient can be paradoxically hypercoagulable despite the abnormally low platelet count. It is also important

to take into consideration that the patient’s hematocrit can affect platelet function. The optimal hematocrit for platelets to function is 30%. This occurs through margination, a process in which the red blood cells push platelets to the periphery of vessels. C The prothrombin time (PT), more commonly referred to as the international normalized ratio (INR), and activated partial thromboplastin time (PTT) are often used as first-line screening for bleeding risk. The PT was originally designed to measure the effects of warfarin or detect liver disease and the PTT to identify hemophilia A/B. However, these plasma-based assays reflect circulating levels of clotting factors in the extrinsic and intrinsic clotting pathways and thus do not represent the physiology of hemostasis in accordance with the now accepted cell-based concept of clotting. Consequently, changes in INR and PTT are relatively nonspecific when applied beyond the measurement of hereditary coagulation abnormalities and medically induced anticoagulation. D Fibrinogen plays a critical role in hemostasis because it is the precursor to fibrin, which binds platelets. Fibrinogen is an acute-phase reactant, and levels are generally preserved even with liver failure. Low levels of fibrinogen are a result of massive blood loss, consumption, dilution, hyperfibrinolysis, or sustained metabolic acidosis. A fibrinogen level, measured by the Clauss assay, of less than 150 mg/dL is usually the threshold for treating active bleeding. Viscoelastic assays also have specific tests that can measure fibrinogen activity (TEG functional fibrinogen and ROTEM FIBTEM). Fibrinogen deficiency in the United States is treated with cryoprecipitate, whereas in Europe, a recombinant fibrinogen product is available. E D-Dimers are a clinical assay to measure degradation products of fibrinolysis. Although an elevated level of D-dimer is concerning for overactivation of the fibrinolytic system (hyperfibrinolysis), this is a nonspecific finding. Any tissue injury related to operative interventions will elevate levels. As a result, they hold limited utility in the postoperative surgical patient. However, in certain circumstances, such as obstetrics and septic patients in the intensive care unit, a rising D-dimer level with concurrent fibrinogen depletion is concerning for disseminated intravascular coagulation, warranting further work-up. The treatment for this pathology is to treat the underlying cause and not give an antifibrinolytic. F Thromboelastography (TEG) or rotational thromboelastometry (ROTEM) are gaining prominence in the assessment of surgical bleeding because these devices reflect the individual components of the cell-based concept of hemostasis. Current indications primarily involve the assessment of abnormalities in the clotting cascade during active blood product replacement for significant bleeding. Measurements provided by TEG can guide ongoing transfusion needs. Specifically, an elevated activated clotting time (ACT > 128 secs) indicates the need for coagulation factors, and thus FFP should be administered. If the angle of the TEG tracing is decreased (48 hours), malignancy, major trauma, and hormone replacement. Malignancies most often associated with hypercoagulability in order of prevalence are lung (17%), pancreas (10%), colorectal (8%), renal (8%), and prostate (7%). Hormone replacement includes the use of oral contraceptives, hormonal replacement therapy (HRT), and testosterone supplementation. E Heparin-induced thrombotic thrombocytopenia (HITT) is another provoked cause of hypercoagulability in patients with recent heparin exposure who possess antibodies against complexes of platelet factor 4 (PF4) and heparin. It may affect

arterial and venous thromboses equally, particularly in vascular and cardiac surgery populations. The associated thrombotic risk is highest in patients with higher levels of PF4-heparin antibodies, drop in platelet count of more than 70%, or both. Although patients can develop HITT after treatment with low-molecularweight heparin, the incidence is much higher in those treated with unfractionated heparin. F Diagnosis of an inherited thrombophilia is often made after presentation with an unprovoked VTE, and rarely with arterial thrombosis. Common inherited hypercoagulable states include factor V Leiden gene mutation, prothrombin G20210A mutation, protein C and S deficiency, antithrombin deficiency, and antiphospholipid syndrome (APS). Factor V Leiden gene mutation is the most inherited thrombophilia and results in resistance to activated protein C. It is diagnosed either by genetic testing to identify the mutation or by functional activated protein C assays. The second most common inherited thrombophilia, prothrombin G20210A mutation results in increased circulating prothrombin levels and is diagnosed by genetic testing (in the presence or absence of anticoagulation). Proteins C and S are vitamin K–dependent anticoagulants, and their deficiency is confirmed by laboratory testing demonstrating decreased levels (50% or less of normal) and free protein S antigen. A functional assay is used to test for antithrombin deficiency; however, this should not be done at the time of initial diagnosis because there may be a transient reduction of antithrombin levels, leading to misinterpretation. APS occurs as either a primary condition or in the setting of another inherited rheumatologic disease, most commonly systemic lupus erythematosus. Diagnosis is made with immunoassays testing for antibodies to cardiolipin and lupus anticoagulant along with dilute Russell viper venom test. G Clinical suspicion for HITT should be raised in patients with recent exposure to heparin with an absolute platelet count of ≤150,000 mm3 or with a relative decrease ≥50% from baseline. The 4 T’s score can be used to estimate HITT likelihood and assesses the degree of thrombocytopenia, timing relative to heparin exposure, presence of a thrombotic event, and other causes of thrombocytopenia. The diagnosis is confirmed with laboratory testing for heparin-dependent antibodies utilizing serologic or functional assays or both. H HITT management should be initiated before laboratory confirmation in those patients felt to have an intermediate or high risk based on their 4 T’s score. Treatment includes removal of all sources of heparin and initiation of anticoagulation with either direct thrombin inhibitors (bivalirudin or argatroban) or factor Xa inhibition (fondaparinux). Warfarin therapy should not be used initially because there is an increased incidence of warfarin-induced skin necrosis in HITT patients; however, once appropriate anticoagulation is reached with another agent and platelet counts have risen above 150,000 mm3, patients can transition to warfarin for continued long-term anticoagulation. I

The gold standard therapy for a newly diagnosed VTE is continuous heparin infusion while transitioning to oral warfarin therapy, a vitamin K antagonist. Warfarin dosage should be titrated to obtain an international normalized ratio (INR) of 2.0 to 3.0. More novel oral anticoagulants include dabigatran, a direct thrombin inhibitor, and direct factor Xa inhibitors such as rivaroxaban and apixaban.

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Chapter 5  ◆  Hypercoagulable Patient  14.e1

Abstract

Keywords

Hypercoagulable patients most commonly present with a new diagnosis of venous thromboembolism (VTE). Virchow’s triad of stasis, vascular injury, and hypercoagulability are the classic risk factors associated with VTE. Patients are further stratified into provoked and inherited hypercoagulable states, with many patients overlapping into both cohorts. Venous duplex ultrasound is the gold standard for VTE diagnosis, and anticoagulation should be initiated in the absence of any contraindications. For patients with provoked VTE, treatment should be continued for 3 months, whereas those with unprovoked DVT or symptomatic pulmonary embolus should be treated for 6 months. Indefinite anticoagulation should be considered in patients with provoked DVT where the underlying risk factor has not been resolved, patients with an unprovoked symptomatic pulmonary embolus, patients with active malignancy with low to moderate bleeding risk, and patients with high-risk inherited thrombophilias. The Vienna Prediction Model can also be used to estimate recurrence risk when establishing an anticoagulation strategy.

hypercoagulable state venous thromboembolism pulmonary embolus thrombophilia heparin-induced thrombotic thrombocytopenia

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Chapter 5  ◆  Hypercoagulable Patient  15 History/physical exam Risk factors - Wells score

D Provoked

I Anticoagulation

Malignancy

A

Symptoms/exam

Recent major surgery Prolonged immobility Major trauma Hormone replacement

B E

Hypercoagulable patient

Heparin-induced thrombotic Thrombocytopenia (HITT)

F Imaging/labs

C

CBC Chemistries Coagulation profile D-dimer ABG EKG Lower extremity duplex U/S CT angiogram chest

J

Inherited

G

H

Diagnosis

Treatment

J Duration of treatment - Vienna calculator

Factor V Leiden Prothrombin 20210A Protein C/S deficiency

Anticoagulation

Antithrombin deficiency Antiphospholipid syndrome

After diagnosis of acute VTE, anticoagulation should be maintained for a minimum of 3 months in all patients. In patients with a provoked VTE in which the prominent risk factor or factors have been removed, cessation of therapy can occur after 3 months. Patients with provoked VTE with persistent risk factors (prolonged immobility, active malignancy, etc.) may benefit from treatment for 6 months; furthermore, those with unprovoked VTE should also be treated for 6 months. In any patient undergoing treatment for more than 3 months, the risk for bleeding versus the risk for recurrence should be considered. Evidence suggests that a normal D-dimer level after 3 months of anticoagulation is associated with decreased recurrence risk; however, it is not recommended to routinely check D-dimer levels to determine the need for continued anticoagulation because of its low specificity. Indefinite anticoagulation beyond 6 months is recommended for patients with unprovoked symptomatic PE, recurrent unprovoked VTE, active malignancy with low to moderate bleeding risk, and patients with high-risk inherited thrombophilias: protein C or S deficiency, antithrombin deficiency, homozygous factor V Leiden mutation, and homozygous

prothrombin gene mutations. Of note, heterozygous factor V Leiden is not felt to be an indication for indefinite anticoagulation. An additional resource for determining the duration of anticoagulation after an initial unprovoked VTE is the Vienna Prediction Model. This model uses a nomogram based on patient gender, location of the initial VTE, and D-dimer levels. Based on point values for each component, the risk for recurrence at 1 and 5 years is determined. The clinician can then use this risk for recurrence to determine the need for continued anticoagulation. REFERENCES Arepally GM, Ortel TL. Heparin-induced thrombocytopenia. N Engl J Med. 2006;355:809–817. Eichinger S, Heinze G, Jandeck LM, Kyrle PA. Risk assessment of recurrence in patients with unprovoked deep vein thrombosis or pulmonary embolism: the Vienna Prediction Model. Circulation. 2010;121:1630–1636. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guidelines and expert panel report. Chest. 2016;149(2):315–352. Stevens SM, Ansell JE. Thrombophilic evaluation in patients with acute pulmonary embolism. Semin Respir Crit Care Med. 2017;38:107–120.

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Chapter

6 

POSTOPERATIVE FEVER David J. Ciesla, MD, and Thomas J. Herron, MD A A careful history and physical examination should direct the radiographic and laboratory work-up in the postoperative period. Close attention should be paid to the pulmonary examination, prosthetic catheters, all surgical wounds, and the extremities. The surgical wound classification and the time elapsed from surgery are important determinants in the probability of the wound being the source of the infectious causes. The incidence of postoperative fever ranges from 15% to 47%. Two temperatures greater than 38.5 °C within a 24-hour period constitute a postoperative fever. Although there are both infectious and noninfectious causes, the presence of a postop fever may herald a serious complication. B Additional diagnostic work-up, including laboratory evaluations of blood, urine, and pulmonary and wound fluids should be guided by the physical examination findings. C Infectious causes in the postoperative period include surgical site infection, pneumonia, urinary tract infection, and intravascular catheter–associated infections. D Most fevers in the early postoperative period are caused by inflammation and resolve spontaneously. Fever is activated by circulating pyrogens. Exogenous pyrogens can directly cause fevers (i.e., endotoxin [lipopolysaccharide]) or stimulate the release of cytokines (TNF alpha, IL-6, IL1beta, INF-alpha, MIP-1) from mononuclear phagocytes. Systemic levels of IL-6 correlate with a postoperative increase in body temperature from baseline. IL-6 is also influenced by the duration and invasiveness of the procedure. Noninfectious causes in the early postoperative period include inflammation from the trauma of surgery, nonhemolytic febrile transfusion reactions (FNHTRs), and drug fevers. FNHTRs are seen 1 to 6 hr post transfusion, and it is important to rule out an acute hemolytic reaction. Antibiotics (i.e., beta-lactam and sulfonamide) account for one-third of drug fevers. Atelectasis is often cited as a noninfectious cause of fever, but its occurrence is felt to be coincidental. E Surgical site infections are classified as incisional or organ/ space. Superficial (skin/soft tissue) and deep (soft tissue/ fascia) incisional are diagnosed by appearance on physical examination. Organ/space surgical site infections are diagnosed with diagnostic imaging, which is most useful 5 to 7 days postoperative when most routine postsurgical fluid collections have resolved. F Critically ill patients in the surgical intensive care unit (ICU) are at risk for infections and may not mount a febrile response given comorbidities and therapy. They are at increased

risk for infection given time on the mechanical ventilator, central venous lines, and indwelling urinary catheters. The frequent use of antibiotics in the ICU puts these patients at risk for multidrugresistant organism infections. The diagnosis of occult sepsis may require additional radiographic evaluation by abdominal ultrasound, computed tomography, or hepatobiliary iminodiacetic acid scan. G The lower genitourinary tract infection is the most common postoperative infectious cause of fever. Female and obese patients are at the highest risk. Bacturia is present in 5% of patients with indwelling catheters and increases at a rate of 3% to 8%/catheter day. Clinical history has a high predictive value in uncomplicated cystitis. A urinalysis should be obtained before a urine culture. A negative result is a strong predictor of a negative urine culture and excludes a urinary tract infection. A positive urine culture is defined as >105 organisms. H Hospital-acquired pneumonia and ventilator-associated pneumonia can be diagnosed clinically or by a bacteriological diagnosis. Quantitative cultures should be drawn before starting antibiotic therapy and tailored to cover organisms based on the patient’s risk for carrying multidrug-resistant organisms. I

Bacteremia in the postoperative patient is not common, with a reported incidence of up to 3%. When present, it carries a 20% to 35% mortality rate and up to 60% mortality rate for ICU patients. Blood culture is the standard diagnostic test but can have a low yield in the first 72 hours after surgery. J

A temperature exceeding 39.4 °C in the early (hours to first few days) postoperative period requires immediate evaluation of the patient. All surgical dressings should be removed to interrogate for evidence of a necrotizing soft tissue infection (NSTI). The diagnosis is typically clinical and requires prompt surgical intervention.

REFERENCES American Thoracic Society; Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005;171:388–416. Aubuchon JP, Dzik WS. Reports on clinical transfusion medicine in the early days of transfusion. Transfusion. 2010;50:963–967. Badillo AT, Sarani B, Evans SR. Optimizing the use of blood cultures in the febrile postoperative patient. J Am Coll Surg. 2002;194(4):477–487. Engoren M. Lack of association between atelectasis and fever. Chest. 1995;107:81–84. Frank SM, Kluger MJ, Kunkel SL. Elevated thermostatic set point in postoperative patients. Anesthesiology. 2000;93:1426–1431. Garibaldi RA, Brodine S, Matsumiya S, Coleman M. Evidence for the non-infectious etiology of early postoperative fever. Infect Control. 1985;6(7):273–277. Lesnikov VA, Efermov OM, Korneava EA, Van Damme J, Billiau A. Fever produced by intrahypothalamic injection of interleukin-1 and interleukin-6. Cytokine. 1991;3:195–198. Mackowiak PA. Drug fever: mechanisms, maxims and misconceptions. Am J Med Sci. 1987;294(4):275–286. Stovall RT, Haenal JB, Jenkins TC, et al. A negative urinalysis rules out catheter-associated urinary tract infection in trauma patients in the intensive care unit. J Am Coll Surg. 2013;217(1):162–166. Ustin JS, Malangoni MA. Necrotizing soft-tissue infections. Crit Care Med. 2011;39(9).

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Chapter 6  ◆  Postoperative Fever  16.e1

Abstract

Keywords

Fever is common after surgery. Although often a normal physiologic response to tissue injury, it can also be a sign of more serious causes that require prompt treatment. The presence of a postoperative fever triggers a workup that directed at identifying a source so that appropriate therapy is selected.

Post-operative Fever Infection Surgical site infection Bacteremia

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Chapter 6  ◆  Postoperative Fever  17

E

A History & physical examination: Postoperative day Wound classification Pulmonary Surgical wound Extremities Intravascular catheters

Surgical site infection

F C Infectious

Surgical critical care: CAUTI CLABSI VAP Acalculous cholecystitis

G Urinary tract infection

Temperature > 38.5 °C

H Pneumonia Labs & radiographic imaging: CBC Urinalysis +/− urine culture Blood cultures Chest X-ray Computed tomography

B

D

I Bacteremia

Noninfectious: Inflammatory response from surgery Febrile, nonhemolytic transfusion reaction Medication/drug fever

J

Necrotizing soft tissue infection

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Chapter

7 

BRIDGE ANTICOAGULATION Lisa Ferrigno, MD, MPH

A For elective procedures, a full history and physical should be performed, including ascertaining which anticoagulant (AC) the patient is taking and the indication for its use. Until recently, vitamin K antagonists (VKAs) were the mainstay of maintenance AC agents. Warfarin is the only VKA available for use in the United States. Direct-acting oral anticoagulants (DOACs) have been increasing in use and will likely continue to do so, especially given their preference in recent AC guidelines. If appropriate to restart the agent based on periprocedural bleeding risk and stable renal and/or hepatic function (depending on mode of clearance), they may be restarted without any bridge given their rapidity of onset. DOACs currently are not recommended for use for mechanical heart valves and should not be considered as a replacement therapy for this indication for VKA or heparin. Current published literature regarding bridging strategies for those on AC do not address interventions performed in urgent or emergent circumstances; therefore extrapolation to those clinical situations should be undertaken with caution, especially because the need for the use of reversal agents for AC in those circumstances may alter subsequent thrombotic potential. B Ascertain whether the patient has an ongoing need for AC, ideally in conjunction with the patient’s primary care provider. If the patient no longer needs AC, it should be stopped in a time period sufficient for the patient to have no increased bleeding risk at the time of the elective procedure. C Relevant labs should be assessed. These include at least baseline prothrombin time (PT)/international normalized ratio (INR) for those on a VKA to ascertain the degree of anticoagulation and duration of time needed for the INR to drift to the desired level before the procedure. Guidelines are clear that cessation of AC in a time frame to allow for normalization is much preferable to the aggressive use of reversal products or agents. If bridging is recommended, this should also be performed with an agent whose duration of action is sufficiently short so as to be ceased just far enough ahead of the procedure that the patient has the shortest time possible without AC. Baseline creatinine is appropriate for those on DOACs that are renally cleared and to assess the suitability of low-molecularweight heparin (LMWH) as a bridge, if indicated. D Assess risk for bleeding associated with the procedure. For procedures that carry a low risk for bleeding, consideration for the continuation of AC should be done. Low-risk procedures are generally considered to be dental and dermatologic procedures and endoscopy and procedures performed via cardiac catheterization.

Some targeted studies have yielded results in this area supporting continuation of AC throughout the procedure. For example, the BRUISE CONTROL trial demonstrated that allowing the INR to drift below 3 before pacemaker or defibrillator placement was associated with fewer bleeding events than the interruption of warfarin and a heparin bridge. Usually, violation of a major body cavity, the axial skeleton, or long bones; peripheral arterial surgery; tissue or organ biopsy; or procedures lasting >1 hour are considered “major” and risk for bleeding significantly higher. Ultimately, bleeding risk assessment for a given procedure is best left to the discretion of the proceduralist. When discussing a bridge to AC, consideration is usually for the use of heparin until which time an oral agent (usually a VKA, given previously noted considerations) becomes therapeutic. To Err Is Human, published by the Institute of Medicine, underscored that medication errors are the most frequent category of inpatient preventable medical errors, and of those, heparin has consistently been one of the top offenders. Mortality rates associated with bleeding events are about 10%, approximately the same or more than a pulmonary embolism. In 2015, the BRIDGE trial was published, a noninferiority trial assessing the use of AC bridging in atrial fibrillation (afib) patients. With more than 1800 subjects, the study demonstrated noninferiority of nonbridging compared with bridging in the perioperative period with respect to thromboembolic (TE) events (three events in each group), whereas rates of major and minor bleeding were significantly higher in the bridged group (major: 3.2% vs. 1.3%; minor 20.9% vs. 12%). Retrospective analyses evaluating perioperative bridging strategies have yielded similar results in the realms of deep venous thrombosis (DVT) and mechanical heart valves. E Thromboembolic (TE) risk will vary based on the indication for AC. Broadly, indications for AC are venous thromboembolic event (VTE), specifically DVT or pulmonary embolism (PE); nonvalvular afib; or mechanical heart valve (MHV). Risk stratification should be performed for each indication, as follows: • VTE/PE: Patients may be categorized as high, moderate, or low risk based on time since the initial event, underlying thrombophilic disorders, and other comorbid conditions. Recent publications suggest that the risks for low- and moderate-risk groups are sufficiently similar that they may be approached in the same fashion and do not necessitate bridging. • Nonvalvular afib: Risk stratification is best performed utilizing the CHA2DS2-VASc score into low-, moderate-, and high-risk groups for TE events. The acronym encompasses variables found to be predictive of stroke risk, and a score is designated in a weighted fashion: Congestive heart failure, Hypertension, Age ≥75 (for 2 points), Diabetes, prior Stroke or transient ischemic attack (TIA) (for 2 points), Vascular disease, Age 65 to 74, and Sex Category. The “2017 Expert Consensus Decision Pathway for Periprocedural Management of Anticoagulation in Patients With Nonvalvular Atrial Fibrillation” notes a CHA2DS2VASc score of 7 to 9 as high risk. • MHV: Considerations include valve location (aortic, mitral, other), type of mechanical valve, and whether other concomitant risk factors exist. The stakes for mechanical

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Chapter 7  ◆  Bridge Anticoagulation  18.e1

Abstract

Keywords

This chapter covers periprocedural anticoagulation bridging.

anticoagulation bridging periprocedural

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Chapter 7  ◆  Bridge Anticoagulation  19 valve thrombosis are sufficiently high that interruptions in AC have dogmatically been avoided. A recent review demonstrated high rates of major bleeding episodes for any bridging strategy (19%). Only two TE events occurred, both of which were preceded by a bleeding event necessitating reversal of bridging AC. F High risk for TE event: High-risk patients are underrepresented in the available literature on bridging. In a recent retrospective analysis specifically evaluating bridging in patients with a history of DVT or PE, there were no thromboembolic rates in the high-risk category, whether they were bridged or not; however, the numbers of patients in this high-risk category were exceedingly low. Ideally, elective procedures would be deferred until the patient reaches a lower risk threshold with respect to time from the acute event. For others who will carry lifelong high risk, a balanced decision weighing risk versus benefit should be performed, and the patient observed closely for bleeding events, should bridging be performed. Those at high risk for TE event should likely be bridged, including the following: • VTE • Acute VTE within past 3 months; or • Severe thrombophilia (deficiency of protein C, protein S, or antithrombin; antiphospholipid antibody syndrome; or multiple abnormalities) • Afib: Those at high risk for stroke or systemic embolism (>10% per year) with • CHA2DS2-VASc score of 7 to 9; or • Recent (within 3 months) ischemic stroke, transient ischemic attack (TIA), or embolic event

A

• MHV • Mitral valve replacement (MVR); or • Aortic valve replacement (AVR) and any TE risk factor: afib/flutter; left ventricular ejection fraction (LVEF) < 35%; severe mitral stenosis (MS); hypercoagulable disorder; left atrial dilation > 50 mm; prior TE; spontaneous contrast in heart on ECHO; or • Older-generation AVR G Moderate-risk individuals vary as to whether they should be bridged or not, as follows: • VTE/PE: Those with moderate risk do not require bridging. • Acute VTE within past 3 to 12 months; or • Nonsevere thrombophilia (heterozygous factor V Leiden, prothrombin 20210 mutation, increased factor VIII activity); or • Recurrent VTE; or • Active cancer • Afib • CHA2DS2-VASc score of 5 to 6; or • Prior history of embolic ischemic stroke, TIA, or systemic embolism (>3 months previously): • High bleed risk: No bridge • Lower bleed risk: Strategy determined based on whether there is a history of prior TE event: • Prior TE event: Likely bridge • No TE event: Bridging not advised • MHV: Bridge recommended • MVR; or • AVR and any TE risk factor: afib/flutter; LVEF < 35%; severe multiple sclerosis (MS); hypercoagulable disorder;

No longer indicated

H&P: - Indication - Agent

DC

F

Yes bridge

High High

E

B Is AC indicated?

Yes

Assess TE risk

D Assess periprocedural bleeding risk

Yes bridge

Valve

G Atrial fibrillation

Moderate

Prior TE event

Moderate NO prior TE event

C

H Low Low

No bridge No bridge

VTE Labs: - PT/INR - GFR

Yes bridge

No bridge Consider no interruption

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20  Part I  ◆  Perioperative Care left atrial (LA) dilation > 50 mm; prior TE; spontaneous contrast in heart on ECHO; or • Older-generation AVR H Low-risk individuals do not require a bridge. • VTE • Acute VTE > 12 months previously and no other risk factors • Afib • CHA2DS2-VASc score ≤ 4 or and no prior history of ischemic stroke, TIA, or other embolic event • MHV • AVR and no other TE risk factor REFERENCES Birnie DH, Healey JS, Wells GA, et al. Pacemaker or defibrillator surgery without interruption of anticoagulation. N Engl J Med. 2013;368(22): 2084–2093. Clark NP, Witt DM, Davies LE, et al. Bleeding, recurrent venous thromboembolism, and mortality risks during warfarin interruption for invasive procedures. JAMA Intern Med. 2015;175(7):1163–1168.

Doherty JU, Gluckman TJ, Hucker WJ, et al. 2017 ACC expert consensus decision pathway for periprocedural management of anticoagulation in patients with nonvalvular atrial fibrillation: a report of the American College of Cardiology clinical expert consensus document task force. J Am Coll Cardiol. 2017;69(7):871–898. Douketis JD, Spyropoulos AC, Kaatz S, et al. Perioperative bridging anticoagulation in patients with atrial fibrillation. N Engl J Med. 2015;373(9):823–833. Douketis JD, Spyropoulos AC, Spencer FA, et al. Perioperative management of antithrombotic therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl): e326S–350S. Hart EA, Jansen R, Meijs TA, et al. Anticoagulant bridging in left-sided mechanical heart valve patients. Int J Cardiol. 2017;232:121–126. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest. 2016;149(2): 315–352. Kohn LT, Corrigan J, Donaldson MS. To Err Is Human: Building a Safer Health System. Washington, D.C.: National Academies Press; 2000. Lip GY, Halperin JL. Improving stroke risk stratification in atrial fibrillation. Am J Med. 2010;123(6):484–488.

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Chapter

8 

INTRAABDOMINAL INFECTION Taryn Hassinger, MD, and Robert G. Sawyer, MD

A Intraabdominal infections (IAIs) are a common problem in surgical patients, and they have a broad range of severity and myriad causes. IAIs affect all ages of patients, including both the healthy and chronically ill. Appendicitis alone afflicts nearly 300,000 patients per year, with significant resulting health-care expenditures. Additionally, IAI is the second leading cause of infectious mortality in intensive care units. Uncomplicated infections involve intramural inflammation of the gastrointestinal tract, whereas complicated IAIs involve infection extending beyond the originating organ and into the peritoneal space, resulting in peritonitis or abscess formation. Presenting symptoms are varied because of the wide range of potential etiologies, but IAI should be suspected in patients with abdominal pain and gastrointestinal dysfunction with or without fever and leukocytosis. Careful history and physical examination should identify those patients requiring further work-up and management. B Laboratory evaluation of patients suspected to have IAI should include a complete blood count and metabolic panel, with further testing—such as liver function tests, total bilirubin, amylase, and lipase—dictated by individual patient presentation. Blood cultures may also be appropriate depending on the patient’s clinical condition and history. C If after physical examination the patient is deemed to exhibit signs of generalized peritonitis, the patient should undergo intravenous fluid resuscitation with the initiation of broadspectrum antibiotics and other medical measures to establish hemodynamic stability. These measures should be rapidly followed by surgical intervention for diagnosis and source control. If there is doubt regarding the diagnosis, often flat and upright plain films of the abdomen and a chest x-ray will be obtained to assess for free intraperitoneal air. D If no signs of generalized peritonitis are present, the patient should undergo intravenous fluid resuscitation. Imaging should be performed to further evaluate the source of suspected IAI. Ultrasonography is preferred for suspected infections of the gallbladder and biliary tree. Otherwise, computed tomography is the most sensitive and specific imaging modality to diagnose IAI. Under special circumstances (e.g., pregnancy), magnetic resonance imaging (MRI) of the abdomen may be used. E After establishing the diagnosis of IAI in the nonperitoneal patient, empiric antimicrobial medications should be started while awaiting procedures to establish source control. Choice of

initial antimicrobials should be based on the location of the source of the IAI and the presence of systemic signs of infection, although coverage will generally include activity against gramnegative, gram-positive, and anaerobic pathogens. Infections originating from the stomach, proximal small bowel, and the biliary tree contain predominantly gram-positive and gramnegative aerobic organisms, whereas IAIs involving the distal small bowel typically include more gram-negative aerobic and facultative bacteria. Infections stemming from the colon involve anaerobes along with high numbers of streptococci, enterococci, and Escherichia coli. Risk factors for multidrug-resistant causative organisms, specifically, recent exposure to the health-care system, and patient-related factors such as immunosuppression, active malignancy, and advanced age, should also be taken into consideration when choosing empiric therapy. F Source control is critical to the management of IAI. For hemodynamically stable patients on appropriate antimicrobial therapy, source-control interventions may be delayed up to 24 hours; however, patients with procedures delayed over 24 hours are at increased risk for treatment failure. Many modalities are available to achieve source control, and the appropriate intervention should be determined by individual patient and infection characteristics. When possible, percutaneous interventions to drain abscesses and fluid collections are preferable. Surgical intervention is likely necessary to control ongoing peritoneal contamination in the presence of perforated viscus via diversion or resection to restore anatomic continuity and physiologic function. Re-laparotomy should be planned only for concerns regarding adequate initial source control, loss of domain so as to prevent definitive abdominal closure, and ongoing bowel ischemia necessitating a second-look operation. For certain IAIs, such as multiple small abscesses or intraabdominal phlegmon, a noninterventional approach is acceptable. G Source-control procedures allow for the collection of specimens for microbiologic analysis. These results can provide guidance regarding the broadening or narrowing of antimicrobial coverage, particularly in patients with risk factors for multidrug-resistant causative organisms. Specimens collected before the administration of antimicrobials are most reliable; however, this is not feasible for many patients with IAI. In the case of specimen collection after initiation of antimicrobial treatment, the earliest specimens are most meaningful. The narrowing of coverage is necessary to decrease the drug resistance. After obtaining definitive source control, patients should generally receive 4 days of antimicrobial therapy. H Treatment failure should be suspected in patients who fail to improve clinically after source control and initiation of appropriate antimicrobial therapy. Reimaging with computed tomography and possible repeat percutaneous or open intervention should be considered in patients who fail to improve at 72 to 96 hours after initial source control. Decisions regarding changes in antimicrobial therapy for treatment failure are complicated and should involve culture results. Given an appropriate spectrum of therapy, however, treatment failure is rarely a result of inadequate antimicrobial treatment. Rather, treatment failure is more likely attributable to inadequate source control, and this should be assessed with repeat imaging as previously discussed.

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Chapter 8  ◆  Intraabdominal Infection  22.e1

Abstract

Keywords

Intraabdominal infections (IAIs) are a common problem in surgical patients, and they have a broad range of severity and myriad causes. IAIs affect patients of all ages, including both the healthy and chronically ill. The presentation is quite varied given its numerous possible etiologies, but IAI should be suspected in patients with abdominal pain and gastrointestinal dysfunction with or without fever and leukocytosis. Patients should first undergo thorough history and physical examination along with laboratory evaluation in an attempt to determine the diagnosis and underlying etiology. All patients with IAIs should receive intravenous fluid resuscitation and any other medical measures required to establish hemodynamic stability. Those patients deemed to have generalized peritonitis should have empiric intravenous antibiotics started, followed by immediate operative source control. Patients without localized pain/peritonitis should undergo imaging evaluation, followed by operative or percutaneous procedures to establish source control. Antibiotics for this population may be started before or after source control is obtained, depending on the patient’s clinical condition and any predicted delays in intervention. Culture results can be used to broaden or narrow antimicrobial coverage, and this is particularly important in patients with risk factors for multidrug-resistant pathogens. Generally, antimicrobial therapy should be continued for 4 days after acquiring definitive source control. Treatment failure should be suspected in patients who fail to clinically improve 72 to 96 hours after source control and initiation of appropriate antimicrobial therapy. Reimaging with repeat sourcecontrol procedure(s) should be considered in these patients because a true treatment failure is more likely attributable to inadequate source control rather than inadequate antimicrobial treatment.

intraabdominal infection peritonitis empiric antimicrobial therapy source control treatment failure

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Chapter 8  ◆  Intraabdominal Infection  23

A History and physical exam Recent surgery/hospitalization Immunosuppression Vital signs changes (fever/hypothermia, hypotension, tachycardia) Altered mental status

C

Generalized peritonitis

+/− Abdominal plain film IV Fluid IV Antibiotics OR for laparotomy or laparoscopy Culture source

G Operative source control

Treat 4 days with source control Adjust antibiotics per cultures

Complaints of abdominal pain Nausea and vomiting with Physical exam dietary intolerance Signs/symptoms of infection

F

D Localized pain/peritonitis

B Laboratory evaluation CBC, metabolic panel LFTs/Tbili Amylase/lipase +/− Blood cultures

REFERENCES Akinci D, Akhan O, Ozmen MN, et al. Percutaneous drainage of 300 intraperitoneal abscesses with long-term follow up. Cardiovasc Intervent Radiol. 2005;28:744–750. Augustin P, Kermarrec N, Muller-Serieys C, et al. Risk factors for multidrug resistant bacteria and optimization of empirical antibiotic therapy in postoperative peritonitis. Crit Care. 2010;14:R20. Blot S, De Waele JJ. Critical issues in the clinical management of complicated intra-abdominal infections. Drugs. 2005;65:1611–1620. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41:580–637.

E IV fluids CT/US/MRI +/− Antibiotics

Percutaneous/ operative source control Culture source Antibiotics

H Treatment failure: recurrent signs/symptoms Stop antibiotics at 4 days Repeat imaging Re-establish source control

Marshall JC, Maier RV, Jimenez M, et  al. Source control in the management of severe sepsis and septic shock: an evidence-based review. Crit Care Med. 2004;32:S513–S526. Mazuski JE, Tessier JM, May AK, et al. The Surgical Infection Society revised guidelines on the management of intra-abdominal infection. Surg Infect (Larchmt). 2017;18:1–76. Sawyer RG, Claridge JA, Nathans AB, et al. Trial of short-course antimicrobial therapy for intraabdominal infection. N Engl J Med. 2015;372:1996–2005.

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Chapter

9 

PREOPERATIVE EVALUATION OF THE GERIATRIC PATIENT Douglas M. Overbey, MD, and Thomas N. Robinson, MD

A

 

GERIATRIC PATIENTS

Older adults have decreased physiologic reserves compared with their younger adult counterparts, a fact that leads to a greater likelihood of developing postoperative complications, functional decline, and death. Geriatric patients’ lack of physiologic reserves to withstand health-care stressors is termed frailty. The comprehensive geriatric assessment is an established clinical assessment targeted at quantifying the well-being of older adults and can identify frail older patients. Chronologic age can be a poor estimate of overall physiologic status but is still used to define the geriatric population. Screening for high-risk geriatric patients is recommended after age 70, and after age 80 frailty often becomes the dominant driver of morbidity rather than preoperative multimorbidity. B

 

ESTABLISHING ADVANCE DIRECTIVES

The older adult’s decision-making capacity must be assessed before obtaining surgical consent and documented in the medical record. In the case of an appointed health-care representative (medical proxy), the individual should be clearly documented in the medical record. Advance directives such as a living will should be reviewed preoperatively, with the discussion focused on the treatment goals and specific risks of the procedure. Potentially life-threatening problems should be discussed, including an approach consistent with the patient’s values and healthcare goals. Do not resuscitate (DNR) orders should be specifically discussed, with emphasis on the perioperative period. C

 

PREOPERATIVE HIGH-RISK SCREENING

Identifying older adults at high risk for postoperative complications and death is important. There are two major components of surgical risk: extrinsic risk (e.g., the extent of the operation), and intrinsic risk (e.g., frailty and comorbidities). In general, healthy older adults undergoing low-risk operations do not require extensive preoperative assessment because their risk for major morbidity and mortality is low. In contrast, frail or comorbid older adults considering a major operation are the population at greatest risk for major morbidity and mortality. These patients should undergo more extensive preoperative evaluation to help reduce the likelihood of adverse postoperative events and to ensure patient-centered surgical decision making. Frailty is defined as reduced a physiologic reserve that leads to the limited capacity of a patient to withstand a health-care stressor. Frailty is driven by age-related biological declines, and the presence of frailty is directly related to increased mortality, postoperative complications, and non-home discharge. Physiologic declines occur in muscle, nutrition, and energy metabolism,

leading to the development of a frail state. The most common clinical approach to quantifying frailty is to measure the characteristics of a frail individual (e.g., impaired cognition, functional dependence, poor mobility, malnutrition, social isolation, and depression). Older adults with multiple abnormal frailty characteristics are determined to be frail. Another strategy to define the frail older adult commonly used in geriatric research is a frailty tool that assesses for weight loss, weakened grip strength, slow mobility, exhaustion, and low activity levels. Cognition describes mental, or brain, function and can be thought of as the ability to think. Older adults can develop impaired cognition, which can be classified clinically as mild cognitive impairment and dementia. Cognition is important to screen in the geriatric assessment. Poor baseline cognition is well recognized to be associated with adverse postoperative events and is one clinical symptom that could help to define the physiologically vulnerable older adult. Screening tools for impaired cognition include the Mini-Cog Test and the Mini-Mental Status Exam. Comorbidities should also be considered. Multimorbidity is the co-occurrence of two or more chronic diseases in the same individual. A higher number of chronic diseases is generally associated with an increased operative risk and is frequently captured by indices such as the Charlson Score or the Cumulative Illness Rating Scale. Medical optimization of individual diseases can mitigate this risk and is an integral part of the preoperative needs assessment. The most common comorbid condition assessed preoperatively is coronary artery disease. The American Heart Association has a well-known guideline statement on the preoperative assessment of heart disease for noncardiac operations. D

 

PATIENT-CENTERED OPERATIVE DECISION MAKING

The older adult’s “patient-centered” health goals specific to the current condition must be considered and should drive the majority of care decisions. These goals can include “living as long as possible,” “living independently,” “remaining comfortable,” and “establishing a diagnosis,” among others. These goals should then be fit with the purpose of the surgical procedure to determine the need for surgery and optimal timing. This should happen before the procedural consent process. E

 

TAILORING OF SURGICAL RECOMMENDATIONS

The decision to undergo an operation results from a conversation between a patient and the provider that the risks versus benefits of the planned operation are in the best interest of the patient. The expected prognosis of the patient with and without the planned procedure should be discussed. If the goals of the patient are found to be inconsistent with the planned operation, tailoring of the surgical recommendations should be considered to better fit any planned health-care intervention with the patient’s desires. Palliative operations are defined as interventions aimed to alleviate pain or other symptoms rather than to address the underlying disease process. Palliative operations should be considered if the curative operation is not feasible or carries an unacceptably high risk for major complication or death. F

 

PREOPERATIVE OPTIMIZATION

The overall goal of effective preoperative assessments is to ensure the surgical course of action best fits within the patient’s desires

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Chapter 9  ◆  Preoperative Evaluation of the Geriatric Patient  24.e1

Abstract

Keywords

This chapter covers the preoperative evaluation of the geriatric surgical patient.

geriatrics gerontology elderly frailty assessment advanced age

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Chapter 9  ◆  Preoperative Evaluation of the Geriatric Patient  25 Revisit need or timing of operation

History Cognition Functional status Social isolation Depression Exhaustion Activity level Co-morbidity

C Intrinsic pre-operative assessment:

B A Geriatric patient presents for elective surgery (>70 years)

High risk patient

1. Frailty 2. Cognitive assessment 3. Co-morbidities

Required in all older adults:

D Patient and/or surgery is high risk

Low risk patient

1. Advance directives 2. DNR status 3. Surrogate decision maker

Patientcentered operative decision making

Operation not consistent with goals Operation aligns with patient values and preferences

E

Optimization High risk surgery Extrinsic pre-operative assessment: Complex or major operation?

Weight loss Grip strength Mobility Malnutrition

REFERENCES

Anticipate additional discharge needs

Low risk surgery

and that all efforts are taken toward maximizing the chance of a successful outcome. The latter is focused on increasing an individual’s physiologic reserve to make it through the planned operative stress without major complication or death. This concept is known as preoperative optimization and can involve preoperative physical therapy, nutritional supplements, cardiopulmonary therapy, medication reconciliation, disease optimization, and anxiety reduction. The term prehabilitation refers to exercise training before an operation with the goal of improving postoperative outcomes.

F

1. Medication review 2. Nutrition 3. Smoking cessation 4. Glycemic control 5. Incentive spirometry

Patient and surgery are low risk

Proceed to OR

Kim S, Brooks AK, Groban L. Preoperative assessment of the older surgical patient: honing in on geriatric syndromes. Clin Interv Aging. 2014;16:13–27. Mohanty S, Rosenthal RA, Russell MM, et al. Optimal perioperative management of the geriatric patient: a best practices guideline from the American College of Surgeons NSQIP and the American Geriatrics Society. J Am Coll Surg. 2016;222:930–947. Partridge JS, Harari D, Martin FC, Dhesi JK. The impact of pre-operative comprehensive geriatric assessment on postoperative outcomes in older patients undergoing scheduled surgery: a systematic review. Anaesthesia. 2014;69(suppl 1):8–16. Robinson TN, Walston JD, Brummel NE, et al. Frailty for surgeons: review of a National Institute on Aging conference on frailty for specialists. J Am Coll Surg. 2015;221:1083–1092.

Hubbard RE, Story DA. Patient frailty: the elephant in the operating room. Anaesthesia. 2014;69(suppl 1):26–34.

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Chapter

10 

CARDIOPULMONARY RESUSCITATION David A. Fullerton, MD

G If the rhythm is not shockable, the patient is most likely asystolic or has experienced an arrest with pulseless electrical activity (PEA arrest). H If the rhythm is shockable, charge the AED and continue CPR until it is charged. Be sure that no responders are touching the patient (tell the responders to “clear”), and then shock the patient. I

If the patient has experienced a PEA arrest, the etiology may be suggested by the QRS complex.

J A Unresponsive patient. Attempt to arouse the patient by shouting and jostling the patient. Call for help or otherwise activate the “code” system. Feel the patient’s neck for up to 10 seconds to determine whether the patient has a pulse. B If a carotid pulse is palpable, assure that the patient is breathing and has a patent airway. If the patient is not breathing, provide ventilation by mouth-to-mouth or mouthto-mask ventilation. Provide 1 breath every 5 to 6 seconds. Each time a breath is to be administered, examine the oral pharynx for a foreign body. However, do not perform a “blind sweep” of the oral pharynx. If the patient does not resume spontaneous ventilations, endotracheal intubation will be required. Establish vascular access. C If the patient does not have a palpable pulse, initiate quality cardiopulmonary resuscitation (CPR). If the patient is in bed, place a backboard behind his or her chest when it is available. Perform chest compressions at a rate of 100 to 120 per minute. Compress the chest to a depth of at least 2 inches, and allow the chest to recoil between compressions. Administer 30 chest compressions and then 2 breaths. Repeat until help arrives. Administer breaths sufficient to raise the patient’s chest, but do not attempt to blow in excessively large tidal volumes. Establish vascular access. Administer epinephrine (1 mg intravenous [IV]) every 3 to 5 minutes during resuscitation. Vasopressin (40 units IV) may be given instead of the first or second dose of epinephrine. Administer amiodarone (first dose 300 mg IV, a possible second dose should be 150 mg IV). D If the patient is hypotensive, administer intravenous normal saline. Initiate an infusion of vasopressin (0.04 units/minute) or epinephrine (0.05 mcg/kg/min). E When an automated external defibrillator (AED) arrives, first, turn it on. Then, place the pads on the skin of the patient’s bare chest. If the patient’s chest is wet, quickly dry it. If the patient has a large amount of chest hair, have it quickly shaved where the pads will be attached. Place one pad over the anterior surface of the right chest in the subclavicular area. Place the other over the anterolateral left chest in the mid- to anterior axillary line at the level of the nipple. F When the AED is ready to interpret the patient’s cardiac rhythm, hold CPR and do not touch the patient. A rhythm that requires an immediate shock will typically be ventricular fibrillation; pulseless ventricular tachycardia; or a pulseless, very rapid supraventricular rhythm.

If the cardiac rhythm is asystole, administer intravenous atropine (0.5 mg IV, may repeat every 3 minutes to a maximum dosage of 3 mg). Begin transcutaneous cardiac pacing via the AED pads. If this mechanism of pacing is not successful, place a transvenous pacing lead into the right ventricle, typically via the right internal jugular vein. K If the QRS complex is narrow, the differential diagnosis includes mechanical causes of hemodynamic collapse. These include tension pneumothorax, pericardial tamponade, and pulmonary embolism. Tension pneumothorax may be suggested by the absence of breath sounds on one side. If this diagnosis is suspected, carefully decompress the respective chest with a needle in the midclavicular line in the second interspace. An ultrasound or echocardiogram may diagnose cardiac tamponade via the demonstration of a pericardial effusion. If so, pericardiocentesis should be performed. Similarly, an ultrasound or echocardiogram may suggest pulmonary embolism if the right ventricle is dilated and the left ventricle is underfilled. If found, consideration of pulmonary embolectomy should be given. L If the QRS complex is wide, the etiology may be from hyperkalemia or sodium channel blocker (antidysrhythmic drugs). In either case, administer calcium chloride (1 mg IV). The differential diagnosis also includes an agonal cardiac rhythm or late-stage, severe cardiac failure. M Immediately resume CPR for 2 minutes or until the patient is responsive. At the end of 2 minutes of CPR, determine if the patient has return of a pulse (return of sustainable circulation [ROSC]). N If there is a pulse, hold chest compression and initiate supportive measures. These will typically include infusion of intravenous normal saline, mechanical ventilation, and infusion of inotropic (epinephrine 0.05 mcg/kg/min) and/or vasoactive (vasopressin 0.04 unit/min) agents. O If there is no pulse, resume CPR. Interrogate the cardiac rhythm after 2 minutes, and shock if the rhythm is shockable. Administer epinephrine (1 mg IV) every 3 to 5 minutes during resuscitation. REFERENCES American Heart Association website for cardiopulmonary resuscitation. www.cpr.heart.org. Chan PS, Drein SL, Tang F, et al. Resuscitation practices associated with survival after in-hospital cardiac arrest: a nationwide survey. JAMA Cardiol. 2016;1:189–197.

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Chapter 10  ◆  Cardiopulmonary Resuscitation  28.e1

Abstract

Keywords

Responders caring for a patient in cardiopulmonary arrest must immediately initiate resuscitative measures. The outcome may be dependent upon prompt recognition of the situation and implementation of the contemporary guidelines of the American Heart Association. This algorithm summarizes those guidelines. Responders to the unresponsive patient should first determine if the patient has a pulse. If so, the focus should be on securing the patient’s airway and maintaining the patient’s blood pressure. But if the patient does not have a pulse, responders should call for help and initiate cardiopulmonary resuscitation (CPR). Once the available equipment has arrived, the patient’s cardiac rhythm should be interrogated and cardioversion performed if indicated. Cardiopulmonary resuscitation, chemical resuscitation and cardioversion should be administered and possibly repeated as outlined in this chapter.

Cardioversion Asystole PEA Arrest CPR Shockable Rhythm

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Chapter 10  ◆  Cardiopulmonary Resuscitation  29

B Has a pulse

A

D Maintain patent airway

Hypotension?

Patient

F E

No pulse

C

CPR

Shockable rhythm?

Epinephrine/ vasopressin IV fluid

Yes

Yes

No Shockable rhythm?

CPR

Shock

CPR

H G

J No

Yes

No

M N

O

ROSC?

Yes?

Support

Atropine pacer

Asystole? No

K Narrow QRS

PEA arrest

I

Giotra S, Nallamothu BK, Spertus JA, et al. American Heart Association get with the guidelines-resuscitation investigators. Trends in survival after in-hospital cardiac arrest. N Engl J Med. 2012;367:1912–1920. Harrison DA, Patel K, Nixon E, et al. National cardiac arrest audit. Development and validation of risk models to predict outcomes following in-hospital cardiac arrest attended by a hospital-based resuscitation team. Resuscitation. 2014;85:993–1000. Koplan BA, Stevensen WG. Ventricular tachycardia and sudden cardiac death. Mayo Clin Proc. 2009;84:289–297. Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, lidocaine, or placebo in out-of-hospital cardiac arrest. N Engl J Med. 2016;374:1711–1722. Nichols G, Leroux B, Wang H, et al. ROC investigators. Trial of continuous or interrupted chest compressions during CPR. N Engl J Med. 2015;373: 2203–2214.

Wide QRS

Consider: • Tension pneumothorax • Cardiac tamponade • Pulmonary embolism Calcium chloride

L

Nolan JP. Cardiac arrest and cardiopulmonary resuscitation. Semin Neurol. 2017;37:5–12. Nolan JP, Hazinski MF, Aickin R, et al. Part 1: executive summary: 2015 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendation. Circulation. 2015;132(suppl 1):S2–S39. Robinson EJ, Smith GB, Power GS, et al. A risk-adjusted survival for adults following in-hospital cardiac arrest by day of week and time of day: observational cohort study. BMJ Qual Saf. 2016;25:832–841.

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Chapter

11 

PERIOPERATIVE ARRHYTHMIA Jason C. Brainard, MD, and Michael Patz, MD

A

 

HISTORY AND PHYSICAL

In the preoperative phase, a complete history and physical should be used to assess perioperative risk. A comprehensive discussion regarding the preoperative cardiac evaluation and prediction for major adverse cardiac events (MACEs) should be considered in parallel with perioperative arrhythmia risk assessment. It is important to note that hemodynamically stable arrhythmias are often not defined as MACEs in the literature, but they are still associated with a substantial increase in morbidity and mortality. Here we review the basic approach to assessing cardiac risk and highlight some additional elements independently relevant to the risk for postoperative arrhythmias. High-risk cardiac conditions warranting further evaluation and treatment preceding surgery include acute coronary syndrome, symptomatic or decompensated heart failure, significant valvular heart disease, and hemodynamically significant arrhythmia. Symptoms of syncope, palpitations, angina, or coronary artery disease or the presence of a new heart murmur on recent examinations should also prompt further inquiry. The history should be accompanied by a complete review of systems and a validated risk-calculating tool, such as the Revised Cardiac Risk Index (RCRI), the Gupta Perioperative Cardiac Risk Calculator, or the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) Myocardial Infarction and Cardiac Arrest (MICA) calculator, to estimate risk for MACE. Additional history relates to the risk for developing postoperative atrial fibrillation (POAF), the most common postoperative arrhythmia. Various patient factors are associated with increased risk for POAF. These include older age, male gender, smoking, American Society of Anesthesiologists (ASA) class 3 or 4, stroke, diabetes, hyperthyroid, alcohol abuse, hypertension, congestive heart failure, chronic obstructive pulmonary disease, obstructive sleep apnea, ischemic heart disease, structural or valvular heart disease, and preexisting atrial fibrillation (AF) or history of paroxysmal AF. Additionally, common preoperative electrocardiogram (EKG) findings such as premature atrial complexes, left anterior fascicular block, and left ventricular hypertrophy are each associated with an increased risk for POAF. Surgical factors are additionally relevant, with abdominal and vascular operations having a higher incidence of POAF compared with other nonthoracic, noncardiac procedures and thoracic and cardiac surgery having a significantly higher incidence than general surgery. Although a validated quantitative POAF risk-calculating tool is not yet available, attention to these risk factors can be used as a rough guide to preoperative risk stratification.

B

 

PREOPERATIVE EVALUATION AND TESTING

Supplemental preoperative diagnostic testing is not routinely indicated and should be ordered on a case-by-case basis. Generally, there are no dedicated studies thought to be helpful for a low-risk patient undergoing low-risk surgery. An ECG is reasonable to obtain for patients who are at >1% risk for MACE, for example, a patient with a history of one or more RCRI risk factors (history of chronic kidney disease [CKD], insulin-dependent diabetes, congestive heart failure, coronary artery disease, or cerebrovascular accident) or any patient undergoing high-risk surgery. For selected patients, a preoperative basic metabolic panel is helpful so that preoperative electrolyte abnormalities can be corrected. Hypocalcemia, hypomagnesemia, and hypo- and hyperkalemia are the most common electrolyte imbalances associated with cardiac arrhythmias. This should be considered for patients with a history of chronic kidney disease or acute kidney injury and may also be useful for any patient on diuretic therapy. Any patient with a high calculated MACE risk is at risk for perioperative arrhythmias; however, the occurrence of hemodynamically stable supraventricular tachycardias (including atrial fibrillation and atrial flutter) is not considered in calculating formal MACE risk. The additional risk factors defined in step A apply to the risk for POAF and warrant independent consideration because the occurrence of POAF is independently associated with a significant increase in morbidity and mortality. Additionally, this risk should be considered in combination with the patient’s stroke risk predicted by the CHADS2 (congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke [double weight]) or CHA2DS2-VASc (vascular disease, peripheral arterial disease, previous myocardial infarction [MI], aortic atheroma; female gender is also included) score to determine the level and duration of monitoring indicated. Beta-blocker therapy has been extensively studied, with the goal of preventing MACE. Although not specific for development of perioperative arrhythmias, current recommendations from the American College of Cardiology and American Heart Association are to continue perioperative beta blockers in those patients on chronic therapy. Beta blockade should not be started on the day of surgery. Similar recommendations for alpha-2 agonists (clonidine) and calcium channel blockers are reasonable, but not enough evidence is available to make a recommendation for management. C

 

CARDIOVASCULAR IMPLANTABLE ELECTRONIC DEVICE (CIED)

The intraoperative challenge in managing patients with CIEDs (pacemakers and implantable cardioverter-defibrillators [ICDs]) is the potential for interaction between the CIED and electromagnetic interference (EMI). The EMI source is usually monopolar electrocautery; however, EMI can be induced by multiple sources, including electroconvulsive therapy, radiofrequency ablation, lithotripsy, and even bipolar cautery. EMI may cause transient inhibition of pacing in pacemaker-dependent patients and inappropriate triggering of shocks and induced ventricular arrhythmias in patients with ICDs. Much less common with today’s devices is the potential for more permanent damage to the CIED, such as electrical reset, inadvertent reprogramming, or hardware malfunction. Before any nonemergency operation, the surgical and anesthesia teams should understand the type of device (pacemaker,

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Chapter 11  ◆  Perioperative Arrhythmia  30.e1

Abstract

Keywords

Perioperative arrhythmias are common in clinical practice and directly associated with increased risk for postoperative morbidity and mortality. Elucidating a history of arrhythmias, preoperative evaluation and risk modification, and postoperative management are critical to reducing this risk. New to the chapter in this edition is a discussion of cardiovascular implantable electronic devices (CIEDs). Specific knowledge about assessment and programming of these devices is essential to providing the best patient care.

cardiovascular implantable electronic devices pacemaker defibrillator atrial fibrillation arrhythmia major adverse cardiac event

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Chapter 11  ◆  Perioperative Arrhythmia  31 ICD, both), the function of the CIED, the response of the CIED to magnet application, and the patient’s underlying cardiac rhythm. When possible, outpatient preoperative evaluation should include the development of a CIED prescription for perioperative device management. If not completed as an outpatient or if device interrogation or reprogramming is required, preoperative evaluation on the day of surgery should include consultation with an electrophysiology (EP) team in collaboration with the anesthesia team in planning for intraoperative and postoperative care of the CIED. It is important to note that the EP team will need to know the device manufacturer to complete bedside interrogation. For pacemakers, planning can involve reprogramming from a synchronous to an asynchronous pacing mode; placing a magnet over the device, inducing temporary asynchronous pacing; temporarily disabling anti-tachycardia therapies; or nothing at all. Tachytherapy can usually be deactivated by applying a magnet over an ICD, but if the device also functions as a pacemaker, the magnet usually will not change the pacer mode. Hence for pacemaker-dependent patients who also have an ICD, the device needs to be reprogrammed before the operation. Preoperative reprogramming in these instances includes temporary deactivation of the tachytherapy and often changing the pacer to an asynchronous mode. Careful coordination and communication with the EP and anesthesia teams are required to ensure the device is reset to baseline settings after the operative procedure. It is important for both the anesthesia and the surgical teams to recognize that any patient undergoing temporary inactivation of ICD tachytherapy is at very high risk for ventricular dysrhythmias. These patients should certainly remain on cardiac monitoring continuously, with external defibrillation equipment readily available, until the device is reprogrammed to the initial settings. Systems should be in place to ensure this sequence is followed because delayed ICD reactivation has resulted in at least several fatalities.

A

History and Physical

PMH: HF, VHD, Arrhythmia, MI, CVA, DM, CKD, COPD, OSA, Old Age, ETOH Abuse Symptoms: SOB, DOE, PND,CP, Palpitations. Signs: Rales, S3, JVD, Peripheral Edema

Intraoperatively, the electrocautery pad should be placed so that the CIED is not in the path between the electrocautery tool and the grounding pad. In some cases, use of a bipolar or an ultrasonic (harmonic) scalpel can minimize the adverse effects on the CIED and leads. Radiofrequency ablation also carries an increased risk for interference with the CIED. Complete guidelines for perioperative care of CIEDs is available in a practice advisory report from the American Society of Anesthesiologists. D   TACHYARRHYTHMIAS

In any patient who develops a tachyarrhythmia, the first step should be an assessment of hemodynamic stability. As described in the advanced cardiac life support (ACLS) guidelines, signs of hypoperfusion, including angina, acute heart failure, hypotension, or altered mentation, direct therapy to the unstable pathway. Although patients with hemodynamically unstable tachyarrhythmias are all managed similarly with electrical cardioversion, the management of a hemodynamically stable patient depends on the specific rhythm. To define the rhythm, the first step is to distinguish the QRS complex as wide or narrow. When the rhythm appears to be a sustained wide-complex tachyarrhythmia, further management should usually include expert cardiology consultation when available. If the QRS complex is wide, the rhythm is either a ventricular tachycardia (VT) or a supraventricular tachycardia (SVT) with aberrancy (i.e., bundle branch block). The QRS complex may change at the onset of the rhythm, but a QRS complex that continues to appear polymorphic is suspicious for torsades de pointes. If suspected, torsades should be treated immediately with magnesium and possible rapid pacing to prevent degeneration to ventricular fibrillation (VF). If the rhythm is clearly SVT with aberrancy, the patient can be managed as a narrow-complex tachyarrhythmia. However, when there is any doubt, the patient should be managed as if the rhythm is VT. Further work-up should include evaluation of ventricular function with echocardiography and ruling out myocardial infarction.

Stable SBP>90 Well Perfused

Tachyarrhythmias Unstable SBP48 hours after admission that may or may not require mechanical ventilation. A community-acquired pneumonia (CAP) is a pneumonia that was present at the patient’s initial presentation. These distinctions may provide clues as to the likely microbial pathogen. C Clinicians can use both invasive and noninvasive techniques to obtain microbiological sampling data to help guide clinical decision making. Invasive techniques include bronchoscopy with bronchoalveolar lavage (BAL) and mini-BAL. Noninvasive techniques include sampling of endotracheal tube aspirate. Guidelines published in 2016 by the Infectious Diseases Society of America and the American Thoracic Society for the diagnosis and management of VAP recommend using noninvasive semiquantitative culture results over invasive quantitative techniques. The Clinical Pulmonary Infection Score (CPIS) and biomarkers such as procalcitonin, soluble Triggering Receptor Expressed on Myeloid (TREM)-1, and C-reactive protein (CRP) can be used to aid in the diagnosis and management of VAP. However, because of suboptimal sensitivities and specificities, the 2016 guidelines recommend against using biomarkers and/or the CPIS score alone to guide clinical decision making. D Ventilator-associated tracheobronchitis (VAT) should not be treated with antibiotic therapy. Unlike VAP, VAT is not associated with radiographic evidence of nosocomial pneumonia, despite fever (without other identifiable cause), new or increased

sputum production, and/or endotracheal aspirate positive for new bacteria. When considering antibiotic therapy for VAT, the risk for developing antibiotic resistance, side effects and drug cost associated with antibiotics, and the development of Clostridium difficile colitis must be weighed against the possibility of decreased duration of mechanical ventilation, which has not been irrefutably demonstrated in the small studies that have been completed. E Empiric antibiotic decisions should be guided by the development and utilization of an institution-specific and, ideally, unit-specific antibiogram. • Patients with suspected VAP should be started on a broadspectrum antibiotic regimen that includes coverage for Staphylococcus aureus, Pseudomonas aeruginosa, and other gram-negative bacilli. Determine the risk for multidrugresistant pathogens such as methicillin-resistant S. aureus (MRSA). • Regimens that include coverage for MRSA should be used in patients with risk factors for MRSA, which include the following: • Prior intravenous antibiotic use within the previous 90 days • Septic shock at the time of VAP • Acute respiratory distress syndrome (ARDS) preceding VAP • >5 days of hospitalization before VAP diagnosis • Patients treated in units where >10% to 20% of S. aureus isolates are methicillin resistant, or where the prevalence of MRSA is not known • Vancomycin or linezolid should be used for empiric coverage of MRSA when indicated. • If empiric coverage of MRSA is not indicated, empiric regimens should include piperacillin–tazobactam, cefepime, levofloxacin, imipenem, or meropenem to achieve adequate coverage of both Pseudomonas and methicillin-sensitive S. aureus (MSSA). • Empiric regimens including two antipseudomonal antibiotics from different classes should be considered for patients with the following risk factors: • Prior intravenous antibiotic use within the previous 90 days • Septic shock at the time of VAP • ARDS preceding VAP • >5 days of hospitalization before VAP diagnosis • Patients treated in units where >10% of gram-negative isolates are resistant to the agent being considered for monotherapy • Aminoglycosides and colistin should be avoided if adequate alternative antipseudomonal antibiotics are available. • Empiric regimens including two antipseudomonal antibiotics from different classes are recommended for patients with the following risk factors: • >History of structural lung disease (i.e., bronchiectasis or cystic fibrosis) • Antimicrobial dosing should be optimized to achieve target pharmacokinetic and pharmacodynamic parameters. F Definitive antibiotic selection for VAP and duration of therapy: Antimicrobial therapy should be narrowed as soon

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Chapter 16  ◆  Ventilator-Associated Pneumonia   48.e1

Abstract

Keywords

Ventilator-associated pneumonia remains a diagnosis that should be considered in critically ill ventilated patients with fever, increased sputum production, decreased oxygenation, and an infiltrate on radiography. An assessment should be made for risk factors associated with multidrug-resistant (MDR) pathogens, and broad-spectrum antibiotics should be initiated, then targeted/ deescalated at 72 hours. Antimicrobials should generally be continued for 7 days.

ventilator-associated pneumonia (VAP) pneumonia antibiotics

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Chapter 16  ◆  Ventilator-Associated Pneumonia   49

History + physical exam findings • Fever • Dyspnea, tachypnea • Increase/change in respiratory secretions • Change in breath sounds

C

A

Invasive sampling • BAL • Mini-BAL

Initiate empiric antibiotics

B Ventilator-associated pneumonia

Onset of symptoms >=48 hours after initiation of mechanical ventilation

E

F

Noninvasive sampling • ET aspirate Use of biomarkers or CPIS score

Labs-CBC, ABG • Leukocytosis/ leukopenia • Hypoxemia Radiographic findings • CXR/CT with new infiltrate +/– worsening effusion

• Assess risk of MDR pathogens (MRSA, Pseudomonas) • Know local microbes

Consider another reason for PNA (HAP, CAP)

Onset of symptoms 2/3 of nutritional needs by mouth. Interruptions in intake because of repeated procedures, operations, sedation, and NPO status should be considered. E When the oral route is unavailable for nutritional support, enteral nutrition is preferred because it is more cost-effective and associated with less risk than parenteral nutrition. Enteral nutrition offers better substrate utilization and maintains gut mucosal integrity and immunocompetence. Recent literature supports its use in pancreatitis. Concurrent parenteral and enteral nutrition is an option in patients with extraordinary demands (e.g., burns) or mild gastrointestinal (GI) intolerance. F Parenteral nutrition is useful when the GI tract is totally nonfunctional. It may also be employed when decreased splanchnic perfusion is suspected (e.g., when high-dose alphaagonists or pressors are used).

G The stomach is accessed by blind nasal or oral intubation. Gastric feedings are suited for stable, nonventilated patients with normal gastric motility who are at low risk for aspiration. The risk for pulmonary aspiration decreases from stomach to duodenum to jejunum. Gastric residuals and abdominal distention should be checked initially every 4 hours and then every 8 hours. An acceptable residual volume is 200 >18 0.1 gm/kg body weight 0.0-0.8

2.8-3.2 180-200 15-18 8-10 g

2.5-2.8 150-180 10-15 10-12 g

92% Spontaneous ventilation mode asap

Perform daily spontaneous awakening and breathing trials (SAT/SBT): Ventilator Rx FiO2 < 0.5 Pplat < 30 PaCO2 40-50 Optimal PEEP by compliance

B

Acute Respiratory Failure

Mechanical Rx ET tube position? Pneumothorax or hydrothorax? Atelectasis or consolidation? Systemic Rx Avoid or treat fluid overload Optimize VO2 and DO2 Hemoglobin > 7 g/dL Treat sepsis Treat underlying conditions

CBC Metabolic panel ABG Cultures CXR

Hemodynamic Rx Optimize perfusion Assess cardiac function (Echo) Assess volume status (Echo, IVC)

Criteria for failure of a SBT: (a) RR > 35 for ≥ 5 min (b) SpO2 < 90% for ≥ 30 seconds (c) HR > 140 or increase/decrease of 20% from baseline (d) SBP > 180 mm Hg or < 90 mm Hg (e) Sustained evidence of respiratory distress (f) Cardiac instability or dysrhythmias (g) Arterial pH ≤ 7.32 SBT Fail: Resume Step #1 Rx

Mechanical Rx No issues noted or adequately treated

Systemic Rx Adequate cardiac function and perfusion I/O and weight stable Sepsis treated Other organ dysfunction or failure treated or managed

SBT Pass: Consider extubation, assess following: (a) does not require suctioning more than Q 4 hours (b) good spontaneous cough (c) endotracheal tube cuff leak (steroids if no leak) (d) no recent upper airway obstruction or stridor (e) no recent reintubation for bronchial hygiene (f) RSBI (f/Vt) < 105

Fails Goal #1 Severe hypoxemia Meets definition for ARDS

Step 2

Fails Goal #1 Fails extubation, reintubated Or requires mechanical ventilation for 10-14 days Consider tracheostomy

C Sedation, Pain Control Maintain light sedation • Analgesia first sedation • Suggest non-benzodiazepine (dexmedetomidine, propofol) • IV vs. enteral Adequate pain control • Opioid vs. non-opioid • IV vs. enteral • Supports early mobilization

E, F

Goal #1

Sedation, Pain Control Adequate sedation Adequate pain control Patient awake and responsive Early mobilization tolerated

G

D

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56  Part II  ◆  Critical Care CI, 0.91 to 1.83; p = 0.02 for comparison with moderate/severe ARDS subgroup). M   RESTRICTIVE FLUID STRATEGY

The FACTT trial randomized 1000 ARDS patients to conservative versus liberal fluid management and confirmed no difference in 60-day mortality, but patients in the fluid-conservative group had significantly more ventilator-free days. N   NEUROMUSCULAR BLOCKADE

Short-course (48 hours) neuromuscular blockade with cisatracurium was associated with a mortality benefit (hazard ratio 0.68, 95% CI 0.48 to 0.98, p = 0.04) in patients (n = 340) with moderate/severe ARDS enrolled early (diagnosis in prior 48 hours) in the ARDS et Curarisation Systematique (ACURASYS) randomized trial after adjustment for baseline P/F ratio, plateau pressure, and Simplified Acute Physiology II score. The PETAL Network is performing a similar trial, Reevaluation of Systemic Early Neuromuscular Blockade (ROSE; see https://clinicaltrials.gov/ ct2/show/NCT02509078). O   INHALED NITRIC OXIDE

Inhaled nitric oxide (iNO) improves oxygenation in ARDS patients but does not improve survival. iNO (10 to 20 ppm) can be used as a rescue strategy in patients with severe hypoxemia. P

 

PRONE POSITION

Prone positioning improves oxygenation via mechanisms of improved ventilation–perfusion matching, alveolar recruitment through alternations in chest wall mechanics, and increased endexpiratory lung volume. Subgroup analysis of prone positioning in patients with more severe hypoxemia confirmed survival benefit. The Proning in Severe ARDS Patients (PROSEVA) randomized trial enrolled patients with P/F ratio < 150 mm Hg (prone 237 vs. supine 229) and confirmed survival benefit with prone-position protocol for a minimum of 16 hours per day: 28-day and 90-day mortality were decreased in the prone versus supine groups (28-day mortality 16.0% vs. 32.8%; 90-day mortality 23.6% vs. 41.0%). ICU staff must be educated about the safe method for prone positioning of critically ill patients; see Guérin et al. Q   RECRUITMENT MANEUVERS

ARDS patients have increased atelectasis, and recruitment maneuvers (RMs) can increase end-expiratory volume, reduce intrapulmonary shunt and increase pulmonary compliance. RMs are performed in multiple methods, including prolonged high continuous positive airway pressure (CPAP; 30 to 40 cm H2O), increased PEEP at constant driving pressure, and high driving pressures. In six randomized trials, RMs were associated with improved oxygenation and lower mortality (n =1423, RR 0.81; 95% CI 0.69 to 0.95). During the use of RMs, clinicians must monitor for the possible complications of transient hypotension and barotrauma. R   ESOPHAGEAL PRESSURE, HIGH-FREQUENCY OSCILLATORY VENTILATION, AND AIRWAY PRESSURE-RELEASE VENTILATION

One small trial (n = 61) documented that PEEP adjusted by esophageal pressures to estimate transpulmonary pressure significantly improved oxygenation and compliance. Two recent large multicenter RCTs confirmed no benefit (Oscillation in

ARDS [OSCAR] trial done in the United Kingdom) or possible harm (higher mortality, RR 1.41; 95% CI 1.21 to 1.79 in the U.S. Oscillation for Acute Respiratory Distress Syndrome Treated Early [OSCILLATE] trial). High-frequency oscillatory ventilation (HFOV) should not routinely be used in patients with moderate or severe ARDS. The potential use of HFOV as a rescue strategy for severe hypoxemia has been successful in some studies and warrants further investigation. Other strategies of high mean airway pressure, such as airway pressure-release ventilation (APRV), have been used in moderate/severe ARDS with success. S

 

EXTRACORPOREAL MEMBRANE OXYGENATION

Patients with severe ARDS who do not respond to other rescue strategies should be considered for extracorporeal membrane oxygenation (ECMO). ECMO techniques and outcomes have improved, in part related to the Conventional Ventilation or ECMO for Severe Adult Respiratory Failure (CESAR) trial and experience gained in the treatment of severe ARDS during the 2009 H1N1 pandemic. Although the CESAR trial reported significantly increased disability-free survival at 6 months in ECMO patients, there was no difference in mortality, and significant study limitations include the following: (1) not all patients randomized to the ECMO cohort received ECMO; (2) no standardized low-tidal-volume ventilation in control cohort; (3) transfer to a single high-volume referral center for the ECMO cohort. ECMO outcomes for adult pulmonary failure were 66% ECMO survival and 57% hospital survival in 12,346 ECMO runs reported by the Extracorporeal Life Support Organization (ELSO) registry from January 2017. The ECMO to Rescue Lung Injury in Severe ARDS (EOLIA, NCT01470703) trial is ongoing to further clarify the role of ECMO in severe ARDS management. The PRedicting dEath for SEvere ARDS on VV-ECMO (PRESERVE) and Respiratory Extracorporeal membrane oxygenation Survival Prediction (RESP) scores can be calculated to assist in outcome prediction in patients undergoing consideration for ECMO for severe ARDS. REFERENCES Adhikari NKJ, Dellinger RP, Lundin S, et al. Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: systematic review and meta-analysis. Crit Care Med. 2014;42(2):404–412. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin definition. JAMA. 2012;307(23): 2526–2533. Barr J, Fraser GL, Puntillo K, et al; American College of Critical Care Medicine. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit: executive summary. Am J Health Syst Pharm. 2013;70(1):53–58. Bellani G, Laffey JG, Pham T, et al. Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA. 2016;315(8):788. Blackwood B, Burns KE, Cardwell CR, O’Halloran P. Protocolized versus non-protocolized weaning for reducing the duration of mechanical ventilation in critically ill adult patients. Cochrane Database Syst Rev. 2014;(11):CD006904. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010;303:865–873. Cabrini L, Landoni G, Oriani A, et al. Noninvasive ventilation and survival in acute care settings: a comprehensive systematic review and metaanalysis of randomized controlled trials. Crit Care Med. 2015;43(4):880–888. Fan E, Del Sorbo L, Goligher EC, et al; American Thoracic Society, European Society of Intensive Care Medicine, and Society of Critical Care Medicine.

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Chapter 18  ◆  Acute Respiratory Failure  57

K, L Ventilator Rx Low tidal volume ventilation (6 mL/kg PBW) Pplat < 30 cm H2O Higher PEEP, by compliance, open lung strategy Limit FiO2 for SaO2 > 88 Permissive hypercapnia

Goal #2

Ventilator Rx FiO2 < 0.6 for SaO2 > 88 Pplat < 30 Optimal PEEP, MAP Permissive hypercapnia Meets Goal #2 Continue step #2 & step #1 Rx Weaning criteria Weaning & extubate vs. tracheostomy if 10-14 days after intubation

M Restrictive Fluid Strategy Diuresis to dry body weight

Step #2 Acute respiratory distress syndrome (ARDS) Berlin definition: Mild ARDS: PaO2/FiO2 201 to 300 Moderate ARDS: PaO2/FiO2 101 to 200 Severe ARDS: PaO2/FiO2 ≤ 100

Evaluate for Correctable Pulmonary Issues: Bronchoscopy: atelectasis, pneumonia, occluded airways Chest ultrasound or CT: necrotizing pneumonia, loculated pneumothorax/hemothorax, abscess

N, O Pharmacologic Rescue Early neuromuscular blockade: • Cisatracurium 48 hours Inhaled nitric oxide (iNO) • Optimal 10ppm if responder

Additional Rx Diuresis achieved Correctable pulmonary issues adequately addressed

S Pharmacologic Rescue Improved oxygenation Discontinued neuromuscular blockade Weaned iNO: as oxygenation improves, fix FiO2 at 0.6, and wean iNO using protocol

P, Q, R Non-Pharmacologic Rescue • Prone position (16 hours/day) • Recruitment maneuvers • Increased PEEP and mean airway Pressures for alveolar recruitment, improved oxygenation • Esophageal pressure-guided PEEP to improve oxygenation • APRV, HFOV for increased mean airway pressures

An official American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine clinical practice guideline: mechanical ventilation in adult patients with acute respiratory distress syndrome. Am J Respir Crit Care Med. 2017;195(9):1253–1263. Fan T, Wang G, Mao B, et al. Prophylactic administration of parenteral steroids for preventing airway complications after extubation in adults: meta-analysis of randomised placebo controlled trials. BMJ. 2008;337: a1841. Ferguson ND, Cook DJ, Guyatt GH, et al; OSCILLATE Trial Investigators; Canadian Critical Care Trials Group. High-frequency oscillation in early acute respiratory distress syndrome. N Engl J Med. 2013;368: 795–805. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (awakening and breathing controlled trial): a randomised controlled trial. Lancet. 2008;371(9607):126–134. Guerin C, Reignier J, Richard J-C, et al. PROSEVA study group. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368:2159–2168. Klompas M, Anderson D, Trick W, et al; CDC Prevention Epicenters. The preventability of ventilator-associated events. The CDC prevention epicenters wake up and breathe collaborative. Am J Respir Crit Care Med. 2015;191(3):292–301. Levy SD, Alladina JW, Hibbert KA, et al. High-flow oxygen therapy and other inhaled therapies in intensive care units. Lancet. 2016;387(10030): 1867–1878. Ni YN, Luo J, Yu H, et al. Can high-flow nasal cannula reduce the rate of endotracheal intubation in adult patients with acute respiratory failure compared with conventional oxygen therapy and noninvasive positive

Fails Goal #2 (Persistent Severe ARDS) Consider ECMO ECMO outcomes for adult pulmonary failure are 66% ECMO survival and 57% hospital survival in 12,346 ECMO runs reported by the Extracorporeal Life Support Organization (ELSO) registry from January 2017

Non-Pharmacologic Rescue Improved oxygenation Improved pulmonary compliance Optimal PEEP and mean Airway pressure

pressure ventilation? A systematic review and meta-analysis. Chest. 2017;151(4):764–775. Papazian L, Forel JM, Gacouin A, et al; ACURASYS Study Investigators. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363(12):1107–1116. Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet. 2009;374(9698):1351–1363. Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Crit Care Med. 2017;45(3):486–552. Schmidt M, Bailey M, Sheldrake J, et  al. Predicting survival after extracorporeal membrane oxygenation for severe acute respiratory failure. The respiratory extracorporeal membrane oxygenation survival prediction (RESP) score. Am J Respir Crit Care Med. 2014;189:1374–1382. Schmidt M, Zogheib E, Roze H, et al. The PRESERVE mortality risk score and analysis of long-term outcomes after extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. Intensive Care Med. 2013;39:1704–1713. Sud S, Friedrich JO, Taccone P, et al. Prone ventilation reduces mortality in patients with acute respiratory failure and severe hypoxemia: systematic review and meta-analysis. Intensive Care Med. 2010; 36:585–599. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359(20):2095–2104. Terragni PP, Antonelli M, Fumagalli R, et al. Early vs. late tracheotomy for prevention of pneumonia in mechanically ventilated adult ICU patients. JAMA. 2010;303:1483–1489.

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58  Part II  ◆  Critical Care The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–1308. Wiedemann HP, Wheeler AP, Bernard GR, et al. National Heart, Lung, and Blood Institute acute respiratory distress syndrome (ARDS) clinical trials network. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006;354:2564–2575.

Young D, Harrison DA, Cuthbertson BH, et al. Effect of early vs. late tracheostomy placement on survival in patients receiving mechanical ventilation: the tracman randomized trial. JAMA. 2013;309:2121–2129. Young D, Lamb SE, Shah S, et al; OSCAR Study Group. High-frequency oscillation for acute respiratory distress syndrome. N Engl J Med. 2013;368:806–813.

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Chapter

19 

ACUTE HYPOXIC EVENT Stephanie Joyce, MD, and Frederic Pieracci, MD

A Acute hypoxia is a decrease in the partial pressure of oxygen in the blood. There are many causes including hypoventilation, ventilation–perfusion (V/Q) mismatch, right-to-left shunt, diffusion impairment, and reduced inspired oxygen tension. Initial evaluation of a patient should include a thorough history and physical examination, noting in particular any recent interventions (e.g., central venous catheter). A focused physical exami­ nation should be performed to rule out any immediate life-threatening pathology such as a tension pneumothorax. Arterial blood gas (ABGs), chest x-ray (CXR), electrocardiography (ECG), and possibly ECHO or a computed tomography pulmonary embolus (CT PE) study can be ordered to distinguish the cause of hypoxia. B The most common cause of hypoxia in the ventilated ICU patient is a problem with either the ventilator circuit (e.g., disconnection) or airway (e.g., plugging). This finding underscores the importance of the physical examination before embarking on costly and potentially dangerous paths such as CT PE. Pulmonary embolism is a rare cause of acute hypoxia and, although morbid, should only be seriously considered after a thorough physical examination and CXR. C Tension pneumothorax is a progressive buildup of air within the pleural space, which pushes the mediastinum into the opposite hemithorax and obstructs venous return to the heart. This can lead to circulatory instability and arrest. The classic physical signs include tracheal deviation (away from the side of injury), absent breath sounds, and hyperresonance to percussion. However, most patients present with tachycardia, tachypnea, and hypoxia. Classically, the management has included needle decompression of the chest with an 18-gauge needle in the 2nd or 3rd intercostal space anterior chest. However, in the ICU setting, formal tube thoracostomy placement is probably faster and more definitive. A tension pneumothorax can develop despite the presence of a chest tube (e.g., if the tube is no longer functional). D In the intubated patient, acute hypoxia should be approached in a stepwise manner. An easy way to evaluate the airway is the ability to pass a suction catheter down the endotracheal tube. If it does not pass easily, the likely cause is an obstruction within the tube itself. This can be a result of a patient biting the tube, a large plug within the tube, or the tube being malpositioned. If this issue cannot be resolved readily, then the tube should be replaced. If the suction catheter passes easily, an upper airway obstruction is essentially ruled out, and further work-up for the cause of hypoxia should continue.

E In the nonintubated hypoxic patient, therapy includes increasing the FiO2 inhaled. There are multiple modes of delivery, but each fulfills the same basic requirements. The modes of delivery can be separated into variable-performance systems (e.g., nasal cannula), fixed performance systems (e.g., Ambu-bag), and high-flow systems (e.g., noninvasive positive-pressure ventilation [NIPPV]). It is imperative to monitor the response to treatment; the decision to intubate is a clinical decision. F Pleural space evaluation is essential to the work-up of acute hypoxia. Chest x-ray and bedside ultrasound are useful in the diagnosis of pleural space pathology. Pneumothorax and pleural effusions are frequently encountered in the ICU setting and should be treated with tube thoracostomy or thoracentesis, respectively. G Two ways to increase oxygenation in the ventilated patient are to increase the FiO2 or PEEP. Depending on the patient’s hemodynamic status, increasing the PEEP not only helps with oxygenation but can improve alveolar recruitment. H Intubated patients with severe hypoxia are often dyssynchronous with the vent because lung-protective strategies can be uncomfortable for patients. The first step to help improve dyssynchrony and thereby oxygenation is the addition of sedation. Depending on the patient’s hemodynamic status, typical agents include propofol, fentanyl, Precedex, or Ativan. Once the patient is adequately sedated and the patient continues to have increased plateau pressures or persistent hypoxia, early use of neuromuscular blockade in patients with acute respiratory distress syndrome (ARDS) has been shown to improve survival. I

Optimal fluid management is essential in patients with acute hypoxia. Studies show that judicious diuresis and fluid restriction can help improve lung function and reduce the duration of mechanical ventilation. One must weigh the risks of injuring extrapulmonary end-organ perfusion versus the benefit of improved pulmonary function. J

The PROSEVA trial showed improved 28-day and 90-day mortality with the use of early, prolonged (at least 16 hours a day) prone ventilation. Prone ventilation significantly improves oxygenation and reduces barotrauma. The technical aspects of prone ventilation are not simple but require skilled teams in the process of turning patients. However, the benefits significantly outweigh the risks in patients with severe refractory hypoxia. REFERENCES Frat JP, Thille AW, Mercat A, et al, FLORALI Study Group; REVA Network. High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N Engl J Med. 2015;372:2185–2196. Guérin C, et al. Prone Positioning in Severe Acute Respiratory Distress Syndrome (PROSEVA). N Engl J Med. 2013;368:2159–2168. Moore FA, Haenel JB, Moore EE, Abernathy CM. Hypoxic events in the surgical intensive care unit. Am J Surg. 1990;160(6):647–651. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wiedemann HP, Wheeler AP, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006;354:2564–2575. Nava S, Hill N. Non-invasive ventilation in acute respiratory failure. Lancet. 2009;374:250–259. Papazian L, Forel JM, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363:1107.

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Chapter 19  ◆  Acute Hypoxic Event  60.e1

Abstract

Keywords

An acute hypoxic event is a common issue in the intensive care unit (ICU). The work-up contains a spectrum of differential diagnoses, but it can be managed with a logical, stepwise approach. Beginning with life-threatening issues such as tension pneumothorax and working through the ABCs, the algorithm progresses. It finishes with various maneuvers the clinician can use in intubated patients to improve oxygenation.

acute hypoxic event hypoxia intubated mechanical ventilation

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Chapter 19  ◆  Acute Hypoxic Event  61 Difficult to pass

D

Check/replace ETT

Pass suction catheter

A Review recent history & interventions physical exam

Passes easily

Chest tube

C

Consider pneumothorax, mucous plug, severe bronchospasm

F

Difficulty bagging

Tension pneumothorax Intubated

Check O2 source Check vent circuit

Acute hypoxemic event Nonintubated

Refractory hypoxemia

G Increase PEEP

H Pharmacologic

ABG, CXR, US, EKG, CTPE

B

Pleural space evaluation

E Supplemental oxygen Hi-flo oxygen Non-invasive ventilation

Intubate

I Diuresis

J Prone ventilation

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Chapter

20 

ACUTE RENAL FAILURE Stephanie Joyce, MD, and Robert C. McIntyre, Jr., MD, FACS

INTRODUCTION Acute kidney injury (AKI) is a common problem in hospitalized patients, with an incidence of up to 22%. It is characterized by an abrupt (within 48 hours) reduction in kidney function based on an elevation of serum creatinine and/or reduction in urine output (UOP). The Acute Kidney Injury Network (AKIN) criteria include the following: • An increase in serum creatinine of 0.3 mg/dL or more (≥26.4 µmol/L), or • An increase in serum creatinine of 50% or more (1.5-fold from baseline), or • A reduction in urine output (documented oliguria of 6 h). A A thorough history and physical examination should be performed. The examination should include determination of volume status, cardiac function, liver disease, or sepsis. Medication history (outpatient and inpatient) must be obtained (e.g., angiotensin-converting enzyme [ACE] inhibitors, nonsteroidal anti-inflammatory drugs [NSAIDs], or aminoglycosides). A history of contrast or other nephrotoxins should be evaluated. The physical examination should focus on the patient’s volume status (i.e., blood pressure, pulse, orthostatics, mucous membranes, axillary sweat, and edema). Intra-abdominal pressures should be measured if there is suspicion for intra-abdominal hypertension. B Initial laboratory evaluation should include complete blood count (CBC), basic metabolic panel (BMP), and urine analysis (UA) with microscopy and urine electrolytes. Imaging studies such as a renal ultrasound (US) can rule out obstruction. The fractional excretion of sodium (FENa) is useful in distinguishing prerenal from intrinsic renal causes of acute kidney injury. FeNa < 1% indicates a prerenal cause with intact tubular function, whereas a value >2% indicates an intrinsic cause resulting from damaged tubules or reflects a history of renal insufficiency, recent administration of diuretics, or osmotic diuresis. After diuretic use, a fractional excretion of urea (FeUrea) may be helpful. Notable findings on urine microscopy include granular casts that are characteristic of acute tubular necrosis (ATN) and white blood cells or casts, which can point to either an infectious or inflammatory cause. Eosinophils suggest interstitial nephritis. C A low FeNa suggests prerenal disorders caused by a decrease in renal blood flow. Supportive findings include compatible history and physical examination, BUN/creatinine ratio of greater than 20, urinary specific gravity greater than 1.020, urine Na less than 20, and a normal urinary sediment with or without

hyaline casts. The volume status of the patient, along with pertinent history and laboratory findings, should help delineate the cause. Prerenal azotemia is often reversible if recognized and treated promptly, but it may lead to ATN if untreated. Prerenal disorders are responsible for 30% to 40% of cases of acute renal failure, with the two most common causes being hypovolemia and low-output cardiac failure. In the surgical patient with worsening renal function as a result of hypovolemia, a volume challenge should be performed. D Intrinsic failure in the surgical patient is most commonly caused by nephrotoxic agents or may be tubular damage as a result of sepsis or shock. The first goal of treatment is to stop the offending agent. Acute tubular necrosis is responsible for ~50% of cases of acute renal failure. It is because of a combination of ischemia, nephrotoxin exposure, and sepsis. Acute interstitial nephritis can be seen in surgical patients, especially after exposure to NSAIDs, antibiotics (e.g., Zosyn), and proton pump inhibitors (PPIs). Eosinophils seen on urine microscopy are pathognomonic for acute interstitial nephritis (AIN), but the absence on microscopy does not exclude the diagnosis. Intrinsic renal failure management is primarily treatment of the underlying disease, discontinuation of the offending agent, and supportive care. E It is important to rule out obstruction in every patient with AKI. Common sites of obstruction include bladder neck and ureteral obstructions. Renal US is the diagnostic test of choice, and a postvoid residual can also help delineate the site of obstruction. Placement of a Foley catheter or percutaneous nephrostomy tubes to relieve the obstruction is usually sufficient treatment. If a Foley is already in place, it should be flushed to ensure patency. F Hypovolemia is treated with fluid resuscitation. US or advanced cardiac monitoring devices can be used to aid in resuscitation. Cardiorenal syndrome can be treated by afterload reduction (i.e., vasodilators or diuretics) and/or improvement of cardiac function (i.e., inotropes). Severe sepsis and septic shock require vasopressors after volume resuscitation to improve renal perfusion. G Indications for dialysis include the following: 1. Fluid overload (refractory to diuretics) 2. Hyperkalemia 3. Metabolic acidosis (pH < 7.1) 4. Uremia (including pericarditis, neuropathy, or encephalopathy) 5. Toxins Current studies in critically ill patients with severe kidney injury show no difference in mortality between early and late initiation of hemodialysis. In fact, these studies have shown that delayed hemodialysis initiation averted the need for renal replacement therapy in some patients. H There are many different modalities for renal replacement therapy, but the two most commonly used in AKI are intermittent hemodialysis (IHD) and continuous renal re­ placement therapy (CRRT). Data do not support one mode in particular, and the selection should be based on individual patient factors. The Kidney Disease: Improving Global Out­ comes (KDIGO) guidelines suggest using IHD and CRRT as

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Chapter 20  ◆  Acute Renal Failure  62.e1

Abstract

Keywords

Acute kidney injury is a common problem in hospitalized patients, with an incidence of up to 22%. It is characterized by an abrupt (within 48 hours) reduction in kidney function based on an elevation of serum creatinine and/or reduction in urine output (UOP). Acute kidney injury can be classified into prerenal, renal, and postrenal causes, and their treatments differ. Once the cause is addressed, dialysis may be indicated depending on renal function.

acute kidney injury acute renal failure oliguria elevated creatinine dialysis

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Chapter 20  ◆  Acute Renal Failure  63

C Pre-renal failure

A History and physical

Acute renal failure

D Intrinsic renal failure

B

F Hypovolemia Hepatorenal syndrome Cardiogenic Distributive shock

Fluid Pressors Afterload reduction

G Vascular Interstitial Glomerular Tubular

CBC, CMP, UA with microscopy, urine electrolytes, renal US

No response to treatment Volume overload Electrolyte abnormalities Uremia Acidosis Toxins

H Dialysis

E Post-renal failure Relieve obstruction

complementary therapies because recovery of renal function appears to be the same in both groups. Advocates for CRRT have claimed enhanced hemodynamic stability, increased net salt and water removal, enhanced clearance of inflammatory mediators, and improved renal recovery when compared with IHD. In patients with acute brain injury and fulminant hepatic failure, CRRT may help preserve cerebral perfusion. In a systematic review of CRRT intensity, intensive CRRT did not improve mortality in critically ill patients with AKI.

CONCLUSIONS Data suggest that patients with preexisting renal disease, multiple comorbidities, advanced age, and higher severity of AKI are more likely to progress to chronic renal disease with subsequent need for long-term dialysis. Also, patients treated with renal replacement therapy (RRT) are more likely to require long-term renal replacement therapy compared with patients managed conservatively. In one study of 1292 patients who needed RRT for AKI, 19% progressed to dialysis dependence.

REFERENCES De Corte W, Dhondt A, Vanholder R, et al. Long-term outcome in ICU patients with acute kidney injury treated with renal replacement therapy: a prospective cohort study. Crit Care. 2016;20:256. Fayad AI, Buamscha DG, Ciapponi A. Intensity of continuous renal replacement therapy for acute kidney injury. Cochrane Database Syst Rev. 2016;(10):Art. No.: CD010613. Gaudry S, Hajage D, Schortgen F, et al. Initiation strategies for renal-replacement therapy in the intensive care unit. N Engl J Med. 2016;375:122–133. Jun M, Bellomo R, Cass A, et al. Timing of renal replacement therapy and patient outcomes in the randomized evaluation of normal versus augmented level of replacement therapy study. Crit Care Med. 2014;42:1756–1765. Navaneethan SD, Singh S, Appasamy S, Wing RE, Sehgal AR. Sodium bicarbonate therapy for prevention of contrast-induced nephropathy: a systematic review and meta-analysis. Am J Kidney Dis. 2009;53:617–627. Vaara ST, Pettila V, Kaukonen KM, et al. The attributable mortality of acute kidney injury: a sequentially matched analysis. Crit Care Med. 2014;42:878–885.

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Chapter

21 

ACID–BASE DISORDERS Gregory M. Borst, MD, and Eric M. Campion, MD Acid–base disorders are among the most complex disorders to fully understand. The following algorithm and discussion are based on the physiologic model of acid–base, which uses the PaCO2 and [HCO3–] to determine pH as in the Henderson– Hasselbalch equation. This model is the simplest and most widely used to explain acid–base disturbances and their secondary responses. The base excess and Stewart models are more complex and beyond the scope of this brief review. A The first step in determining if an acid–base disorder is present is a history and clinical examination, which may provide clues of an underlying disorder. Symptoms such as altered mental status, tachypnea, vomiting, fever, or alteration in other vital signs may be evidence of an acid–base disorder. To establish the presence of an acid–base disorder, an arterial blood gas should be obtained to determine the pH, PaCO2, and [HCO3–]. Normal pH ranges from 7.38 to 7.42; a pH less than 7.38 indicates acidosis, and a pH greater than 7.42 is diagnostic of alkalosis. B The normal range of [HCO3–] is 22 to 26 mEq/L, and that for PaCO2 is 36 to 44 mm Hg. Use pH, [HCO3–], and PaCO2 to determine the primary acid–base disorder. Respiratory disorders are the result of a change in primary respiratory function that results in an alteration in PaCO2. Metabolic disorders occur when the primary change is attributed to a change in [HCO3–]. A normal pH most commonly indicates that there is no acid–base disorder but rarely can be seen when a mixed disorder is present with no dominant primary disorder. A normal pH with an abnormal PaCO2 or [HCO3–] indicates a mixed disorder with equal and opposite strengths. For example, with a low PaCO2, there is a respiratory alkalosis balanced by a metabolic acidosis (low [HCO3–]) and vice versa. C Secondary responses (disorders) are homeostatic reactions to the primary disorder that attempt to normalize pH. These responses are predictable and can be calculated. Secondary responses do not completely compensate for the primary disorder (pH will not return to normal). Respiratory compensation is quick to develop (minutes to hours), whereas metabolic compensation evolves more slowly (2 to 5 days). If the observed PaCO2 or [HCO3–] is as expected, there is full compensation. If it is greater or less than the expected, a superimposed acidosis or alkalosis is present. Respiratory disorders may be acute or chronic and can typically be distinguished with the history and clinical examination. Metabolic compensation for chronic respiratory disorders is larger in magnitude than that for acute disorders because of the chronic compensation to maintain homeostasis. Renal failure impairs metabolic compensation; therefore, patients may not compensate appropriately or as quickly as a patient with normal kidney function.

D Respiratory disorders result from an aberration in ventilation, acidosis results from hypoventilation, and alkalosis results from hyperventilation. Causes of hyperventilation include broad categories of hypoxia, lung diseases, drugs, and stimulation of respiratory drive. Hypoxia may be caused by a variety of factors, including any cause of ventilation/perfusion (V/Q) mismatch, congestive heart failure, pulmonary edema, pneumonia, and pulmonary emboli. The most common drugs that may cause hyperventilation include salicylates, progesterones, and nicotine. Respiratory drive may be stimulated by cirrhosis of the liver, gram-negative sepsis, or psychogenic causes. Overventilation by ventilators is a common cause of respiratory alkalosis in the intensive care setting. Respiratory acidosis is caused by hypoventilation, which may come from the broad categories of airway obstruction, neuromuscular disorders, central respiratory depression, and respiratory disorders. Airway obstruction may occur for a variety of reasons, such as obstructive sleep apnea, laryngospasm, chronic obstructive pulmonary disease (COPD), or asthma. Neuromuscular disorders that impair ventilation include Guillain–Barré syndrome, botulism, spinal injuries, and morbid obesity. Centrally, respiratory drive can be impaired by a variety of—most commonly narcotics and benzodiazepines—but also can be caused by brain injury of either traumatic or ischemic etiology. Respiratory disorders may also cause acidosis when ventilation is impaired. Respiratory disorders can be further characterized by calculating the alveolar-arterial (Aa) gradient with the following equation, where Pb is barometric pressure, PH O is the partial pressure of water in the atmosphere, and RQ is the respiratory quotient: 2

Aa gradient = FiO2 (Pb − PH2 0 ) − (PaCO2 RQ) − PaO2 At sea level, on room air = 150 − 1.25 × PaCO2 − PaO2

The normal Aa gradient increases with age and can be calculated based on the following formula: Normal expected Aa gradient = (Age 4) + 4

When the Aa gradient is higher than expected, there is likely underlying lung pathology causing the respiratory disorder. A normal Aa gradient (less than or equal to the expected gradient for age) indicates normal lung function; thus, another cause for the observed acid–base disorder is likely, which should prompt a search for an extrapulmonary source. The treatment of respiratory disorders should be directed at the underlying cause for the disorder. E The presence of metabolic acidosis requires calculation of the anion gap to determine the etiology. The anion gap is the difference between the cations and anions measured on routine chemistry labs. Because the anion gap varies with the albumin concentration, the albumin level should also be checked, and a corrected anion gap should be calculated if the albumin is low. The calculations are as follows: Anion gap (AG) = [Na + ] − [Cl − ] − [HCO3− ] Corrected AG (AG c ) = AG + 2.5 × (4 − [Albumin])

If the corrected gap is within the normal range of 8 to 12, the acidosis is said to be a non-gap acidosis, and if the anion gap is over 12, it is said to be an anion-gap or gap acidosis. Non-gap acidosis is caused by loss of bicarbonate, decreased renal acid

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Chapter 21  ◆  Acid–Base Disorders  64.e1

Abstract

Keywords

This chapter presents a simple algorithm for acid–base analysis. The algorithm starts with arterial blood gas and differentiates the primary acid–base disturbances, the secondary responses, and further classification of the respiratory and metabolic disturbances to determine the underlying causes.

acid–base disorders respiratory acidosis respiratory alkalosis metabolic acidosis metabolic alkalosis anion gap

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Chapter 21  ◆  Acid–Base Disorders  65

pH < 7.38 Acidosis

B

C

[HCO3−] < 22 Primary Metabolic Acidosis

Expected PaCO2 = 1.5 [HCO3−] + 8 ± 2

PaCO2 > 42 Primary Respiratory Acidosis

A Arterial Blood Gas

pH = 7.38 to 7.42 Normal

PaCO2 = 38 to 42 No Acid/Base disorder PaCO2 < 38 or > 42 Mixed Acid/Base disorder PaCO2 < 38 Primary Respiratory Alkalosis

pH > 7.42 Alkalosis [HCO3−] > 26 Primary Metabolic Alkalosis

Acute: Expected [HCO3−] is 1 mmol/L higher for every increase in PaCO2 of 10 mm Hg over 40 Chronic: Expected [HCO3−] is 4−5 mmol/L higher for every increase in PaCO2 of 10 mm Hg over 40 Acute: Expected [HCO3−] is 2 mmol/L lower for every decrease in PaCO2 of 10 mm Hg below 40 Chronic: Expected [HCO3−] is 4 to 5 mmol/L lower for every decrease in PaCO2 of 10 mm Hg below 40

Expected PaCO2 = 0.7 × ([HCO3−] − 24) + 40 + 2

E

• PaCO2 Observed = PaCO2 Expected Pure Metabolic Acidosis • PaCO2 Observed > PaCO2 Expected Secondary Respiratory Acidosis • PaCO2 Observed < PaCO2 Expected Secondary Respiratory Alkalosis

Determine Anion Gap (normal is 8 to 12 mEq/L) AG = [Na+] − ([CI−]) + [HCO3−]) If low albumin, calculated AG: AGc = AG + 2.5 × (4 − [Albumin])

• [HCO3−] observed = [HCO3−] expected Pure Respiratory Acidosis • [HCO3−] observed < [HCO3−] expected Secondary Metabolic Acidosis • [HCO3−] observed > [HCO3−] expected Secondary Metabolic Acidosis

D

• If Anion Gap < 12 Non-Gap Metabolic Acidosis • If Anion Gap > 12 Anion Gap Metabolic Acidosis

Calculate Aa gradient

• [HCO3−] observed = [HCO3−] expected Pure Respiratory Alkalosis • [HCO3−] observed < [HCO3−] expected Secondary Metabolic Acidosis • [HCO3−] observed > [HCO3−] expected Secondary Metabolic Acidosis

• PaCO2 Observed = PaCO2 Expected Pure Metabolic Alkalosis • PaCO2 Observed > PaCO2 Expected Secondary Respiratory Acidosis • PaCO2 Observed < PaCO2 Expected Secondary Respiratory Acidosis

• If Urine [CI−] > 40 mEq/L Chloride-resistant metabolic alkalosis • If Urine [CI−] < 25 mEq/L Chloride-resistant metabolic alkalosis

Measure Urine [CI−] ∗If exogenous alkali or severe hypercalcemia diagnosis is milk alkali syndrome

F excretion, or other iatrogenic causes. The most common non-gap acidosis is hyperchloremia, when the body attempts to retain electroneutrality by excreting bicarbonate in response to exogenous administration of chloride. Common causes of non-gap acidosis besides hyperchloremia include renal tubular acidosis, the use of carbonic anhydrase inhibitors (most commonly acetazolamide), ureteroenterostomy, diarrhea, pancreatic fistulae or pancreaticoenterostomy, and early renal insufficiency. A common mnemonic used to remember the causes of non-gap acidosis is HARDUP: hyperchloremia, acetazolamide, renal tubular acidosis, diarrhea, ureteroenterostomies, pancreaticoenterostomies. Anion-gap acidosis (>12) is characterized by overproduction of acid—most commonly lactic acid in the setting of tissue hypoxia. Other causes of gap acidosis include ketoacidosis, administration of acidic drugs/chemicals or those that cause acidosis, and underexcretion or impaired clearance of acid by the kidneys or liver. A common mnemonic used to remember the causes of anion-gap acidosis is MUDPILES: methanol, uremia, DKA (and other ketoacidosis), paraldehyde (paracetamol/acetaminophen), isoniazid, lactic acid, ethylene glycol, salicylates. F Metabolic alkalosis typically results from an increase in alkali and impairment of renal excretion of bicarbonate. It also requires further classification to determine the underlying

cause and direct treatment. Urinary chloride should be measured and used to determine if the alkalosis is chloride-sensitive or resistant. Urinary chloride values of less than 20 meq/L indicate chloride-sensitive alkalosis, which responds to treatment with infusion of chloride-rich intravenous (IV) fluid. Chloride-sensitive alkalosis is typically from gastric acid loss or overdiuresis (contraction alkalosis). A urinary chloride value of over 40 meq/L is indicative of chloride-resistant alkalosis, which is rare and does not respond to resuscitation with saline. The most common causes of chlorideresistant alkalosis include severe hypokalemia and mineralocorticoid excess. Less common causes include Bartter syndrome, Gitelman syndrome, severe hypercalcemia, and magnesium deficiency. REFERENCES Achinger Steven G, Ayus Juan Carlos. Blood gas analysis and acid-base disorders. In: Gabrielli Andrea, Layon A. Joseph, Yu Mihae, eds. Civetta, Taylor, & Kirby’s Critical Care. Philadelphia: Lippincott Williams & Wilkins; 2009:631–649. Berend K, de Vries APJ, Gans ROB. Physiological approach to assessment of acid-base disturbances. N Engl J Med. 2014;371:1434–1445. Marino Paul L. “Acid-base analysis,” “organic acidoses,” and “metabolic alkalosis.” In: The ICU Book. 4th ed. Philadelphia: Wolters Kluwer; 2014.

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Chapter

22 

SODIUM DISORDERS Lauren Steward, MD, and Catherine Velopulos, MD

INTRODUCTION The osmoregulatory system of the human body acts to maintain the sodium plasma concentration within its normal range of 135 to 145 mEq per liter (mEq/L). Hyponatremia is a plasma sodium concentration of less than 135 mEq/L, and hypernatremia is a plasma sodium concentration of greater than 145 mEq/L. Inability of the osmoregulatory system to maintain the plasma sodium concentration within its normal range can cause significant stress to cells. The consequence of hypernatremia and hyponatremia is encephalopathy. The most severe clinical manifestations of hyponatremic encephalopathy include cerebral edema, increased intracranial pressure, and the potential for brain herniation. It often presents with nausea, vomiting, and ultimately seizures. The most severe clinical manifestation of hypernatremic encephalopathy is coma. Symptoms of hypernatremic encephalopathy range from significant agitation to lethargy. In both hyponatremic and hypernatremic encephalopathy, the risk for and severity of symptoms are related to the time for the development of the metabolic derangement, with more acute presentations (less than 48 hours) more likely to develop symptoms. A Hyponatremia is defined as a plasma sodium concentration of less than 135 mEq/L. It occurs secondary to excess water in relationship to sodium. B The first step in the evaluation of hyponatremia is the evaluation of the serum osmolality. Increased levels of lipids or protein can significantly lower the plasma sodium. This usually occurs with lipid levels > 1500 mg/dL or protein levels > 12 to 15 g/dL. In addition, significant hyperglycemia can also falsely lower the plasma sodium. This phenomenon is referred to as pseudohyponatremia. In all of these instances, the diagnosis can be confirmed by evaluating the plasma osmolality. Plasma osmolality will be normal (>280 mOsm/kg) in patients with pseudohyponatremia. It will be low in patients with “true” hyponatremia. a. The formula to calculate plasma osmolality is as follows: Plasma osmolality = (2 × serum Na + ) + (serum glucose 18) + (serum blood urea nitrogen [BUN] 2.8)

b. The formula to correct plasma sodium for hypertriglyceridemia is as follows: Estimated (corrected) plasma sodium = measured plasma sodium + [(0.21 × triglycerides) − 0.6] × (plasma Na + 100)]

c. The formula to correct plasma sodium concentration for hyperglycemia is as follows:

Estimated (corrected) plasma sodium = measured plasma sodium + 0..016 × (serum glucose − 100)

C The next step in the evaluation of the hyponatremic patient is the evaluation of volume status. The physical examination should determine if a patient is hypovolemic, euvolemic, or hypervolemic. D Evaluating the urine sodium can help differentiate the cause of hypovolemic hyponatremia. Patients with a urine sodium of less than 20 mEq/L have extrarenal causes of sodium loss, which are usually gastrointestinal-related losses. Hyponatremic patients with a urine sodium of greater than 20 mEq/L potentially have hyponatremia related to diuretics (particularly the thiazide diuretics), cerebral salt wasting, or primary adrenal insufficiency. Cerebral salt wasting can be seen in patients with traumatic brain injuries. In addition to having a urine sodium greater than 20 mEq/L, patients with cerebral salt wasting will also have a urine osmolality greater than 100 mOsm/kg. E Euvolemic hyponatremia occurs because of excess water intake or retention. Excess water retention usually occurs as a result of inappropriate or nonosmotic release of antidiuretic hormone (ADH). This can occur with the syndrome of inappropriate ADH (SIADH), which is seen with various malignancies, infections, drugs, and/or trauma, and in times of physiologic stress, such as sepsis, major surgery, pain, or respiratory distress (hypoxia/hypercapnia). Excess water intake can occur with psychogenic polydipsia or water intoxication. Urine osmolality will differentiate between the etiologies of euvolemic hyponatremia. Urine Osm < 100 mOsm/kg or dilute urine indicates a state of excess water intake. Urine Osm > 100 mOsm/kg indicates a state of inappropriate/nonosmotic ADH secretion. F Hypervolemic hyponatremia is the result of excess water retention that occurs with advanced congestive heart failure, cirrhosis, and renal failure (cardiacosis, cirrhosis, nephrosis). Presumably, the patient’s history will be able to help differentiate the etiology of hypovolemic hyponatremia. However, urine sodium can be used as well. A urine sodium of less than 20 mEq/L in a patient with hypervolemic hyponatremia indicates either cirrhosis or congestive heart failure as the etiology of hypervolemic hyponatremia. A urine sodium of greater than 20 mEq/L indicates renal failure as the etiology. G Regardless of the cause of hypovolemic hyponatremia, the method of correction depends on if the patient is symptomatic or asymptomatic. For the patient with symptomatic hypovolemic hyponatremia, the sodium should be corrected with hypertonic saline. For patients with acute-onset or symptomatic hyponatremia, the plasma sodium should be corrected with 100-mL boluses of 3% NaCl but should not increase by more than 2 to 6 mEq/L over the first 2 hours. However, the total change in the serum sodium should not exceed 15 to 20 mEq/L over the first 48 hours. The patient should have the sodium level checked frequently (every 2 hours) to evaluate for rapid overcorrection. Rapid overcorrection (>15 to 20 mEq/L over 48 hours) can lead to cerebral pontine myelinolysis, which is characterized by significant damage to the pons region of the brainstem, leading to dysphagia, dysarthria, acute paralysis, and pseudocoma. Asymptomatic hypovolemic hyponatremia

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Chapter 22  ◆  Sodium Disorders  66.e1

Abstract

Keywords

The osmoregulatory system of the human body acts to maintain the sodium plasma concentration within its normal range of 135 to 145 mEq per liter (mEq/L). Hyponatremia is a plasma sodium concentration of less than 135 mEq/L, and hypernatremia is a plasma sodium concentration of greater than 145 mEq/L. Inability of the osmoregulatory system to maintain the plasma sodium concentration within its normal range can cause significant stress to cells. The consequence of hypernatremia and hyponatremia is encephalopathy. The most severe clinical manifestations of hyponatremic encephalopathy include cerebral edema, increased intracranial pressure, and the potential for brain herniation. It often presents with nausea, vomiting, and ultimately seizures. The most severe clinical manifestation of hypernatremic encephalopathy is coma. Symptoms of hypernatremic encephalopathy range from significant agitation to lethargy. In both hyponatremic and hypernatremic encephalopathy, the risk for and severity of symptoms are related to the time for the development of the metabolic derangement, with more acute presentations (less than 48 hours) more likely to develop symptoms.

sodium sodium disorders hyponatremia hypernatremia

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Chapter 22  ◆  Sodium Disorders  67 should be corrected with isotonic saline to correct the patient’s volume status.

overload. Asymptomatic patients with euvolemic hyponatremia should be placed on fluid restriction, usually less than 800 mL per day, to correct their sodium.

H Similar to hypovolemic hyponatremia, the method of correction of the plasma sodium concentration is dependent on whether the patient is symptomatic or asymptomatic. Symptomatic euvolemic hyponatremic patients should be corrected with hypertonic saline, as described previously. However, these patients may also need furosemide to prevent volume

Signs and symptoms Nausea and vomiting Headache Confusion Loss of energy and fatigue Restlessness Muscle weakness, spasms or cramps Seizures Coma

I

Symptomatic hypervolemic hyponatremic patients should be treated with hypertonic saline and furosemide to correct the plasma sodium. Asymptomatic patients with hypervolemic hyponatremia should be treated with fluid restriction and diuretics.

B

Pseudohyponatremia - Hyperglycemia - Hyperlipidemia - Hyperproteinemia

Serum Osmolality > 280 mOsm/kg

Fluid management

D Hypovolemia

A

Basic metabolic panel Serum and urine Osm Urine Na

Check volume status

E Euvolemic

Extrarenal Na+ loss - GI losses

> 20

Renal Na+ losses - Thiazides - Primary adrenal insufficiency - Cerebral salt wasting - Urine Osm > 100

Urine Na (mEq/L)

Hyponatremia Na < 135 mEq/L

C

< 20

< 100

Urine Osm (mOsm/kg) > 100

F Hypervolemic

< 20

Urine Na (mEq/L) > 20

Signs and symptoms Lethargy Weakness Irritability Twitching Seizures Coma

J Hypernatremia Na > 145 mEq/L

Basic metabolic panel Urine Osm Urine Na

G

Symptomatic - Hypertonic saline Asymptomatic - Isotonic saline to correct volume status

H

Symptomatic - Hypertonic saline, +/− lasix Asymptomatic - Fluid restriction

I

Symptomatic - Hypertonic saline, +/− lasix Asymptomatic - Fluid restriction, diuretics

- Psychogenic polydipsia - Water intoxication -

SIADH U Na > 20 Hypothyroidism Stress

- Congestive heart failure - Cirrhosis Renal failure

Fluid management - GI losses + impaired thirst - Vomiting - Diarrhea - Diuretics - Excessive sweat loss in heat related illness - Sepsis

L Hypovolemia

K Check volume status

M Euvolemic

P Diabetes Insipidus Urine Osm < 200

O

Central DI - CNS insult - Concentrated urine after desmopressin Nephrogenic DI • Nephrotoxic drugs • Failure to concentrate urine after water deprivation

N Hypervolemic

- Sodium bicarbonate infusion - Hypertonic saline

S

- Resuscitate with isotonic fluid - Then replace free water deficit (slowly)

Q

- DDAVP/vasopressin - Replace free water deficit

R - Replace free water deficit

- Diuresis - If Na increases, then replace urine output w/¼ NS

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68  Part II  ◆  Critical Care Hypernatremia is defined as a plasma sodium > 145 mEq/L. It occurs secondary to hypotonic fluid loss, free water loss, or excess sodium gain. J

K The assessment of hypernatremia, similar to hyponatremia, begins with an assessment of the patient’s volume status. L Hypovolemic hypernatremia is usually caused by loss of hypotonic fluid, where both sodium and water are lost, but water is lost in excess of sodium. Gastrointestinal losses, diuretics, excessive sweating, and sepsis are examples of situations that may lead to hypovolemic hyponatremia. M Euvolemic hypernatremia is a result of the loss of free water. Diabetes insipidus (DI) is the most common cause of euvolemic hypernatremia and is characterized by dilute urine despite having hypertonic plasma. It comes in two forms: central and nephrogenic DI. Central DI is the result of damage to the hypothalamus or pituitary, which occurs with trauma, surgery, tumors, infections, and so forth. Nephrogenic DI occurs when the kidneys do not respond to vasopressin, which may result from lithium toxicity, electrolyte abnormalities such as hypokalemia or hypercalcemia, chronic kidney disease, or urinary tract obstruction. N Hypervolemic hypernatremia usually occurs secondary to exogenous administration of sodium via hypertonic saline administrations for the treatment of elevated intracranial pressure or sodium bicarbonate infusions. It may also be caused by excessive salt intake as seen in some psychiatric disorders. O As stated before, hypernatremia may lead to nausea/vomiting, altered mental status, and even coma. As a result, it should be corrected. For hypovolemic hypernatremic patients, the first step in management is fluid resuscitation with isotonic fluid to restore volume status. Once the patient’s volume status has been restored to euvolemia, the patient’s free-water deficit can be calculated and subsequently slowly replaced with free water. The calculation for a patient’s free-water deficit is as follows: a. Free-water deficit = (total body water) × [(current Na – goal Na)/goal Na] i. Total body water = 0.6 × (weight in kg) for men or 0.5 × (weight in kg) for women

Sodium correction should occur at less than 0.5 to 1 mEq/L per hour. As a result, plasma sodium should be measured frequently. Rapid correction of plasma sodium may lead to cerebral edema, seizures, brain damage, and potentially death. P The management of central versus nephrogenic DI is different. As a result, it is important to differentiate between the two conditions. If administration of desmopressin results in the ability to concentrate urine, central DI is implicated. Failure to concentrate urine after a water-deprivation test is indicative of nephrogenic DI. Q The treatment for central DI is to administer desmopressin, an analog for vasopressin, in addition to replacing the free-water losses using the equations listed previously. Multiple doses of desmopressin may be required. Urine osmolality should increase by at least 50% with each dose of desmopressin. R Treatment for nephrogenic DI is free-water replacement per the correction strategy listed previously. S The treatment of hypervolemic hypernatremia is diuresis. However, a side effect of the diuresis may be elevation of the plasma sodium. As a result, the urine output may be replaced with 1 4 normal saline.

CONCLUSION Sodium disorders are very common in surgical patients. Evaluation of the patient’s volume status is key to the determination of the nature of the patient’s hyper- or hyponatremia. A single variable may be used to further delineate the cause of the patient’s sodium abnormality, which will dictate a fluid-management strategy. It is important to correct both hyper- and hyponatremia slowly to avoid adverse neurologic consequences. REFERENCES Achinger SG, Ayus JC. Fluids and electrolytes. In: Gabrielli AG, Layon AJ, Yu M, eds. Civetta, Taylor, and & Kirby’s Critical Care. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:609–630. Marino PL. Osmotic disorders. In: Marino PL, ed. Marino’s the ICU Book. 4th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2014:652–672. Sterns RH. Disorders of plasma sodium—causes, consequences, and correction. N Engl J Med. 2015;372:55–65.

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Chapter

23 

POTASSIUM DISORDERS Ryan A. Lawless, MD

HYPERKALEMIA A The increased release of potassium from cells has multiple etiologies: pseudohyperkalemia, metabolic acidosis; insulin deficiency, hyperglycemia, and hyperosmolality; tissue catabolism; nonselective beta blockers, particularly following a potassium load; exercise. B Decreased urinary excretion of potassium occurs in four situations: decreased aldosterone secretion, aldosterone resistance, decreased sodium and water delivery to the distal nephron, and acute and chronic kidney disease. C The evaluation of patients with hyperkalemia includes history, physical exam, laboratory studies, and an electrocardiogram (ECG). D Clinical findings include muscle weakness, generally distally and progressing proximal, and possibly flaccid paralysis. Arrhythmias include sinus bradycardia/arrest, slow idioventricular rhythms, ventricular tachycardia/fibrillation, and asystole. Conduction abnormalities include left and/or right bundle branch block and advanced AV block. Tall peaked t-waves, P-R interval and QRS lengthening, P-wave disappearance, and a sine wave can be seen on ECG. Lab studies may indicate a metabolic acidosis. E Emergent therapy: a. Intravenous calcium: calcium gluconate 1000-mg push over 2 to 3 minutes; calcium chloride 500- to 1000-mg push over 2 to 3 minutes. Give higher concentrations through central vein. b. Insulin: 10 to 20 units in 500 mL D10 solution over 60 minutes (no dextrose if serum glucose ≥ 250 mg/dL); 10 units regular insulin IV + 50 mL D50 solution, recommend following with D10 solution at 50 to 75 mL/hr to prevent hypoglycemia. c. Potassium removal: loop diuretic IV in patients without severe renal impairment; hemodialysis; gastrointestinal (GI) tract cation exchanges (not recommended in postoperative period, ileus, narcotic use, bowel obstruction, underlying bowel disease). d. β-2 adrenergic agonist: albuterol 10 to 20 mg in 4 mL saline nebulizer or 0.5-mg IV push. e. Sodium bicarbonate: 150 meq in 1 L D5W (isotonic) over 2 to 4 hours; 50-meq IV bolus f. Treat reversible causes: i. Volume status ii. Medications

F

Prompt therapy (correction within 6 to 12 hours): a. Isotonic bicarbonate infusion b. Dextrose infusion overnight in preoperative patient c. Hemodialysis

G

Slow correction (≥12 hours): a. Dietary modification b. Diuretic use c. Stop all nonsteroidal anti-inflammatory drugs (NSAIDs) d. Correct volume status

REFERENCES Ashurst J, Sergent SR, Sergent BR. Evidence-based management of potassium disorders in the emergency department. Emerg Med Pract. 2016;18(11): 1–24. Kovesdy CP. Management of hyperkalemia: an update for the internist. Am J Med. 2015;128(12):1281–1287. McDonough AA, Youn JH. Potassium homeostasis: the knowns, the unknowns, and the health benefits. Physiology. 2017;32:100–111. Palmer BJ, Cleff DJ. Physiology and pathophysiology of potassium homeostasis. Adv Physiol Educ. 2016;40:480–490.

HYPOKALEMIA A Etiology of hypokalemia: movement of potassium into the cell; decreased potassium intake in conjunction with another cause; increased urinary excretion; GI loss, including upper and lower GI issues; dialysis; excessive sweating or loss in sweat (cystic fibrosis); plasmapheresis. B The evaluation of hypokalemia includes history; physical exam; laboratory studies, including blood and urine testing; and an ECG. C Clinical findings include weakness and muscle cramps, starting more distally and progressing proximally and worsening in nature; rhabdomyolysis; myoglobinuria; ileus; +/– diarrhea; renal dysfunction (structural and functional); and glucose intolerance. Arrhythmias include premature atria and/ or ventricular beats. Conduction abnormalities include ST depression, decreased T-wave amplitude, increased U-wave amplitude (V4 to V6), and QT prolongation. D Emergent therapy: a. Potassium chloride (KCl) 40 meq orally 3 to 4 times daily plus KCl 20 meq IV every 2 to 3 hours (up to 40 meq per hour if necessary), with careful monitoring in intensive care unit (ICU) setting (laboratory testing every 2 to 3 hours until K+ ≥ 3.0). b. For patient with renal potassium wasting, add a potassium-sparing diuretic (spironolactone/eplerenone). c. Use saline for fluid resuscitation because dextrose fluid will worsen hypokalemia. d. Identify any reversible/underlying cause for the hypokalemia. e. Once the K+ ≥ 3.0 and the symptoms have resolved, continue with the mild/moderate algorithm. E Mild/moderate hypokalemia due to GI loss with metabolic acidosis: a. Potassium bicarbonate (acetate if IV is needed) 10 to 20 meq oral 2 to 4 times daily is the treatment of choice.

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Chapter 23  ◆  Potassium Disorders  70.e1

Abstract

Keywords

Disorders of potassium homeostasis are common in the surgical population. A stepwise and careful approach is necessary to the work-up, and management is crucial for patient care.

hyperkalemia hypokalemia rhabdomyolysis cardiac arrhythmia potassium

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Chapter 23  ◆  Potassium Disorders  71

D

A History and Exam

Emergent Therapy -calcium -insulin, dextrose -B2-adrenergic agonist -NaHCO3 -Loop diuretic/HD

C Acute symptoms

Serum K+ ≥ 6.5

E

Hyperkalemia

Prompt Therapy -NaHCO3 -Dextrose -HD

All following present: • K+ ≥ 5.5 • Significant renal impairment • Ongoing tissue breakdown

Asymptomatic

Severe renal impairment

B Basic metabolic panel ABG EKG

History and Exam -Intracellular shift -Decreased intake -Increased excretion

A

Slow Correction -Diuretic -Volume -Resin

D

C

Insulin

E Emergent Therapy

K+ ≤ 3.0 Asymptomatic

Basic metabolic panel ABG Magnesium EKG

Saline Potasium

Diabetic ketoacidosis/Nonketotic hyperglycemia

Clinical signs/symptoms

Hypokalemia

B

F

Serum K+ 4.5 – 5.5

Signs/symptoms resolved K+ ≥ 3.0 GI losses Mild/moderate hypokalemia

F Mild/moderate hypokalemia due to GI loss with metabolic alkalosis or normal serum bicarbonate level: a. KCl 10 to 20 meq orally 2 to 4 times daily. G Check magnesium level and replace accordingly. Potas­sium levels will not be restored if the patient also has hypomagnesemia. In the setting of diabetic ketoacidosis (DKA) or nonketotic hyperglycemia, the initial serum potassium may be elevated; however, the patient is truly hypokalemic due to high urinary losses. Early insulin therapy will worsen the hypokalemia by

F Metabolic acidosis

KHCO3

Metabolic alkalosis

KCl

G Renal potassium wasting

Spironolactone Primary hyperaldosteronism Chronic diuretic use

Amiloride

driving K+ into cells; therefore, saline resuscitation and delay of insulin therapy until the serum K+ ≥ 3.3 is advised. REFERENCES Ashurst J, Sergent SR, Sergent BR. Evidence-based management of potassium disorders in the emergency department. Emerg Med Pract. 2016;18(11): 1–24. Palmer BF. A physiologic-based approach to the evaluation of a patient with hypokalemia. Am J Kidney Dis. 2010;56(6):1184–1190. Palmer BJ, Cleff DJ. Physiology and pathophysiology of potassium homeostasis. Adv Physiol Educ. 2016;40:480–490. Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a clinical perspective. Nat Rev Nephrol. 2011;7(2):75–84.

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Chapter

24 

CALCIUM DISORDERS Maria B. Albuja-Cruz, MD, and Robert C. McIntyre, Jr., MD, FACS A Malignancy and primary hyperparathyroidism account for more than 80% of the cases of hypercalcemia. Other causes include thyrotoxicosis, granulomatous disease, medications, total parenteral nutrition, and immobilization. Hypercalcemia affects nearly every organ in the body and, in particular, the central nervous system and the kidneys. Neurologic symptoms include fatigue, depression, weakness, confusion, cognitive dysfunction, seizures, hallucinations, and coma. Renal effects include nephrolithiasis and nephrogenic diabetes insipidus. Gastrointestinal manifestations of hypercalcemia are nausea, vomiting, anorexia, abdominal pain, constipation, and pancreatitis. Cardiovascular effects include cardiac arrhythmias and shortening of the QT interval. B Hypocalcemia is defined as a total serum calcium (TSC) < 8.5 mg/dL. Half of the serum calcium is bound to albumin; therefore a low calcium level could simply reflect hypoalbuminemia. For this reason, calcium should be corrected to the serum albumin level (corrected calcium [CCa] = serum calcium + 0.8 [4-serum albumin]). Hypoalbuminemia—caused by cirrhosis, nephrosis malnutrition, burns, chronic illness, and sepsis—is the most common cause of hypocalcemia that has no clinical significance and requires no treatment. Hypoparathyroidism is another important cause of hypocalcemia, which most commonly results from anterior neck surgery, constituting 75% of all cases. Other causes of hypocalcemia are renal failure, hungry bone syndrome, liver disease, acute pancreatitis, hyperphosphatemia, medications, severe hypomagnesemia, and vitamin D deficiency. Clinical manifestations of hypocalcemia are paresthesia, muscle cramps, circumoral numbness, tetany, bronchospasm, laryngospasm, seizures, hyperirritability, anxiety, depression, Chvostek and Trousseau signs, prolonged QT and ST interval, coma, congestive heart failure, cataracts, alopecia, and xeroderma. C Mild hypercalcemia is defined by a TSC from 10.5 to 11.9 mg/ dL. There is no need for immediate treatment; however, it warrants a work-up to identify the cause and treatment tailored to the origin of hypercalcemia (e.g., parathyroidectomy for primary hyperparathyroidism). The patient needs to drink at least 6 to 8 glasses of water per day to minimize the risk for nephrolithiasis. D Moderate hypercalcemia is a TSC from 12 to 13.9 mg/dL. Chronic moderate hypercalcemia may not require immediate treatment; however, as with mild hypercalcemia, a work-up to identify and correct its cause is needed, as is good hydration. Acute symptomatic moderate hypercalcemia requires more aggressive therapy, as described for severe hypercalcemia. E Severe hypercalcemia is a TSC ≥ 14 mg/dL and requires immediate and aggressive treatment. The goals of therapy are as follows: (1) correct dehydration and increase renal calcium

excretion, (2) lower calcium levels, and (3) decrease osteoclastmediated bone resorption. F Acute hypocalcemia can be an endocrine emergency requiring rapid intervention. After thyroidectomy, determination of immediate postoperative calcium and parathyroid hormone (PTH) can help guide treatment. Patients with severe hypocalcemia (CCa < 7 mg/dL) or severe symptoms require immediate intravenous (IV) calcium (2 g of calcium gluconate in 100 mL IV of over 1 h) and oral calcium and vitamin D3 supplementation (calcium carbonate 1000 mg or calcium citrate 1900 mg QID plus calcitriol 0.5 mcg BID). If there is no resolution of symptoms, start calcium drip (5 g calcium in 500 mL normal saline [NS] at 50 cc/h). For patients with asymptomatic hypocalcemia (CCa 7.1 to 7.9 mg/dL) and PTH > 10, we recommend oral calcium supplementation TID. If PTH ≤ 10, we add vitamin D3 to the oral calcium supplementation. For patients with mild symptomatic hypocalcemia, we recommend oral calcium and vitamin D3 supplementation. Evaluation for hypomagnesemia and its correction are very important in the management of hypocalcemia. G Chronic hypocalcemia is mainly treated with oral calcium and vitamin D. The goals in the management of chronic hypocalcemia are to prevent signs and symptoms of hypocalcemia, maintain calcium levels between 8 and 8.5 mg/dL, maintain the calcium-phosphate product below 55 mg2/dL2, avoid hypercalciuria, avoid hypercalcemia, and avoid renal and extraskeletal calcifications. The patient should be evaluated for vitamin D deficiency (25-hydroxyvitamin D < 20 ng/mL); if present, the patient should be treated with 50,000 international units (IU) of vitamin D2 once a week for 8 weeks to achieve a blood level of 25 (OH) D above 30 ng/mL, followed by maintenance therapy of 1500 to 2000 IU/daily. H Hypercalcemic crisis is defined by severe hypercalcemia with the presence of multiorgan dysfunction. Primary hyperparathyroidism is the most common underlying etiology. In the majority of patients, definitive curative therapy requires surgical parathyroidectomy. The exact timing of parathyroidectomy is not definitively established; recent case series favor early surgery after medical optimization. I

Vigorous hydration with isotonic saline corrects dehydration and hyponatremia. Intravenous fluid (IVF) needs to be adjusted on an individualized basis, depending on both the degree of dehydration and underlying cardiac and other comorbid disease. The goal is to maintain a urinary output of 100 to 150 mL/ hr. Saline infusion reduces hypercalcemia in most patients but will not restore normocalcemia in individuals with severe hypercalcemia. Generally, a reduction of 1.6 to 2.4 mg/dL in the serum calcium may be expected with isotonic saline infusion. Calcitonin (4 to 8 IU/kg every 6 to 12 hours) lowers calcium levels by reducing osteoclastic bone resorption and promoting calciuresis. Calcitonin has a rapid onset of action within 4 to 6 hours but a modest effect, with reductions in calcium levels of approximately 1 to 2 mg/dL. The efficacy of calcitonin is limited to the first 48 hours because of the development of tachyphylaxis from downregulation of calcitonin receptors in target cells in bone and the kidney. Calcitonin is most beneficial in patients with severe hypercalcemia when combined with hydration and bisphosphonates.

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Chapter 24  ◆  Calcium Disorders  72.e1

Abstract

Keywords

Acute symptomatic calcium disorders—hypercalcemia and hypocalcemia—require immediate attention and treatment.

hypercalcemia hypocalcemia hypercalcemia crisis bisphosphonates calcitriol vitamin D

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Chapter 24  ◆  Calcium Disorders  73 Signs and Symptoms Hypercalcemia Nausea & vomiting Abdominal pain Muscular weakness Depression & Anxiety Cognitive dysfunction Pancreatitis Shortening of QT interval Nephrogenic diabetes insipidus Hypocalcemia Paresthesias Muscle cramps Tetany Bronchospasm & laryngospasm Seizures Depression & Anxiety Chvostek & Trousseau sign Prolonged QT and ST interval

C

No need for immediate treatment

Mild: Ca < 12 mg/dL

D

Chronic

Moderate: 12-14 mg/dL

A

Asymptomatic Symptomatic

Acute

E

HYPERCALCEMIA

I

Severe: >14 mg/dL

Require immediate treatment

H

Vigorous hydration Calcitonin Bisphosphonates Glucocorticoids Dialysis

HYPERCALCEMIA CRISIS Profound volume depletion Coma Cardiac decompensation Acute abdomen

CALCIUM DISORDERS Asymptomatic

B

CCa 7.1-7.9 mg/dL

HYPOCALCEMIA

Labs Calcium Albumin Ionized calcium Vitamin D Creatinine BUN Phosphorus PTH/PTHrp

F

Mild Symptoms

Acute Severe Symptoms CCa < 7 mg/dL

G Chronic

PTH > 11 PTH < 10 or > 60% drop Oral calcium supplementation Oral vitamin D3 Replace magnesium IV Calcium Oral calcium supplementation Oral vitamin D3 Replace magnesium

Oral calcium supplementation Oral calcium supplementation Oral vitamin D3 (calcitriol)

No resolution of symptoms

No resolution of symptoms

IV calcium drip

CCa 8-8.5 mg/dL Ca x Phosphate < 55 m2/dL/g2 24H Urine Ca < 300 mg/D Avoid hypercalcemia Avoid calcifications

Bisphosphonates inhibit calcium release by interfering with osteoclast-mediated bone resorption. Bisphosphonates are effective in treating hypercalcemia resulting from excessive bone resorption of any cause and are more potent than calcitonin and saline for patients with moderate or severe hypercalcemia. Their maximum effect occurs in 2 to 4 days. Zoledronic acid (ZA) and pamidronate are the bisphosphonates of choice. ZA (4 to 8 mg IV) is favored by some because it is more potent than pamidronate (60 to 90 mg IV) and can be administered over a shorter period of time (15 minutes vs. 2 hours). Glucocorticoids (prednisone 20 to 40 mg/day) may be useful in a limited subset of individuals with hypercalcemia secondary

to chronic granulomatous diseases (e.g., sarcoidosis), multiple myeloma, and lymphoma. Dialysis is a last-resort treatment for severe hypercalcemia and may be indicated in patients with severe malignancyassociated hypercalcemia and renal insufficiency or heart failure, in whom hydration cannot be safely administered. REFERENCES Albuja-Cruz MB, et al. A “safe and effective” protocol for management of post-thyroidectomy hypocalcemia. Am J Surg. 2015;210(6):1162–1169. Brandi ML, et al. Management of hypoparathyroidism: summary statement and guidelines. J Clin Endocrinol Metab. 2016;101:2273–2283. Goltzman D. Approach to hypercalcemia. NCBI Bookshelf. NIH; 2016.

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Chapter

25 

HYPOTHERMIA Bruce C. Paton, MD Hypothermia is defined as a core temperature of 32° C

Transport to nearest hospital

G Confused

CV stable

H Hypothermia core temperature >35° C

B Labs Core temperature Basic metabolic panel ECG Urine Toxicology screen Echocardiogram X-rays CT scans

CV unstable

D Vital signs present Unconscious 15. B Risk factors for the development of skin cancer include exposure to ultraviolet (UV) radiation through sun exposure (varying by geography), tanning beds, and therapeutic exposure, for example, in the treatment of psoriasis. Those with increased sensitivity to UV light are also at greater risk, including those with a fair complexion, blue or green eyes, and propensity for sunburn. Genetic syndromes such as xeroderma pigmentosum, basal cell nevus syndrome, Muir-Torre syndrome (a subset of Lynch syndrome), syndrome of multiple trichoepitheliomas, and dysplastic nevus syndrome predispose to skin cancers, often at an early age. Conditions associated with skin cancer include oral lichen planus, history of solid organ transplant, and chronic immunosuppression. Actinic keratosis (AK), Bowen’s disease, and keratoacanthoma are predisposing or pre-malignant lesions. AK lesions are scaly, circumscribed, rough, erythematous, sun-induced pre-malignant lesions that histologically may mimic squamous cell cancer. They are typically found on the head and neck of middle-aged and elderly individuals. Malignant conversion to squamous cell carcinoma is estimated at 0.1% per year. C A histological diagnosis is needed to ensure proper identification and adequate treatment. The microscopic features of each lesion are predictive of clinical behavior, recurrence, and metastasis. The treatment for melanoma, for example, differs significantly from that of basal cell carcinoma; thus, diagnosis should be confirmed by biopsy before treatment. Although biopsy technique (punch, shave, incisional, excisional) may vary between medical specialties, a full-thickness skin biopsy consisting of epidermis, dermis, and a portion of the subcutaneous tissue including a margin of uninvolved skin is indicated. Biopsies are easily performed in a clinic setting. D Cutaneous neoplasms are the most commonly diagnosed malignancy, with the majority arising on sun-exposed regions of the head and neck. Ninety-six percent of these are nonmelanoma skin cancers (NMSCs), with basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) comprising nearly the entirety of this subset at a 4 : 1 ratio. The incidence of skin cancer

has been rising rapidly since the 1960s, with more than 1 million cases of NMSC in the United States each year. The mortality caused by NMSC is low, with an estimated 95% 5-year survival rate. NMSCs, however, can be locally aggressive and result in considerable disfigurement, loss of function, and health-care costs. Staging: The staging of both basal and squamous cell carcinomas is based on the American Joint Commission on Cancer’s TNM system. The presence of certain high-risk factors plays into the tumor burden (T) staging: depth > 2 mm, Clark level ≥ IV, perineural invasion, location on the ear or hair-bearing lip, and poorly differentiated or undifferentiated lesions. Tumors of the eyelid are excluded from this staging system. T1 lesions are staged as stage I if the tumor is 2 cm or less in greatest dimension and has zero or only one high-risk feature. T2 lesions (more than 2 cm or any size with two or more high-risk features) are considered stage II. Stage III lesions have either a lesion invading the maxilla, mandible, orbit, or temporal bone (T3) or metastasis measuring 3 cm or smaller to a single ipsilateral lymph node (N1) with T1–T3 tumor. Stage IV lesions have more significant nodal involvement or a T4 lesion (invasion of axial or appendicular skeleton or perineural invasion of the skull base). Locoregional evaluation: The most common sites for metastasis of cutaneous SCC are regional lymph nodes. BCC metastasizes even less frequently than SCC, and as a result, the data for evaluation of nodes are sparser. All patients should undergo lymph node examination by palpation at the time of diagnosis and during follow-up. Patients with palpable nodes or suspicious nodes on imaging should undergo fine-needle aspiration (FNA) or surgical excision. There are no definitive guidelines for management of patients without palpable nodes. The presence of a large tumor > 2 cm or multiple high-risk features may prompt the clinician to obtain additional imaging to evaluate locoregional metastasis—typically computed tomography (CT) or magnetic resonance imaging (MRI)—but there are insufficient data to guide management. The modality depends on preference and institutional experience, but CT may be better for discriminating bony involvement. Although sentinel lymph node (SLN) biopsy is common in the management of cutaneous melanoma, SLN biopsy has not shown any benefit to patient outcomes in BCC or SCC, and it is not routinely recommended. E Basal cell carcinoma is the most common cutaneous malignancy and represents 75% of all NMSCs. More than 2 million BCCs are treated annually in the United States. The lifetime risk for the development of BCC in Caucasians is approximately 30%, and the incidence is increased in men and with increasing age. Seventy percent of BCCs arise on the head and neck, and 30% alone are found on the nose, making it the most common site for BCC. Although metastasis is very rare, without treatment, BCCs are characterized by slow, locally destructive invasion that can result in high morbidity. BCCs can be divided into several subtypes based on clinical and histologic patterns: nodular (most common, 75%), superficial, micronodular, infiltrative, morpheaform, and basosquamous carcinoma. Nodular BCC clinically presents as a well-defined, pearly, translucent nodule with a rolled border. Telangiectasias are commonly seen on the surface of the nodule. Central ulceration or bleeding may be present. Superficial BCCs (10%) are erythematous, scaly, discrete macules or slightly elevated papules that can resemble an eczematous dermatitis. Micronodular, infiltrative, and morpheaform BCCs (10%) have a more aggressive

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Chapter 27  ◆  Nonmelanoma Skin Cancer of the Face  82.e1

Abstract

Keywords

Cutaneous neoplasms are the most commonly diagnosed malignancy, with the majority arising on sun-exposed regions of the head and neck. Most are nonmelanoma skin cancers (NMSCs), with basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) comprising 95% of this subset. The incidence of skin cancer has been rising rapidly since the 1960s, with more than 1 million cases of NMSC in the United States each year. The mortality caused by NMSC is low, with an estimated 95% 5-year survival rate. NMSCs, however, can be locally aggressive and result in considerable disfigurement, loss of function, and health-care costs.

skin cancer squamous cell carcinoma basal cell carcinoma dermatofibrosarcoma protuberans angiosarcoma Merkel cell carcinoma head and neck scalp face sentinel lymph node biopsy

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Chapter 27  ◆  Nonmelanoma Skin Cancer of the Face  83 Re-excision Mohs surgery

A Prevention

Positive margin

J E

Suspicious lesion

Standard excision

Surveillance Negative margin

Basal cell carcinoma

History and physical examination Risk factors Syndromes Predisposing lesion

F D NON-MELANOMA SKIN CANCER OF THE FACE

Biopsy

Mohs micrographic surgery

Squamous cell carcinoma

B

M

Non-surgical therapies

K

L

G Merkel cell carcinoma

C

Wide local excision/Mohs micrographic surgery Radiation

H Dermatofibrosarcoma protuberans (DFSP)

Wide local excision/Mohs micrographic surgery

I Angiosarcoma

histologic appearance and clinical course. They appear as flat, white or yellow plaques or have a scar-like appearance with ill-defined margins. Basosquamous carcinomas are rare, showing histologic evidence of both basal cell and squamous cell differentiation with increased rates of growth and metastasis compared with BCC. Location of the tumor also can influence the chance of incomplete excision and recurrence. Areas like the ear and inner canthus region have little protective fat, and consequently, BCCs invade quickly through the dermis into deeper tissues. Significantly more BCCs recur in the midface or around the ears. Recurrence rates also increase with tumor size, duration, and neglected or inadequately excised tumors. F Squamous cell carcinoma comprises approximately 20% of NMSCs and presents with varied clinical manifestations and can correlate with the level of tumor differentiation. Welldifferentiated lesions can appear firm or indurated as hyperkeratotic papules, plaques, or nodules. Poorly differentiated lesions are typically ill-defined, fleshy, soft nodules with or without ulceration, hemorrhage, or necrosis. For primary cutaneous SCC, the 5-year cure rate is more than 90%. The risk for metastasis is 2% to 5% and occurs in local or regional lymph nodes. Overall 5-year survival in patients with nodal disease is as low as 50%, improved with the addition of radiation therapy. Fifty-five percent of SCCs are located on the head and neck, but specific areas are at higher risk for recurrence and metastasis: eyelid, eyebrow, periorbital skin, nose, lip, chin, mandible, ear, and pre- and postauricular skin. As with

Surgical excision Radiation

BCC, the eyelids, periorbital areas, and ears are more susceptible to rapid invasion of deeper tissues resulting from a lack of protective fat. On the lower lip, the accompanying dense inflammatory infiltrate makes an assessment of the true depth of invasion difficult. On the nasal septum, SCCs frequently invade to the bone of the nasal spine. SCCs can also arise in areas that were previously scarred or ulcerated, as in burns and chronic ulcers. Tumors that arise in scars or chronic wounds are more aggressive, with a metastatic rate between 18% and 38%. SCCs arising in immunocompromised patients may be multiple, grow rapidly, and have aggressive clinical courses. G Merkel cell carcinoma (MCC) is a very rare, highly malignant tumor derived from neuroendocrine cells. At presentation, 26% have regional lymph node involvement, and 8% have distant metastases. It predominantly affects fair-skinned men with a mean age of diagnosis of 74 years. However, in patients who are immunocompromised, including those with solid organ transplants, HIV, and B-cell malignancies, MCC occurs at a younger age. They typically present as a rapidly growing, painless, firm nodule that may be shiny, flesh-colored, or bluish-red. Forty-three percent are located on the head and neck and are associated with a worse prognosis. Although biopsy-confirmed MCC in other locations would warrant sentinel lymph node biopsy, the utility is unclear in head and neck primary lesions because of highly variable lymphatic drainage. Treatment includes wide local excision, although areas of the head and neck are typically prohibitive of wide margins. Mohs micrographic surgery can ensure total excision of the lesion.

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84  Part III  ◆  Head & Neck Radiation therapy has also been shown to increase overall survival and improve local and regional tumor control. H Dermatofibrosarcoma protuberans (DFSP) is a rare, locally aggressive cutaneous soft tissue sarcoma. In the United States, the incidence is estimated to be 0.8 to 4.5 cases per million persons per year. DFSP most commonly arises in adults in their 30s as an asymptomatic and slow-growing indurated plaque with varying color appearance. Thirteen percent are located on the head and neck. Surgical resection is the optimal treatment for DFSP. There is no consensus on adequate margin for a wide local excision, and tumors on the face are typically prohibitive of large margins; 33% to 50% of patients have local recurrence after excision, typically within 3 years. Given that DFSP is a locally aggressive tumor with high local recurrence rates, Mohs micrographic surgery on lesions of the face allows for the lowest recurrence and narrowest margins. Very rarely do the lesions metastasize, rendering lymph node dissection unnecessary. I

Angiosarcomas arise in blood or lymphatic vessels and are associated with poor prognosis, local recurrence, and distant metastases. Five-year survival is less than 40%. They tend to be seen in older Caucasian men, and 5% to 20% of patients report prior history of radiotherapy to the face or scalp. On presentation, the lesions appear as a purple papule or nodule for early lesions and a large, flat, bruise-like plaque for more delayed cases. Small lesions can be treated with wide local excision and immediate reconstruction combined with either pre- or postoperative radiation therapy. Radiation is the primary therapy for larger lesions not amenable to surgery. Adjuvant chemotherapy has no proven value for local disease. J

For most cases of BCC and SCC, the treatment of choice is surgical excision. In SCCs with low risk for recurrence, a 4-mm resection margin is adequate. Low-risk lesions are well defined; nonrecurrent; 1, and a shave biopsy that is broadly positive at the base, should be considered for sentinel node biopsy. The use of sentinel node biopsy in melanomas > 4 mm may be used to risk stratify patients. Sentinel lymph node status was found to be an independent prognostic indicator, with 3-year overall survivals of 89.8% and 66.4% for sentinel lymph node negative and positive, respectively. This may have particular significance in the head and neck where local, regional control is of the utmost importance. K   SENTINEL NODE NEGATIVE

Patients with a sentinel node negative biopsy are placed in a surveillance program. The most important predisposing factor for melanoma is the history of a previous melanoma. Careful skin evaluation three to four times a year is indicated. A false-negative

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Chapter 28  ◆  Management of Melanoma of the Head and Neck  86.e1

Abstract

Keywords

In cutaneous lesions of the head and neck, suspicion is based on size greater than 6 mm, border irregularity, uneven distribution of color, asymmetric shape, or bleeding. Any preexisting lesion that is identified by the patient as having undergone some change (size, shape, color, texture) may be considered as suspicious.

head and neck melanoma

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Chapter 28  ◆  Management of Melanoma of the Head and Neck  87

C

Observation

Benign lesion Excision, minimal margin

D Premalignant lesion

A Suspicious lesion Biopsy

E

Hyperplasia

Excision, 2−3 mm margin

Severe dysplasia

Excision, 5 mm margin

Early stage Tis&T1

J

F Head & Neck Melanoma

Invasive melanoma > 1 mm

Excision, 2 cm margin

G Positive FNAB

K

Excision, 1 cm margin

Completion lymphadenectomy

SLNB

Positive SLNB

Completion lymphadenectomy

Negative SLNB

Surveillance

H Palpable mass Parotid or Neck

FNAB

B

Negative FNAB

L

Treat primary disease & surveillance

I Non-diagnostic FNAB

rate of less than 1% is possible with the use of radioactive tracer for lymphoscintigraphy and vital blue dye. L   POSITIVE SENTINEL NODE

Completion lymphadenectomy is the standard of care for these patients with proven regional metastatic disease. In the head and neck, this is complicated by a number of factors. A positive sentinel node in the parotid gland is managed with a superficial parotidectomy. There are no randomized controlled trials looking at the extent of dissection needed for regional control distal to the parotid bed. Because the standard parotidectomy incision extends into the neck, it is reasonable to extend the dissection into the neck to clear the contiguous cervical basin. Dissection of levels I, II, and III is carried out along with a superficial parotidectomy. For positive cervical sentinel nodes, the patient will need a selective neck dissection. The levels most at risk will need to be addressed. With a positive sentinel node in level V, levels II, III, IV, and V will need to be dissected. Level I, the submandibular

Open biopsy

nodes, is low risk and can be spared. A positive sentinel node in level I or submental nodes will require lymphadenectomy of levels I, II, III, and IV. Level V is a low-risk basin in these patients and can be spared in the dissection. REFERENCES Gershenwald JE, Mansfield PF, Lee JE, Ross MI. Role for lymphatic mapping and sentinel lymph node biopsy in patients with thick (> or = 4 mm) primary melanoma. Ann Surg Oncol. 2000;7(2):160–165. Kenady DE, Brown BW, McBride CM. Excision of underlying fascia with a primary malignant melanoma: effect on recurrence and survival rates. Surgery. 1982;92(4):615–618. Rosko AJ, Vankoevering KK, McLean SA, Johnson TM, Moyer JS. Contemporary management of early-stage melanoma: a systematic review. JAMA Facial Plast Surg. 2017;19(3):232–238. Sagebiel RW. Diagnosis and management of premalignant melanocytic proliferations. Pathology. 1985;17(2):285–290. Tufaro A, Califano J, Mithani S, Shah S. Neck dissection and parotidectomy in melanoma. In: Balch C, Houghton A, Sober A, et al, eds. Cutaneous Melanoma. 5th ed. St. Louis MO: Quality Publishing; 2009.

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Chapter

nodules. Follow-up imaging ranges from 3 to 12 months, with earlier imaging needed for more suspicious nodules.

29 

LUNG NODULE Patrick D. Kohtz, MD, and Michael Weyant, MD A Cigarette smoking remains the dominant risk factor for the development of lung cancer. The only current indications for the use of computed tomography (CT) scans to identify lung cancer is in patients 55 to 80 years old, with a smoking history of 30 pack-years or greater, and currently smoke or who have quit within 15 years (National Lung Cancer Screening Trial). Symptoms of early-stage lung cancer are rare, and when symptoms such as cough, dyspnea, weight loss, and chest pain present, it may indicate a more advanced malignancy. Paraneoplastic syndromes are seen in small-cell lung carcinomas (SCLCs), such as Lambert-Eaton, syndrome of inappropriate antidiuretic hormone secretion (SIADH), carcinoid syndrome, and Cushing’s syndrome (adrenocorticotropic hormone [ACTH]-secreting). Occupational and environmental exposures that are linked to lung cancer include arsenic, chromium, nickel, cadmium, silica, radon, and asbestos. B The widespread utilization of CT scans of the chest and abdomen illustrates the importance of managing incidentally found nodules appropriately. It is estimated that approximately 150,000 pulmonary nodules are detected annually in the United States, and 90% of these are found incidentally. Incidentally discovered pulmonary nodules ( 2 L (>60% predicted), VO2Max > 15 mL/kg/min, and DLCO > 50% predicted will tolerate up to a pneumonectomy. Patients are at higher risk for significant morbidity and mortality with pulmonary anatomic resection if their FEV1 < 1.2 L (4-6 mm

• • • • • •

• • • • • • • •

>6-8 mm >8 mm

CT at 12 months If stable, no further follow-up Initial CT at 6-12 months If stable, repeat CT at 18-24 months CT at 3, 9, and 24 months Consider PET or biopsy

CT at 12 months If stable, no further follow-up Initial CT at 6–12 months If stable, repeat CT at 18–24 months Initial CT at 3–6 months If stable, repeat CT at 9–12 months and 24 months CT at 3, 9, and 24 months Consider PET or biopsy

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Chapter 29  ◆  Lung Nodule  90.e1

Abstract Lung cancer is the leading cause of cancer death in the United States and all lung nodules must be considered cancerous until proven otherwise. Recent developments in the treatment of non-small cell lung cancer can make managing this disease more challenging compared to the past. This chapter will help surgeons diagnose, treat and monitor lung nodules in a rapidly changing field of thoracic surgery.

Keywords lung Nodule fleischner Society Surveillance non-small cell lung cancer small cell lung cancer

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Chapter 29  ◆  Lung Nodule  91 squamous cell carcinoma (SCC), large-cell carcinoma, and adenosquamous, among other less common histologies. Table 29.2 outlines the most recent International Association for the Study of Lung Cancer (IASLC) lung cancer TNM staging, and Table 29.3 outlines the American Joint Committee on Cancer (AJCC) 8th edition anatomic staging and prognostic groups for NSCLC. The clinical management of neuroendocrine tumors (carcinoid, large cell) is done in the same manner as for NSCLCs. Carcinoid lung cancers account for 2% of all lung cancers and are centrally located 40% of the time, and carcinoid syndrome presents in only 2% of cases when metastatic disease is present (usually liver). Five-year survival rates are 90% for typical carcinoids and 60% for atypical carcinoids. Large-cell neuroendocrine tumors are high-grade tumors with 5- and 10-year survival rates of 27% and 9%, respectively. Neuroendocrine tumors share the same TNM/anatomic staging classifications as SCLCs (Tables 29.2, 29.4).

I

All patients with known lung cancer should undergo some form of mediastinal lymph node staging, usually with endobronchial ultrasound (EBUS) or mediastinoscopy. Patients with proven mediastinal lymph node involvement should undergo a multidisciplinary evaluation to determine the appropriate form of therapy, whether it is neoadjuvant therapy before surgery or definitive chemoradiotherapy without surgery.

H SCLC is highly responsive to chemotherapy (response rates 75% to 90%), depending on the extent of disease, when compared with NSCLCs. Fewer than 10% of all patients diagnosed with SCLC are seen by a surgeon because of most patients having advanced disease. The AJCC 7th edition SCLC and neuroendocrine TNM staging is analogous to the NSCLC TNM staging system (IASLC, Table 29.2) and is applied to the AJCC anatomic staging classification. Table 29.4 displays the AJCC 7th edition anatomic staging/prognostic groups for both SCLC and neuroendocrine lung cancers.

K Patients with T1-2N0 disease, diagnosed in less than 5% of all SCLC patients, are managed surgically in a similar fashion to NSCLC; however, almost universally, chemotherapy and radiotherapy are added adjuvantly. Patients without mediastinal disease who receive surgery have a 5-year survival rate of 30% to 50%.

J

Patients with superior sulcus or Pancoast tumors usually are offered neoadjuvant combined chemotherapy and radiation therapy before surgery. This increases the chances of a complete R0 resection. Patients with a complete response to this therapy have a 2-year and 5-year survival of 70% and 53%, respectively. Other lung cancers with chest wall involvement should undergo en bloc resection of the chest wall and lung. Adjuvant therapy is then determined by the true pathologic findings.

L Patients with advanced disease in excess of T1-2N0 disease receive definitive chemoradiation. If a partial or complete response occurs to systemic therapy, response assessment with N3 Disease

History & Physical A - Age - Weight loss - Smoking history - Previous cancer history - Occupational/Infectious exposure history - Family history - Lung disease

Radiologic surveillance

T1-3, N0-3 (Stage I-IIIA)

Radiographic D CT Chest/Abdomen PET-CT Brain MRI Bone scan

Lung Nodule

Laboratory CBC, BMP Genetic markers PFTs

E

F Pathologic Sputum cytology Bronchoscopy TBNA, EBUS, EUS FNA Radiologic Studies Thoracentesis Mediastinoscopy - Chest X-ray B VATS - Chest CT - Incidental nodules Open surgical biopsy - High-risk patient imaging Smoking cessation Nutrition assessment

Chemo

M

I

C

ChemoRT

Surgery

ChemoRT alone

N

Surgery

Chemo ± RT

N1 Disease

Surgery

Chemo

N0 Disease

Surgery Inoperable

O1

Q

R

Observe/Surveillance

Margin Negative Resection

Surveillance

Chemo ± RT

O2

J

Margin Positive Resection

Re-resection ± Chemo ± RT Chemo ± RT

Superior sulcus tumor Chest wall/proximal airway tumor Unresectable Stage IIIA (T4, N0-1) Stage IIIB (T1-3N3, T4N2-3) Stage IV P Metastatic disease

H

Surgery

N2 Disease

G Non-Small Cell Lung Cancer - Adeno CA - SCC - Carcinoid - Neuroendocrine

Reassess Progress

Chemo ± RT

K

Small Cell Lung Cancer

L

Clinical stage T1-2, N0

ChemoRT En bloc resection

Surgery Adjuvant therapy

Chemo ± RT

S Surgery

Chemo ± RT

Surveillance

Clinical stage in excess of T1-2, N0

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92  Part IV  ◆ Thoracic TABLE 29.2  The International Association for

TABLE 29.3  American Joint Committee on

Primary Tumor (T)

When T is…

And N is…

And M is…

Then the Stage group is…

TX Tis t1mi t1a t1a t1a t1a t1b t1b t1b t1b t1c t1c t1c t1c t2a t2a t2a t2a t2b t2b t2b t2b t3 t3 t3 t3 t4 t4 t4

N0 N0 N0 N0 n1 n2 n3 N0 n1 n2 n3 N0 n1 n2 n3 N0 n1 n2 n3 N0 n1 n2 n3 N0 n1 n2 n3 N0 n1 n2 n3 Any N Any N Any N

m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m0 m1a m1b m1c

Occult carcinoma 0 IA1 IA1 IIB IIIA IIIB IA2 IIB IIA IIIB IA3 IIb IIIA IIIB IB IIB IIIA IIIB IIa IIB IIIA IIIB IIB IIIA IIIB IIIC IIIA IIIA IIIB IIIC IVA IVA IVB

the Study of Lung Cancer (IASLC) TNM staging of NSCLC.

Tx T0 Tis T1a (mi) T1a T1b T1c T2aa T2ba T3

T4

Description Cannot be assessed; malignant cells in sputum/ bronchial washings but not visualized No evidence of primary tumor Carcinoma in situ Minimally invasive adenocarcinoma Tumor ≤ 1 cm in greatest dimension, not invading main bronchus >1 cm but ≤2 cm, not invading main bronchus >2 cm but ≤3 cm, not invading main bronchus >3 cm but ≤4 cm >4 cm but ≤5 cm >5 cm but ≤7 cm, separate tumor nodule(s) in a different ipsilateral lobe or directly invades one of following: chest wall (parietal pleura, superior sulcus tumor), phrenic nerve, parietal pericardium >7 cm, separate tumor nodule(s) in different ipsilateral lobe or invading any of the following: diaphragm, mediastinum, heart, great vessels, trachea, recurrent laryngeal nerve, esophagus, vertebral body, carina

Regional Lymph Nodes (N) Nx Cannot be assessed N0 No regional lymph node metastasis N1 Metastasis in ipsilateral peribronchial and/or ipsilateral hilar lymph nodes and intrapulmonary nodes, including involvement by direct extension N2 Metastasis in ipsilateral mediastinal and/or subcarinal lymph node(s) N3 Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph node(s) Distant Metastasis (M) Mx Cannot be assessed M0 No distant metastasis M1a Separate tumor nodule(s) in a contralateral lobe; tumor with pleural or pericardial nodule(s); malignant pleural or pericardial effusion M1b Single extrathoracic metastasis M1c Multiple extrathoracic metastases in one or more organs a T2 tumors may invade the main bronchus, regardless of distance from the carina, but do not invade the carina; they invade the visceral pleura and are associated with atelectasis or obstructive pneumonitis extending to the hilar region involving part of or the entire lung.

CT imaging (chest/liver/adrenals) and brain MRI should take place. Prophylactic cranial irradiation should be administered in limited disease, with the addition of thoracic radiation therapy in extensive disease. If metastatic brain disease is present, wholebrain radiation therapy with chemotherapy should be given. M N3 disease undergoes chemotherapy with or without radiation therapy (Stage IIIA shows no survival benefit) as initial treatment. Stage IIIA (T3N2M0) disease is under debate about

Cancer (AJCC) 8th edition anatomic staging and prognostic groups for NSCLC.

Any T Any T Any T

From the AJCC Cancer Staging Manual 8th edition, Springer

which treatment route is the best for surgery first versus neoadjuvant chemoradiation. Patients should be part of a multidisciplinary clinic for all therapeutic and follow-up treatment plans. Some randomized trials have shown no overall survival benefit with resection, but this patient population is heterogeneous, and case-by-case decisions should be made for N2 disease. Multiple randomized trials have been completed that show some improvement in resectability and survival for neoadjuvant therapy when compared with surgery or radiation alone. It is accepted that patients with this stage disease and one N2 lymph node smaller than 3 cm would benefit from surgical resection and lymph node dissection. N Patients with N0/N1 disease (after mediastinal lymph node biopsy) and resectable disease undergo surgery as the primary therapy for lung tumors Stage IIIA (T3N1) or less. O The mainstay of treatment for Stage I and II lung cancers is surgical resection with systematic lymph node sampling

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Chapter 29  ◆  Lung Nodule  93 TABLE 29.4  AJCC 7th edition anatomic

staging for both SCLC and neuroendocrine lung cancers. Anatomic Staging

TNM Stage(s)

Occult carcinoma Stage 0 Stage IA

Tx Tis T1a T1b T2a T2b T1A T1b T2a T2b T3 T1a T1b T2a T2b T3 T3 T4 T4

Stage IB Stage IIA

Stage IIB Stage IIIA

Stage IIIB

Stage IV

T1a T1b T2a T2b T3 T4 T4 Any T Any T

N0 N0 N0 N0 N0 N0 N1 N1 N1 N1 N0 N2 N2 N2 N2 N1 N2 N0 N1 N2 N3 N3 N3 N3 N3 N3 N3 Any N Any N

M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M1a M1b

AJCC Cancer Staging Manual, 7th edition, Springer Verlag 2010

or dissection. Patients should have N1 and N2 lymph node dissection with a minimum of 3 stations of N2 lymph nodes removed from the ipsilateral side of resection. Adequate mediastinal lymphadenectomy depends on the side of the primary tumor (right—2R, 4R, 7 to 9; left—4L, 5 to 9), but no survival advantage exists for complete mediastinal lymph node dissection versus sampling. Tumors extending into adjacent structures (e.g., chest wall, pericardium, diaphragm) should have en bloc resection along with the pulmonary resection. Segmentectomy and wedge resections should have margins of greater than 2 cm or greater than the size of the nodule, and sleeve lobectomy (lung-sparing), when possible, is preferred over pneumonectomy (improved operative mortality and 5-year survival) if margin-negative resection is possible. Lobectomy is performed for Stage IB (and larger) tumors unless centrally located invading vital bronchial/ vascular structures. The surgical approach should be dictated by surgeon experience; however, minimally invasive resections should be used when possible in early-stage lung cancer. O1. Margin-negative (R0) disease undergoes observation only in Stage IA disease, whereas Stage IB, IIA (T2bN0) will be observed unless high-risk features (e.g., poorly

differentiated, vascular invasion, wedge resection, tumor > 4 cm, visceral pleural involvement, Nx disease) exist; then adjuvant chemotherapy treatment may be considered. All other Stage IIA, IIB, and IIIA (T1 to T3, N1 to N2) R0 resections undergo adjuvant chemotherapy with radiation therapy added only for N2 disease. O2. Margin-positive (R1 = microscopic, R2 = macroscopic) resections should undergo re-resection when feasible, with adjuvant radiotherapy being used to treat residual disease focally. In some cases, chemoradiation may be the only option if no further surgical intervention is possible. P These are all advanced disease clinical scenarios where surgery is generally excluded and combinations of chemotherapy and radiotherapy are often used as the mainstay of treatment. Q If the primary tumor is inoperable but mediastinal staging (typically by EBUS-TBNA) does not show node-negative disease, patients will undergo definitive radiation therapy with the addition of chemotherapy in Stage IB (or higher staging) and N1 disease. Patients then enter a supportive/palliative management care program. R Surveillance for NSCLC requires patients to be evaluated with history and physical, chest CT (+/– contrast) every 3 to 6 months for the first 3 years and then every 6 months for the next 2 years to screen for locoregional recurrence or metastatic disease. PET/CT and brain MRI is not routinely recommended for reassessment. Recurrent or persistent disease is managed with further chemotherapy and/or radiation. If no progression is present, surgical resection is warranted with adjuvant therapy, particularly in Stage IIIA (i.e., T3N2M0) disease. S Surveillance after primary therapy for SCLC requires patients to follow up every 3 to 4 months for the first 1 to 2 years and then every 6 months for the next 3 to 5 years. Patients at these visits should have a history and physical, CT chest/liver/ adrenal, and blood work as clinically indicated. If new primary pulmonary nodules are discovered, they should receive full work-up because patients who survive SCLC can develop NSCLC primary lung tumors. The average risk for developing a new primary pulmonary tumor in SCLC patients is 6% annually. REFERENCES Darling GE, Allen MS, Decker PA, et al. Randomized trial of mediastinal lymph node sampling versus complete lymphadenectomy during pulmonary resection in the patient with n0 or n1 (less than hilar) non-small cell carcinoma: results of the American College of Surgery oncology group z0030 trial. J Thorac Cardiovasc Surg. 2011;141:662–670. Howington JA, et al. Treatment of stage I and II non-small cell lung cancer: diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013;143(5 suppl):e278S–e313S. Narsule CK, Ebright MI, Fernando HC. Sublobar versus lobar resection: current status. Cancer J. 2011;17:23–27. Rivera MP, Mehta AC, Wahidi MM. Establishing the diagnosis of lung cancer: diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013;143:e142S–e165S. Whitson BA, Groth SS, Duval SJ, et al. Surgery for early-stage non-small cell lung cancer: a systematic review of the video-assisted thoracoscopic surgery versus thoracotomy approaches to lobectomy. Ann Thorac Surg. 2008;86:2008–2016, discussion 2016–2008.

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Chapter

30 

MEDIASTINAL TUMORS Hai Nguyen Salfity, MD, Thomas A. D’Amico, MD, and DuyKhanh Ceppa, MD INTRODUCTION Primary mediastinal tumors are rare, and the epidemiology of these neoplasms differs between children and adults (Table 30.1). Overall, the prevalence in adults has steadily increased secondary to the rise in the use of computed tomography (CT) in clinical practice (lung cancer screening programs). More than 50% of these masses are incidental findings on radiography, and thus treatment is directed by and dependent on the type of tumor and symptoms. A Approximately 62% of patients are symptomatic with chest pain (30%), fever (20%), cough (16%), fatigue (6%), or dysphagia (4%). Compression and/or invasion of adjacent structures can lead to pain, hoarseness, and a variety of associated syndromes (superior vena cava, Horner’s, or Cushing’s syndrome). Hormone production can manifest systemically in the form of myasthenia gravis, thyrotoxicosis, hypertension, and hypercalcemia. Patients with malignant disease are more likely to be symptomatic than patients with benign disease (85% vs. 46%). The initial step in evaluating a patient suspected to have a mediastinal tumor is performing a thorough history and physical. B Symptomatic patients can first be evaluated by plain radiography of the chest; however, clinical practice has moved toward recommending CT as the initial test. Localization and characterization of these neoplasms with cross-sectional TABLE 30.1  Mediastinal Tumors, Locations,

and Frequencies in Adult Versus Pediatric Population Thymoma, % Neurogenic tumors, % Cysts, %   Bronchogenic   Esophageal   Pericardial Germ cell tumors, %   Teratoma   Seminoma   Nonseminoma Lymphoma, % Endocrine tumors, %

Adult

Pediatrics

26.5 20

8000 mm Hg•s•cm. Hypercontractility may involve, or even be localized to, the LES. Absent contractility: Normal median IRP and 100% failed peristalsis. Achalasia should be considered with borderline IRP values and when there is evidence of esophageal pressurization. Premature contractions with DCI values less than 450 mm Hg•s•cm meet criteria for failed peristalsis. F Minor Motility Disorders is a category of disorders that continues to be debated and was simplified for the updated Chicago Classification v3.0. These disorders include ineffective esophageal motility and fragmented peristalsis. The clinical significance and treatment of these disorders are areas of active clinical research. Ineffective esophageal motility (IEM): Defining feature is poor bolus transit in the distal esophagus. It is defined by HRM as ≥50% infective swallows. Ineffective swallows can be failed or weak swallows with DCI < 450 mm Hg•s•cm. Fragmented peristalsis: ≥50% fragmented contractions with DCI > 450 mm Hg•s•cm. This disorder pertains to large breaks in the normal peristaltic wave. It is thought that large breaks (>5 cm) may have clinical significance. G In patients with a documented primary motility disorder, whose primary symptom is dysphagia or chest pain, a trial of calcium channel blocker (diltiazem 60 mg four times a day as needed, switch to extended release if symptoms improve) is the initial treatment of choice. Calcium-channel-blocker therapy requires close monitoring of the patient’s blood pressure and coordination with the primary care provider if the patient is already taking another antihypertensive. A tricyclic antidepressant (trazodone 100 to 150 mg/day or imipramine 25 to 50 mg at bedtime) is another option in patients primarily presenting with chest pain. Some patients may experience symptom relief with the smooth muscle relaxation of a nitric oxide–donating drug (sildenafil 50 mg PRN). Additionally, high-concentration peppermint oil may relieve chest pain in DES. For refractory patients, upper endoscopy with injection of botulinum toxic (Botox) can improve dysphagia but has not been shown to significantly improve chest pain, reflux, or regurgitation. It has the disadvantage of temporary effect, requiring repeat endoscopy (usually every 6 months).

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Chapter 33  ◆  Esophageal Motility Disorders (Other Than Achalasia)  104.e1

Abstract

Keywords

Esophageal motility disorders other than achalasia are seen in patients presenting with dysphagia, noncardiac chest pain, or refractory heartburn or regurgitation. The diagnosis is made with high-resolution manometry as defined by the 2015 Chicago Classification v3.0. Optimal patient management remains controversial and an active area of research, with medical, surgical, and endoscopic treatment options available.

esophageal motility disorders high-resolution manometry diffuse esophageal spasm jackhammer esophagus

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Chapter 33  ◆  Esophageal Motility Disorders (Other Than Achalasia)  105 Achalasia (see achalasia)

H

G A History

E

C B

Esophageal motility disorder

Trial of medical therapy

Carcinoma (see carcinoma of the esophagus)

Dysphagia Chest pain regurgitation reflux

Upper gastrointestinal endoscopy +/− biopsy

Major motility disorder Distal esophageal spasm

D No carcinoma or structural abnormality

Highresolution manometry

Hypercontractile esophagus (Jackhammer) Absent contractility

Labs EKG CXR Barium swallow Upper GI series Esophageal pH/Impedance

No improvement

Consider surgical therapy Heller myotomy POEM (long myotomy)

Evidence of GERD Esophagitis Barrett’s esophagus (see GERD)

H For patients who do not respond to medical treatment, there are limited data about the efficacy of surgical options for esophageal motility disorders other than achalasia. Data for laparoscopic or thoracoscopic Heller myotomy for the treatment of esophageal motility disorder other than achalasia predate the current disease definitions based on the Chicago Classification v3.0. For DES, a long myotomy (extension of the myotomy onto the level of the thoracic aorta) has been shown to improve dysphagia symptoms in 80% to 86% of patients, and chest pain can be relieved in 75% to 80% of patients. Per-oral endoscopic myotomy (POEM) is emerging as a potential treatment for spastic esophageal disorders, including DES and jackhammer esophagus. POEM is a flexible endoscopic approach to the LES providing access for myotomy to relieve dysphagia. In the case of spastic esophageal disorders, a longer myotomy (approximately 14 to 16 cm) is performed to address the spastic esophageal body and the LES. In a series of 100 patients who underwent a POEM procedure, 25 had nonachalasia esophageal motility disorders; within this group, 70% experienced dysphagia relief over a mean follow-up of 23 months, and 75% reported relief of chest pain. In an international case series of POEM for spastic esophageal disorders, 100% of DES patients and 70% of jackhammer patients experienced a clinical response, defined as improvement in chest pain and Eckardt score. Overall, DES appears to be more amenable to surgical and endoscopic treatment when compared with jackhammer esophagus. The treatment of absent contractility is disappointing and relies mainly on lifestyle and dietary modifications because there

Lifestyle modification Dietary changes

F Minor motility disorder Ineffective esophageal motility Fragmented peristalsis

Individualized treatment based on patient symptoms and clinical presentation

are no effective esophageal prokinetic agents. There is little information available about the efficacy and necessity of medical or surgical treatment for the minor motility disorders, and treatment should be based on clinical presentation and patient symptoms. REFERENCES Castell D. Esophageal motility disorders: clinical manifestations, diagnosis, and management. UpToDate. 2017. Topic updated: March 02, 2017. Topic 2256 Version 18.0. Herbella FA, Tineli AC, Wilson JL, Del Grande JC. Surgical treatment of primary esophageal motility disorders. J Gastrointest Surg. 2008;12: 604–608. Kahrilas PJ, Bredenoord AJ, Fox M, et al. The Chicago classification of esophageal motility disorders, v3.0. Neurogastroenterol Motil. 2015;27: 160–174. Khashab MA, Messallam AA, Onimaru M, et al. International multicenter experience with peroral endoscopic myotomy for the treatment of spastic esophageal disorders refractory to medical therapy. Gastrointest Endosc. 2015;81(5):1170–1177. Patti MG, Pellegrini CA, Arcerito M, et al. Comparison of medical and minimally invasive surgical therapy for primary esophageal motility disorders. Arch Surg. 1995;130:609–615. Ravi K, Friesen L, Issaka R, Kahrilas PJ, Pandolfino JE. Long-term outcomes of patients with normal or minor motor function abnormalities detected by high-resolution esophageal manometry. Clin Gastroenterol Hepatol. 2015;13(8):1416–1423. Sharata AM, Dunst CM, Pescarus R, et al. Peroral endoscopic myotomy (POEM) for esophageal primary motility disorders: analysis of 100 consecutive patients. J Gastrointest Surg. 2015;19:161–170. Zerbib F, Roman S. Current therapeutic options for esophageal motor disorders as defined by the Chicago classification. J Clin Gastroenterol. 2015;49(6):451–460.

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Chapter

34 

ESOPHAGEAL PERFORATION Erinn Ogburn, MD, Brittany A. Zwischenberger, MD, Jordan D. Miller, DO, and Joseph B. Zwischenberger, MD A Esophageal perforation is a challenging clinical emergency, with delays in diagnosis and treatment resulting in significant effect on patient morbidity and mortality. More than 70% of esophageal perforations are iatrogenic, with other common causes including trauma, foreign-body ingestion, tumor, postemetic, and spontaneous perforation. Presentation with pain, emesis, hematemesis, dysphagia, or subcutaneous emphysema should generate a high level of clinical suspicion, although signs and symptoms will vary by the location, severity, and etiology of the perforation. Cervical perforations may present with neck pain, stiffness, and subcutaneous emphysema and are less likely to present with systemic symptoms because of containment within the soft tissue planes of the neck. Thoracic perforations often present with dyspnea and retrosternal pain that can lateralize to the side of the perforation. Abdominal perforations may present with subxiphoid or epigastric pain and signs of peritonitis, which may radiate to the back in posterior perforations. Initially, patients with thoracic and abdominal perforations usually present with nonspecific systemic symptoms and signs, such as tachypnea, tachycardia, and low-grade fever. As the course progresses, increased mediastinal and pleural contamination can lead to hemodynamic instability and shock. B When history and physical examination are suggestive of esophageal perforation, initial work-up should begin with laboratory work-up, including complete blood count (CBC), basic metabolic panel (BMP), lactate, and imaging. Although imaging may be unremarkable in the period immediately after a perforation, chest x-ray findings include mediastinal widening, subcutaneous emphysema, pneumomediastinum, pleural effusion, pneumothorax, or pneumoperitoneum. C The keys to diagnosis and surgical planning for esophageal perforation are esophagram and computed tomography (CT) scan. The gold standard for diagnosis is an esophagram with water-soluble contrast. However, water-soluble esophagrams have a false-negative rate of approximately 10%; therefore, patients should subsequently receive thin barium esophagram if the clinical suspicion is high. Commonly, patients arriving through the emergency department have already undergone CT scanning, which may provide adequate information for diagnosis and management. Importantly, the CT scan should include chest, abdomen, and pelvis with oral contrast. Esophagoscopy carries a risk for worsening of existing perforation and should be performed in the operating room. D Patients with contained perforations may be managed nonoperatively. Patients must be hemodynamically stable

and without signs of progressive sepsis. Nonoperative management for contained perforations includes nil per os (NPO), broadspectrum intravenous antimicrobials (including bacterial and fungal coverage), intravenous (IV) fluid resuscitation, and consideration of nutritional access. Importantly, all fluid collections should be drained (i.e., chest tube). If the patient clinically deteriorates or the perforation is no longer contained, then surgical intervention is warranted. E Surgery remains the treatment of choice for patients with transmural or free perforations. All patients with transmural or free perforations should receive broad-spectrum IV antibiotics with IV fluid resuscitation and remain NPO. Additional choices for management of these patients are determined by the degree of tissue inflammation, hemodynamic stability, perforation location, and underlying etiology. F The choice of surgical approach varies by the location of the perforation. Cervical perforations are approached through an oblique left neck incision. Right thoracotomy is performed for perforations to the upper two-thirds of the esophagus, whereas perforations to the lower third are approached with a left thoracotomy. Importantly, the location of contrast extravasation and pleural effusion can also direct the approach. Abdominal perforations may be approached through either the left chest or the abdomen, although the abdominal approach is preferred when there is contamination of the peritoneal space without intrathoracic component. Recent case series have suggested comparable outcomes with the use of a video-assisted thoracoscopic surgery (VATS) approach; however, the open approach remains the current standard. G Hemodynamically stable patients who present with iatrogenic perforations or small perforations less than 1 cm may be managed endoscopically with esophagoscopy and stent placement. Over the past decade, endoscopic management of esophageal perforations has gained popularity, with encouraging results. The European Society of Gastrointestinal Endoscopy recommends endoscopic treatment with stents, clips, or other devices, especially for perforations 50, Male, Obese Caucasian, Sx >5 years

Improvement

Continue Rx

Endoscopic Eradication

O Achalasia or Diffuse Spasm

No Reflux

EGD

L Alarm Symptoms Dysphagia Hematemesis Unintentional weight loss

Barrett’s Esophagus High Grade Dysplasia

Normal Esophagitis Barrett’s Esophagus No Dysplasia OR Low Grade Dysplasia Hiatal Hernia Peptic Stricture

M

pH Study Acid Reflux

N Manometry No Significant Abnormalities

P

Esophagogram

Q

Re-evaluate for Surgery

R

Laparoscopic Antireflux or Bariatric Surgery

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114  Part V  ◆  Alimentary Tract in the first 6 weeks, and most surgeons recommend the slow advancement of diet from liquids to soft foods over the first 2 to 4 weeks. Patients can then be advanced to thicker foods, reserving dry bread and meat until recovery is complete (typically 6 weeks to 3 months). Persistent dysphagia should not be intervened upon (endoscopically dilated) until recovery is complete because the vast majority of patients will experience resolution of dysphagia by 3 months.

Bello B, Zoccali M, Gullo R, et al. Gastroesophageal reflux disease and antireflux surgery-what is the proper preoperative work-up? J Gastrointest Surg. 2013;17(1):14–20. discussion p. 20. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol. 2013;108(3): 308–328. quiz 329. Singhal V, Khaitan L. Preoperative evaluation of gastroesophageal reflux disease. Surg Clin North Am. 2015;95(3):615–627. Worrell SG, Greene CL, DeMeester TR. The state of surgical treatment of gastroesophageal reflux disease after five decades. J Am Coll Surg. 2014;219(4):819–830.

REFERENCES ASGE Standards of Practice Committee. The role of endoscopy in the management of GERD. Gastrointest Endosc. 2015;81(6):1305–1310.

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Chapter

37 

BARRETT’S ESOPHAGUS Alessandro Paniccia, MD, and Michael Weyant, MD A Barrett’s esophagus (BE) is an acquired condition in which the normal stratified squamous epithelium of the esophagus is replaced with metaplastic, intestinal-type columnar epithelium containing goblet cells. The prevalence of BE is estimated to be 1% to 2% in the North American population. BE is the only known precursor lesion of esophageal adenocarcinoma (EAC), and the progression from BE to EAC occurs in a stepwise manner through increasing histopathologic stages of mucosal dysplasia. B Chronic (>5 years) gastroesophageal reflux disease (GERD) is the main risk factor for the development of BE, and the metaplastic transformation—pathognomonic of BE—can be observed in up to 15% of patients with chronic GERD. Other risk factors associated with the development of Barrett’s esophagus include age > 50 years old, male gender, central obesity, tobacco use, Caucasian (white) race, and family history of BE. Of note, no definitive association exists between Helicobacter pylori infection or alcohol consumption and Barrett’s esophagus. C The diagnosis of Barrett’s esophagus requires both (1) macroscopic visualization, on endoscopy, of abnormalappearing distal esophageal mucosa (salmon-colored) extending ≥1 cm proximal to the gastroesophageal junction and (2) histologic confirmation of a change from normal esophageal squamous epithelium to metaplastic columnar epithelium in a biopsy specimen. D BE can present solely as abnormal flat columnar mucosa, or, more insidiously, it can be accompanied by mucosal nodules or lesions. Therefore at the time of the first endoscopic evaluation, it is paramount to survey the entire esophagus. The goal here is to identify any suspicious nodules or lesions (because these commonly harbor the highest grade of dysplasia) along the visually abnormal segment of BE mucosa. E An esophageal biopsy must be obtained in accordance with the Seattle protocol, which consists of targeted biopsies of macroscopically visible nodules or lesions—or, preferentially, endoscopic mucosal resection (EMR; see decision point F)—and then four-quadrant random biopsies every 2 cm. At least 8 random biopsies may be needed for detection of intestinal metaplasia (yield 67.9%); however, >16 biopsies per endoscopy is associated with 100% yield. Additionally, it is important to note (1) the length of the Barrett’s segment and (2) the presence and size of a hiatal hernia. We also recommend obtaining a videoesophagram to assess esophageal motility (it can be compromised in the setting of chronic GERD), to identify the presence and severity of any esophageal stricture, and to evaluate the size and reducibility of a hiatal hernia.

F All nodules or lesions less than or equal to 2 cm should undergo EMR in addition to systematic mucosal biopsy of the remaining segment of Barrett’s. EMR of all visible nodules or lesions is preferred to biopsy because EMR specimens are deeper and larger, with limited distortion of tissue, in comparison with traditional biopsies. Moreover, submucosa and muscularis mucosa are present in the majority of EMR specimens, making it a useful tool for diagnosis, staging, and choice of therapeutic approach. Please note that routine staging of patients with nodular BE with endoscopic ultrasound (EUS) or other imaging modalities before EMR has no demonstrated benefit. Furthermore, given the possibility of overstaging and understaging, the findings of these modalities should not preclude the performance of EMR to stage early neoplasia. It is important to understand that the size of the nodule or lesion can pose some diagnostic and therapeutic challenges. In fact, lesions greater than 2 cm are often not amenable to EMR because of the high risk for incomplete resection, esophageal strictures, or esophageal perforation. These lesions represent a real challenge and can require surgical resection even for diagnostic purposes. Although more advanced endoscopic techniques, such as endoscopic mucosal dissection (EMD) are currently being investigated, their utility in BE is still limited to very few centers of expertise. When faced with BE associated with large mucosal nodules or lesions greater than 2 cm, a multidisciplinary discussion is mandatory to guide the most appropriate diagnostic and therapeutic approach on a case-by-case basis. G If there is evidence of esophagitis at the time of the initial EGD, the biopsies obtained in this setting have a notoriously low accuracy for the diagnosis of BE. Therefore repeat endoscopic assessment after proton pump inhibitor (PPI) therapy for 8 to 12 weeks is recommended to ensure healing of esophagitis and exclude the presence of underlying BE. If there is no evidence of esophagitis and no intestinal metaplasia on histology, a repeat EGD should be considered in 1 to 2 years if there is a high pretest index of suspicion for BE. H The treatment for BE depends mainly on the grade of histologic dysplasia identified in the biopsy specimen and the length of the metaplastic segment (i.e., particularly, ultra-long segment ≥ 8 cm). Treatment strategies are tailored based on three broad categories of BE: (1) BE without dysplasia, (2) BE with dysplasia (this can be low-grade or high-grade dysplasia, with or without nodules), and (3) BE with adenocarcinoma (intramucosal or invasive). I

Nondysplastic BE (NDBE) is associated with a 0.2% to 0.5% per-year risk for developing esophageal adenocarcinoma and can be treated similarly to GERD, with primary goals of symptom relief and improvement in quality of life. All patients diagnosed with NDBE should be initiated on antacid medication therapy. Most importantly, patients with NDBE should enroll in an endoscopic surveillance program performed with highresolution/high-definition white-light endoscopy at 3-year to 5-year intervals. The main goal of surveillance is the detection of dysplasia. J

Dysplastic BE can vary from low-grade dysplasia to high-grade dysplasia, with or without areas of adenocarcinoma.

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Chapter 37  ◆  Barrett’s Esophagus  116.e1

Abstract

Keywords

Barrett’s esophagus is an acquired condition of metaplasia in which normal squamous epithelium is replaced with metaplastic intestinal columnar epithelium. It is a precursor of adenocarcinoma. Chronic gastroesophageal reflux is the main risk factor. The diagnosis requires endoscopic visualization and biopsy. Treatment depends on the grade of histologic dysplasia and the length of the metaplastic segment. Management options could include proton pump inhibition, anti-reflux surgery, endoscopic mucosal resection, endoscopic radiofrequency ablation, and esophagectomy.

barrett’s esophagus metaplasia dysplasia gastroesophageal Reflux Disease endoscopic mucosal resection radiofrequency ablation esophagectomy anti-reflux surgery

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Chapter 37  ◆  Barrett’s Esophagus  117 K BE with low-grade dysplasia (BE-LGD) is associated with a 0.7% per-year risk for developing esophageal adenocarcinoma. When LGD is identified, one must ensure that the biopsies were obtained according to the Seattle protocol, and if not, biopsies should be repeated to exclude additional lesions of higher grade dysplasia, and diagnostic confirmation must be obtained by a second expert GI pathologist. It is important to understand that making a histologic diagnosis of LGD in the setting of BE is particularly difficult. In fact, a study that included 147 patients with LGD from six community hospitals whose slides were reviewed by two expert pathologists showed that 75% of the patients who were initially diagnosed with LGD were downgraded to NDBE. • Treatment: • Antacid medication must be initiated; alternatively, if the patient is already being treated with antacid medication, the dose should be maximized. • Antireflux surgery can be offered to select patients with BE-LGD because there is evidence that after a gastric fundoplication, LGD regresses—in some patients—to NDBE. In addition to BE-LGD, eligible surgical candidates must have severe GERD symptoms inadequately controlled with antacid medication and impaired quality of life resulting from the dietary or lifestyle modifications necessary to control severe GERD. Patient selection dictates the success of the antireflux surgery, and the best outcomes are obtained in patients with absent or small hiatal hernia, good esophageal motility, and symptomatic improvement with antacid therapy.

• Surveillance: • Independent of what treatment strategy is employed, endoscopy and biopsies should be repeated in 6 months. • If LGD is resolved, routine surveillance can resume at 3-year to 5-year intervals. • Please note that the persistence of LGD is an indication for endoscopic radiofrequency ablation (RFA) of the BE segment. However, if RFA is not performed, annual endoscopic surveillance is recommended until two consecutive examinations are negative for dysplasia; thereafter, surveillance can be resumed at 3-year to 5-year intervals. L BE with high-grade dysplasia (BE-HGD) is associated with a 7% per-year risk for developing EAC. Furthermore, a focus of concurrent adenocarcinoma is often already present in these patients in approximately 40% of cases. Moreover, the presence of high-risk features along the BE segment, such as ulcerations, visible lesions, or multifocal HGD, carries a risk for concurrent adenocarcinoma in up to 60% to 78% of cases. • Treatment: • In the absence of visible nodules or lesions, the first therapeutic choice is endoscopic eradication therapy (EET) obtained via RFA of the entire BE segment, followed by surveillance. RFA treatments are often delivered in multiple sessions (every 2 to 3 months) to achieve eradication of dysplasia and intestinal metaplasia. • Alternatively, multimodality endoscopic eradication therapy (MEET) is the preferred choice in the setting of BE-HGD presenting with associated mucosal nodules

Q Endoscopic ultrasound

Submucosal (T1b)

M

P

EAC

N Intramucosal (T1a)

D

B GERD

A

F Endoscopic mucosal resection + Systematic biopsy

Endoscopically visible nodularity in BE

C

Suspected BE

B

H

EGD with high resolution/white light

J

Abnormal histology consistent with BE

D

Other risk factors

L Confirmed BE-HGD

Dysplastic BE

E

Flat columnar mucosa

No evidence of BE If high index of suspicion for BE consider repeat EGD + Biopsy in 1-2 years

No

G

Esophagitis Yes

I Non-dysplastic BE

Favorable prognostic factors - No lymphovascular invasion - Moderate to well differentiated EAC - Negative resection margin (EMR) Endoscopic eradication therapy (RFA +/− EMR) +/− Anti-reflux surgery

K Confirmed BE-LGD

Systematic mucosal biopsy

O

Unfavorable prognostic factors - Poorly differentiated EAC - Positive lymphovascular invasion - Positive resection margin (EMR)

Discussion at multidisciplinary oncology; Systemic staging and evaluation for systemic therapy and esophagectomy

Consider Esophagectomy (only in specific situation)*

Surveillance endoscopy every 3 months for the 1st year following EET, every 6 months in the 2nd year, and annually thereafter

Endoscopic ablation therapy (RFA) PPI therapy +/− Anti-reflux surgery

Surveillance: repeat endoscopy in 6-12 months x 2 then every 3-5 years

PPI therapy +/− Anti-reflux surgery

Surveillance: repeat endoscopy in 3-5 years

PPI therapy for 12 weeks then repeat EGD + Biopsy

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118  Part V  ◆  Alimentary Tract

•

•

•

•

•

•

or lesions. MEET consists of a combination of EMR of all nodules or lesions, if not performed during the diagnostic process (see decision point F), followed by endoscopic ablation (via RFA) of the entire BE segment. EMR is accomplished by excising an area of full-thickness mucosa and submucosa, leaving an intact muscularis propria. Scrupulous pathologic evaluation of the resected specimens is mandatory; EMR will change the diagnosis in ~50% of patients when compared with endoscopic biopsies, given the larger tissue sample available for review by the pathologist. The primary objective here is to identify any evidence of occult adenocarcinoma (EAC). If EAC is identified, one must accurately assess the tumor characteristics (i.e., depth of invasion, grade of differentiation, lymphovascular invasion, and margin of resections) to inform the next diagnostic or therapeutic choice (see decision point M). Commonly reported complications after EMR include an overall rate of stricture formation of 6% and a rate of perforation of 0.6%; the most common complication after RFA is chest pain, occurring in 25% to 50% of cases and usually treated with nonsteroidal anti-inflammatory drugs (NSAIDs). The reported rates of complete eradication of intramucosal metaplasia after a combination of EMR and RFA ranges between 72% and 97%. However, recurrence rates of 0% to 15% for dysplasia and 5% to 39.5% for intestinal metaplasia are reported. One must be cognizant that intensive endoscopic surveillance—as an alternative to endoscopic ablation therapy (EAT) for BE-HGD—should not be recommended because of the high risk for progression of BE-HGD to EAC. Antireflux surgery can be recommended in the presence of refractory GERD symptoms despite maximal therapy and large hiatal hernia (>4 cm) because this is a significant predictor of recurrence of BE-HGD or EAC. Nevertheless, esophagectomy can be offered to patients unwilling to undergo an intensive surveillance program, patients with ultra-long BE segment (i.e., ≥ 8 cm because RFA of long segment has decreased efficacy) or in high-risk patients (young, family history of esophageal adenocarcinoma, poorly controlled GERD symptoms despite maximal medical treatment). Surveillance: • Although surveillance after EET is of critical importance, no definitive agreement exists. A common strategy is to perform endoscopic surveillance every 3 months in the first year after successful EET, every 6 months in the second year, and annually thereafter.

M BE with esophageal adenocarcinoma (EAC) can be identified in a mucosal biopsy or EMR specimen during the diagnostic process of BE. For the purpose of this chapter, we will limit our discussion solely to intramuscular EAC (T1a) and submucosal EAC (T1b). N If BE with intramucosal EAC (T1a) is identified on a biopsy specimen, then an EMR of the EAC site should be performed when appropriate (if it was not previously performed; see decision point F) to precisely assess the depth of tumor invasion. Moreover, the EMR specimen must be carefully analyzed for the presence

of unfavorable tumor-specific prognostic factors that would preclude endoscopic therapy. Unfavorable prognostic factors include (1) poorly differentiated tumor, (2) lymphovascular invasion, and (3) positive deep margin of excision for adenocarcinoma (after EMR). Nevertheless, known pathologic lymphadenopathy is a contraindication to EET even in the setting of a T1a EAC. O In the case of favorable tumor-specific prognostic factors (absence of unfavorable prognostic factors), multimodality EET (i.e., combination of EMR and RFA) is the preferred treatment choice in the setting of known EAC (T1a). In this setting, multimodality EET is considered the definitive treatment. P If unfavorable tumor-specific prognostic factors exist, then local eradication therapy should not be performed. The patient must be referred for consultation with a multidisciplinary oncology team for systemic staging and treatment; depending on the staging findings, this could include systemic treatment followed by esophagectomy (refer to esophageal adenocarcinoma chapter). • Importantly, esophagectomy is the treatment of choice when faced with multifocal EAC, high-grade (poorly differentiated) EAC, positive deep margin of excision for EAC (after EMR), presence of lymphovascular invasion, or submucosal tumor invasion (T1b). Q In cases where adenocarcinoma with submucosal invasion (T1b) is identified on a biopsy specimen, then endoscopic ultrasound to evaluate for the depth of invasion and for the presence of any enlarged regional lymph nodes should be completed first. Documented adenocarcinoma with invasion in the submucosa (T1b) carries a risk for metastatic nodal disease in excess of 25%; therefore fine-needle aspiration of any suspicious lymph nodes must be performed. Local eradication therapy should not be performed in this scenario, and the patient must be referred for consultation with a multidisciplinary oncology team for systemic staging and treatment; depending on the staging findings, this could include systemic treatment followed by esophagectomy (refer to esophageal adenocarcinoma chapter). REFERENCES Brimhall B, Wani S. Current endoscopic approaches for the treatment of Barrett esophagus. J Clin Gastroenterol. 2017;51(1):2–11. Conio M, Cameron AJ, Chak A, Blanchi S, Filiberti R. Endoscopic treatment of high-grade dysplasia and early cancer in Barrett’s oesophagus. Lancet Oncol. 2005;6(5):311–321. DeMeester SR. Barrett’s oesophagus: treatment with surgery. Best Pract Res Clin Gastroenterol. 2015;29(1):211–217. Grant KS, DeMeester SR, Kreger V, et al. Effect of Barrett’s esophagus surveillance on esophageal preservation, tumor stage, and survival with esophageal adenocarcinoma. J Thorac Cardiovasc Surg. 2013;146(1):31–37. Shaheen NJ, Falk GW, Iyer PG, Gerson LB. American College of Gastroenterology. ACG clinical guideline: diagnosis and management of Barrett’s esophagus. Vol. 111. Am J Gastroenterol. 2016;30–50, quiz 51. Wani S, Muthusamy VR, Shaheen NJ, et al. Development of quality indicators for endoscopic eradication therapies in Barrett’s esophagus: the TREAT-BE (treatment with resection and endoscopic ablation techniques for Barrett’s esophagus) consortium. Am J Gastroenterol. 2017;112(7):1032–1048. Wani S, Rubenstein JH, Vieth M, Bergman J. Diagnosis and management of low-grade dysplasia in Barrett’s esophagus: expert review from the clinical practice updates committee of the American Gastroenterological Association. Gastroenterol. 2016;151:822–835. Zehetner J, DeMeester SR, Hagen JA, et al. Endoscopic resection and ablation versus esophagectomy for high-grade dysplasia and intramucosal adenocarcinoma. J Thorac Cardiovasc Surg. 2011;141(1):39–47.

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Chapter

38 

ESOPHAGEAL DIVERTICULUM Michael Schweitzer, MD, and Sepehr Lalezari, MD A Symptoms: • Regurgitation: Regurgitation is one of the most common complaints associated with esophageal diverticula. Usually patients will complain of regurgitation of undigested food. Food that has been masticated but not acted upon by gastric juice will be stored in the pouch and regurgitated at a later time. • Dysphagia: Dysphagia is the most common complaint associated with esophageal diverticula. Patients will complain of food getting “stuck” in the throat. Although the differential for dysphagia is broad, dysphagia as it pertains to diverticular disease is the result of food impacting within the diverticula. • Recurrent aspiration: Patients with a history of recurrent aspiration should raise the suspicion of esophageal diverticula. B Esophageal diverticula are epithelial-lined outpouchings from the esophagus. There are two broad categories of diverticula: pulsion type and traction type. Pulsion diverticula usually result from increased intraluminal pressure and are false diverticula that do not involve all layers of the esophageal wall. Pulsion-type diverticula usually occur at either the proximal or distal esophagus and account for most esophageal diverticula. Traction diverticula are true diverticula where all layers of the esophagus bulge out, and they tend to occur in the mid-esophagus. C Diagnostic testing: • Barium esophagram: An esophagram should be the first study performed in all patients complaining of dysphagia. This study provides information on diverticula location/ diameter and other esophageal luminal abnormalities. • Upper endoscopy: An upper endoscopy should be the second study ordered in patients complaining of dysphagia. This study provides information on the presence of inflammation, evidence of luminal irritation, strictures of peptic or neoplastic origin, and other esophageal luminal abnormalities. It also allows for direct visualization of the diverticula. If a pharyngeoesophageal diverticulum is noted on esophagram in the absence of other concerning findings, then upper endoscopy may be foregone. D Although Zenker was not the first to describe this type of pharyngoesophageal pulsion diverticulum, it bears his name. Zenker’s diverticula occur secondary to increased intraluminal pressure at the upper esophageal sphincter and are thought to be caused by disordered muscle contractions. A natural weakness at Killian’s triangle between the thyropharyngeus and cricopharyngeus muscles is where most occur.

The most important aspect of any operation for treating esophageal diverticula is to address the underlying pathophysiology. Therefore a cricopharyngeal myotomy is considered to be the most crucial aspect of surgical therapy for a Zenker’s diverticulum. • Rigid endoscopic management: A standard laparoscopic stapling device introduced transorally with the aid of a diverticuloscope is used to staple and transect the diverticulum from the esophagus. This is the treatment of choice of most surgeons, and success is achieved in about 90% of patients. Stapling may not be suitable in small diverticula (5 cm) may require diverticulectomy as opposed to diverticulopexy. F Epiphrenic diverticula are pulsion-type diverticula and tend to occur at the last 10 cm of the esophagus. Although any iatrogenic pathologic process at the lower esophageal sphincter that causes increased intraluminal pressure can result in an epiphrenic diverticulum, they are usually a result of esophageal motor abnormalities. G Esophageal manometry should be obtained in all patients with epiphrenic diverticulum. Most patients with this type of diverticulum will have an associated esophageal dysmotility

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Chapter 38  ◆  Esophageal Diverticulum  120.e1

Abstract

Keywords

Esophageal diverticulum are epithelial lined outpouchings from the esophagus. There are two broad categories of diverticulum – pulsion type and traction type. Diagnosis usually involves an esophogram and/or esophagogastroduodeoscopy (EGD). Treatment depends on the type, symptoms, size and location of the diverticulum. Depending on the etiology of the diverticulum treatment of the underlying of the diverticulum should be addressed.

diverticulum epiphrenic phrenoesophageal midesophageal zenker’s diverticulum pulsion traction dysphagia myotomy diverticulopexy diverticulectomy regurgitation reflux aspiration

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Chapter 38  ◆  Esophageal Diverticulum  121

D Pharyngoesophageal (Zenker’s Diverticulum)

A

Symptoms Regurgitation Aspiration Dysphagia

E

≤2 cm

Myotomy alone Myotomy and diverticulectomy Myotomy and diverticulopexy

>2 cm

Myotomy and diverticulectomy Myotomy and diverticulopexy

Surgery

Asymptomatic

Monitor

Symptomatic

Surgery

Midesophageal

B

Myotomy and diverticulectomy Diverticulopexy

Esophageal Diverticulum

L Associated GERD

K

I Symptomatic

C

Diagnostic Testing Esophagram EGD

F Epiphrenic

Surgery

G

M Associated dysmotility disorder

Myotomy Diverticulectomy and antireflux procedure Myotomy and diverticulectomy

N

Manometry pH study

H

Other Pathology

J Asymptomatic

>5 cm

Address and correct underlying pathology

Monitor

14.72 on a 24-hour pH study; this is in addition to repair of the PEH. E In patients with symptomatic type 2, 3, or 4 PEH, a 24-hour pH study is typically not needed because only one-half of symptomatic patients will have abnormal pH findings. More advanced stages of PEH are associated with a higher incidence of symptoms (and complications) from gastric volvulus, including entrapment and obstruction. Clinical presentation (and associated risk) are therefore directly related to gastric volvulus and include bleeding, incarceration, pain, strangulation, and perforation. Bleeding and anemia are commonly caused by gastritis and ulceration that occur in PEH as a result of poor gastric emptying and gastric torsion, which cause gastric mural ischemia and inflammation. F SURGICAL MANAGEMENT

Historically and significantly as a result of the 1980s recommendations of Dr. Ronald Belsey, prophylactic surgery was advised as standard practice for any PEH on presentation because it was thought that up to 25% of untreated PEHs would have incarceration or other serious complications, including strangulation. G A change in philosophy occurred because of experience and further outcome assessments, which demonstrated that serious complications did not occur as frequently as previously thought and that a more selective approach to PEH repair was required. Stylopoulos et al. (2002) compared watchful waiting (WW) and elective laparoscopic PEH repair (ELHR) using all data available in the literature. The lifetime risk for developing acute symptoms requiring emergency surgery was found to decrease significantly with age; the mortality rate associated with ELHR was 1.4%. With WW, it was found that the likelihood of urgent surgery was 1.1% per year. The authors concluded that if ELHR were to be routinely recommended for asymptomatic or minimally symptomatic PEHs, it would only be more beneficial than WW in fewer than one of every five patients, and therefore WW is the more reasonable recommendation for the initial management in these patients. Also, if emergency surgery is required, the risk of the procedure is not as severe as was thought in the past, for a variety of reasons (e.g., improved imaging, minimally invasive options, better intensive care).

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Chapter 39  ◆  Paraesophageal Hiatal Hernia  122.e1

Abstract

Keywords

Paraesophageal hiatal hernias and recurrences are becoming an increasingly important and common entity for minimally invasive and robotic surgeons.

paraesophageal hiatal hiatus hernia volvulus dysphagia recurrence crural

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Chapter 39  ◆  Paraesophageal Hiatal Hernia  123 H Patients with symptomatic PEHs should be referred for surgery. Findings that may prompt more urgent surgery include signs of more advanced gastric volvulus—progressive symptoms of obstruction, reflux symptoms, anemia or hematemesis, or other systemic findings that would raise the concern of gastric ischemia. Oftentimes, the patient retches but cannot vomit, and/or there is an inability to pass a decompressive nasogastric tube. The goal in these patients is to avoid aspiration, hemorrhage, transfusion requirements, and the rare gastric necrosis, which has an associated mortality of 50%. I

Standard and best practice has found that the surgical approach has changed in the past two decades to the transabdominal approach using minimally invasive techniques, including laparoscopy and, more recently, robotic surgery. In most centers, the transthoracic approach has been replaced by the transabdominal approach even when done by thoracic surgeons. Standard surgical principles are similar to those of other hernia operations and include the reduction of hernia contents and excision of the sac from the stomach and mediastinum. Standard PEH repair principles include the following: (1) mediastinal mobilization of the lower esophagus to ensure adequate intraabdominal esophageal length; (2) closure of the hiatus primarily with a permanent suture, typically without mesh or suture buttress; and (3) fundoplication with collar sutures and a posterior gastropexy. J

Several technical controversies exist regarding PEH surgical technique, including the following:

A

History & physical examination Symptoms Postprandial fullness and pain Vomiting and regurgitation Dysphagia GERD and heartburn Bleeding Pulmonary dysfunction

C Paraesophageal Hernia

1. Gastropexy. Gastric reduction and anchoring alone, without fundoplication or hiatoplasty, using either an anterior or posterior (Hill) gastropexy or Stamm gastrostomy, is not recommended as a primary repair. It should be reserved for high-risk or unstable patients as a fallback procedure or for patients with recurrent PEH and significant perihiatal or mediastinal adhesions where dissection and an attempt to mobilize the esophagogastric (EG) junction and proximal stomach would be detrimental or unsafe. Anterior gastropexy can be rapidly performed with several interrupted, permanent sutures to the intraabdominal fascial structures. Stamm gastrostomy fixes the stomach to the abdominal wall and may prevent volvulus and concurrently eliminates the need for long-term NG tube placement. Thus gastrostomy may be an alternate option for gastropexy or concurrent option for formal PEH repair. 2. Concurrent fundoplication. Although this was previously controversial, it is less so now because partial or complete fundoplication has been found to be beneficial for most patients with PEH to diminish or resolve postoperative symptoms of GERD following EGJ mobilization, which disrupts the natural antireflux mechanism, which may cause a high (>30%) incidence of GERD following PEH repair. An added benefit is that fundoplication facilitates intraabdominal gastric fixation and crural anchoring with the associated expected decrease in PEH recurrence rates. 3. The “short esophagus.” Many surgeons do not feel that this historical entity actually exists. With a high, circumferential mobilization of the mediastinal esophagus and posterior crural approximation, adequate intraabdominal

D Esophageal manometry 24-hour pH probe Upper endoscopy

DeMeester score > 14.72

Antireflux surgery

F Prophylactic surgery for all PEH − historically significant only G Watchful waiting for PEH − symptomatic or minimally symptomatic

Type 1 − sliding (common)

E Degree of gastric volvulus = Type 2 − rolling (rare) risk and indication for surgery Type 3 − Type 1 + Type 2 Type 4 − Type 3 + other organs H

PEH repair – symptomatic PEH Urgent surgery for progressive symptoms

B

Labs & studies Complete blood count Chest radiograph Upper GI contrast study CT scan chest/abdomen

I Standard surgical technique: transabdominal, minimally invasive J 1. 2. 3. 4.

PEH Controversies Gastropexy Gastrostomy Fundoplication Collis gastroplasty

K Reoperative PEH surgery: should be only performed by experienced hiatal surgeons when possible

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124  Part V  ◆  Alimentary Tract esophageal length is almost always possible. An esophageal lengthening procedure, termed Collis gastroplasty, should be very rarely, if ever, required. K Reoperative PEH repair should be performed by experienced surgeons when possible. REFERENCES Dallemagne B, Kohnen L, Perretta S, et al. Laparoscopic repair of paraesophageal hernia. Long-term follow-up reveals good clinical outcome despite high radiological recurrence rate. Ann Surg. 2011;253(2):291–296. Hashemi M, Peters JH, DeMeester TR, et al. Laparoscopic repair of large type III hiatal hernia: objective followup reveals high recurrence rate. J Am Coll Surg. 2000;190:553.

Kaplan JA, Schecter S, Lin MY, Rogers SJ, Carter JT. Morbidity and mortality associated with elective or emergency paraesophageal hernia repair. JAMA Surg. 2015;150(11):1094–1096. Oelschlager BK, Pellegrini CA, Hunter J, et al. Biologic prosthesis reduces recurrence after laparoscopic paraesophageal hernia repair: a multicenter, prospective, randomized trial. Ann Surg. 2006;244:481. Oelschlager BK, Pellegrini CA, Hunter JG, et al. Biologic prosthesis to prevent recurrence after laparoscopic paraesophageal hernia repair: long-term follow-up from a multicenter, prospective, randomized trial. J Am Coll Surg. 2011;213:461. Ponsky J, Rosen M, Fanning A, Malm J. Anterior gastropexy may reduce the recurrence rate after laparoscopic paraesophageal hernia repair. Surg Endosc. 2003;17:1036. Stylopoulos N, Gazelle GS, Rattner DW. Paraesophageal hernias: operation or observation? Ann Surg. 2002;236:492, discussion 500–501.

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Chapter

40 

GASTRIC ULCER Akshay Pratap Chauhan, MD, and Dmitry Oleynikov, MD, FACS

A Epigastric pain, the most frequent symptom of a gastric ulcer, occurs in 70% of patients. Typically, pain is nocturnal and is worsened by eating. Dyspepsia is manifested as epigastric discomfort, nausea, belching, and bloating. Anorexia is present in 40% to 60% of patients. The pain may be so severe that patients lose weight from a fear of food inciting pain, although weight loss in a gastric ulcer may harbor underlying malignancy. Nausea and vomiting are more common with gastric ulcers. This may represent an underlying antropyloric ulcer causing gastric outlet obstruction. Anemia may be the only sign or symptom of a malignant gastric ulcer. Physical examination may reveal board-like rigidity and tympanic abdomen (perforation) or succussion splash (gastric outlet obstruction), or it may portend advanced disease with malignancy, such as a hard lymph node in the left supraclavicular fossa (Virchow node), umbilical nodule (Sister Mary Joseph nodule), enlarged left axillary lymph node (Irish node), metastatic tumor high on the anterior rectal wall on rectal examination (Blumer’s shelf), or fluid thrill of malignant ascites. B A complete blood count (CBC) may demonstrate anemia, and a chemistry panel may reveal hypokalemic hypochloremic metabolic alkalosis in the presence of gastric outlet obstruction. Guaiac-positive stool indicates a bleeding ulcer. The choice of imaging should be tailored to the acuity of presentation. In emergent cases, an upright chest and abdominal films can detect free air in 70% of cases. Computed tomography (CT) or ultrasound can be useful to detect small amounts of free air or fluid. Upper gastrointestinal (GI) radiography is useful in detecting gastric ulcer and gastric outlet obstruction. Transcatheter angiography is useful in a bleeding ulcer in a high-risk patient. C At this point, if the patient had a stable, uncomplicated ulcer, refer the patient to GI for further evaluation and endoscopy. D If any concerning signs present, such as unstable vital signs, orthostatic hypotension, signs of increased blood loss, or abnormal initial laboratory results (complicated peptic ulcer disease [PUD]), send the patient to the emergency room for an urgent surgical consult. E Endoscopy remains the standard diagnostic and therapeutic procedure against which other modalities are measured. It is 90% accurate in diagnosing a gastric ulcer. Johnson classified five types of gastric ulcers: Type 1: Lesser curvature Type 2: Gastric and duodenal Type 3: Pyloric or prepyloric Type 4: Juxtacardiac

Type 5: Occurring anywhere in the stomach and is a result of chronic ingestion of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs) Virtually all gastric ulcers lie within 2 cm of the histologic transition zone between fundic and antral mucosa. All gastric ulcers should have multiple biopsies taken from the perimeter and central pit to exclude malignancy. Adding lesional brushings to the biopsy increases diagnostic accuracy to 95%. Approximately 75% of cases of gastric ulcers are caused by Helicobacter pylori (Hp) infection, and the remaining by NSAIDs. The diagnosis of H. pylori can be established by invasive or noninvasive methods. During endoscopy, one of three tests can be performed: biopsy urease test, histology, and, less commonly, bacterial culture. Noninvasive tests for the diagnosis of H. pylori are available, which include urea breath testing (UBT), stool antigen testing, and serology. F Perforation carries a mortality rate of 10% to 40%, depending on the presence of preoperative shock, significant underlying medical illness, perforation > 24 hours’ duration and age > 65 yr. Initial management of the patient with gastrointestinal perforation includes intravenous (IV) fluid therapy, cessation of oral intake, and broad-spectrum antibiotics. G Bleeding from a gastric ulcer is rare. About 20% of patients present with melena, 30% with hematemesis, and 50% with both. As many as 5% of patients with bleeding ulcers present with hematochezia. Hemodynamic assessment and, if necessary, institution of resuscitative measures are the first steps in the management of ulcer bleeding. H Chronic inflammation from an ulcer may result in obstruction of the gastroduodenal junction. I

Multiple regimens have been evaluated for H. pylori therapy in randomized controlled trials. For initial therapy, triple therapy with a proton pump inhibitor (PPI), amoxicillin (1 g twice daily), and clarithromycin (500 mg twice daily) for 14 days is recommended, if the prevalence of clarithromycin resistance in the population is less than 15%. Quadruple therapy is for retreatment or initial treatment in areas where clarithromycin resistance is high (≥15%) or in patients with recent or repeated exposure to clarithromycin or metronidazole. Bismuth-containing quadruple therapy consists of a PPI, bismuth subsalicylate (524 mg four times daily), and two antibiotics (e.g., metronidazole 250 mg four times daily and tetracycline 500 mg four times daily) given for 14 days. Drugs can heal ulcers by neutralizing acid secretion or by restoring mucosal defenses. Prostaglandins increase mucus, bicarbonate, and blood flow. Sucralfate and low-dose antacids promote ulcer healing by unknown mechanisms. The histamine (H2) receptor antagonists are structurally similar to histamine and differ in potency, half-life, and bioavailability. Oral doses produce equivalent inhibition of parietal cell secretion. Continuous IV infusion of H2 receptor antagonists produces more uniform acid inhibition than intermittent administration. The H+–K+– adenosine triphosphatase (ATPase) pump is the gastric pump responsible for the final step in parietal cell acid secretion. A PPI like omeprazole inhibits acid secretion more completely than an H2 receptor antagonist and produces more prolonged inhibition of acid secretion than H2 blockers. Smoking cessation should be encouraged. Ulcer recurrence is increased by heavy alcohol use. Misoprostol, a prostaglandin analogue, is effective

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Chapter 40  ◆  Gastric Ulcer  126.e1

Abstract

Keywords

Gastric ulcer is one of the common causes of dyspepsia. This chapter discusses the etiology, pathogenesis, work-up, clinical presentation, and surgical decision making in the management of benign and complicated gastric ulcers.

gastric ulcer patch closure vagotomy complications

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Chapter 40  ◆  Gastric Ulcer  127

A Epigastric pain, dyspepsia, nausea Board-like rigidity, succussion splash

C Uncomplicated gastric ulcer

E Upper Endoscopy, Biopsy ulcer and Test H pylori

F Perforated Ulcer

Gastric ulcer

D Complicated gastric ulcer

I Treat with Anti H pylori and Anti Ulcer Drugs Treat for 8-12 weeks and repeat Endoscopy to confirm healing

J Omental patch + biopsy of ulcer + testing for Hp and treatment Definitive ulcer surgery if recurrent or failed Hp treatment

G Bleeding Ulcer

M

K Upper Endoscopy, angioembolization

B CBC, CMP, FOBT, PT/INR, and PTT AXR, CT, UGI, angiography

H Obstruction

L Endoscopic Balloon Dilation

in NSAID-induced ulcers. The gastric ulcer should be treated for 8 to 12 weeks and then reevaluated for healing. If the ulcer has healed, maintenance therapy should be considered if the patient is not taking NSAIDs and does not have H. pylori infection. J

The choice of operation for gastric ulcer perforation depends on hemodynamic stability, Hp treatment, and the chronicity of the ulcer. In a patient with known perforated chronic ulcer or priorly treated Hp infection, a definite antiulcer operation should be contemplated if hemodynamic stability allows. In such a patient, a type I ulcer is treated by a partial gastrectomy. Type II and III ulcers should undergo truncal vagotomy and antrectomy. Type IV ulcers should be patched along with an intraoperative biopsy because of the close proximity to the gastroesophageal (GE) junction. If the patient is unstable, the standard of care is an omental patch with ulcer biopsy regardless of the type of ulcer. On the other hand, in a patient with recent onset of symptoms, without known Hp infection, a definite antiulcer operation is not warranted. In such patients, a type I, II, or IV ulcer should undergo omental patch, ulcer biopsy, and Hp testing and treatment. However, a type III ulcer is best treated by antrectomy and vagotomy because patch closure in the prepyloric region is associated with a high incidence of gastric outlet obstruction. K Most patients with bleeding gastric ulcers should undergo endoscopy after stabilization. It enables identification of the site of bleeding, allows therapeutic attempts at stopping the bleeding, and predicts the risk for rebleed. A success rate of 90% is reported. A repeat attempt at endoscopy should be done in the case of a rebleed in a stable patient. Continued hemodynamic instability with shock, massive transfusion, failure of index endoscopy to control bleeding, and a failed second attempt are indications for angiography and embolization or surgery.

Type I: Wedge resection. Type ll and III: Truncal vagotomy and antrectomy Type IV and V: Gastrotomy and oversewing

N Truncal Vagotomy and antrectomy

M Bleeding type I gastric ulcers are best treated with a wedge resection. Type II and III ulcers are best treated with truncal vagotomy and antrectomy. Type IV ulcers are best treated with oversewing of the ulcer or ligation of the left gastric artery. Type V ulcers are best treated with gastrotomy and oversewing of the vessel. N Endoscopic failure of gastric outlet obstruction usually requires surgery. A truncal vagotomy and antrectomy with a feeding jejunostomy is the ideal procedure. Sometimes inflammation and scarring may preclude a safe antrectomy. In such situations, a Jaboulay side-to-side duodenoplasty plus highly selective vagotomy (HSV) or a gastrojejunostomy with HSV may be performed. REFERENCES Biecker E. Diagnosis and therapy of non-variceal upper gastrointestinal bleeding. World J Gastrointest Pharmacol Ther. 2015;6(4):172–182. Cherian PT, Cherian S, Singh P. Long-term follow-up of patients with gastric outlet obstruction related to peptic ulcer disease treated with endoscopic balloon dilatation and drug therapy. Gastrointest Endosc. 2007;66(3): 491–497. Hahn M, Fennerty MB, Corless CL, et al. Noninvasive tests as a substitute for histology in the diagnosis of Helicobacter pylori infection. Gastrointest Endosc. 2000;52(1):20–26. Johnson HD. Etiology and classification of gastric ulcers. Gastroenterology. 1957;33(1):121–123. Kurata JH, Nogawa AN. Meta-analysis of risk factors for peptic ulcer. Nonsteroidal antiinflammatory drugs, Helicobacter pylori, and smoking. J Clin Gastroenterol. 1997;24(1):2–17. Nykanen T, Peltola E, Kylanpaa L, Udd M. Bleeding gastric and duodenal ulcers: case-control study comparing angioembolization and surgery. Scand J Gastroenterol. 2017;52(5):523–530. Schmocker RK, Lidor AO. Management of non-neoplastic gastric lesions. Surg Clin North Am. 2017;97(2):387–403. Turner IB, Jones M, Piper DW. Factors influencing mortality from bleeding peptic ulcers. Scand J Gastroenterol. 1991;26(6):661–666. Xin Y, Manson J, Govan L, et al. Pharmacological regimens for eradication of Helicobacter pylori: an overview of systematic reviews and network meta-analysis. BMC Gastroenterol. 2016;16(1):80.

L In the absence of malignancy, endoscopic balloon dilation has emerged as the most effective first-line therapy in most patients.

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Chapter

41 

DUODENAL ULCER Brandon C. Chapman, MD, and Gregory Van Stiegmann, MD

A More than 90% of duodenal ulcers are caused either by infection of the stomach with Helicobacter pylori or by long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs). Appropriate antimicrobial drug regimens to eradicate H. pylori and improved medical therapy with proton pump inhibitors (PPIs) have significantly reduced annual hospitalizations by 37% and overall mortality to 2.1%. B All patients with duodenal ulcers should be tested for infection with H. pylori. Noninvasive testing with serologic or breath tests accurately identifies those patients who have an underlying H. pylori infection. Subsequent therapy in these patients with a variety of short-term, multiple-drug regimens can eradicate most such infections and produces a cost-effective, durable cure of the ulcer in up to 98% of successfully treated cases. The urea breath test is the most reliable nonendoscopic test to document clearance of H. pylori infection and should be performed at least 4 weeks after completion of treatment. C In patients with uncomplicated duodenal ulcers, all patients should receive medical management to facilitate ulcer healing. PPIs have superior rates of ulcer healing compared with histamine-2 receptor antagonists (H2RAs) and are the antisecretory drug of choice. Patients who are H. pylori positive should receive a 14-day course of either clarithromycin-based triple therapy (PPI, clarithromycin, and amoxicillin or metronidazole) or bismuth quadruple therapy (PPI or histamine blocker, bismuth, metronidazole, and tetracycline). Patients with NSAID-associated ulcers should be treated with a PPI for a minimum of 8 weeks and indefinitely in patients requiring long-term NSAID use. In H. pylori–negative and non–NSAID-induced ulcers, long-term PPI therapy should be used. D Serum gastrin levels should be measured when the diagnosis of gastrinoma is suggested by massive hypersecretion (diarrhea), prominent rugae, multiple and/or distal ulcers, or medical/ surgical refractory ulcer. Fasting gastrin levels may be slightly elevated in patients who are taking antisecretory medications. If a patient is able to stop PPI without difficulty for a week, then a fasting serum gastrin and a gastric fluid pH is measured after 1 week. If the patient has severe symptoms with discon­ tinuation of PPI, an H2RA can be used for 1 week. Then the H2RA is discontinued for 30 hours and the fasting gastrin and gastric fluid pH obtained. The diagnosis of gastrinoma is made if the gastric fluid pH is 1000 pg/mL. Gastrinoma is excluded in a patient with a serum gastrin level 2.5 (hypochlorhydria/achlorhydria). If the patient has moderate gastrin elevation (101 to 999 pg/mL) and a pH < 2.5, then a secretin stimulation test should be performed.

E Hemorrhage is the most frequent complication, occurring in up to 73% of patients hospitalized for peptic ulcer disease, and is associated with a mortality rate of 2.5%. When aggressively treated, ulcer bleeding is self-limited in 80% of patients. Initial medical therapy includes large-bore intravenous access, the administration of appropriate transfusions, correction of coagulopathies, and nasogastric lavage. F Gastric outlet obstruction occurs in up to 3% of patients with peptic ulcer disease and presents with symptoms of gastric retention including early satiety, bloating, nausea, vomiting, and epigastric pain as a result of edema or scarring adjacent to prepyloric or channel ulcers. Endoscopy confirms the benign nature of the lesion and affords appraisal of the severity of obstruction. A short-term trial of nasogastric tube decompression combined with medical management of the ulcer relieves the obstruction in some patients. The remainder will require endoscopic dilation or surgical correction. G Perforated PUD occurs in up to 9% of patients and is associated with the highest mortality (11%) of all complications. Most patients with perforated duodenal ulcers present with the abrupt onset of severe abdominal pain and rigidity. The symptoms tend to be subtler in elderly patients and in persons who take steroids. Pneumoperitoneum may be absent on plain radiographs in 20% of patients. Initial medical management includes nasogastric tube insertion, fluid resuscitation, broadspectrum antibiotics, and intravenous PPI therapy. H In patients with uncomplicated disease who fail medical management after 6 to 8 weeks of optimal therapy, diagnostic endoscopy with biopsy for H. pylori should be performed to confirm the diagnosis and redirect therapy. Patients with persistent H. pylori who have not been previously treated with clarithromycin should be treated with triple therapy. Bismuth quadruple therapy can be used in patients previously treated with a clarithromycincontaining regimen. Recent evidence suggests that treatment with a PPI, levofloxacin, and amoxicillin is a suitable alternative in patients failing previous therapy. Additionally, other serious lesions should be sought, including gastrinomas, gastric ulcers or tumors, inflammatory bowel disease, and hepatobiliary or pancreatic disorders. Renewed attention should be given to the avoidance of such risk factors as smoking, ethanol, aspirin, and NSAIDs. I

After initial stabilization of patient with a bleeding duodenal ulcer, endoscopy should be performed. The endoscopic appearance of the ulcer helps predict its course. Clean-based ulcers rarely rebleed and do not require intervention but should receive standard oral PPI therapy after endoscopy. Duodenal ulcers with an adherent clot or a nonbleeding visible vessel have a higher risk for rebleeding (22% and 43%, respectively) and require aggressive endoscopic intervention. Epinephrine injections may slow or stop bleeding and improve visualization but should not be used alone. Combination therapy with bipolar electrocoagulation, heater probe therapy, or mechanical clips is significantly more effective in reducing recurrent bleeding. After successful endoscopic hemostasis, intravenous PPI therapy with an 80-mg bolus and subsequent 8-mg/hour continuous infusion for 72 hours should be given. Eradication of H. pylori has been shown to significantly reduce the frequency of recurrent bleeding. A meta-analysis reported that recurrent bleeding from peptic

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Chapter 41  ◆  Duodenal Ulcer  128.e1

Abstract

Keywords

Greater than 90% of duodenal ulcers are caused either by infection of the stomach with Helicobacter pylori or by long-term use of non-steroidal anti-inflammatory drugs. Appropriate antimicrobial drug regimens to eradicate H. pylori and improved medical therapy with proton pump inhibitors have significantly reduced the morbidity and mortality associated with the disease. The management of duodenal ulcers is based upon the presentation of uncomplicated or complicated disease and may include endoscopic, interventional radiology, or surgical intervention.

duodenal ulcer peptic ulcer Helicobacter pylori nonsteroidal anti-inflammatory drugs (NSAIDs) bleeding ulcer perforated ulcer

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Chapter 41  ◆  Duodenal Ulcer  129 ulcers occurred in only 1% of patients after successful H. pylori eradication compared with 5.6% in patients treated with maintenance antisecretory therapy alone.

are avoided. Open vagotomy with antrectomy is recommended for severe obstruction and for giant ulcers (>2 cm). As an alternative, the laparoscopic approach with highly selective vagotomy and gastrojejunostomy also yields satisfactory results. Gastroenterostomy without vagotomy may be advisable in elderly patients to avoid postoperative gastric atony.

J

Historically, truncal vagotomy and antrectomy was performed in patients with intractable disease. However, removal of the pylorus is associated with a high incidence of postgastrectomy complications. Laparoscopic highly selective vagotomy avoids these complications and is currently the treatment of choice for intractability.

M In patients with no history of ulcer disease, simple closure of the perforation with a Graham patch and subsequent H. pylori eradication is associated with a recurrence rate of only 4.8%, thus obviating more extensive ulcer surgery in the majority of patients. Laparoscopic methods are highly effective and well tolerated when combined with appropriate medical therapy. Definitive operation should be considered in patients who are H. pylori negative, have failed adequate H. pylori therapy, or are NSAID-dependent. Highly selective vagotomy is the treatment of choice and may be performed using an open or laparoscopic approach. Hemodynamic instability and heavy peritoneal con­ tamination are recognized as contraindications.

K Persistent bleeding after endoscopic therapy may be treated with repeat endoscopy, angiographic embolization, or surgery depending on patient fitness and availability of services. Failed repeat endoscopic therapy or angiographic embolization requires an operation. Oversewing of the bleeding site with a “U-stitch” to control the proximal and distal gastroduodenal artery and the transverse pancreatic branch is essential. Some patients may benefit from vagotomy and pyloroplasty in addition to the oversewing.

N Operations for duodenal ulcer have decreased in frequency as nonoperative measures have improved. Nonetheless, surgical therapy may become necessary if ulcer disease is complicated or intractable. Most operative approaches have two major objectives: to relieve specific ulcer-related problems and to prevent recurrence. The defined risks and benefits of the different procedures vary and can be used to determine their respective

L Patients with gastric outlet obstruction that fails to resolve with medical management require more aggressive therapy. Endoscopic balloon dilation may be indicated in high-risk surgical patients but is associated with a risk for perforation. Although multiple dilations are commonly required, excellent long-term results can be achieved when H. pylori is eradicated and NSAIDs

History and physical examination Epigastric pain/dyspepsia Relief with food NSAIDs Aspirin Uncomplicated Ethanol Smoking Ulcer history

Medical management

Atypical

Other pathology

Persistent or recurrent symptoms

Diagnostic endoscopy

Unhealed ulcer

Asymptomatic

Observe

Repeat medical management

Serum Gastrin

E Complicated

Highly selective vagotomy Or Vagotomy and antrectomy

Normal

K Elevated

See Zollinger-Ellison syndrome

B Lab Serologic or breath test for H. pylori

J

Intractable ulcer

D

A Duodenal ulcer

C

H

Bleeding

F Obstruction

G Perforation

Transfusion Gastric lavage Medical management

Nasogastric tube Fluid resuscitation Medical management

Nasogastric tube Fluid resuscitation Antibiotics IV PPI Medical management

I Therapeutic endoscopy

Bleeding persists or recurs

Reapeat therapeutic endoscopy Or Angiographic embolization Or Ligation of bleeder, vagotomy and pyloroplasty

Bleeding stops

Medical management

L Obstruction clears Diagnostic endoscopy

Obstruction persists

Risk factors

No ulcer history Ulcer history Good risk

Endoscopic dilation Or Vagotomy and antrectomy Or Vagotomy and gastroenterostomy Or Gastroenterostomy

M Graham patch

N Highly selective vagotomy Or Vagotomy and antrectomy

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130  Part V  ◆  Alimentary Tract TABLE 41.1  Risks and benefits of procedures

to manage duodenal ulcers

Recurrence Morbidity Mortality

Vagotomy/ Pyloroplasty

Vagotomy/ Antrectomy

Highly Selective Vagotomy

12% 15-20% 1%

1% 15-20% 1-2%

10-15% 5% 0.5%

roles (Table 41.1). All such procedures can be successfully performed laparoscopically, but this approach should be limited to specialized centers and/or to surgeons who have completed advanced laparoscopic training.

Laine L, Jensen DM. Management of patients with ulcer bleeding. Am J Gastroenterol. 2012;107:345–360. Lau JYW, Sung JJY, Lam YH, et al. Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding. N Engl J Med. 1999;340:751–756. Leodolter A, Kulig M, Brasch H, et al. A meta-analysis comparing eradication, healing and relapse rates in patients with Helicobacter pylori-associated gastric or duodenal ulcer. Aliment Pharmacol Ther. 2001;15:1949–1958. Kyaw M, Tse Y, Ang D, Ang TL, Lau J. Embolization versus surgery for peptic ulcer bleeding after failed endoscopic hemostasis: a meta-analysis. Endosc Int Open. 2014;2(1):E6–E14. Schwesinger WH, Page CP, Sirinek KR, et al. Operations for peptic ulcer disease: paradigm lost. J Gastrointest Surg. 2001;5:438–443. Tan S, Wu G, Zhuang Q, et al. Laparoscopic versus open repair for perforated peptic ulcer: a meta-analysis of randomized controlled trials. Int J Surg. 2016;33(Pt A):124–132.

REFERENCES Chey WD, Wong BCY. Practice parameters committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808–1825.

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Chapter

42 

MORBID OBESITY Bria Meyer, MD, Akshay Pratap Chauhan, MD, and Jonathan A. Schoen, MD A The initial surgical history and physical examination will determine a person’s eligibility for bariatric surgery. The patient must meet the 1991 National Institutes of Health (NIH) Consensus Conference weight criteria discussed further in the next section. The patient must have had prior counseling and a referral from the primary care physician for surgical evaluation. Endocrine disorders such as hypothyroidism and Cushing’s disease must be ruled out, as should any medications causing weight gain. A documented history of the failed prior weight-loss attempts through dietary, behavioral, lifestyle, and/or medical interventions must be reviewed. Last but most important, the patient must be motivated and have a basic understanding of the procedure and its risks, benefits, complications, and long-term outcomes before any further evaluation for surgery. B Morbid obesity was just recently recognized as a disease by the American Medical Association (AMA) because of its increasing prevalence in the United States and negative associated health outcomes and costs. Approximately 300,000 Americans die each year from causes related to obesity, and it is the second leading cause of preventable death in the United States (tobacco use is first). Close to 10% of U.S. health-care expenditures result from obesity and physical inactivity. Bariatric surgical procedures are superior to medical therapies for weight loss and treatment of obesity-related medical comorbidities. The 1991 NIH Consensus Conference on GI Surgery for severe obesity established the current weight guidelines. Patients must have a body mass index (BMI) between 35 and 39.9 kg/m2 and either high-risk or lifestyle-limiting comorbid conditions or a BMI of 40 kg/m2 or greater to be candidates for obesity surgery. Obesity-related comorbidities include pseudotumor cerebri, hypertension (HTN), coronary artery disease (CAD), cardiomyopathy, pulmonary hypertension, stroke, obstructive sleep apnea (OSA), obesity hypoventilation syndrome (Pickwickian syndrome), gastroesophageal reflux disease, cholelithiasis, nonalcoholic steatohepatitis (NASH), cirrhosis, diabetes mellitus (DM), hyperlipidemia, metabolic syndrome, uterine cancer, breast cancer, colon cancer, venous stasis disease, asthma, hypercoagulability, peripheral vascular disease, degenerative joint disease, osteoarthritis, ventral hernias, skin infections, dysmenorrhea, hirsutism, infertility, chronic kidney disease, and stress urinary incontinence. There has been a recent push to lower the accepted minimum BMI to 30 kg/m2 in the setting of inadequately controlled type 2 diabetes mellitus, as evidenced by American Diabetes Association (ADA) and International Diabetes Federation (IDF) guidelines endorsing metabolic surgery for this lower-BMI group. C Routine laboratory results will be obtained, including liver function tests to evaluate for NASH and advanced liver disease. A right upper quadrant (RUQ) ultrasound should be considered if a gallbladder is still present and the patient reports any prior episodes of RUQ pain. If gallstones are present, a

cholecystectomy should be performed at the time of surgery. If gallstones are not present, then prophylactic treatment with ursodiol acid postoperatively can be given to decrease the rate of gallstone formation. In addition, thyroid function tests should be considered to assess that the patient’s excess weight and subsequent weight loss are not impacted by hypothyroidism. An upper GI contrast study and upper endoscopy are usually performed selectively on patients presenting with GERD to rule out Barrett’s esophagitis, ulcer, or hiatal hernia. The results may change the recommended operation. D Patients will first be counseled in a weight-loss program, and most insurance payors will mandate a 3- to 6-month program. Examples of these programs include supervised diets alongside a clinical nutritionist; drug therapy such as phentermine, phentermine-topiramate, or orlistat; or a combined diet and exercise program. Unfortunately, the reported rates of long-term success of keeping a BMI below 35 kg/m2 with medical weight-loss programs alone are less than 5%. It is not unusual for patients, especially those with NASH and hepatomegaly, to be put on a calorie-restrictive diet preoperatively so that the laparoscopic portion of the surgery can be done with more ease. Occasionally, an obesity comorbidity may be so severe (e.g., venous stasis ulcer, pseudotumor cerebri, obesity hypoventilation) that one will proceed with bariatric surgery without a medical weight-loss trial. E For those who fail nonoperative weight loss and meet all criteria for surgery, a multidisciplinary preoperative evaluation is done. Bariatric surgery will alter the patient’s anatomy and metabolism, appetite, and many metabolic processes in the patient’s body. The multidisciplinary team includes the surgeon, dietician, primary care physician, nurse care coordinator or educator, psychologist/psychiatrist, exercise specialist, and any medical specialists needed to evaluate and assist with cardiac, pulmonary, endocrine, or other comorbidities as needed. This team is necessary in both the preoperative and postoperative periods. F The dietician is instrumental in teaching the patient how the procedure will change his or her eating habits and what behavioral and lifestyle changes are needed to maintain a healthy diet and ultimately be successful with the procedure. The dietician will reinforce what supplements are necessary. Proximal gastric bypass patients will require a daily multivitamin, calcium, iron, folic acid, and B12 supplements at a minimum. Patients undergoing biliopancreatic diversion (BPD) will also require fat-soluble vitamins, and menstruating women will require additional iron supplementation. The dietician will continue to see the patient postoperatively to assist with maintaining weight-loss goals, follow vitamin and mineral levels, and provide additional dietary interventions needed. G Routine psychological screening is important to establish the stability of the patient and verify the motivation for the surgery. This patient population tends to have a history of mental health conditions and emotionally traumatic events. Patients should be questioned about substance abuse and alcoholism. Formal psychiatric evaluation is necessary in cases of active ongoing psychiatric disease or prior psychiatric hospitalizations. Adolescents undergoing bariatric surgery will be formally evaluated by a psychologist to establish their level of maturity and

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Chapter 42  ◆  Morbid Obesity  132.e1

Abstract

Keywords

Bariatric surgery remains the treatment of choice for the extremely obese patient, with an exponential growth in the number of procedures performed in response to the obesity epidemic. There are a variety of bariatric procedures available, which differ according to the method by which they achieve sustained weight loss. Proper evaluation of the patient for weight loss requires an understanding of the physiologic effect of different bariatric procedures, with particular knowledge of potential long-term nutritional complications, and a multidisciplinary approach.

bariatric surgery evaluation weight-loss surgery

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Chapter 42  ◆  Morbid Obesity  133 their knowledge of the procedure, risks, benefits, complications, and outcomes. They should be available to provide the patient with postoperative support.

position. The arm boards should also be wide and have extra padding. Sequential compression device (SCD) stockings need to be extra-large, and a footboard should be available. Care must be taken with extra foam padding to reduce the risk for pressure ulcers or neurologic deficits. If the case may exceed 3 hours, the patient should have a Foley catheter. In the more complex cases or patients with significant cardiac history, a radial artery line should be placed. The anesthesia team must have experience with this patient population, including difficult airway management.

H Cardiac evaluation includes assessing for a history of chest pain and the patient’s functional activity. A preoperative electrocardiogram (ECG) is done for all patients. Formal cardiac evaluation is reserved for those patients with a history of recent chest pain, abnormal ECGs, recent decrease in exercise tolerance, or prior history of myocardial infarction. Further evaluation may require an echocardiogram or a cardiac stress test.

L The most commonly performed restrictive procedure is the vertical sleeve gastrectomy (VSG). The adjustable gastric band (AGB) has seen a considerable decrease in popularity because of its variable and often poor long-term weight-loss results combined with a relatively high rate of explantation. The verticalbanded gastroplasty (VBG) is no longer performed because of its high rate of complications and poor long-term weight loss. The VSG has become more popular in recent years. It has close to the same profile in terms of long-term weight loss and quality of life as the Roux-en-Y gastric bypass (RYGB) with fewer longterm complications and has better results for weight loss and appetite control than AGB. Advantages of the VSG include preservation of the pylorus and decreased ulcers, internal hernias, and malabsorption of vitamins and minerals compared with the RYGB, and it can be converted to an RYGB if needed. The VSG promotes reflux and is not the best option for those with a large hiatal hernia or severe reflux. It also may not be the best option for those with a high BMI > 50 kg/m2 or those with severe diabetes.

I

Undiagnosed sleep apnea is common in the morbidly obese. A history of multiple night-waking episodes, early morning headaches, loud snoring, somnolence while driving, daily afternoon naps, or witnessed apnea is suggestive, and these patients should undergo a preoperative sleep study. Consideration should be given to patients with a BMI greater than 50 kg/m2 or those with suggested Pickwickian syndrome for arterial blood gas testing or an echocardiogram to rule out pulmonary hypertension. Involvement of a pulmonologist in the perioperative care of these patients may be helpful, along with possible planned postoperative intensive care unit (ICU) admission if severe obesity hypoventilation syndrome is present. J

Hypertension and metabolic abnormalities such as hyperlipidemia and diabetes mellitus are common in the obese. Close follow-up with the patient’s primary care physician and endocrinologist is important to ensure that the patient’s medications are adjusted and blood pressure and glucose are well controlled.

M The first malabsorptive procedure performed starting in the 1960s was the jejunoileal bypass (JIB). The JIB had significant late complications, including protein-calorie malnutrition, cirrhosis, severe osteoporosis, and interstitial nephritis. This

K In the operating room (OR), the morbidly obese patient requires special considerations. The OR table should be wide and able to accommodate >500 lb, especially in the tilted

History and Physical Examination - Comorbidities A - Weight history

Nutrition

D Medical Therapy - Diet/exercise program - Drug therapy

B Morbid Obesity BMI ≥ 40 kg/m2 BMI 35-39.9 kg/m2 with comorbidity

F

Surgical Therapy - Multidisciplinary preoperative evaluation

G Restrictive - VSG - AGB L

Psychiatric/Psychology

Cardiac

H

Operating Room

K

E

I Pulmonary

Labs C - CBC, chemistries, LFTs, TSH, EKG, +/− RUQ US, +/− Upper GI, +/− EGD

Malabsorptive - JI Bypass (historic)

Technique Laparoscopic vs. Open

M

O

Combination - RYGB (largely restrictive) - BPD (largely malabsorptive) - BPD-DS (largely malabsorptive)

N J Metabolic/Endocrine

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134  Part V  ◆  Alimentary Tract procedure is no longer an approved procedure and has been completely abandoned. N The RYGB, the BPD, and the biliopancreatic diversion– duodenal switch (BPD-DS) are all restrictive and malabsorptive. The RYGB is composed of a small proximal gastric pouch that holds 15 to 20 mL that is anastomosed to the distal divided end of the jejunum (Roux limb), cut 25 to 50 cm from the ligament of Treitz. The proximal divided end of the jejunum (biliopancreatic limb) is then reconnected to the Roux limb 60 to 150 cm from the pouch. The most serious of its complications are leak ( 4 to 5 mm, sludge or stones, and pericholecystic fluid. F Cholecystenteric fistulas arise when large stones > 2 cm enter the intestine and cause obstruction. Most patients are women, average age 70, and are asymptomatic. Pneumobilia is seen in most patients. Computed tomography (CT) has a sensitivity of 93%. Treatment is surgery to remove the stone proximal to the site of obstruction (enterolithotomy), with closure of the fistula and cholecystectomy at the index procedure in good-risk patients. In high-risk patients, cholecystectomy and fistula closure may be done at a second stage. G Serum amylase levels greater than 3 times the upper limit of normal in patients with cholelithiasis and elevated liver function tests (LFTs) are associated with gallstone pancreatitis. Cholecystectomy should be performed in the index hospitalization after resolution of clinical pancreatitis. H Elective laparoscopic cholecystectomy is standard of care in patients with symptomatic cholelithiasis. Laparoscopic cholecystectomy and selective open cholecystectomy are indicated for acute cholecystitis. The optimal timing of laparoscopic cholecystectomy is within 24 to 48 hours of admission. Delayed surgery is associated with increased conversion rate, risk for bile duct injury, mortality, infection, and costs. The rate of bile duct injury for laparoscopic cholecystectomy is estimated at 0.5%, twice as much as in open cholecystectomy, with one-third to one-half of all surgeons having an injury during their career. Risks for bile duct injury include anatomic variation, acute inflammatory processes, and chronic scarring. Indications for open surgery include the inability to complete a laparoscopic procedure safely because of anatomy or exposure, intolerance for pneumoperitoneum, refractory coagulopathy, or suspected malignancy. I

Antibiotics should be given to patients with acute cholecystitis. Existing guidelines offer coverage of mild cases with a first- through third-generation cephalosporin, and in these cases, antibiotics should be complete after a 24-hour postoperative course. In more severe cases, antibiotics should be continued until clinical resolution of infection, and coverage should also cover Enterococci and anaerobes. J

Conversion to open cholecystectomy should be done as soon as it is realized that a safe laparoscopic procedure cannot be performed. Conversion rates in the United States approach 9%. Predictors of a difficult laparoscopic cholecystectomy include male patients, elderly patients, inflammation, longer duration of symptoms, impacted stones, repeated cholecystitis, and contracted gallbladder. Subtotal cholecystectomy can also be performed in instances of increased injury risk. K Intraoperative ultrasonography and transcystic cholangiography have a similar sensitivity of 0.87 and a specificity of ~0.99 in detecting choledocholithiasis. The use of both

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Chapter 47  ◆ Cholelithiasis  144.e1

Abstract

Keywords

Cholelithiasis is a common problem that often requires surgery. Treatment is based on symptoms and severity and includes minimally invasive surgery, open surgery, and nonsurgical management.

gallstones gallbladder cholelithiasis

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Chapter 47  ◆ Cholelithiasis  145 History and Physical Exam - Pain - RUQ tenderness - Postprandial discomfort

C

H

Asymptomatic

Laparoscopic cholecystectomy Or Selective open cholecystectomy

D Chronic cholecystitis

A

Cholelithiasis

E B Diagnosis - CBC - Liver function studies - RUQ US - HIDA - MRCP

Acute cholecystitis

I Medical management: IV Fluids Antibiotics Analgesia

F G

K Intraoperative ultrasonography or Selective cholangiogram

See choledocholithiasis

Improving

L Emergency cholecystectomy Worsening

M

Gallstone ileus

Gallstone pancreatitis

J Open cholecystectomy

See acute pancreatitis

intraoperative methods for assessing the biliary anatomy and identifying injury is dependent on user familiarity. If choledocholithiasis is identified, laparoscopic common bile duct exploration (CBDE), open CBDE, or postoperative ERCP are all options. If a bile duct injury occurs that appears readily correctable, an open primary duct repair over a T-tube with the placement of a drain may be attempted. For the more common extensive injury, an end-to-side Roux-en-Y hepaticojejunostomy may be necessary. However, this anastomosis may be very difficult in the acute setting with small, normal-size bile ducts. If injury is identified after surgery, the biliary tree should be drained and the patient transferred to a specialized center for later definitive treatment. L Emergency cholecystectomy increases perioperative risk considerably and should be reserved for patients with gangrenous or emphysematous cholecystitis with systemic symptoms overweighing the operative risk. Mortality rates in emergency cholecystectomies can be 10% or greater, especially in elderly patients. M In recent years, there has been an increase in the use of percutaneous cholecystostomy tubes (PCTs) for cholecystitis patients who have poor surgical risk. Cholecystostomy tubes can also be placed intraoperatively. No well-defined guidelines have been established for their use; broadly, PCTs are used in instances of failure of antibiotic management of severe cholecystitis involving end-organ effects, late presentation, critical illness, and

Enterolithotomy ± Cholecystectomy and fistula closure

Cholecystostomy

contraindications to general anesthesia. Mortality is historically high for these procedures because of their use in a more unstable patient population; however, there has been improving mortality, likely as a result of recent use in less morbid patients. The need for delayed cholecystectomy after resolution of cholecystitis and removal of the cholecystostomy tube is controversial. REFERENCES Agresta F, et al. Laparoscopic cholecystectomy: consensus conference-based guidelines. Langenbecks Arch Surg. 2015;400(4):429–453. Cabarrou P, et al. Prophylactic cholecystectomy during abdominal surgery. J Vasc Surg. 2013;150(4):229–235. Ingraham AM, et al. A current profile and assessment of North American cholecystectomy: results from the American national surgical quality improvement program. J Am Coll Surg. 2010;211(2):176. Kaafarani HM, et al. Trends, outcomes and predictors of open and conversion to open cholecystectomy in Veterans Health Administration hospitals. Am J Surg. 2010;200(1):32–40. Luu MB, Deziel DJ. Unusual complications of gallstones. Surg Clin North Am. 2014;94(2):377–394. Peitzman AB, et al. Acute cholecystitis: when to operate and how to do it safely. J Trauma Acute Care Surg. 2015;78(1):1–12. Smith TJ, et al. Changing trends and outcomes in the use of percutaneous cholecystectomy tubes for acute cholecystitis. Ann Surg. 2013;257(6): 1112–1115. Tabone LE, et al. To ’gram or not? Indications for intraoperative cholangiogram. Surgery. 2011;150(4):810–819. van Baal MC, et al. Timing of cholecystectomy after mild biliary pancreatitis: a systematic review. Ann Surg. 2012;255(5):860–866. Zafar SN, et al. Optimal time for early laparoscopic cholecystectomy for acute cholecystitis. JAMA Surg. 2015;150(2):129–136.

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Chapter

48 

CHOLEDOCHOLITHIASIS Laura A. Harmon, MD, and Paulesh K. Shah, MD A It is important to approach the patient with a wide differential; history, physical clinical examination, labs and imaging can lead to a number of similar symptoms but with vastly different pathology. Typical symptoms are often indistinguishable from cholelithiasis or cholecystitis (see Cholelithiasis chapter) but right upper quadrant (RUQ) pain, elevated bilirubin, alkaline phosphatase, ALT, AST, and dilated common bile duct are all signs that point to choledocholithiasis and should prompt you to move this higher on your differential. (Incidentally, these signs can also be seen in a patient with cirrhosis, hepatitis, or primary biliary cirrhosis.) B Common bile duct (CBD) stones are primarily (95%) from the gallbladder (usually cholesterol stones) and are present in about 10%–15% of the patients undergoing cholecystectomy (25% for age >60 years). Conversely, 5% of CBD stones are associated with no stones in the gallbladder. The most common mechanism of choledocholithiasis is the passage of stones from the gallbladder through the cystic duct and into the CBD. However, gallstone formation can occur even after a patient has had a cholecystectomy. These are referred to as primary duct stones and are generally composed of pigmented calcium bilirubinate and are usually the result of biliary stasis. C Ultrasound is the best technology for evaluating the common bile duct with a reported 80% accuracy for detecting CBD stones or ductal dilatation. When the picture is unclear, CT scan is often used to determine if there are any other intraabdominal sources for clinical symptoms (i.e., pancreatic head mass, biliary duct mass, duodenal ulcer). D Presentation of choledocholithiasis may range from no symptoms to septic shock. From a clinical standpoint choledocholithiasis in and of itself may not be emergent in nature; however, the sequelae of untreated choledocholithiasis can prove to be catastrophic. The branch point in management for choledocholithiasis is dependent primarily on the acuity of the patient. A patient with choledocholithiasis and ascending cholangitis is a medical emergency. If a patient presents with symptoms of choledocholithiasis (RUQ pain, elevated liver enzymes, dilated CBD) but is otherwise hemodynamically stable, without fever or white blood cell count, you have time to make a plan. However, in the presence of Charcot’s triad (RUQ pain, fever, and jaundice) or Reynolds’s pentad (Charcot’s triad plus hypotension and CNS changes), initial management of acute cholangitis should be emergent. These are both signs of ascending cholangitis resulting from occlusion of the biliary tree. Your goal in therapy is twofold: (1) source control by ductal decompression and (2) sepsis treatment with fluid resuscitation antibiotic therapy. E In a patient with choledocholithiasis without signs of cholangitis the patients should be admitted to the hospital and treated but does not necessitate emergent intervention.

However, patients should not be discharged home and instructed to follow up for further treatment because asymptomatic choledocholithiasis can escalate to ascending cholangitis. F In the presence of cholangitis, about 5%–10% of patients progress to septic shock, a condition that demands aggressive fluid resuscitation with hemodynamic monitoring in addition to antibiotics. Broad-spectrum antibiotic agents should cover gram negatives (E. coli, Klebsiella) and anaerobes (Bacteroides, Clostridia). G Preoperative endoscopic retrograde pancreatocholan­ giography (ERCP) may be reserved for cases of elevated bilirubin, jaundice, or evidence of dilated ducts to search for tumor or stone (especially with history of prior gallbladder removal). Magnetic resonance cholangiopancreatography (MRCP) shows promise in detecting CBD stones before laparoscopic cholecystectomy. If a CBD stone is suspected, non-invasive MRCP may be an ideal alternative to the invasive diagnostic ERCP and thereby determining the need for either a CBD exploration or preoperative ERCP and sphincterotomy. The limitation to MRCP is that it is diagnostic only and patients with choledocholithiasis detected on MRCP will still require an intervention. H In instances with limited availability, an interventionalist who performs ERCP proceeding with cholecystectomy and intraoperative cholangiography (IOC) is a reasonable alternative. Indications for IOC are elevated liver function enzymes and CBD dilation. I

The availability of resources at your institution will dictate how you treat choledocholithiasis with associated cholangitis because there is typically a multi-disciplinary approach to managing these patients. If you are at an institution with gastroenterology support, the first step would be emergent ductal decompression with endoscopic retrograde pancreatocholangiography (ERCP) and sphincterotomy. This is both diagnostic and therapeutic and affords the opportunity to evaluate the biliary tree endoscopically to identify etiology of obstruction (mass vs. stone), clear the common bile duct (stone extraction), and perform sphincterotomy of the sphincter of Oddi to allow for passage of stones into the duodenum. J

Another viable option is percutaneous transhepatic cholangiography (PTCA). This is usually performed by an interventional radiologist under fluoroscopy and involves placing a drain through the liver antegrade into the common bile duct. This does not clear the obstruction; however, it does afford decompression of the duct. Transhepatic drainage is most successful in patients with intrahepatic ductal dilation. This is a different procedure from a percutaneous cholecystostomy tube. A percutaneous cholecystostomy tube is a drain placed directly into the gallbladder and is used as a mode of source control in patients with cholecystitis who would otherwise not tolerate a cholecystectomy. Placing a cholecystostomy tube in a patient with ascending cholangitis from choledocholithiasis does not decompress the biliary tree and therefore is not treating the underlying disease. In a patient with choledocholithiasis, the goal is to decompress the biliary tree—not the gallbladder. K Finally, surgical intervention is an option and would be done with a common bile duct exploration.

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Chapter 48  ◆ Choledocholithiasis  146.e1

Abstract

Keywords

Choledocholithiasis is a complex and often multidisciplinary disease process. It is important to first recognize the clinical acuity of illness in the patient. Availability of resources at your institution will then dictate your approach to management.

choledocholithasis ERCP gallstones cholangitis

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Chapter 48  ◆ Choledocholithiasis  147

I ERCP & Sphincterotomy

A History and exam RUQ Pain Fever Jaundice Shock Altered mental status

F Resuscitation Antibiotics

Emergent Ductal Decompression

Transhepatic decompression (PTCA)

J

D

K

Surgical Decompression

Acute Cholangitis

Emergent Open T-tube Decompression Transduodenal Sphincteroplasty Common Bile Duct Exploration

B CHOLEDOCHOLITHIASIS

G C CBC Electrolyes Liver function tests Lipase US

ERCP & Sphincterotomy

E No Cholangitis

N

Elective Ductal Decompression

L H Cholecystectomy and Intraoperative cholangiogram (IOC)

Positive IOC

M

Common Bile Duct Exploration Post-Op ERCP

Intraoperative ERCP

Negative IOC

L If the patient has a positive IOC, saline irrigation through the cholangio-catheter coupled with intravenous glucagon for ampullary relaxation may clear the stone. If this does not clear the duct you must then decide, based on your institutional support, to proceed with laparoscopic or open common bile duct exploration. M A negative IOC is documented by five findings: (1) flow of contrast from the cystic duct into the common bile duct, (2) filling of the common bile duct, (3) retrograde filling of the right and left hepatic ducts, (4) no filling defects, and (5) flow of contrast into the duodenum or post-operative versus intraoperative ERCP. N After exposing the common bile duct (and taking care not to disrupt the blood supply to the CBD at the 3 and 9 o’clock positions) make a 0.5 cm–1 cm longitudinal choledochotomy. There are a variety of tools available to clear the duct. Start with a choledochoscope to visualize the inside of the duct and identify the obstruction. With the ductal lumen under video monitoring, the stone is either retrieved or pushed using a No. 3 French helical basket. The CBD stone is either flushed with

irrigation or pushed with instruments as mentioned previously. If you are unable to clear the duct because of constriction at the ampulla, transductal balloon catheter dilation or transduodenal sphincteroplasty may be required. When closing the choledocotomy, a T-tube should be placed into the common bile duct at the time of initial surgery and allowed to mature for a minimum of 6 weeks. This allows for the formation of a biliary enteric tract that can later be used for instrumentation. Additionally, it allows for biliary diversion if the stone cannot be cleared. REFERENCES Aleknaite A, Simutis G, Stanaitis J, Valantinas J, Strupas K. Risk assessment of choledocholithiasis prior to laparoscopic cholecystectomy and its management options. United European Gastroenterol J. 2018;6(3):428–438. Dasari BV, Tan CJ, Gurusamy KS, et al. Surgical versus endoscopic treatment of bile duct stones. Cochrane Database Syst Rev. 2015;(2):CD010339. Doshi B, Yasuda I, Ryozawa S, Lee GH. Current endoscopic strategies for managing large bile duct stones. Dig Endosc. 2018;30(suppl 1):59–66. Jang SE, Park SW, Lee BS, et al. Management for CBD stone related mild to moderate acute cholangitis: urgent versus elective ERCP. Dig Dis Sci. 2013;58(7):2082–2087. Manning A, Frazee R, Abernathy S, et al. Protocol driven management of suspected common duct stones. J Am Coll Surg. 2017;224(4):645.

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Chapter

49 

HEPATIC ABSCESS Jad Abou-Khalil, MD, and Scott Helton, MD A The most common cause of pyogenic liver abscess is biliary tract obstruction or cholangitis (35%) caused by gallstones or malignancy. In the past, the most common cause was portal pyemia because of diverticulitis, inflammatory bowel disease, or perforated appendicitis (now accounting for 20% of cases). Approximately 20% of hepatic abscesses are cryptogenic and associated with other morbid medical conditions. Cryptogenic liver abscesses in the absence of hepatobiliary disease or intraabdominal septic foci should undergo a colonoscopy to rule out an occult colon cancer. B A history of travel to an endemic area should raise suspicion of an amebic abscess or hydatic cyst. Hydatid disease occurs in sheep-rearing countries, the Mediterranean basin, central Asia, Mexico, New Zealand, and the subalpine zones of northern Europe and North America. Tropical climate is associated with amebiasis. C There is increased risk associated with chronic granulomatous disease, Job’s syndrome, and inflammatory bowel disease. D Classic symptoms include night sweats, vomiting, anorexia, weight loss, diarrhea, and right upper quadrant (RUQ) pain. The presentation is often varied. Single abscesses present gradually and insidiously, whereas multiple abscesses are associated with more systemic symptoms. On examination, the liver can sometimes be palpated, and percussion over the ribs may aggravate the pain. E Leukocytosis is present in most patients. Liver function tests are abnormal in most patients, but the elevations are seldom marked. In recent years, the percentage of patients with abnormal liver function tests has decreased. This difference may reflect the increased incidence of abscesses in patients with biliary stents. Alkaline phosphatase elevations tend to be higher when compared with other liver function tests. F If a hepatic abscess is detected, serologic tests should be performed to rule out active amebiasis or echinococcal infection as called for by a history of travel to an endemic region. Entamoeba histolytica–specific antigen detection or polymerase chain reaction (PCR) is preferred to confirm the diagnosis of amebiasis. Echinococcal infection can be confirmed by serologic and antigen testing. G Blood cultures and/or bile cultures (obtained at endoscopic retrograde cholangiopancreatography [ERCP]) are important because they are positive in half of patients and can aid in directing antimicrobial therapy. Cultures from abscess cavities are frequently sterile because of prior antimicrobial therapy. Presence of Streptococcus milleri in the blood may be associated with a visceral abscess.

H Ultrasonography is the study of choice in patients with suspected biliary disease and in patients who must avoid intravenous contrast or radiation exposure. It has excellent sensitivity (80% to 90%) and can demonstrate lesions as small as 2 cm. Most liver abscesses occur in the right lobe: 40% are 1.5 to 5 cm in diameter, 40% are 5 to 8 cm in diameter, and 20% are more than 8 cm in diameter. Computed tomography (CT) scanning is superior to ultrasound for evaluating the presence of air and abscesses as small as 0.5 cm in diameter, especially near the hemidiaphragm. Abdominal CT is the method of choice in the postoperative patient. CT imaging is the best guide for complex drainage procedures. ERCP is indicated when gallstones or biliary malignancy is the potential source of the abscess. Percutaneous transhepatic cholangiography/drainage is indicated when ERCP is nondiagnostic or unavailable. I

Establishing the presence of an infectious etiology is important in making management decisions. It is essential to differentiate hydatid cysts from amebic or pyogenic abscess because special precautions are required for the drainage of echinococcal cysts because of the risk for spillage and anaphylaxis. Less common infectious agents such as fungi and mycobacterium may also cause hepatic abscesses in immunosuppressed patients. J

Diagnostic percutaneous aspiration is critical in cases where the etiology is unclear but should be performed after ruling out the possibility of a hydatid cyst through serological studies. Aspiration can be both diagnostic and therapeutic. Aspirated material should always be cultured. K Amebic liver abscesses follow intestinal infection with Entamoeba histolytica, endemic to subtropical and tropical climates and in developing countries. Immigration and travel between countries have increased the incidence of this disease in developed countries. The cystic form enters the human through oral ingestion of contaminated material. Trophocytes are released and multiply in the colon, especially the cecum, where they cause a diarrheal illness. The trophocytes reach the liver through the portal vein, through the lymphatics, or by direct extension through the colon wall into the peritoneum and then through the liver capsule. Amebic abscess tends to be solitary and is known to display a male predominance. The clinical signs and symptoms of an amebic liver abscess are similar to those of pyogenic abscesses. There are often no detectable parasites in the stool of patients with an amebic liver abscess. Serologic testing for antibodies to E. histolytica is more useful. It is important to note that a positive titer can represent a previous infection rather than current illness. Therefore imaging techniques are important in the diagnosis. In addition to ultrasound (US) and CT, 99mTc scanning may be useful for differentiating an amebic liver abscess from a pyogenic abscess. Amebic abscesses do not contain leukocytes and consist of amebic cells around dead and dying hepatocytes; they therefore appear as “cold” lesions, whereas pyogenic liver lesions contain leukocytes and may be visualized as “hot” lesions on the nuclide scan. L Pyogenic abscesses are the most common hepatic abscess in the United States. Mortality is as high as 30%. The incidence has slowly increased from 13 to 20 per 100,000 hospital admissions. Aggressive operative and nonoperative approaches to the management of hepatobiliary and pancreatic neoplasms (e.g., hepatic artery embolization and biliary stenting) may be

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Chapter 49  ◆  Hepatic Abscess  148.e1

Abstract

Keywords

Liver abscesses are increasing in frequency because of increasing interventions and instrumentations of the biliary tree and increasing travel to areas where endemic organisms cause a variety of bacterial and parasitic liver abscesses. This chapter illustrates an algorithm for the diagnosis and treatment of liver abscesses.

hepatic abscess echinococcal cyst amebic abscess invasive Klebsiella pneumoniae liver abscess

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Chapter 49  ◆  Hepatic Abscess  149 contributing to this trend. Most patients with pyogenic abscess present with fever and abdominal pain. With the exception of alkaline phosphatase and leukocyte count, most laboratory findings are normal. Most pyogenic abscesses are located in the right lobe of the liver. Pyogenic liver abscesses tend to be multiple.

or amebic abscess. The diagnosis can be difficult when there is no evidence of extrahepatic tuberculosis. Tuberculous liver abscess occurs more often in patients being treated for extra-hepatic tuberculosis who have acquired drug resistance or who are noncompliant with the medication. The patient’s history and percutaneous diagnostic aspiration may serve as the only indicators for tuberculous abscess. The tuberculin test and other serological examinations may be noncontributory.

M Hepatosplenic candidiasis is less common than pyogenic or amebic liver abscesses and should be considered in patients with hematological malignancies and prolonged neutropenia or immunosuppression. The most common causative organism is Candida albicans. Others include Aspergillus, Cryptococcus, Histoplasma, and mucormycosis; the lesions are multiple and may appear as hypoechoic areas on ultrasound and hypodense on CT, with their appearance evolving as the neutrophil counts wax and wane. These lesions can be difficult to distinguish from pyogenic liver abscesses. Percutaneous aspiration under US or CT guidance is indicated for definitive diagnosis. Amphotericin B or fluconazole are most commonly used, but caspofungin or other echinocandins are used where fluconazole resistance is endemic.

O Hydatid cysts are caused by the tapeworm Echinococcus granulosus. The disease is endemic to areas of the world where humans, ungulates, and canids coexist, such as sheepherding societies and sub-boreal areas. Infection occurs when ingestion of ova leads to invasion through the intestinal wall and passage through the portal vein to the liver. Infected patients have symptoms similar to those with pyogenic or amebic abscesses. Rupture of the cyst into the peritoneum may result in urticaria, anaphylactic shock, eosinophilia, and implantation into the surrounding abdominal viscera. Percutaneous aspiration of cysts that could be echinococcal should not be performed for this reason. The diagnosis is confirmed using hemagglutination and complement fixation tests.

N Tuberculous liver abscess is rare and occurs most often in areas where tuberculosis is still prevalent. Tuberculosis in the liver usually presents in diffuse form (miliary) or as multiple caseating granulomas. Imaging studies can be diagnostic in these cases. Occasionally, a hepatic abscess thought to be pyogenic or amebic in etiology is discovered to be caused by mycobacteria. It is thought that the organisms reach the liver by hematogenous spread from tuberculous foci in the lungs or via the hepatic artery or through the portal vein from tuberculous foci in the gut. Most patients present with symptoms similar to a pyogenic

P Patients with a high risk for abscess rupture, cavity size greater than 5 cm, left lobe abscess (associated with higher mortality and higher frequency of peritoneal leak or rupture into the pericardium), and those who fail to respond clinically to drug therapy within 5 to 7 days benefit from percutaneous drainage. Q Complicated cases of pyogenic liver abscess require operative treatment. These include failed percutaneous drainage, very

History and Physical

A B C D

Previous abdominal infection: cholangitis, diverticulitis, pancreatitis, cholecystitis, appendicitis

U

Cryptogenic: diabetes, malignancy, cirrhosis, AIDS, transplant, immune suppression

K Amebic

Country of origin and/or recent travel

L Pyogenic

J

I Hepatic Abscess

Etiology Unclear

Percutaneous Diagnostic Aspiration

M Fungal

N Mycobacterial

E

P Flagyl + Percutaneous aspiration/Catheter drainage US- or CTguided

Q

Fever, night sweats, vomiting, anorexia, weight loss, diarrhea, RUQ pain, enlarged and tender liver, jaundice

Labs and Imaging WBC ESR, LFTs, Bili, Alk Phos

Bacterial-specific antibiotic treatment Antibiotic treatment only

R

Empirical Broad Spectrum Antibiotics

complicated uncomplicated

Antifungal

W

S Systemic Antituberculous Chemotherapy + Percutaneous Catheter drainage US or CTguided

X

Surgical drainage/ resection

PAIR

T

Eosinophilia, hemagglutination and complement fixation test

G

Cultures

H

Imaging

IKLAS

US CT ERCP

V

Hydatid

Percutaneous aspiration/ Catheter drainage US- or CT-guided

Biliary Rupture

F

O

Y

Flagyl

complicated

History: chronic granulomatous disease, Job’s syndrome, inflammatory bowel disease

Infectious Etiology

uncomplicated

Small calcified cyst, elderly patient

Anti-helminthic medication

Anti-helminthic medication

Drainage and extendedspectrum cephalosporins

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150  Part V  ◆  Alimentary Tract large and/or multiple loculated abscesses, patients with concurrent intraabdominal disease, and impending rupture or rupture into the pericardium or peritoneum.

infection of the liver in the absence of predisposing hepatobiliary disease and with the potential for metastatic infection. Treatment consists of drainage and extended-spectrum cephalosporins.

R Early empiric antibiosis should be instituted and include coverage for anaerobes, gram-negative bacilli, and Streptococcus species, and the activity spectrum should be narrowed once a pathogen is identified, with continuing therapy for 4 to 6 weeks. If the abscess is polymicrobial, anaerobic coverage should be continued. The empiric regimen can include beta-lactamase inhibitors, third-generation cephalosporin or fluoroquinolone and metronidazole, or a carbapenem. Repeat imaging should be obtained to ensure resolution. Antibiotic treatment only may have a role in selected patients. Indications for antibiotics alone may include high-risk patients who cannot tolerate procedures or those with multiple small liver abscesses.

W Surgery is reserved for hydatid disease not amenable to treatment by PAIR and complicated pyogenic, amebic, fungal, and tuberculosis cases that cannot be treated by percutaneous techniques. Operations for hydatid disease include capitonnage, omentoplasty, cyst excision, cystoenterostomy, and laparoscopic deroofing.

S Treatment consists of a multidrug regimen, such as rifampicin, isoniazid, pyrazinamide, and ethambutol, along with a drainage procedure. Most recommend using percutaneous catheter drainage. The abscess usually resolves after 2 to 3 weeks. There are also reports of combined treatment using catheter drainage with transcatheter infusion of anti-tuberculous drugs into the cavity. T Echinococcal cysts require surgical removal or percutaneous aspiration-injection-reaspiration (PAIR) with a scolicidal agent, as well as treatment with anti-helminthic medications such as albendazole, flubendazole, or praziquantel. After surgical removal, anti-helminthic drugs are continued for at least 2 weeks postoperatively to prevent recurrence. PAIR results in equivalent cure rates to surgery but is contraindicated when the cyst communicates with the biliary tree, contains daughter cysts, or is superficial and at risk for rupture. Small, calcified echinococcal cysts in elderly patients can be treated medically. U Metronidazole is the treatment of choice for uncomplicated amebic liver abscess. It is effective against both systemic and intestinal manifestations, and clinical improvement usually occurs within 3 days. Patients failing this therapy should receive chloroquine therapy. After the patient has been treated, a luminal agent such as iodoquinol, paromomycin, or diloxanide furoate should be administered for treatment of the asymptomatic colonization state. Failure to use luminal agents will lead to relapse of infection in approximately 10% of patients. Patients failing medical therapy should undergo percutaneous drainage. Operative drainage is indicated only when medical and percutaneous therapy fails. Invasive Klebsiella pneumoniae liver abscess syndrome V (IKLAS) is a distinct clinical entity observed in Asia and increasingly since the 1990s in Europe and North America. It manifests as a community-acquired monomicrobial invasive

X Surgical treatment of pyogenic, amebic, fungal, and tuberculous abscess—performed open or laparoscopically— consists of either a drainage procedure or resection. Resection (wedge, segment, or lobe) is defined by the extent of the disease and the amount of destruction in the surrounding liver parenchyma. Y The preferred treatment of hepatic abscess secondary to bacteria, fungus, or mycobacteria is US- or CT-guided percutaneous drainage. Drainage is preferable to aspiration for abscesses > 5 cm, with aspiration being acceptable for smaller abscesses but requiring reaspiration in half of the patients. REFERENCES Cheng HP, Siu LK, Chang FY. Extended-spectrum cephalosporin compared to cefazolin for treatment of Klebsiella pneumoniae-caused liver abscess. Antimicrob Agents Chemother. 2003;47(7):2088–2092. Fang CT, Chuang YP, Shun CT, Chang SC, Wang JT. A novel virulence gene in Klebsiella pneumoniae strains causing primary liver abscess and septic metastatic complications. J Exp Med. 2004;199(5):697–705. Jeong SW, Jang JY, Lee TH, et al. Cryptogenic pyogenic liver abscess as the herald of colon cancer. J Gastroenterol Hepatol. 2012;27(2):248–255. Junghanss T, da Silva AM, Horton J, Chiodini PL, Brunetti E. Clinical management of cystic echinococcosis: state of the art, problems, and perspectives. Am J Trop Med Hyg. 2008;79(3):301–311. Kao WY, Hwang CY, Chang YT, et al. Cancer risk in patients with pyogenic liver abscess: a nationwide cohort study. Aliment Pharmacol Ther. 2012;36(5):467–476. Krige JE, Beckingham IJ. ABC of diseases of liver, pancreas, and biliary system. BMJ. 2001;322(7285):537–540. Lederman ER, Crum NF. Pyogenic liver abscess with a focus on Klebsiella pneumoniae as a primary pathogen: an emerging disease with unique clinical characteristics. Am J Gastroenterol. 2005;100(2):322–331. Nunnari G, Pinzone MR, Gruttadauria S, et al. Hepatic echinococcosis: clinical and therapeutic aspects. World J Gastroenterol. 2012;18(13): 1448–1458. Pappas PG, Kauffman CA, Andes DR, et al. Clinical practice guideline for the management of candidiasis: 2016 update by the Infectious Diseases Society of America. Clin Infect Dis. 2016;62(4):e1–e50. Salles JM, Salles MJ, Moraes LA, Silva MC. Invasive amebiasis: an update on diagnosis and management. Expert Rev Anti Infect Ther. 2007;5(5): 893–901. Stanley SL Jr. Amoebiasis. Lancet (London, England). 2003;361(9362): 1025–1034. Zerem E, Hadzic A. Sonographically guided percutaneous catheter drainage versus needle aspiration in the management of pyogenic liver abscess. AJR Am J Roentgenol. 2007;189(3):W138–W142.

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Chapter

50 

CYSTIC LIVER DISEASE Ana Gleisner, MD, PhD, and Benedetto Mungo, MD

A Cystic liver lesions are a broad entity encompassing a vast array of benign and malignant processes that originate primarily in the liver or are hepatic manifestations of systemic disease. As with solid liver lesions, the diagnostic work-up should start with a thorough history and physical examination. Simple cysts are the most common diagnosis (>95%). Cystic neoplasms should be suspected in the presence of thick or irregular walls, septations, or nonhomogeneous content, as well as rapid growth on follow-up, although some of these features can be seen in simple cysts, especially with previous bleeding. Presence of calcifications or daughter cysts and/or a history of travel to endemic areas are suggestive of echinococcal cysts. In patients with a known primary malignancy, cystic metastasis should be considered in the differential diagnosis. B Simple liver cysts (cystic bile duct hamartomas) are cystic formations that contain clear fluid. They are present in approximately 1% of the population but only rarely cause symptoms. Because symptoms are often vague, aspiration can be performed to confirm the association between the cyst and the symptoms. Asymptomatic simple cysts can be followed up with imaging in 6 months and at 12 months. No further imaging is required if no increase in size is noticed. Patients whose symptoms are clearly associated with the cyst, patients whose symptoms improved with aspiration, and patients with a significant increase in the size of the cyst on follow-up should be offered surgical treatment. Cyst unroofing, preferably done laparoscopically, is associated with low recurrence rates ( 1.5 cm in size in patients with cirrhosis and/or chronic liver disease, especially hepatitis B, should be evaluated with an MRI to attempt to establish the diagnosis of HCC. In patients with smaller lesions or with no clear features of HCC, follow-up imaging in 3 months is recommended, although biopsy could also be considered. In the absence of

cirrhosis and/or chronic liver disease, patients with lesions ≤ 1.5 cm should be reimaged in 6 months, whereas those with larger lesions should undergo prompt MRI; if that is not diagnostic, the recommendation is for either repeat imaging in 3 months or biopsy of the lesion. The management of hypovascular uncharacterized lesions will depend on the presence or absence of benign features on imaging. Benign features are sharp margins, homogeneity, lack of enhancement, low attenuation on CT, and either very low signal intensity in T1 or very high signal intensity in T2 on MRI. When these are present, the lesion is characterized as benign, and no further follow-up is needed. In the absence of reassuring features, lesions of any size in low-risk individuals or lesions equal to or smaller than 1.5 cm in high-risk individuals can be followed up with CT or MRI in 6 months. Low-risk individuals are defined as asymptomatic patients who are 40 years old or younger, with no known malignancy or hepatic dysfunction. Average- and high-risk individuals with lesions larger than 1.5 cm should instead be directed toward either close follow-up with reimaging in 3 months or biopsy of the lesion. E Hemangiomas and FNHs should be considered for resection in the presence of symptoms. Symptoms are most commonly pain and/or derived from compression of nearby organs, such as early satiety. Symptoms can be vague, and a clear association between the lesion and the symptoms is often not easy to establish, with up to a quarter of patients experiencing persistent symptoms after the surgical treatment of hemangiomas. Hemangiomas can be enucleated. Patients with FNHs or those operated for an unclear diagnosis should undergo liver resection. For asymptomatic FNHs or hemangiomas, follow-up imaging in 3 months is recommended. If at that time there is no significant growth and the diagnosis is clear, there is no need for further imaging. Otherwise, biopsy, resection, or repeat imaging in 3 months should be discussed. F Adenomas are benign liver tumors that have the potential for malignant transformation and spontaneous bleeding. This is especially true when the size of the lesion is ≥ 5 cm. Measures such as discontinuation of OCP and weight loss in obese patients can lead to a decrease in the size of adenomas and therefore should be the initial step when managing these patients. Patients with symptoms other than those caused by active bleeding and asymptomatic patients with lesions ≥ 5 cm should be considered for surgical resection. If there is active bleeding, embolization should be performed first, followed by elective resection after the patient recovers. For patients for whom surgery would be associated with high morbidity (poor clinical performance or centrally located lesions that would require a major resection), treatment may be guided by the histologic subtype of the adenoma. There are four histologic subgroups of adenomas: inflammatory, HNF1 alpha mutated, beta-catenin mutated, and unclassified. HNF1 alpha mutated adenomas are typically steatotic and have a very low risk for malignant transformation. Therefore these patients could be considered for observation. Patient with lesions < 5 cm should undergo annual follow-up with CT or MRI for 5 years and then every 2 years until age 55. G Metastases are by far the most common malignant neoplasm of the liver. The management of hepatic metastases depends largely on the nature of the primary malignancy, and it is not

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Chapter 51  ◆  Solid Liver Lesion  154.e1

Abstract

Keywords

In this chapter, we describe the diagnostic and treatment approach for patients that are found to have a solid liver lesion. Based on the imaging features, these can be classified into hypervascular or hypovascular lesions. Hypervascular lesions include hemangioma, focal nodular hyperplasia (FNH), adenomas and hepatocellular carcinoma. Hemangioma and FNH are benign lesions that should only be resected in the presence of symptoms. Adenomas have potential for bleeding and malignant transformation and, therefore, should be resected if 5 cm or greater. Hypovascular lesions include liver metastasis, focal steatosis and cholangiocarcinoma. In patients with no known primary malignancy, a biopsy can point to the occult primary. Upper endoscopy, colonoscopy, mammogram and PAP smear are often necessary to confirm the diagnosis.

hemangioma focal nodular hyperplasia hepatocellular adenoma liver metastasis

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Chapter 51  ◆  Solid Liver Lesion  155 Consider MRI for further evaluation (if not already obtained)

D

m 5c ≤1. Size >1 .5 cm

Treat accordingly

s Ye

Follow-up with CT or MRI in 3 months or Biopsy

Follow-up with CT or MRI in 3 months or Biopsy Hepatocellular carcinoma

Evaluate with MRI

No

s Ye

E Symptoms N

Hemangioma

Ye o

Suggest discontinuation of estrogen-containing preparations

o

Discontinuation of Size < estrogen-containing 5c preparations and weight m loss if obese Follow-up with CT or MRI in 6 months Hepatocellular carcinoma

Surgical resection; anatomic resection if confirmed malignant degeneration

o

o cm ≥5

CBC with platelet count Liver function, coagulation Hepatitis screen Tumor markers (CEA, AFP, CA 19-9)

Liver biopsy

N

Active bleeding

N

Labs

s Ye

Symptoms

Consider observation

N

F Adenoma

Embolization

Consider biopsy/ resection/repeat imaging in 3 months No further imaging

s Ye

HNF1 alpha mutated/ steatotic HCC

Hypervascular lesions

s Ye

s Ye

o

Focal Nodular Hyperplasia

B

Diagnosis unclear and/or significant growth

N

Follow-up with CT or MRI in 3–6 months

A

Treat accordingly

Resection

s

E Solid Liver Lesion

Diagnosis

o

History of hepatitis, cirrhosis, alcohol use, transfusions Cancer history OCP/hormone use Jaundice, hepatomegaly, stigmata of portal hypertension

Cirrhosis and/or chronic liver disease

Evaluate with MRI

N

Unable to characterize

Size > 1.5 cm

No

s Ye

History and physical examination

Follow-up with CT or MRI in 6 months

cm .5 ≤1

Consider resection

Centrally located, highrisk resection

Annual follow-up with CT or MRI for 5 years, then every 2 years until age 55

See chapter 82

G Metastasis from enhancing malignancy (i.e. neuroendocrine, melanoma, renal cell and breast cancer)

G Metastasis

Known primary malignancy No

Yes Occult primary work-up: EGD Colonoscopy Mammogram Gyn/PAP smear

Biopsy (?)

C Focal hepatic steatosis

Hypovascular lesions

Cholangiocarcinoma

See chapter 81

Benign features: Sharp margins Homogenous No enhancement No CT: low attenuation (≤20 HU) MRI: very low signal intensity on T1; very high signal intensity on T2

Unable to characterize Yes

Consider MRI for further evaluation (if not already obtained)

No further follow-up

cm .5 ≤1

Size >1 .5

cm

Follow-up with CT or MRI in 6 months

Low risk individual: ≤ 40 years old, no known malignancy or hepatic dysfunction, no symptoms

Follow-up with CT or MRI in 3 months or Biopsy

No

s Ye

D

Treatment according to primary tumor, resectability

Rule out extrahepatic disease

Follow-up with CT or MRI in 6 months

Benign, no further follow-up

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156  Part V  ◆  Alimentary Tract uncommon that the metastasis is incidentally discovered before the primary is diagnosed. If there is no known primary, a biopsy can be performed, and diagnostic efforts should be targeted toward characterization of the occult primary; tools such as esophagogastroduodenoscopy (EGD), colonoscopy, mammogram, and Papanicolaou (Pap) smear can all be invaluable in this process. In addition, before focusing on treatment of the hepatic metastases, the presence of extrahepatic disease should be ruled out. Treatment will then vary depending on resectability and on the nature of the primary tumor.

Berland LL, et al. Managing incidental findings on abdominal CT: white paper of the ACR incidental findings committee. J Am Coll Radiol. 2010;7(10):754–773. Gore RM, et al. That liver lesion on MDCT in the oncology patient: is it important? Cancer Imaging. 2012;12:373–384. Nault JC, et al. Molecular classification of hepatocellular adenoma associates with risk factors, bleeding, and malignant transformation. Gastroenterology. 2017;152(4):880–894.e6. Nguyen BN, et al. Focal nodular hyperplasia of the liver: a comprehensive pathologic study of 305 lesions and recognition of new histologic forms. Am J Surg Pathol. 1999;23(12):1441–1454. Ozden I, et al. Long-term results of surgery for liver hemangiomas. Arch Surg. 2000;135(8):978–981.

REFERENCES Assy N, et al. Characteristics of common solid liver lesions and recommendations for diagnostic workup. World J Gastroenterol. 2009;15(26):3217–3227.

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Chapter

52 

ACUTE PANCREATITIS Damian James Mole and O. James Garden

A Acute pancreatitis (AP) is a sudden-onset, painful acute inflammatory disease of the pancreas usually triggered by gallstones or excess alcohol consumption. The incidence is approximately 50 per 100,000 population per year. The diagnosis is made based on a combination of two of the following: a clinical history of acute abdominal pain and/or vomiting with an elevated serum amylase or lipase greater than threefold the upper limit of the laboratory reference range or imaging findings diagnostic of AP. Overall, the individual case fatality rate is 5%. The key factor that determines outcome in AP is the presence or development of extrapancreatic organ dysfunction, most commonly acute lung injury and acute kidney injury, and often multipleorgan failure. This severe form occurs in approximately 1 in 4 episodes. The case fatality rate for AP with organ failure is 20%. The key decision-making node is to identify the patient with actual, impending, or high risk for organ dysfunction and consider the need for organ support or monitoring in a critical care environment. Scoring systems, for example, the Ranson score, Glasgow score, C-reactive protein > 100 mg/dL at 48h, and APACHE II score, can be helpful in identifying these patients and at the very least can direct an organ systems–based approach to the assessment of the patient presenting with AP. B Both serum amylase and lipase are equally valid alternatives as a biochemical diagnostic in the presence of a compatible history. It is important to note that the magnitude of either amylase or lipase is not predictive of the severity of an attack. Routine blood tests, as listed, help to gauge the degree of inflammation and may indicate biliary obstruction or sepsis as confounders, and an arterial blood gas is a helpful tool to measure respiratory and metabolic compromise. Together, the investigations listed allow any of the standard predictive scoring models to be applied. A targeted ultrasound scan of the gallbladder should always be performed and should be repeated at least once at an interval if no gallstones are seen on the first scan and alcohol is not the obvious initiator. In case of diagnostic uncertainty, early computed tomography (CT) is indicated. Endoscopic retrograde cholangiopancreatography (ERCP) should never be used as a diagnostic test in this setting, and there is no benefit (and a risk for harm) in ERCP in AP unless there is quite clearly biliary sepsis (cholangitis) as a result of an obstructing calculus. C Organ-supportive strategies in critical care should be based on specific organ system requirements and developed in close liaison with critical care colleagues as local protocol specifies. The least invasive, most organ-friendly strategies should be used wherever possible. Enteral feeding is preferable to parenteral nutrition where possible, but the parenteral route should be

used if the gut is not working. Contrast-enhanced CT should be performed in all patients at around 4 days into an episode of severe AP and whenever there is a clear deterioration in clinical state. In improving or stable patients, there is no advantage to be gained by intervening on acute fluid collections or developing necrosis. D If the critically ill patient is failing to progress clinically or is deteriorating, with increasing organ support requirements, and there is evidence on cross-sectional imaging of intraabdominal complications that are technically amenable to intervention, this should be considered. It is generally advisable to resist the temptation to drain or otherwise intervene when the patient is improving spontaneously with conservative management. E Patients who have suffered acute pancreatitis secondary to gallstones should have a same-admission cholecystectomy if they are clinically fit to do so or should have an urgent scheduled cholecystectomy as soon as possible (i.e., after discharge, ideally within 2 to 3 weeks of the acute attack). For those patients unfit for general anesthesia, ERCP as prophylaxis against repeat episodes of gallstone AP is warranted. F Where indicated (nearly always because of proven or suspected superadded infection of local pancreatic complications), drainage of fluid collections or walled-off pancreatic necrosis may be considered. Increasingly the transluminal (transgastric) route is favored, guided by endoscopic ultrasound (EUS), because this reduces the complications and discomfort associated with external pancreatic fistulas. However, complications of EUS-guided drainage (perforation and bleeding) can be serious, especially early during AP, and stent migration remains a risk at any time. For patients where the anatomy is not favorable for transluminal drainage, percutaneous drainage is chosen. This is best done under CT guidance through a flank approach to allow for upsizing and minimally invasive retroperitoneal pancreatic necrosectomy (MIRP) if required in due course. G The etiology of AP is not always clear. If neither gallstones (at least two negative gallbladder ultrasounds) nor alcohol (being mindful of the occasional downplaying of alcohol intake by some historians) is the cause, a careful look for prescribed medicines thought to be associated with AP should be made, and alternative prescriptions should be made if possible. Exclude a family history of pancreatic disease. EUS can be useful to detect microlithiasis or ultrasound scan repeated at a later date if there remains clinical suspicion of underlying gallstone disease. Hyperlipidemia should be excluded, as should derangements in calcium. Always be aware that an episode of AP can be the first presentation with pancreatic cancer, albeit unusual. H Failure to progress clinically and deterioration that, on repeat imaging (usually repeat CT), can be attributed to a further drainable collection are indications for further intervention. For patients with transluminal drainage in place, this can be through repeat stenting; clearance of stent blockage; and formal transluminal cavity endoscopy, washout, and endoscopic debridement. For those with percutaneous drains in situ, it is most usual to upsize the drain to a larger diameter drain under radiology guidance or place additional drains. If there is no further upsizing option available, then consideration can be given to an MIRP.

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Chapter 52  ◆  Acute Pancreatitis  158.e1

Abstract

Keywords

Acute pancreatitis is a sudden- onset, painful inflammatory disease of the pancreas. The most common etiologies are excess alcohol or gallstones. Serum amylase and lipase are equally valid diagnostic tests. Supportive strategies should be based on patient requirements. Cross-sectional imaging of the abdomen is indicated for severe disease or deteriorating patients. Gallstone pancreatitis should have same admission cholecystectomy if the patient is fit. When indicated for infection, drainage of fluid collections or walled off necrosis may be considered. Increasingly a transluminal route is favored.

acute pancreatitis pancreas

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Chapter 52  ◆  Acute Pancreatitis  159

History and examination • Epigastric abdominal pain • Nausea and vomiting • Medication • Known gallstones • Alcohol history • Previous attacks of AP • Heart rate, respiratory rate, blood pressure, oxygen sats

A

C Consider admission to critical care for organ support/monitoring High risk of developing or has extrapancreatic organ dysfunction—e.g., respiratory failure, renal dysfunction

Organ-specific support • Invasive/non-invasive ventilation • Vasopressors • Hemofiltration • Enteral tube feeding • Define any local pancreas complications by contrast-enhanced CT at 4 days

F D Failure to progress or obvious sepsis

If clearly a drainable collection, consider • EUS-guided transluminal cystgastrostomy • Percutaneous CTguided (flank) drainage

H

Failure to progress or obvious sepsis

Step-up as required • Transluminal necrosectomy • Upsize drain • Consider retroperitoneal debridement (minimally invasive)

Acute pancreatitis

B

Low risk or no extrapancreatic organ dysfunction

Investigations • Serum amylase or lipase • Hematocrit • WBC • Arterial blood gases • Calcium • Lipid profile • BUN • Glucose • LDH • SGOT (AST) • C-reactive protein • Abdominal USS for gallstones • If diagnosis unclear, abdominal CT

Ward level care • Normal diet and fluids as wishes • Symptom control • Analgesia • Anti-emetics • DVT prophylaxis • Define any local pancreas complications by contrast-enhanced CT at 4-7 days if needed

REFERENCES Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis– 2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62(1):102–111. Mole DJ, Gungabissoon U, Johnston P, et al. Identifying risk factors for progression to critical care admission and death among individuals with

Alcohol etiology • Alcohol withdrawal protocol +/– B vitamins +/– lifestyle advice if alcoholrelated and necessary Gallstone etiology • Consider same admission laparoscopic cholecystectomy if physically well • MRCP if LFTs deranged

E

G If neither alcohol or gallstones, investigate for unusual causes (can often be done as an outpatient) • review medications • EUS for microlithiasis • Lipid profile • Calcium/PTH profile • Pancreas cancer

acute pancreatitis: a record linkage analysis of Scottish healthcare databases. BMJ Open. 2016;6(6):e011474. van Santvoort HC, Besselink MG, Bakker OJ, et al for the Dutch Pancreatitis Study Group, A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010;362:1491–1502.

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Chapter

53 

CHRONIC PANCREATITIS Damian James Mole and O. James Garden A Chronic pancreatitis is a progressive fibro-inflammatory disorder characterized by loss of normal acinar cell exocrine function, acinar cell atrophy, increasingly abnormal ductal morphology, heterotopic calcification, and secondary damage to the hormone-producing islet cells, leading to exocrine and endocrine insufficiency. Excess alcohol use and smoking are the most important etiological factors. Trauma (including iatrogenic at endoscopic retrograde cholangiopancreatography) and repeated attacks of acute pancreatitis may result in a partially or completely obstructed pancreatic duct, which in turn may result in chronic pancreatitis upstream. Inherited genetic defects in pancreatic enzyme deactivation mechanisms are exceedingly rare. The incidence of chronic pancreatitis is approximately 5 per 100,000 population, and the prevalence is approximately 40 per 100,000 population. B Recurrent episodic epigastric pain radiating through to the back is reported by 85% of people with chronic pancreatitis. Pain may have triggering or exacerbating factors, often associated with repeated episodes of alcohol use. Exocrine insufficiency, particularly reduced pancreatic lipase, leads to undigested or partially digested fats reaching the colon and triggering steatorrhea. Inability to fully digest and use ingested carbohydrates, fats, and protein leads to malnutrition. This can manifest as loss of fat and muscle bulk but also specific nutritional defects, for example, fat-soluble vitamins A, D, E, and K and trace elements. Secondary damage to the islet cells can lead to type 3c diabetes mellitus, presenting with polyuria, glycosuria, and polydipsia. A careful history should be taken for medications associated with pancreatic injury (e.g., anticonvulsants), a thorough alcohol history (which can be downplayed by the patient), smoking history, and previous admissions with acute pancreatitis, and gallstones or cholecystectomy and a family history of pancreatic disease should be considered in the younger patient in excluding hereditary causation. C Endocrine insufficiency should be diagnosed with a combination of measurement of urine glucose, fasting blood glucose, and progression to a formal oral glucose tolerance test in cases where a diagnosis of diabetes is suspected but not clear. Nutritional assessment, including body mass index and estimations or formal measurement of muscle strength and bulk, is essential, and it is often helpful to include specialist dietetic assessment. Biochemical assays supplement the clinical picture, with overall nutritional state reflected in the serum albumin concentration and more specific nutritional defects (e.g., vitamin K deficiency) reflected in the coagulation profile. Liver function tests are contributory to the diagnosis of biliary stricture and can reflect long-standing alcohol misuse. In cases where steatorrhea is suspected, measurement of low fecal elastase can be helpful to confirm the diagnosis.

Ultrasound of the gallbladder to detect stones is mandatory. Magnetic resonance cholangiopancreatography (MRCP) is helpful to delineate the pancreatic ductal architecture and evaluate the presence of a secondary biliary structure. Magnetic resonance imaging (MRI) of the pancreas may be done instead, according to local protocol. If there is any concern of pancreatic malignancy, pancreas-protocol computed tomography (CT) with contrast is essential. In situations where the diagnosis is unclear or where a discrete abnormality is detected on cross-sectional imaging, endoscopic ultrasound with the option of biopsy is invaluable. D A holistic, multidisciplinary approach to managing patients with chronic pancreatitis is essential. It is important for the clinical team and the patient to realize that there is rarely a quick-fix solution and that all parties will be working together to improve the patient’s overall quality of life and health. Coordinated involvement of specialist nurses, alcohol liaison teams, dieticians, pain specialists, surgeons, gastroenterologists, diabetologists, and endoscopists is usually the best strategy. E Exocrine function replacement is the mainstay of management and is best achieved with oral preparations of pancreatic enzymes (e.g., pancrelipase). It is important to prescribe a sufficiently large dose (e.g., 50,000 units with meals) and include a prescription for snacks (e.g., 25,000 units). General healthy eating advice is important, and multivitamin replacement, especially B vitamins in those with heavy alcohol use, is important. Specific nutritional defects identified during the diagnostic work-up should be addressed appropriately. As with any patient with diabetes mellitus, good diabetic control is critical for quality of life and health and to avoid secondary complications of diabetes. F Chronic pancreatitis pain management is often challenging. The intractable nature of pancreatic pain may be partly contributed to by long-standing changes in central pain-processing areas in the brain, compounded by ongoing fibro-inflammatory progression locally in the pancreas. The pancreas is highly innervated through the visceral nerves, and pancreatic pain is notoriously unpleasant. Simple analgesia, with progression according to the World Health Organization (WHO) pain ladder algorithm, is the best initial approach, but specialist chronic pain management is frequently required. The side effects of long-term opioid use can be troublesome, and wherever possible, attempts to avoid or reduce the risk for opioid dependence should be made. Historically, direct denervation strategies have been used to ameliorate chronic pain, but with limited efficacy, high financial cost, and significant patient complications. Transcutaneous electrical nerve stimulation (TENS) is available. It is fundamentally important to counsel the patient on reducing the exposure to pain triggers, specifically smoking and alcohol use, and to reinforce the fact that smoking will drive the fibro-inflammatory process underlying chronic pancreatitis. In the presence of gallstones, it is sometimes difficult to distinguish pancreatic pain from biliary colic, and consideration should be given to cholecystectomy. G Chronic pancreatitis and recurrent bouts of acute pancreatitis can leave anatomical complications in the pancreas and nearby structures. Pseudocysts may directly cause abdominal fullness or pain or, more usually, may indirectly cause problems through mass effect leading to gastric outlet obstruction, biliary

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Chapter 53  ◆  Chronic Pancreatitis  160.e1

Abstract

Keywords

Chronic pancreatitis is a progressive inflammatory disorder. Alcohol and smoking are the most common etiologies. Recurrent pain is the most common symptom. Endocrine and exocrine insufficiency along with malnutrition are possible sequela. A multidisciplinary approach is essential. Pain management is often challenging. Anatomic complications may require endoscopic or surgical intervention.

chronic pancreatitis endocrine insufficiency exocrine insufficiency pancreatic enzyme pseudocyst stricture thrombosis varicies Pseudoaneurysm cystgastrostomy stent

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Chapter 53  ◆  Chronic Pancreatitis  161 obstruction, or rupture or become infected, leading to sepsis. Asymptomatic pseudocysts should be ignored. Secondary stricturing of the common bile duct and/or duodenum can occur through fibrosis of the duct itself or by extrinsic compression from a pseudocyst, inflammatory mass, or importantly, malignant tumor. The management of each of these is different (see paragraph J). Portal vein thrombosis can lead to the development of varices and cavernous transformation. The evidence base for anticoagulation to encourage recanalization of the portal vein in this circumstance is limited, and clinician judgment on a case-by-case basis is warranted. Splenic vein thrombosis is common in chronic pancreatitis and leads to left-sided portal hypertension. Anticoagulation for isolated splenic vein thrombosis is not recommended. Portal and splenic vein thrombosis can lead to portal gastropathy and varices, which may present with catastrophic hemorrhage. Splenic artery pseudoaneurysm is an infrequent complication and does not usually require prophylactic intervention if asymptomatic and 3 cm or if bleeding complications occur, interventional radiological therapy is highly effective.

B

History and examination • Epigastric abdominal pain • Back pain • Steatorrhea • Weight loss

D

C

Investigations Endocrine insufficiency • Fasting blood glucose (or formal glucose tolerance test) Exocrine insufficiency • Nutritional assessment • BMI • Muscle strength/bulk • Serum albumin • Coagulation screen • Liver function tests • Fecal elastase test Imaging • USS to exclude gallstones • MRI/MRCP • CT scan • EUS

Endoscopic intervention for chronic pancreatitis is becoming more frequent. Pseudocysts that are closely applied to the posterior stomach can be drained relatively straightforwardly

E

Endocrine insufficiency • Diabetic control • Metformin • Oral hypoglycemics • Insulin

• Medication • Alcohol history • Tobacco-smoking history • Previous attacks of pancreatitis • Consider gallstone symptoms

Chronic pancreatitis

I

Exocrine insufficiency • Pancreatic enzyme replacement • Nutritional support

• Polyuria/polydipsia

A

H It is preferable to avoid intervention in chronic pancreatitis where conservative symptom control is effective. Surgery for symptom control is effective in only a small proportion of cases, and endoscopic therapy has limited efficacy; both modalities should be reserved for patients who have intractable pain or local anatomical complications. The exception is when a change in symptoms or unexpected deviation from an individual’s disease trajectory raises the suspicion of an underlying malignancy. The risk for developing pancreas cancer on a background of chronic pancreatitis is two to three times that of the general population, and risk is increased in smokers. Alarm signals include new biliary obstruction, increased weight loss, and increased pain, especially back pain. Cross-sectional imaging with contrastenhanced CT should be done urgently and any equivocal imaging findings further evaluated with endoscopic ultrasound (EUS) biopsy.

Manage in parallel

Pain control • Simple analgesia • Chronic pain management • Specialist pain management • Managing/avoiding opioid dependency • Lifestyle advice (avoid smoking and alcohol) • Healthy diet and exercise

F

Local anatomical complications • Pseudocysts • Common bile duct stricture • Duodenal stricture • Portal vein thrombosis • Splenic vein thrombosis • Varices secondary to portal hypertension – especially portal gastropathy • Splenic artery G pseudoaneurysm

I

H Careful patient selection and only when conservative measures fail, or suspicion of cancer

Endoscopic intervention • EUS-guided cystgastrostomy • Endoscopic biliary stent • Endoscopic pancreatic duct stent

J Surgical intervention • Pancreatic decompression with pancreaticojejunostomy +/– excision of pancreatic head • Bypass (gastrojejunostomy and/or hepaticojejunostomy) • Total pancreatectomy with islet autotransplantation

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162  Part V  ◆  Alimentary Tract under EUS guidance with plastic pigtail or double-flanged metal stents. These should be removed or replaced after 2 to 3 months. Complications are related to bleeding, perforation, and endoscopic stent migration. Extrinsic biliary compression causing jaundice is effectively managed by endoscopic retrograde cholangiopancreatography (ERCP) and stenting, especially as a temporary measure while the cause of the extrinsic compression is dealt with. Uncovered metal stents (nonremovable) should be avoided if possible if further surgery and endoscopic intervention are likely. Pancreatic duct stents do not usually help with pain control or exocrine insufficiency but do have a place in the management of recurrent pseudocyst reaccumulation and particularly to gain antegrade control of pancreatic duct fistulas. Although once commonplace, the role for neurolytic therapies—for example, laparoscopic splanchnicectomy or celiac plexus neurolysis—is diminishing. J

Surgery in chronic pancreatitis should be reserved for malignant disease or considered a last resort in benign disease. For benign disease or inoperable malignancy, simple biliary bypass can be effective to relieve obstructive jaundice (particularly where repeated endoscopies have failed or where the patient wishes), and surgical bypass of gastric outlet ob­ struction (optimally with a Roux-en-Y reconstruction) can be done in cases of duodenal stricturing. It should always be borne in mind that the patient will have many years to live with the reconstruction, so care should be taken to avoid configurations that predispose to biliary reflux or blind loops. Pancreatic decompression is advocated by some to ameliorate chronic pain symptoms, and there are randomized control trial data to suggest that this is effective as first-line therapy.

However, in the presence of portal hypertension and malnutrition, surgery should be undertaken with due respect for the challenging nature of these operations in a specialist unit. There is a surgical aphorism that there are as many variants of pancreatic decompression operation in chronic pancreatitis as there are patients who are operated on! Outcomes should be carefully audited and reported. There is an intermittent vogue for total pancreatectomy and islet cell auto-transplantation, which may prove effective in the future as islet cell transplantation improves (particularly with autologous stem cell islet technology), although the surgical difficulty of total pancreatectomy in chronic pancreatitis and the physiological consequences are not to be underestimated. Again, these treatments should be restricted to specialist units. REFERENCES Bellin MD, Freeman ML, Gelrud A, et al. Total pancreatectomy and islet autotransplantation in chronic pancreatitis: recommendations from PancreasFest. Pancreatology. 2014;14(1):27–35. Fitzpatrick J, Bhat R, Young JA. Angiographic embolization is an effective treatment of severe hemorrhage in pancreatitis. Pancreas. 2014; 43(3):436–439. Löhr JM, Dominguez-Munoz E, Rosendahl J, et al. United European gastroenterology evidence-based guidelines for the diagnosis and therapy of chronic pancreatitis (HaPanEU). United European Gastroenterol J. 2017;5(2):153–199. Majumder S, Chari ST. Chronic pancreatitis. Lancet. 2016;387(10031): 1957–1966. Sheth SG, Conwell DL, Whitcomb DC, et al. Academic Pancreas Centers of Excellence: guidance from a multidisciplinary chronic pancreatitis working group at PancreasFest. Pancreatology. 2017. Solomon S, Whitcomb DC. Genetics of pancreatitis: an update for clinicians and genetic counselors. Curr Gastroenterol Rep. 2012;14(2): 112–117.

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Chapter

54 

PANCREATIC PSEUDOCYSTS Attila Nakeeb, MD

A Pancreatic pseudocysts are defined as a collection of fluid in the peripancreatic or intrapancreatic tissues that are surrounded by a well-defined wall and contain no solid debris. These collections can result from an episode of acute pancreatitis, chronic pancreatitis, pancreatic surgery, endoscopic retrograde cholangiopancreatography (ERCP), or abdominal trauma. B The revised Atlanta classification categorizes acute pancreatic fluid collections based on the presence of necrosis within the collection, the presence of a well-defined wall, and the time from the index episode of pancreatitis. The four categories are (1) acute peripancreatic fluid collections, (2) acute necrotic collections, (3) pseudocysts, and (4) walled-off necrotic collections (WONCs). Acute peripancreatic fluid collections are defined as fluid collections with no necrosis and no well-defined wall occurring within 4 weeks of a bout of pancreatitis. The majority of acute peripancreatic collections will resolve spontaneously, and a small percentage will develop into a pseudocyst. A pseudocyst is defined as a circumscribed collection of fluid with minimal or no solid debris or necrosis surrounded by a welldefined nonepithelialized inflammatory wall that has persisted for more than 4 weeks. Acute necrotic collections develop within 4 weeks of an episode of acute pancreatitis and are characterized by both liquid and solid necrosis without a well-defined wall. A walled-off necrotic collection is more than 4 weeks old and is a well-circumscribed walled-off collection containing both liquid and solid necrosis. Patients with asymptomatic necrosis may be observed, whereas symptomatic necrosis or infected collections will mandate intervention. C Serum amylase and lipase levels may be persistently elevated in 50% to 75% of patients with pseudocysts. Transabdominal ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MRI) can all be used to diagnose and characterize pancreatic pseudocysts. US is inexpensive and can be used to follow patients serially. Intravenous (IV) contrastenhanced CT scanning is an excellent way to characterize associated necrosis and secondary complications such as hemorrhage, infection, and involvement of surrounding structures. MRI is useful in defining pancreatic and bile duct anatomy and is more sensitive than CT in differentiating fluid from solid components of a peripancreatic collection. D A pseudocyst is defined as a circumscribed collection of fluid with minimal or no solid debris or necrosis surrounded by a well-defined nonepithelialized inflammatory wall that has persisted for more than 4 weeks. E Acute necrotic collections develop within 4 weeks of an episode of acute pancreatitis and are characterized by both liquid and solid necrosis without a well-defined wall.

F The majority of patients with pseudocysts are asymptomatic and can be simply followed clinically for the development of symptoms or with serial imaging (US or CT) to document either increase in size or resolution. Patients with chronic ductal obstruction or disconnected left-sided pancreatic duct are less likely to resolve spontaneously. Intervention should be reserved for patients who become symptomatic, develop complications, or show evidence of an enlarging pseudocyst. G Patients without a precedent history of pancreatitis with a cystic lesion in or near the pancreas must be evaluated for a possible cystic neoplasm of the pancreas. Clinical history, symptoms, imaging characteristics, and endoscopic ultrasound evaluation with fine-needle aspiration biopsy and cyst fluid analysis can be useful in differentiating a cystic neoplasm from a pseudocyst. On cyst fluid analysis, pseudocysts will demonstrate high amylase and low carcinoembryonic antigen (CEA) levels without evidence of mucin. Biopsy will demonstrate inflammatory cells with no epithelial cells. Mucinous neoplasms will tend to have a high cyst CEA level with or without an elevated amylase level and evidence of mucin and epithelial cells. H Symptoms result from mass effect of the pseudocyst on the pancreas or surrounding viscera and blood vessels. Symptoms include abdominal fullness, nausea, vomiting, and early satiety from gastric outlet or duodenal obstruction, jaundice from biliary obstruction, gastrointestinal (GI) bleeding from erosion into surrounding viscera, peritonitis from pseudocyst rupture, hemorrhagic shock from erosion into adjacent arteries, and sepsis from infection of the pseudocyst. I

Patients presenting with jaundice should undergo ERCP for endoscopic biliary stenting. The jaundice may be a result of direct compression of the biliary tree by the pseudocyst or a result of inflammatory changes or fibrosis in the head of the pancreas. Biliary-enteric bypass may be necessary if a biliary stricture persists after cyst decompression or biliary stenting. J

Hemorrhage can result from direct erosion into adjacent blood vessels. Bleeding can occur in the cyst, the retroperitoneum, or into the GI tract if there has been erosion into the stomach, duodenum, or colon. CT arteriography can demonstrate active arterial bleeding and may demonstrate a pseudoaneurysm of peripancreatic blood vessels (splenic artery, gastroduodenal artery). Visceral angiography and embolization are highly effective in controlling hemorrhage. K Infection should be suspected in patients who are febrile, have an elevated white blood cell (WBC) count, or develop sepsis. CT imaging may demonstrate an air–fluid level in the pseudocyst. Broad-spectrum antibiotics should be initiated, and percutaneous drainage of the pseudocyst should be accomplished. L A walled-off necrotic collection is more than 4 weeks old and is a well-circumscribed walled-off collection containing both liquid and solid necrosis. Patients with asymptomatic necrosis may be observed, whereas symptomatic necrosis or infected collections will mandate intervention. M Management options for a patient with a pancreatic pseudocyst include percutaneous drainage, endoscopic drainage

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Chapter 54  ◆  Pancreatic Pseudocysts  164.e1

Abstract

Keywords

Pancreatic pseudocysts are fluid collections arising from pancreatic and or peripancreatic tissues that have a well-defined wall, contain no solid debris, and have persisted for more than 4 weeks. Asymptomatic pseudocysts can be observed and symptomatic pseudocysts may require intervention. Pancreatic pseudocysts can be effectively managed by either percutaneous, endoscopic or operative interventions

pancreas pseudocyst percutaneous drainage endoscopic drainage operative drainage

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Chapter 54  ◆  Pancreatic Pseudocysts  165

L

A History and exam Pancreatitis Pancreatic surgery or ERCP Abdominal trauma

E

> 4 weeks

Walled-off Pancreatic necrosis (WOPN)

Acute necrotic Collection

Observe Decreasing or Stable size

Observe

B Acute peripancreatic Fluid collection

Increasing size

F

M

Asymptomatic

D

Percutaneous drainage

Pancreatic pseudocyst

H

N Endoscopic drainage

Symptomatic Pain

O

Obstruction

C Labs Amylase, Lipase Imaging CT scan, US, MRI

Rule out cystic pancreatic neoplasm

G

I

Jaundice

Surgical drainage ERCP + Biliary stenting

Rupture

J

Hemorrhage

Angiography + embolization

K

Infection

Percutaneous Drainage

(transgastric, transduodenal, or transpapillary), operative internal and external drainage, and resection. Success rates for percutaneous drainage range between 40% and 90%. Patients with persistent ductal disruptions or strictures are unlikely to be successfully managed percutaneously. Complications of percutaneous drainage include secondary infection, bleeding, catheter dislodgment, inadvertent puncture of the pleura or surrounding viscera, and the development of a persistent pancreato-cutaneous fistula. N Endoscopic drainage has become the preferred choice for the management of most pancreatic pseudocysts. Endoscopic therapy usually requires that the pseudocyst be located in the head or body of the pancreas and that it be well opposed to the stomach or duodenum. Endoscopic ultrasound can be used to drain cysts that do not manifest an obvious bulge into the lumen of the stomach or duodenum. Success rates for endoscopic drainage range between 60% and 90%. Relative contraindications to endoscopic drainage include pseudocysts that contain extensive necrotic material, have a thin or immature wall, or are adjacent to a pseudoaneurysm or other vascular structures.

drainage. The three standard options include cystojejunostomy to a Roux-en-Y jejuna limb, cystogastrostomy, and cystoduodenostomy. Cystojejunostomy is the most versatile technique of operative drainage and is particularly appropriate when a pseudocyst is located at the base of the transverse mesocolon and is not adherent to the posterior gastric wall. Cystogastrostomy is a faster and less technically demanding procedure that is used when the pseudocyst is adherent to the posterior wall of the stomach. These operations can be performed via an open or laparoscopic approach, depending on the surgeon’s expertise. REFERENCES Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62:102–111. Park AE, Heniford BT. Therapeutic laparoscopy of the pancreas. Ann Surg. 2002;236:149–158. Varadarajulu S, Bang JY, Sutton BS. Equal efficacy of endoscopic and surgical cystogastrostomy for pancreatic pseudocyst drainage in a randomized trial. Gastroenterology. 2013;145:583–590. Zerem E, Hauser G, Loga-Zec S, et al. Minimally invasive treatment of pancreatic pseudocysts. World J Gastroenterol. 2015;21:6850–6860.

O The preferred operative approach for most uncomplicated pseudocysts requiring surgical intervention is internal

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Chapter

55 

PANCREAS DIVISUM Carrie D. Walsh, BA, Charles J. Yeo, MD, FACS, and Harish Lavu, MD, FACS

A

 

HISTORY AND PHYSICAL EXAMINATION

Pancreas divisum is the most common congenital anomaly of the pancreas. Autopsy and radiographic studies suggest that it affects up to 10% of the population. Typically, patients are asymptomatic, and the anomaly is often discovered incidentally. In patients presenting with symptoms of abdominal pain/ distention, chronic recurring pancreatitis, nausea, anorexia, and food intolerance (particularly in the postprandial state), pancreas divisum should be considered in the differential diagnosis. B   DIFFERENTIAL DIAGNOSIS

Patients presenting with such symptoms should undergo a complete work-up to rule out other causes of pancreatitis and abdominal pain before treatment for pancreas divisum is begun. The differential diagnosis includes acute pancreatitis, chronic pancreatitis, chronic abdominal pain, pancreatic cancer, hyperamylasemia, sphincter of Oddi dysfunction, gastritis, gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and cholecystitis. C

 

PHYSICAL FINDINGS, IMAGING, AND LABS

Physical findings at abdominal examination are usually normal. However, abdominal distention, epigastric tenderness, and even a palpable pseudocyst may be evident when there is associated pancreatitis. Computed tomography (CT) and transcutaneous or endoscopic ultrasound can be used to evaluate for dorsal duct dilation and pancreatitis. However, they may not be sensitive enough to confirm the presence of pancreas divisum.

Endoscopic Retrograde Cholangiopancreatography The traditional method of evaluation and diagnosis of pancreas divisum has been via endoscopic retrograde cholangiopancreatography (ERCP), which involves cannulation of the major papilla at the ampulla of Vater to perform a contrast injection, which can delineate the pancreatic ductal anatomy. This provides visualization of the ventral pancreatic duct. In pancreas divisum, a short (10 to 6 mm) and thin (2-mm-diameter) duct will be visualized, whereas cannulation of the minor papilla will demonstrate filling of the dorsal duct (2 to 4 mm in diameter) that drains the majority of the pancreas. Although the ERCP technique provides a conclusive diagnosis of pancreas divisum, it is an invasive and expensive technique with a complication rate reported at 5% to 15%. Therefore magnetic resonance pancreatography (MRCP) is preferred as the initial imaging modality to diagnose pancreas divisum.

Magnetic Resonance Pancreatography MRCP is a noninvasive imaging technique that does not require the use of ionizing radiation. It uses T2-weighted pulse sequences to contrast between stationary, fluid-filled structures and adjacent soft tissue. Patients are usually required to fast for 4 hours before the procedure to minimize fluid secretions within the abdomen. Additionally, MRCP can be augmented with secretin, which is injected intravenously. Secretin stimulates the production of pancreatic juice and bicarbonate, thereby increasing the volume of fluid in the pancreatic ducts and making pancreatic ductal visualization more obvious.

Secretin-Stimulated Ultrasonography Secretin can also be used in secretin-stimulated ultrasonography (US), which is an additional noninvasive test that involves sequential measurement of pancreatic ductal fluid secretion before and after secretin administration. However, the technique does not provide conclusive evidence related to ductal anatomy, but it can provide evidence of ductal stenosis. D   PANCREATIC DIVISUM

Pancreas divisum is a common congenital anomaly where the ventral and dorsal pancreatic ducts fail to fuse in the eighth week of gestation. In development, the dorsal pancreatic anlage migrates from the medial wall of the duodenum to connect with the ventral anlage on the lateral side of the duodenum as it emerges from the liver bud. The ventral anlage becomes the uncinate process and caudal pancreatic head, which is drained by the duct of Wirsung and enters the duodenum at the ampulla of Vater. The dorsal pancreas is drained by the duct of Santorini, which enters the duodenum at the minor papilla. When the two ducts properly fuse, the majority of the pancreatic exocrine secretion is drained through the ventral duct and the major papilla. In pancreas divisum, the dorsal and ventral pancreatic anlages merge into a single structure, but fusion of the ducts of Wirsung and Santorini is incomplete, resulting in pancreatic secretions draining primarily through the smaller dorsal pancreatic duct and the minor papilla. This is hypothesized to lead to poor ductal drainage and increased pressure within the pancreatic duct, causing symptoms of pancreas divisum in some patients.

Classifications There are three subtypes of pancreas divisum: • Type 1/Classic: no connection between the ventral or dorsal ducts • Type 2: absent ventral duct • Type 3: filamentous connection between the ventral and dorsal ducts In classic pancreas divisum (type 1; Fig. 55.1), the ventral duct, which feeds into the larger, major papilla, drains only about 20% of the pancreas. In contrast, the dorsal duct, which drains into the duodenum via the smaller, minor papilla, is responsible for drainage of the majority of the pancreas. The restricted opening into the duodenum through the minor papilla can give rise to a functional obstruction, where the pancreatic juice is unable to pass efficiently into the duodenum. This can result in chronic abdominal pain and pancreatitis as a result of the high intrapancreatic dorsal ductal pressure. Additionally, the obstruction of the minor papilla by proteinaceous plugs provides an alternative mechanism for obstruction. It should be noted that

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Chapter 55  ◆  Pancreas Divisum  166.e1

Abstract

Keywords

Pancreas divisum is the most common congenital anomaly of the pancreas, where the ventral and dorsal pancreatic ducts fail to fuse in the eighth week of gestation. Autopsy and radiographic studies suggest that it affects up to 10% of the population. However, patients are typically asymptomatic, and the anomaly is often discovered incidentally. In symptomatic patients, it is hypothesized that the abnormal fusion of the ducts of Wirsung and Santorini results in pancreatic secretions draining primarily through the smaller dorsal pancreatic duct and the minor papilla, which in some patients can lead to symptoms of recurring abdominal pain and pancreatitis. Treatment for symptomatic patients with pancreas divisum includes the endoscopic approach of minor papillary balloon dilation or sphincterotomy and, in select cases, operative minor duct sphincteroplasty.

pancreas divisum acute pancreatitis chronic pancreatitis endoscopic retrograde cholangiopancreatography (ERCP) magnetic resonance pancreatography (MRCP) secretin-stimulated ultrasonography (US) Bedside Index for Severity in Acute Pancreatitis (BISAP) score endoscopic minor papilla sphincterotomy (EMPS) minor duct sphincteroplasty

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Chapter 55  ◆  Pancreas Divisum  167 a chief complaint of abdominal pain can be present with or without chemical pancreatitis. The pain typically has a rapid onset; it begins as a dull, steady ache, becoming more severe. In the majority of cases it is located in the upper abdomen and may radiate to the posterior spine. In type 2 pancreas divisum, the duct of Wirsung is absent, which results in complete dorsal duct drainage. In type 3 pancreas divisum, or incomplete pancreas divisum, a small filamentous communication exists between the dominant dorsal duct of Santorini and the duct of Wirsung.

E   ASYMPTOMATIC/INCIDENTAL FINDING

Pancreas divisum is usually asymptomatic, and it is not known why some patients with this congenital anomaly have symptoms. Treatment is only necessary if the patient is symptomatic, and therefore the incidental finding of pancreas divisum should be ignored. F   SYMPTOMATIC

There are three types of symptomatic pancreas divisum. G

 

MILD SYMPTOMS WITHOUT PANCREATITIS

Observation and conservative management are preferred rather than treatment of the narrowed papilla. This should include a low-fat diet, anticholinergics, analgesics, and, in certain cases, pancreatic enzyme supplements. H

 

SEVERE ACUTE PANCREATITIS AND ABDOMINAL PAIN

In patients with confirmed pancreas divisum and symptoms of acute pancreatitis, an evaluation of the severity of the patient’s pancreatitis can be performed using the Bedside Index for Severity in Acute Pancreatitis (BISAP) score. The BISAP is an updated evaluation of pancreatitis, requiring fewer variables than the Ranson’s criteria, and uses data from the first 24 hours of the patient’s admission. In the scoring system, a point is allocated for each variable present. A score of 0 to 2 indicates a low mortality rate (less than 2%), whereas a score of 3 to 5 suggests a higher mortality rate (more than 15%). The BISAP variables: Fig. 55.1  MRCP image of the dorsal pancreatic duct draining the majority of the pancreas and emptying into the duodenum at the minor papilla. The common bile duct is labeled for reference.

B: Blood urea nitrogen (BUN) > 25 mg/dl (8.92 mmol/L) I: Impaired mental status

E A

History and physical exam Abdominal pain/distention Chronic recurring pancreatitis Nausea Anorexia Food intolerance (particularly in the postprandial state)

Incidental finding — Asymptomatic

G Mild symptoms without pancreatitis

B

Differential diagnosis Acute pancreatitis Chronic pancreatitis Chronic abdominal pain Pancreatic cancer Hyperamylasemia Sphincter of Oddi dysfunction Gastritis Gastroesophageal reflux disease (GERD) Peptic ulcer disease (PUD) Cholecystitis

D Pancreas divisum

H

F Symptomatic

Severe acute pancreatitis and abdominal pain BISAP score

I Chronic pancreatitis and abdominal pain

C

Physical findings, Imaging and Labs Amylase/lipase US CT MRCP ERCP Secretin US

Disregard until symptomatic

Inconclusive findings for pancreas divisum

Observation

Stable

J Endoscopic approach EMPS Balloon dilation

K Surgical approach Minor duct Sphincteroplasty

Observe

L Post-procedure management

M Post-Op management

Rule out pancreas divisum — consider differential diagnosis

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168  Part V  ◆  Alimentary Tract S: Systematic inflammatory response syndrome (SIRS)—≥ 2 SIRS criteria A: Age > 60 P: Pleural effusion present (excess fluid in the thoracic cavity) Severe acute pancreatitis can result in life-threatening organ failure; therefore, patients with a high-risk BISAP score should begin treatment for pancreatitis immediately.

Medical Treatment for Pancreatitis 1. Fluids: Intravenous (IV) fluid resuscitation should be begun immediately upon admission to prevent dehydration. 2. Nutritional support: For the first 24 to 48 hours, the patient should be placed on bowel rest. After this 48-hour period of abstinence, oral intake is permitted to maintain nutritional needs. If patients are unable to tolerate an oral diet, they are candidates for IV total parenteral nutrition (TPN) or enteral nutrition (EN) via a nasojejunal feeding tube. 3. Pain control: IV and then oral narcotic medications should be provided to relieve pain. 4. Nausea control: IV and then oral antiemetic medications may be used. I

 

CHRONIC PANCREATITIS AND ABDOMINAL PAIN

Medical treatment: Refer to the medical treatment section for severe, acute pancreatitis (point H). J   TREATMENT: ENDOSCOPIC APPROACH Primary Treatment Option— the Endoscopic Approach

The most common endotherapy for symptomatic pancreas divisum patients is minor papilla sphincterotomy and temporary dorsal duct stent placement, which is termed endoscopic minor papillary sphincterotomy (EMPS). A study conducted by Fujimori et al. at Kyushu University in Fukuoka, Japan, demonstrated that EMPS is technically feasible in 50% to 86% of patients when using a wire-guided cannulation (WGC) technique. However, the two most common causes of problematic ventral duct cannulation were found to be pancreas divisum and distortion of Wirsung’s duct, and therefore high-volume referral centers with experienced endoscopists are preferred and often more successful. There are several variations of EMPS techniques; the first is to use a pull-type sphincterotomy over a guidewire. This is performed after cannulation, with the sphincterotome advanced over a guidewire and inserted into the papilla at a 10- to 12-o’clock angle. The sphincterotomy is performed with electrocautery. An alternative method is the use of a needle knife cut, which is sometimes preferred because it provides better cutting control and limits injury to the surrounding papillary tissue. A temporary plastic pancreatic ductal stent, straight or pig-tailed, is frequently placed at the conclusion of the sphincterotomy procedure. These stents often dislodge on their own and pass into the gastrointestinal (GI) tract. Some patients may require a stent exchange, which is usually performed within 3 to 12 months, and the endoscopic minor papillary sphincterotomy may be repeated. A systematic review conducted by Kanth et al. in 2014 evaluated 22 retrospective studies, with a total of 838 patients, and found that a mean of 62% of patients “responded” to an endoscopic approach (range from 31% to 92%). The review

suggested that in the setting of pancreas divisum, patients with acute pancreatitis are more likely to show improvement compared with patients with chronic pancreatitis or abdominal pain. Typically, interventional procedures like EMPS or surgery are timed for when a patient is completely healed after a recent attack.

Endoscopic Dilation of the Minor Papilla (an Alternative to EMPS) High-pressure polyethylene balloons ranging from 4 to 10 mm have been designed to relieve obstruction of the minor duct. After identification of the minor duct, a guidewire and catheter are inserted through the stricture, with the catheter then exchanged for a balloon over the guidewire. The balloon contains radiopaque markers, which assist in the correct positioning of the device. When in position, the balloon is inflated to its specified diameter to dilate the minor papilla. In this scenario, no formal sphincterotomy is performed. K   TREATMENT: SURGICAL

Patients with chronic pancreatitis, chronic pain, or recurring episodes of acute pancreatitis (detailed categorization) may be responsive to surgical therapy. It should be reiterated that surgical treatment should not be performed without confirmation of pancreas divisum by ERCP or a high-quality, unequivocal MRCP.

Minor Duct Sphincteroplasty The abdomen can be accessed via either a midline incision or a right subcostal incision. If the gallbladder is still present, a cholecystectomy is usually performed to eliminate any possibility that the gallbladder is linked to the patient’s pancreatitis (gallstone-associated pancreatitis) or abdominal symptoms. After a wide Kocher maneuver is completed, a longitudinal duodenectomy is performed and the accessory papilla identified. The minor papilla typically lies proximal to the major papilla and may be difficult to identify. Extreme care is required for cannulation of the minor papilla. If there is any trauma to the tissue, edema and hematoma may make further cannulation attempts difficult. After cannulation, a lacrimal probe is inserted into the duct, and a papillotomy is performed using needle-tip electrocautery. Because of the perpendicular orientation of the dorsal pancreatic duct, which enters the duodenal wall and accessory papilla at a 90-degree angle, the papillotomy can only be extended for approximately 3 to 5 mm in length. Once completed, the pancreatic ductal and duodenal mucosa are anastomosed with interrupted 5-0 or 6-0 synthetic absorbable suture (we prefer polydioxanone). To prevent postoperative anastomotic edema or stenosis from occluding the pancreatic juice drainage through the minor papilla, a temporary pancreatic duct stent can be left in place at the conclusion of the procedure and secured into place with single 5-0 synthetic absorbable suture (we typically use a 3.5 or 5 French pediatric feeding tube, cut to a length of 5 cm). This stent will subsequently be passed through the gastrointestinal tract by the patient postoperatively. To complete the minor duct sphincteroplasty, the duodenotomy is closed in a transverse fashion in two layers: an inner layer of running absorbable 3-0 synthetic sutures such as polyglactin placed in a Connell style and an outer layer of interrupted 3-0 silk Lembert sutures. The duodenotomy can then be drained via a closed suction drain placed posteriorly. However, in most cases, no drains are placed.

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Chapter 55  ◆  Pancreas Divisum  169 L   POSTPROCEDURE MANAGEMENT

ERCP Postprocedure Management The majority of patients can be discharged 1 to 2 hours after the procedure if there are no symptoms warranting concern for post-ERCP pancreatitis. If symptoms of pancreatitis persist, IV fluids should be administered during the recovery period. Approximately 10% to 15% of patients will require overnight observation. However, the majority of these patients will show improvement within 72 hours. The myriad complications of ERCP and EMPS are beyond the scope of this chapter. M   SURGICAL POSTOPERATIVE

MANAGEMENT

Routine postoperative care includes maintenance IV fluids, analgesics, and early ambulation. We no longer leave a nasogastric (NG) tube in place. Most patients are ready for discharge on postoperative day 3 or 4. Postoperative pancreatitis may occur but tends to be uncommon. However, it may present with tachycardia, pain, elevated serum amylase or lipase, and an elevated white blood cell count.

Other Complications Pancreas divisum can also be associated with choledochal cysts and intestinal malrotation and, rarely, a Santorinicoele, which refers to a cystic dilation at the distal end of the dorsal pancreatic duct. Santorinicoele is thought to be an acquired condition rather than a congenital defect, and it requires no intervention. REFERENCES Adler Douglas G. Advanced Pancreaticobiliary Endoscopy. 1st ed. Salt Lake City: Springer; 2016. Print. Bülow R, Simon P, Thiel R, et al. Anatomic variants of the pancreatic duct and their clinical relevance: an MR-guided study in the general population. Eur Radiol. 2014;24(12):3142–3149. doi:10.1007/ s00330-014-3359-7. Cameron John L, Sandone Corinne. Atlas of Gastrointestinal Surgery. 1st ed. Hamilton: BC Decker; 2007. Print. Fujimori N, Igarashi H, Asou A, et al. Endoscopic approach through the minor papilla for the management of pancreatic diseases. World J Gastrointest Endosc. 2013;5(3):81–88. doi:10.4253/wjge.v5.i3.81. Kanth R, Samli N, Inaganti A, et al. Endotherapy in symptomatic pancreas divisum, A systematic review. Pancreatology. 2014;14(4):244–250. Web. Scott-Conner Carol E.H. The SAGES Manual Fundamentals of Laparoscopy, Thoracoscopy, and GI Endoscopy. 2nd ed. Iowa City: Springer; 2006. Print.

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Chapter

56 

SMALL BOWEL OBSTRUCTION Eliza E. Moskowitz, MD, Eric M. Campion, MD, and Robert C. McIntyre, Jr., MD, FACS

INTRODUCTION The incidence of adhesive small bowel obstruction (SBO) following all types of abdominal operations is approximately 2.5%. In North America, there are more than 300,000 annual hospital admissions for SBO, accounting for 850,000 days of inpatient care, costing more than $2.7 billion in medical expenditure. SBO accounts for 3.5% of all emergency admissions that lead to laparotomy, and 3% of all laparotomies performed in the United States are for SBO. Approximately 30% to 60% of adhesive SBOs require operation. The recurrence after lysis of adhesion is 10% to 20%. Additional causes of SBO include incarcerated hernia, tumor, inflammatory bowel disease, intussusception, radiation fibrosis, and gallstone ileus. Large bowel obstruction (LBO) can sometimes be difficult to differentiate from SBO. A Typically, patients present with gradual-onset crampy abdominal pain, followed by nausea, emesis, and obstipation. Signs and symptoms will depend on site of obstruction, whether it is partial or complete, and length of time between onset of symptoms and presentation. The most common causes of mechanical small bowel obstruction include adhesions, hernias, and cancer. Physical examination should focus on evaluating for palpable masses, focal tenderness, the presence of hernias, and signs of peritonitis. B No single laboratory test confirms bowel ischemia or necrosis. Leukocytosis, acidosis, and electrolyte abnormalities (hyponatremia, hypokalemia) are frequently present. Metabolic alkalosis can result from vomiting; metabolic acidosis (lactic acidosis) can also result if bowel becomes ischemic or if the hypovolemia is severe enough to cause organ hypoperfusion. Clinical parameters for prediction of bowel strangulation are notoriously inaccurate. Patients who present with a complete bowel obstruction and evidence of systemic inflammatory response syndrome, metabolic acidosis, and leukocytosis have bowel strangulation in only 40% to 60% of cases. Absent these clinical signs, the incidence of strangulation is still 10%. C Plain radiographs should include an upright view of the chest and upright and supine views of the abdomen. Plain x-rays have a sensitivity of 70% to 85% in establishing the diagnosis. These may demonstrate findings that indicate an urgent need for operative intervention—namely, pneumoperitoneum (best seen on upright chest x-ray) or volvulus. The site and etiology of the obstruction are not always apparent on plain films because a transition point between dilated proximal and nondilated distal bowel cannot always be appreciated.

D Computed tomography (CT) of the abdomen and pelvis (A/P) aids in the diagnosis of SBO with a sensitivity of 78% to 100% for high-grade obstructions. A CT scan will help identify the transition point. Moreover, a CT scan will delineate the severity of obstruction (partial vs. complete) and will help identify etiology (hernia, mass lesions, inflammatory changes). A CT scan may also provide additional information as to potential complications (ischemia, necrosis, perforation) necessitating urgent operative intervention. E Small bowel obstructions have the propensity to cause metabolic derangements. The metabolic effects (electrolyte abnormalities, metabolic alkalosis or acidosis) of small bowel obstruction are a result of decreased fluid intake, vomiting, and a shift of fluid from the vascular and extracellular spaces into the lumen of the proximal bowel (third spacing). Immediate treatment is resuscitation with intravenous fluid therapy and replacement of depleted electrolytes. The effectiveness of resuscitation is gauged by hemodynamic parameters and urine output. A nasogastric tube (NGT) should be placed to decompress the stomach and proximal small bowel and reduce the risk for aspiration of gastric contents. NGT placement also minimizes patient discomfort and the passage of swallowed air, which can worsen distention. F A groin hernia can cause a small bowel obstruction. If reduction of a groin hernia relieves the signs and symptoms of SBO, the patient is observed to rule out bowel necrosis, and then a herniorrhaphy is performed on an elective basis. A nonreducible hernia causing small bowel obstruction warrants urgent surgical interventions to evaluate the bowel and repair the hernia. This can be performed in either an open or laparoscopic approach based on surgeon preference. G Emergent surgical indications may include fever, shock, acidosis, leukocytosis, and peritonitis. Any or all of these signs and symptoms may indicate ongoing bowel ischemia and/ or necrosis, in which case an operation is warranted. In addition to clinical signs, there are radiologic signs that will identify 70% to 96% of patients who will benefit from surgical intervention. These include free air (indicating bowel perforation), pneumatosis or portal venous gas (indicating intestinal ischemia), and evidence of complete or closed-loop obstruction. Additionally, any patient with SBO initially treated with conservative therapy who develops any of these signs or symptoms should be considered for immediate operation. H Adhesive obstructions are the most common etiology for SBO. Many of these obstructions will resolve with decompression. In the absence of clinical improvement, additional radiographic studies may be indicated. Any patient with worsening signs or symptoms should undergo immediate operation and lysis of adhesions (LOA). I

Gallstone ileus is obstruction of the small bowel caused by an intraluminal gallstone. Treatment is enterotomy and removal of the stone. Swallowed objects or bezoars can also cause bowel obstruction. If endoscopic retrieval is not feasible, these may require removal via enterotomy. J

Intussusception of the small bowel is uncommon in adults. The lead point for an intussusception is a tumor in most

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Chapter 56  ◆  Small Bowel Obstruction  170.e1

Abstract

Keywords

The incidence of adhesive small bowel obstruction (SBO) following all types of abdominal operations is approximately 2.5%. In North America, there are more than 300,000 annual hospital admissions for SB accounting for 850,000 days of inpatient care, costing more than $2.7 billion in medical expenditure. SBO accounts for 3.5% of all emergency admissions that lead to laparotomy, and 3% of all laparotomies performed in the United States are for SBO. Approximately 30% to 60% of adhesive SBOs require operation. The recurrence after lysis of adhesion is 10% to 20%. Additional causes of SBO include incarcerated hernia, tumor, inflammatory bowel disease, intussusception, radiation fibrosis, and gallstone ileus. Large bowel obstruction (LBO) can sometimes be difficult to differentiate from SBO.

small bowel obstruction ileus adhesions adhesiolysis

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Chapter 56  ◆  Small Bowel Obstruction  171 patients, although less often, adhesive bands or inflammatory lymph nodes may also be causative. Patients with tumors require resection of the mass after reduction of the intussusception. The extent of resection remains controversial. In patients with ileocolic, ileocecal, and colocolonic intussusceptions, formal resection is indicated. If intussusception is found incidentally on CT A/P and the patient is without symptoms, laparotomy is not indicated. K Inflammatory bowel disease (IBD) can present with intestinal obstruction either during an acute inflammatory episode or from chronic stricture formation. Acute inflammatory obstructions usually resolve with bowel rest and medical treatment of IBD. Operation is frequently required for obstruction from chronic stricture formation in Crohn’s disease. Because frequent obstructive episodes are the rule rather than the exception in this chronic inflammatory disease, operations that preserve small bowel length (stricturoplasty or limited resections) are preferred. L An ileus is a functional obstruction secondary to decreased motility of the small intestine, usually associated with an underlying condition. Despite the lack of a true obstruction, these patients are also volume/electrolyte depleted and uncomfortable from abdominal distention. Treatment modalities should therefore be aimed at volume resuscitation and electrolyte replacement. All medications that cause decreased motility (e.g., narcotics and anticholinergics) should be decreased in dose or withheld until resolution of the ileus. Treatment may include NGT decompression until the underlying etiology for decreased motility can be addressed. Pseudo-obstruction is a chronic condition often characterized by symptoms of recurrent distention, associated with nausea and emesis. The large intestine is more often affected than the small intestine. No mechanical

HISTORY/PHYSICAL - Pain - Distention - Nausea/vomiting - Obstipation - Focal tenderness - Peritonitis - Hernia - Mass

PLAIN FILMS

CONTRASTED CT A/P No emergent findings

E ETIOLOGY ADMIT KNOWN NPO/NGT IVF Monitor UOP Optimize electrolytes

F

P For a partial obstruction, further observation can extend for another 24 to 48 hours with few adverse sequelae. If there is still failure to improve, abdominal exploration and adhesiolysis should be considered. If patients do not improve

SURGERY

Reducible

Q Laparoscopy or laparotomy + LOA

Overnight observation and NGT ETIOLOGY UNKNOWN/ decompression PRESUMED ADHESIVE OBSTRUCTION

D

LABS - Metabolic panel - CBC - Lactate

O Failure of Gastrografin to reach the colon within 24 hours of ingestion suggests a complete obstruction, and this patient will benefit from immediate laparotomy and LOA.

Decompensation or signs of peritonitis

Observation

Persistent obstruction

M

H

No emergent findings

B

N Passage of contrast to the colon, combined with the return of bowel function (passing flatus or bowel movements), is an indication that the patient’s diet can be advanced, and disposition plans can be considered with the resolution of pain.

EMERGENT FINDINGS - Free fluid - Pneumoperitoneum - Perforation - Ischemia

C SUSPECTED SBO

M Nonoperative management (NOM) with the performance of a water-soluble contrast challenge is warranted in patients with suspected adhesive obstruction who present without indications for immediate surgical intervention. Clinical evaluation including physical examination and review of radiographic findings should be performed to preclude the need for immediate surgery. After overnight observation with NGT decompression and barring any aspiration risk factors (hiatal or paraesophageal hernia, severe chronic obstructive pulmonary disease [COPD], advanced frailty), a water-soluble small bowel contrast challenge is performed. Water-soluble contrast agents may be therapeutic because they draw fluid into the lumen of the bowel because of its hypertonicity and, by doing so, decrease intestinal wall edema and stimulate peristalsis. Abdominal plain films should be obtained at 12 and 24 hours to evaluate for contrast passage to the colon.

G

EMERGENT FINDINGS - Acute abdomen - Pneumoperitoneum - Volvulus

A

cause may be demonstrated. The patient may have a history of previous negative laparotomies for bowel obstruction.

Remain stable

WATER SOLUBLE CONTRAST CHALLENGE

N

O Complete P Partial Observation

Resolution

I

Intraluminal mass/bezoar

SURGERY

Enterotomy

J

Intussusception

SURGERY

Resuction +/− Resection

K

Inflammatory bowel disease

SURGERY

Limited resection

L

Ileus, pseudoobstruction

No improvement Improvement

Advance diet as tolerated

Stricturoplasty Observation + symptom management

Elective repair

Anterior repair +/− Laparotomy

Hernia Non-Reducible

Laparoscopic repair (TAPP) Pre-peritoneal repair

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172  Part V  ◆  Alimentary Tract by 72 hours, it is unlikely that they will do so with continued NOM. Q Minimally invasive management of small bowel obstructions has become more prevalent. Laparoscopic surgical management of adhesive SBOs is associated with shorter length of stay but slightly longer operative times. Patient-related factors and surgeon preference should be taken into account when deciding whether a laparoscopic or open approach for adhesiolysis is to be undertaken. Difficulties encountered include a lack of a free area for initial port insertion, lack of free space in the abdomen resulting from bowel distention, injury to the bowel wall, and limited ability to place traction on the bowel and exposure. Relative contraindications to laparoscopy include multiple previous operations, history of dense adhesion, excessive bowel distention, malignancy, and peritonitis. REFERENCES Beardsley C, Furtado R, Mosse C, et al. Small bowel obstruction in the virgin abdomen: the need for a mandatory laparotomy explored. Am J Surg. 2014;208(2):243–248. Bilderback PA, Massman JD, 3rd, Smith RK, La Selva D, Helton WS. Small bowel obstruction is a surgical disease: patients with adhesive small bowel obstruction requiring operation have more cost-effective care when admitted to a surgical service. J Am Coll Surg. 2015;221(1):7–13. Broek RP, Stommel MW, Strik C, van Laarhoven CJ, Keus F, van Goor H. Benefits and harms of adhesion barriers for abdominal surgery: a systematic review and meta-analysis. Lancet. 2014;383(9911):48–59.

Catena F, Di Saverio S, Kelly MD, et al. Bologna guidelines for diagnosis and management of adhesive small bowel obstruction (ASBO): 2010 evidence-based guidelines of the world society of emergency surgery. World J Emerg Surg. 2011;6:5. Ceresoli M, Coccolini F, Catena F, et al. Water-soluble contrast agent in adhesive small bowel obstruction: a systematic review and meta-analysis of diagnostic and therapeutic value. Am J Surg. 2016;211(6):1114–1125. Keenan JE, Turley RS, McCoy CC, Migaly J, Shapiro ML, Scarborough JE. Trials of nonoperative management exceeding 3 days are associated with increased morbidity in patients undergoing surgery for uncomplicated adhesive small bowel obstruction. J Trauma Acute Care Surg. 2014;76(6):1367–1372. Loftus T, Moore F, VanZant E, et al. A protocol for the management of adhesive small bowel obstruction. J Trauma Acute Care Surg. 2015;78(1):13–21. Maung AA, Johnson DC, Piper GL, et al. Evaluation and management of small-bowel obstruction: an eastern association for the surgery of trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 suppl 4):S362–S369. Prost AlDJ, Douard R, Malamut G, Mecheri F, Wind P. Small bowel obstruction in patients with a prior history of cancer: predictive findings of malignant origins. World J Surg. 2014;38(2):363–369. Scotte M, Mauvais F, Bubenheim M, et al. Use of water-soluble contrast medium (Gastrografin) does not decrease the need for operative intervention nor the duration of hospital stay in uncomplicated acute adhesive small bowel obstruction? A multicenter, randomized, clinical trial (adhesive small bowel obstruction study) and systematic review. Surgery. 2017.

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Chapter

57 

ACUTE MESENTERIC VASCULAR OCCLUSION James H. Black, III, MD, FACS, and Courtenay M. Holscher, MD A Although acute mesenteric ischemia (AMI) is an uncommon cause of abdominal pain (fewer than 1 in 1000 hospital admissions), the mortality rate approaches 100% without intervention. Severe abdominal pain out of proportion to examination should trigger concern for AMI. Accompanying symptoms of nausea, vomiting, diarrhea, and bloody stools may or may not be present; their absence should not preclude prompt evaluation in patients with extensive risk factors. B Acute mesenteric vascular occlusion can be categorized into arterial embolism, arterial thrombosis, venous occlusion, and nonocclusive mesenteric ischemia. Although all types of AMIs share risk factors of older age, female sex, preexisting atherosclerotic disease, and hypercoagulable states, each has unique risk factors as well. Patients with atrial fibrillation, other arrhythmias, or recent myocardial infarction are at risk for arterial embolism, which is the most common type of AMI, accounting for 40% to 50% of cases. Arterial thrombosis, which accounts for 20% to 35% of cases of AMI, can be seen in patients with chronic mesenteric ischemia who thrombose a diseased native vessel. Other risk factors for arterial thrombosis include recent endovascular interventions, which may have caused dissection or local trauma. Mesenteric venous occlusion accounts for 5% to 15% of cases and causes bowel ischemia from inadequate venous outflow. Risk factors for venous thrombosis include hypercoagulable states, trauma, and inflammation, which may include biliary, pancreatic, or gastrointestinal etiologies. Finally, nonocclusive mesenteric ischemia (5% to 15% of cases) results from low-flow states or vasospasm, and risk factors include hemodialysis, hemodynamic shock, and drug use, including vasopressors, ergots, and cocaine. C Given the nonspecific history, examination, and laboratory results seen in AMI, maintaining a high index of suspicion for AMI is critical in prompt diagnosis. Many vascular surgeons believe that the critical barrier to decreasing the high mortality rate of AMI is simply making the diagnosis. Less than 30% of AMI patients are diagnosed before surgical exploration. With AMI on the differential diagnosis, appropriate computed tomographic (CT) imaging can be performed. Early resuscitation en route to CT should include crystalloid administration, electrolyte management, and treatment of arrhythmia when present. D Laboratory studies are nonspecific in the evaluation of AMI. Leukocytosis is common and is often greater than 20 K/ mm3. Lactic acidosis is typically a late development and should raise concern for bowel ischemia. Electrolyte derangements and elevated amylase can be seen. Underlying hypercoagulable states

should be identified with a panel of laboratory tests, including factor V Leiden; prothrombin 20210 mutation; protein C activity; protein S activity and free protein S antigen; antithrombin deficiency; an antiphospholipid panel, including dilute Russell viper venom test, anti-B2-glycoprotein antibodies, and anticardiolipin antibodies; and a complete blood count with flow cytometry to evaluate for myeloproliferative disorders and paroxysmal nocturnal hemoglobinuria. Finally, drugs that could cause a hypercoagulable state include estrogen, cocaine, anabolic steroids, and heparin, in which case a heparin-induced thrombocytopenia panel including PF4 and serotonin release assay should be performed. E An electrocardiogram (ECG) can identify arrhythmia or recent myocardial infarction (MI). Although echocardiography may also be helpful in identifying a source of emboli such as left ventricular thrombus after MI, it should not delay mesenteric revascularization. F Abdominal x-ray and ultrasound have low yield in the diagnosis of AMI. Findings of pneumoperitoneum, portal venous gas, pneumatosis, and bowel wall thickening on plain x-ray demonstrate bowel ischemia but are nonspecific for AMI. Duplex ultrasonography, although useful in chronic mesenteric ischemia, is low yield in the setting of bowel edema, highly operator-dependent, and not recommended to diagnose AMI because an acute clot may be difficult to diagnose in limited ultrasound windows. G Computed tomographic angiography (CTA) has >90% sensitivity and specificity in the diagnosis of AMI. The inclusion of arterial and venous contrast phases provides critical information about both mesenteric vasculature and bowel ischemia. Although magnetic resonance angiography (MRA) can avoid the radiation and iodinated contrast required for CTA, MRA takes longer, has lower resolution, and is not recommended to diagnose AMI. H Once the diagnosis of AMI is made, anticoagulation (intravenous [IV] heparin 80 to 100 units/kg bolus) and broad-spectrum antibiotics should be administered, and revascularization should be performed without delay. If examination, laboratory, and imaging suggest a low concern for bowel infarct, initial endovascular revascularization can be considered. However, if bowel ischemia is suspected, laparotomy for bowel resection will be a critical component of management. Revascularization of segments of infarcted bowel is not recommended because the release of endotoxins can lead to sudden hemodynamic collapse. I

Endovascular techniques are increasingly used for revascularization and are associated with a lower mortality and shorter length of stay. Despite much debate in the literature, the key in pursuing endovascular-first revascularization is a low threshold for laparotomy in addition to endovascular intervention if revascularization is inadequate or if bowel ischemia is suspected. Selection of the endovascular intervention depends on the etiology of AMI. Emboli can be managed with transcatheter suction embolectomy (e.g., 8F Export catheter) and anticoagulation. Mesenteric arterial thrombosis can be managed with catheterdirected thrombolysis. If underlying vessel stenosis has caused acute thrombosis, angioplasty and stenting can assist in

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Chapter 57  ◆  Acute Mesenteric Vascular Occlusion  174.e1

Abstract

Keywords

Acute mesenteric ischemia is an uncommon cause of abdominal pain with high mortality if unrecognized. Caused by superior mesenteric artery embolism or thrombosis, venous thrombosis, or nonocclusive mesenteric ischemia, early resuscitation and diagnosis through computed tomographic imaging are critical. Once identified, anticoagulation and revascularization are the cornerstones of management for superior mesenteric artery embolism or thrombosis. A hybrid operating room/endovascular suite allows for flexibility in both endovascular and open interventions. Bowel resection for infarcted bowel may be necessary, with a low threshold for second-look laparotomy. After successful revascularization, lifelong aspirin is indicated and patients should be educated on symptoms of stenosis and re-occlusion to avoid delay in diagnosis of recurrence.

acute mesenteric ischemia embolism thrombosis nonocclusive mesenteric ischemia

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Chapter 57  ◆  Acute Mesenteric Vascular Occlusion  175 revascularization. Venous occlusion is typically managed with anticoagulation alone, but if this is unsuccessful, mechanical thrombectomy or thrombolysis can be attempted. Nonocclusive mesenteric ischemia (NOMI) is similarly medically managed with fluid resuscitation, limitation of vasopressors, and anticoagulation; however, intra-arterial papaverine or vasodilators can be used. A minority of NOMI will have a mesenteric stenosis that may benefit from angioplasty or stenting to improve inflow. J

A hybrid operating room/endovascular suite allows for flexibility in both endovascular and open interventions and should be used when available. K Laparotomy is performed in the majority of cases of AMI. Preparation of the patient should include access to the greater saphenous vein, which is preferred over prosthetic graft in the setting of bowel ischemia. Bowel viability should be established at the time of laparotomy with fluorescein dye or mesenteric Doppler. Clearly infarcted bowel should be resected. Bowel with questionable viability should be revascularized and re-evaluated. If there is still questionable viability, a second-look laparotomy can be planned for 24 to 48 hours after revascularization. The pattern of bowel ischemia may suggest the location of occlusion: thrombosis of the origin of the superior mesenteric artery (SMA) will affect the entire small bowel to the midtransverse colon, whereas embolic occlusion may spare the proximal SMA branches that provide blood flow to the proximal jejunum. L During laparotomy, selection of a revascularization technique depends on the etiology of occlusion. Embolism is managed with anticoagulation and embolectomy via transverse arteriotomy in the mid-SMA; longitudinal arteriotomy with patch repair may be required for a smaller or diseased SMA. Similarly, arterial thrombosis can be managed with thrombectomy. Arterial bypass to the SMA is performed using vein or artificial graft if thrombectomy or embolectomy are unsuccessful. Options for graft inflow include the supraceliac aorta, infrarenal aorta, or iliac arteries. There are successful reports of a hybrid approach of open retrograde mesenteric stenting, but this is not well established. Venous occlusion and nonocclusive mesenteric ischemia are managed similarly to endovascular techniques if medical management has failed.

A B

History and physical examination Pain out of proportion to exam Risk factors Cardiac disease

C Concern for acute mesenteric vascular occlusion

D E F

Resuscitation

Labs/imaging CBC/amylase/chemistries ABG/Lactate Hypercoagulation panel ECG Echocardiogram Abdominal x-ray or ultrasound

M In the setting of endovascular revascularization where suspicion for infarcted bowel is low, laparoscopy can rule out bowel ischemia and may spare select patients a laparotomy. N After revascularization and bowel resection when necessary, continued resuscitation in an intensive care unit (ICU) is critical. This includes hemodynamic monitoring, broad-spectrum antibiotics, and anticoagulation. It is not uncommon for patients to require large volume fluid resuscitation (10 to 20 liters of crystalloid) in the first 24 hours. Vasopressors should be avoided unless necessary for the maintenance of systemic pressure. O If segments of possibly viable bowel were noted at initial operation, a planned second-look laparotomy should be done 24 to 48 hours after initial laparotomy. Again, Doppler and fluorescein injection can establish bowel viability, and necrotic or marginally perfused bowel should be resected. Colonoscopic evaluation can be considered in select patients for whom the isolated concern is colon ischemia. P Lifelong anticoagulation is indicated in those patients who presented with embolus or thrombus resulting from arrhythmia or hypercoagulation disorders. Lifelong aspirin is indicated after revascularization of any type. Clopidogrel may be appropriate if angioplasty or stenting is performed. Q Initial parenteral nutrition may be required if patients experience prolonged ileus after ischemia. If significant bowel resection has been required, malabsorption and short bowel syndrome can result. Small bowel transplant can be considered for relatively healthy patients after total enterectomy. R Comorbid hypertension and atherosclerosis should be managed medically and smoking cessation encouraged to decrease the risk for recurrent mesenteric stenosis. S After successful revascularization, follow-up duplex ultrasonography of the mesenteric vessels and any bypass graft should be done every 6 months in the first year, then yearly. Patients should be educated on the symptoms of stenosis and re-occlusion to avoid delay in diagnosis of recurrence.

Endovascular revascularization Embolic – catheter aspiration embolectomy Thrombotic – thrombolysis/stenting Venous occlusion – anticoagulation/ thrombolysis Nonocclusive – intra-arterial papaverine

I

H

Low concern for bowel infarction

M

Laparoscopy

O

G CTA

Acute mesenteric vascular occlusion

J

Hybrid OR/endovascular suite availability

ICU resuscitation

N Exclude non-vascular causes

Laparotomy with revascularization ± bowel resection Embolic – embolectomy Thrombotic – thrombectomy/bypass/ open retrograde stenting Venous occlusion – anticoagulation Nonocclusive – intra-arterial papaverine

K L

Second-look Laparotomy ± colonoscopy

P

Continued management Anticoagulation Antiplatelet agents

Q R S

Nutrition Risk factor mitigation Follow-up imaging

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176  Part V  ◆  Alimentary Tract REFERENCES Beaulieu RJ, Arnaoutakis KD, Abularrage CJ, et al. Comparison of open and endovascular treatment of acute mesenteric ischemia. J Vasc Surg. 2014;59(1):159–164. Björck M, Orr N, Endean ED. Debate: whether an endovascular-first strategy is the optimal approach for treating acute mesenteric ischemia. J Vasc Surg. 2015;62(3):767–772. Branco BC, Montero-Baker MF, Aziz H, Taylor Z, Mills JL. Endovascular therapy for acute mesenteric ischemia: an NSQIP analysis. Am Surg. 2015;81(11):1170–1176. Clair DG, Beach JM. Mesenteric ischemia. N Engl J Med. 2016;374(10): 959–968. Cudnik MT, Darbha S, Jones J, et al. The diagnosis of acute mesenteric ischemia: a systematic review and meta-analysis. Acad Emerg Med. 2013;20(11):1087–1100.

Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA task force on practice guidelines (writing committee to develop guidelines for the management of patients with peripheral arterial disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation. 2006;113(11): e463–e654.

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Chapter

58 

SHORT BOWEL SYNDROME Jon S. Thompson, MD

A Short bowel syndrome (SBS) is characterized by malnutrition, weight loss, dehydration, diarrhea, and electrolyte abnormalities. This clinical syndrome and its associated complications are related primarily to the length of the remaining functioning intestine. However, the site of resection, underlying intestinal disease, presence or absence of the ileocecal valve, functional status of the remaining digestive organs, and adaptive capacity of intestinal remnant are important factors as well. Patients left with less than 60 cm of the small intestine are almost uniformly dependent on parenteral nutrition (PN) long term. Those with greater than 120 cm of intestine can usually be rehabilitated to enteral nutrition (EN). Those with 60 to 120 cm of intestine will usually require PN for up to a year but will often be rehabilitated to EN, depending on the other factors mentioned previously. B SBS occurs when resection of the intestine results in an absorptive capacity that does not meet the needs of the patient. This generally occurs when less than 120 cm of the small bowel is remaining in the adult, but patients with up to 180 cm may require specialized nutrition support depending on anatomy and intestinal disease. Conditions that lead to the SBS include mesenteric vascular disease, Crohn’s disease, malignancy and/ or radiation therapy, and a variety of benign causes, including trauma and postoperative complications such as intestinal obstruction. Seventy-five percent of incidents result from single massive intestinal resection and 25% from multiple sequential resections. The anatomy of the residual intestine and function of gastrointestinal organs need to be assessed to evaluate prognosis and guide management. C The early management of patients with SBS is often that of the care of a critically ill surgical patient. Maintaining fluid and electrolyte balance and initiation of nutritional support are important. Sepsis is often present. D During the initial phase, nutrition support usually requires PN, particularly until the patient’s condition stabilizes. Initiation of enteral therapy will be important during this period as soon as feasible. Approximately 70% of patients will survive massive intestinal resection. E Adaptation of the remaining intestinal remnant occurs over a period of months after resection. Luminal contents, such as pancreaticobiliary secretions, nutrients, and hormonal factors, appear to be important in this process. The initial dietary management should include frequent small feedings, although continuous therapy may be useful in very short remnants. Hyperosmolar solution should be avoided early on. Oral rehydration solution may optimize fluid absorption in the proximal intestine and should be employed in patients with proximal remnants. A

low-oxalate (no cola, tea, spinach), low-fat, lactose-free diet is recommended if the colon is in continuity. Separating the ingestion of solids and liquids may decrease the frequency of bowel movements. F Patients with SBS are at risk for several complications. Metabolic complications are present particularly in patients requiring PN. These include metabolic acidosis and alkalosis, hypocalcemia, hyper- and hypoglycemia, and D lactic acidosis. Specific nutrient deficiencies may also occur depending on absorption and replacement therapy. Bacterial overgrowth may exacerbate diarrhea and impair absorption. Intestinal obstruction should be sought and treated if present. Cholelithiasis occurs in at least one-third of patients. Prophylactic cholecystectomy should be considered in patients with SBS. Gastric hypersecretion occurs transiently during the first several months after resection and should be managed with acid suppression (proton pump inhibitors). Kidney stones develop in one-third of patients and are usually calcium oxalate stones. This occurs primarily in patients with remaining colon where the free oxalate is absorbed. Diarrhea can be treated generally with agents such as loperamide, codeine, or Lomotil. Octreotide is useful short term in selected patients. Using cholestyramine to bind bile acids may also be helpful. Treating gastric hypersecretion and bacterial overgrowth, as mentioned previously, is also important. G Patients who successfully transition to total EN will require long-term monitoring and care to prevent complications. Patients who do not successfully transition to EN require further efforts at intestinal rehabilitation. The initial step is to optimize dietary intake. This is done to maximize absorption from the intestinal remnant. However, the diet can also be modified, and other treatment introduced, to maximize the intestinal adaptive response. Provision of fat and dietary fiber may be important in this regard. Pharmacologic therapy, such as glucagon-like peptide-2 analogues, have some efficacy in reducing fluid and PN requirements. Surgical therapy may also be helpful. Intestinal obstruction should be sought as a cause of bacterial overgrowth and stasis. Intestinal continuity should be restored whenever feasible to recruit downstream intestine. However, this may result in worsening diarrhea and perianal complications that may limit the diet in patients with shortened remnants. H Patients who cannot be successfully rehabilitated during a 1- to 2-year period after their resection are considered to have irreversible intestinal failure. These patients are anticipated to be permanently dependent on PN. The 5-year survival for this therapy is approximately 85%. Complications of long-term PN include line sepsis, thrombosis with difficulty maintaining vascular access, and PN-related liver failure. Hepatic failure occurs in approximately one-third of patients on long-term PN. This can be minimized by maximizing delivery of nutrients via the enteral route. I

Selected patients who have intestinal failure may become candidates for nontransplant operations to improve intestinal function. Patients who have a dilated intestinal remnant may be considered for intestinal tapering and lengthening to improve their motility and intestinal absorption and to lengthen the intestinal remnant. This has been more commonly performed in children. The success rate of this approach is approximately 75%. Patients who have a moderate intestinal remnant and rapid

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Chapter 58  ◆  Short Bowel Syndrome  178.e1

Abstract

Keywords

Short bowel syndrome (SBS) is characterized by malnutrition, weight loss, dehydration, diarrhea, and electrolyte abnormalities. This clinical syndrome and its associated complications are related primarily to the length of the remaining functioning intestine. However, the site of resection, underlying intestinal disease, presence or absence of the ileocecal valve, functional status of the remaining digestive organs, and adaptive capacity of intestinal remnant are important factors as well. Patients left with less than 60 cm of small intestine are almost uniformly dependent on parenteral nutrition (PN) long term. Those with greater than 120 cm of intestine can usually be rehabilitated to enteral nutrition (EN). Those with 60 to 120 cm of intestine will usually require PN for up to a year but will often be rehabilitated to EN, depending on the other factors mentioned previously. Patients who cannot be successfully rehabilitated during a 1- to 2-year period after their resection are considered to have irreversible intestinal failure. These patients are anticipated to be permanently dependent on PN. The 5-year survival for this therapy is approximately 85%. Complications of long-term PN include line sepsis, thrombosis with difficulty maintaining vascular access, and PN-related liver failure. Hepatic failure occurs in approximately one-third of patients on long-term PN. This can be minimized by maximizing delivery of nutrients via the enteral route. Patients with irreversible intestinal failure who develop complications of long-term PN are candidates for intestinal transplantation.

short bowel syndrome intestinal transplantation parenteral nutrition

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Chapter 58  ◆  Short Bowel Syndrome  179 History and physical examination Weight loss Diarrhea Steatorrhea Malnutrition Ostomy Perianal disease

B SHORT BOWEL SYNDROME

A

Restore C Electrolytes Nutrition Minerals Vitamins

Laboratory Electrolytes Albumin Glucose Phosphate Calcium Magnesium Zinc Liver function Radiographic studies GI contrast studies Ultrasound

Successful

D PN

Observe

Successful

H

G

E Unsuccessful

Enteral feeding

F

Complications Bacterial overgrowth Gallstones Gastric hypersecretion Kidney stones Metabolic

Enhance intestinal adaptation

Irreversible intestinal failure

Surgical rehabilitation Ostomy closure Relieve obstruction Recruit additional intestine

Home TPN Complications Line sepsis Hepatic failure

Nontransplant operation Tapering/lengthening Reversed segment

I

J

Intestinal transplantation Isolated or combined with liver

Cholecystectomy Relieve intestinal obstruction

transit with significant diarrhea and electrolyte problems may be candidates for procedures such as a reversed intestinal segment. The success rate of procedures designed to slow motility is only 50%. J

Patients with irreversible intestinal failure who develop complications of long-term PN are candidates for intestinal transplantation. Isolated intestinal transplantation is acceptable for patients who have recurrent sepsis and difficulty with vascular access but reversible liver disease. Patients with irreversible liver disease will require combined liver-intestinal or multivisceral transplantation. These procedures are successful in 75% of patients at 1 year and 50% at 5 years. REFERENCES Amiot A, et al. Determinants of home parenteral nutrition dependence and survival of 268 patients with non-malignant short bowel syndrome. Clin Nutr. 2013;32:368–374.

Beyer-Berjot L, et al. Segmental reversal of the small bowel can end permanent parenteral nutrition dependency: an experience of 38 adult patients with short bowel syndrome. Ann Surg. 2012;256:739–744. Dray X, et al. Incidence, risk factors and complications of cholelithiasis in patients with home parenteral nutrition. J Am Coll Surg. 2007;204: 13–21. Grant D, et al. Intestinal Transplant Association. Intestinal transplant registry report: global activity and trends. Am J Transplant. 2015; 210–219. Jeppesen PB, et al. Teduglutide reduces need for parenteral support among patients with short bowel syndrome with intestinal failure. Gastroenterology. 2012;143:1473–1481. Sudan D. The current state of intestine transplantation: indications, techniques, outcomes and challenges. Am J Transplant. 2014;14: 1976–1984. Sudan D, Thompson JS, Botha J, et al. Comparison of intestinal lengthening procedures for patients with short bowel syndrome. Ann Surg. 2007;246:593–601. Thompson JS, Rochling FA, Weseman RA, Mercer DF. Current management of short bowel syndrome. Curr Probl Surg. 2012;49:41–116.

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Chapter

59 

ENTEROCUTANEOUS FISTULA Paul Norbert Montero, MD, FACS

A Enterocutaneous fistula (ECF) remains a complex condition to manage, with subsequent mortality risk (up to 40%) and substantial morbidity. Death is usually a result of sepsis, malnutrition, or electrolyte imbalance. Satisfactory results require judgment, meticulous care, and often innovation and patience. ECF resulting from inflammatory bowel disease requires special expertise and specific considerations, including the use of biological agents and a tendency to not tolerate enteral feeds. B Sepsis is the main etiology of death with ECF. Computed tomography enables visualization and percutaneous drainage of abscesses. Subsequent sinograms with water-soluble contrast enable detailed information about fistula anatomy. The Surviving Sepsis guidelines should dictate antibiotic management, including limited duration of empiric antibiotics. C Generally, parenteral nutrition is initially required, but most patients can transition to enteral nutrition sources, with the goal of achieving an anabolic state (positive nitrogen balance). Sepsis control is mandatory to achieve adequate nutritional status. Nutritional requirements vary according to fistula location and output and should be monitored with weekly serum markers. Successful enteral nutrition requires adequate bowel length and may require elemental or immunomodulated formulas, although data are scarce. Enteroclysis (feeding distal to fistula) is an option in some circumstances but requires an enterostomy tube and ostomy appliance and may result in abdominal discomfort and diarrhea. D The goals of wound care are to protect the skin, control/ measure fistula output, and improve quality of life. Options range from simple dry gauze for low-output fistulas to ostomy appliances, wound managers, and innovative care for high-output or complex fistulas. Negative-pressure wound therapy, although not indicated for ECF, has mixed results in the literature but may serve certain patients well, particularly with quality of life. Sump drains and feeding tubes have also been used successfully for complex fistulas. E Computed tomography, sinogram, and contrast studies (small bowel follow-through, contrast enema) are useful to assess for distal obstruction, location and size of fistula, and tract length. Foreign body, radiation, infection, epithelialization, neoplasm, and distal obstruction (FRIEND) are associated with a poor prognosis for spontaneous closure.

F Albumin, prealbumin, C-reactive protein, and transferrin are acute-phase reactants with limited accuracy in the initial assessment of nutritional status. Normalization of these serum markers signals adequate nutritional status and is associated with improved outcomes after surgical intervention. G Nasogastric decompression does not decrease fistula output and may result in esophagitis, sinusitis, decreased mobility, and decreased quality of life. Proton pump inhibitors and H2 antagonists decrease fistula output and acidity. Sucralfate also reduces acidity and can have a constipating effect. Loperamide, codeine, and tincture of opium have been shown to decrease fistula output. Somatostatin and associated analogues have been shown in some studies to decrease fistula output and improve subsequent fistula closure rate (with no change in mortality rate). Consideration should be given for a 72-hour trial to assess output effect, with continuation if efficacious. H Fibrin sealant is often successful when employed in long, narrow, low-output fistulas, although it may require several treatments. Endoscopic clips have been used successfully in small, acute fistulas in the setting of sepsis control but have a limited role in chronic fistulas and necessitate accessibility endoscopically. Fistula plugs (porcine small intestine submucosa) have been described with some success in case reports and series, typically involving enteroatmospheric fistulas (fistulas opening into a surgical wound rather than to skin). I

Operative intervention must be preceded by complete sepsis control and adequate nutrition. Evidence of scar softening (“pinch test”) is desirable to facilitate dissection in an otherwise hostile abdomen. Historically, surgical timing involved a minimum of 6 weeks; current trends are for longer delays to allow spontaneous closure, adequate nutrition, and resolution of “obliterative peritonitis.” A key principle for surgical intervention is to avoid/ repair further enterotomies because the risk for recurrent ECF is substantial. The preferred surgical intervention is resection of affected bowel and primary anastomosis. Poorer outcomes are associated with primary repair or wedge resection of the fistula. A diverting ostomy carries risks of continued malnutrition/fluid balance and the need for subsequent surgery for takedown. REFERENCES Bobkeiwicz, et al. Management of enteroatmospheric fistula with negative pressure wound therapy in open abdomen treatment: a multicentre observational study. Int Wound J. 2017;14(1):255–264. Gribovskaja-Rupp, et al. Enterocutaneous fistula: proven strategies and updates. Clin Colon Rectal Surg. 2016;29(2):130–137. Leang, et al. Enterocutaneous fistula: analysis of clinical outcomes from a single victorian tertiary referral centre. ANZ J Surg. 2016. July 24 epub. Rogalski, et al. Endoscopic management of gastrointestinal perforations, Leaks, and fistulas. World J Gastroenterol. 2015;21(37):10542–10552. Yin J, et al. Is it feasible to implement enteral nutrition in patients with enteroatmospheric fistulae? A single-center experience. Nutr Clin Pract. 2014;29(5):656–661.

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Chapter 59  ◆  Enterocutaneous Fistula  180.e1

Abstract

Keywords

Enterocutaneous fistula (ECF) remains a complex condition to manage, with subsequent mortality risk (up to 40%) and substantial morbidity. Death is usually a result of sepsis, malnutrition, or electrolyte imbalance. Satisfactory results require judgment, meticulous care, and often, innovation and patience.

enterocutaneous fistula enteroatmospheric fistula

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Chapter 59  ◆  Enterocutaneous Fistula  181

Clinically Unstable History and Physical Exam Crohn’s Disease Previous Operations Sepsis Electrolyte Imbalance Malnutrition Nutrition Fluid Resuscitation Radiation C Electrolyte Repletion Initial TPN Enteral > Parenteral Strict I/Os ENTEROCUTANEOUS FISTULA

A

Labs Elecrolytes LFTs Albumin Bacterial Cultures Imaging

Wound Care Control Sepsis Perc Drainage Antibiotics

B

Urgent Laparotomy and Repair Prognosis for Spontaneous Closure

D

Define Anatomy Serum Markers

E F

Medical Management

G

Poor: Distal Obstruction Short Tract Proximal Fistula Radiated Bowel High Output Fistula Malnutrition

Good: Distal Fistula Long Tract Low Output Fistula Adequate Nutrition

Non-Surgical Interventions

H

GI interventions IR interventions

Operative Intervention

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I

Chapter

60 

CROHN’S DISEASE OF THE SMALL BOWEL Tracy L. Hull, MD

A Patients with small bowel Crohn’s disease may present with abdominal pain, diarrhea, fever, weight loss, fatigue, anal pain, or an abdominal mass. If lesions are present that bleed, either overtly or occultly, anemia may be present. B The etiology of Crohn’s disease is unknown. It can affect the GI tract anywhere from the mouth to the anus. The ileocolic region is most often affected. Neither medical nor surgical treatment is curative. The aim of management is to maintain quality of life and to foster the longevity of the bowel, not simply to deal with the current problem. C Upper and lower intestinal contrast x-rays outline the location of disease. Colonoscopy allows visualization of the disease process and the opportunity to do biopsies. Patients with duodenal disease can have biopsies done via an esophagogastroduodenoscopy (EGD). In patients without obstruction, capsule video endoscopy may help locate disease that is difficult to see on contrast studies. This test may be useful for occult bleeding and when looking for ulcers in the small bowel. Experience is being gained with magnetic resonance imaging (MRI) to locate and evaluate disease. D Medical treatment should be started in patients with nonacute problems. The aim is to alleviate symptoms, restore nutrition, and provide emotional support. Steroids are usually the mainstay of initial treatment. Antibiotics such as metronidazole are commonly used. Azathioprine and 6-mercaptopurine are used for steroid-sparing effects, although such effects can take up to 6 months to appear. These drugs are used if a patient cannot be weaned from steroids or has had multiple small bowel resections. Oral 5-ASA compounds (but not sulfasalazine) are also used to treat small bowel Crohn’s disease. Intravenous infliximab has gained support for induction of remission and maintenance treatment of inflammatory disease. E Acute ileitis can mimic an acute flare-up of Crohn’s disease. The bowel is spongy, edematous, and violaceous. The lumen is not narrowed, and the cecum is normal. Should appendectomy be done, fistulization from the appendiceal stump or diseased ileum is rare, in contrast with appendectomy associated with Crohn’s ileitis. F Vagotomy and gastrojejunostomy are used when medical treatment of gastroduodenal Crohn’s disease fails. Revision

rates in some studies approach 70% at 10 years. When feasible, strictureplasty can be done with better long-term outcomes in some cases. G Resection of diseased small bowel is favored over bypass procedures in almost all patients with intractable disease or obstruction. In the few instances when resection is too hazardous, and bypass of the ileum to the side of the transverse colon is done, the bypassed segment is resected at a second stage. Midline incisions are favored to preserve the right and left lower quadrants for stoma sites, which may be needed later in the patient’s lifetime. Patients should have physiologic deficits such as anemia and electrolyte imbalances corrected before surgery. At 10 years after surgery, 30% of patients with distal ileal disease need more than one operation, and 5% need more than three for recurrent disease. H It is optimal to drain abscesses before abdominal surgery in stable patients. This avoids free contamination of pus in the abdominal cavity at surgery. Drainage can be done with computed tomography (CT) guidance by the radiologists, and a drain can be placed. If persistent sepsis or a fistula develops, surgery is done. I

When resection is done, wide resection margins (2 to 3 cm) are not needed, and microscopic margins need not be checked. Patients presenting for elective first operations for ileocecectomy may be ideal candidates for laparoscopic-assisted surgery. Open surgery is usually selected for those who have had multiple operations or enterostomies that preclude safe, timeefficient laparoscopy. J

Patients who are malnourished or cannot have their sepsis cleared before surgical intervention should be considered for a resection with an ileostomy and no anastomosis. The distal end may be closed and placed in the upper incision or positioned close to the stoma, which will facilitate stoma closure when the patient regains his or her health. Sometimes the bowel is fragile and the distal end is matured as a mucous fistula to avoid a staple line in the abdomen. K Strictureplasty is used instead of resection to treat all feasible strictures. It is usually not considered with active sepsis or fistula or when transverse closure of the enterotomy is vulnerable to leakage. This procedure allows for small bowel preservation. Short strictures (less than 10 cm) are treated with a Heinke– Mikulicz type of construction. Longer strictures are corrected with Finney-type reconstruction. Strictureplasty can be combined with resection of the small intestine. Rates of complications such as abdominal sepsis (6%) and reoperation for new strictures (28% at a median of 7 years’ follow-up) compare favorably with resection. The decision to perform an anastomosis or to divert the intestine after resection is based on the patient’s condition with respect to residual sepsis, malnutrition, and other factors that affect dehiscence. Preoperative total parenteral nutrition in a debilitated patient may decrease the risk for primary anastomotic dehiscence. Preoperative stoma marking should be done if there is a possibility that a stoma may be needed.

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Chapter 60  ◆  Crohn’s Disease of the Small Bowel  182.e1

Abstract

Keywords

Crohn’s disease commonly affects the small bowel. Because there is no cure, the goal is to control symptoms and maintain quality of life. Management balances medical and surgical therapy. Except in emergent situations, all treatment begins with medical therapy. Elective surgery is geared toward managing symptoms and preserving small bowel length.

Crohn’s disease strictureplasty small bowel enterography

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Chapter 60  ◆  Crohn’s Disease of the Small Bowel  183

A History and physical exam Abdominal pain Diarrhea Fever Weight loss Fatigue, anemia Abdominal mass

Gastroduodenal

Unsuccessful

D

Small bowel Crohn’s disease

+/– vagotomy or strictureplasty

Patient in good condition minimal or no sepsis

Obstruction

H

Fistula

Medical treatment

Surgery Sepsis +/− malnutrition

Intractability

Successful

I

F Gastroenterostomy

B C

Evaluation Colonoscopy CT enterography MRI enterography +/− EGD Labs

Complete small bowel obstruction

Short lesion no fistula or sepsis

Emergent surgery

Resect long segment with primary anastomosis +/− proximal stoma

J Resect with ileostomy

K Strictureplasty

Perforation

G Abscess

Drainage +/− resection +/− ileostomy

E RLQ pain not appendicitis

REFERENCES Delaney CP, Fazio VW. Crohn’s disease of the small bowel. Surg Clin North Am. 2001;81:137–158. Dietz DW, Fazio VW, Laureti S, et al. Strictureplasty in diffuse Crohn’s jejunoileitis. Dis Colon Rectum. 2002;45:764–770. Hoffmann JC, Zeitz M. Treatment of Crohn’s disease. Hepatogastroenterology. 2000;47:90–100.

Milsom JW, Hammerhofer KA, Bohnm B, et al. Prospective, randomized trial comparing laparoscopic vs. conventional surgery for refractory ileocolic Crohn’s disease. Dis Colon Rectum. 2001;44:1–9. Reiber A, Nussle K, Reinshagen M, et al. MRI of the abdomen with positive oral contrast agents for diagnosis of inflammatory bowel disease. Abdom Imaging. 2002;27:394–399. Strong SA. Surgical treatment of inflammatory bowel disease. Curr Opin Gastroenterol. 2002;18:441–446.

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Chapter

61 

RIGHT LOWER QUADRANT PAIN Maggie McQueen Hodges, MD, MPH, and Clay Cothren Burlew, MD

A In the majority of patients, history and physical examination point to the etiology of right lower quadrant (RLQ) pain. Appendicitis, the most common etiology of RLQ pain, is characterized by progressive periumbilical discomfort that intensifies and localizes to McBurney’s point. In contrast, gynecologic sources of RLQ pain are often sudden in onset, such as in the case of a ruptured ovarian cyst or ovarian torsion. Associated symptoms may help differentiate the etiology; nausea and vomiting after the onset of pain suggest appendicitis, whereas emesis before the onset of pain is more consistent with gastroenteritis. Diarrhea, although nonspecific, is more suggestive of inflammatory bowel disease (IBD) or regional/infectious enteritis. Dyspareunia or changes in vaginal discharge point to a gynecologic etiology, whereas dysuria is consistent with cystitis, and flank pain may indicate pyelonephritis; hematuria suggests renal or ureteral stones. Physical examination should rule out such sources as an incarcerated hernia, epididymitis or testicular pathology, musculoskeletal complaints, or a rectus sheath hematoma. B Laboratory studies should routinely include white blood cell (WBC) count and urinalysis, as well as a beta human chorionic gonadotropin (βHCG) in women. Leukocytosis with a left shift is indicative of inflammatory conditions. If a patient has a normal WBC count, the incidence of significant intraabdominal pathology is lower, and a trial of observation may be warranted. C Imaging is often helpful in evaluating equivocal cases of RLQ pain (e.g., patients presenting without a classic history, examination, or laboratory findings), in female patients, and in patients at either extreme of age. Pelvic ultrasound is the preferred first-line test in patients with suspected gynecologic pathology, whereas appendicitis, diverticulitis, and IBD are best visualized by computed tomography (CT) scan. In pregnant women with suspected appendicitis not well visualized on ultrasound, magnetic resonance imaging (MRI) should be considered to further aid diagnosis. D Thorough evaluation may not reveal an obvious cause of the patient’s RLQ pain. Patients with a normal WBC count and negative imaging who are able to tolerate a diet may be considered for outpatient management with repeat evaluation in 24 hours. Alternatively, patients with a concerning examination, equivocal imaging or laboratory results, or continued PO intolerance may be admitted for close observation, serial abdominal examinations, and repeat laboratory studies. E Mesenteric adenitis or infectious ileitis are often diagnoses of exclusion, but may be suggested by CT scan findings of

enlarged mesenteric lymph nodes or a thickened ileum. Conservative therapy is warranted. Meckel’s diverticulitis may be noted on CT scan but is often discovered at the time of operation when a normal-appearing appendix is identified, resulting in further exploration. The morphology of the diverticulum determines diverticulectomy versus segmental resection. Some surgeons advocate appendectomy at the time of diverticulectomy; however, there is no evidence-derived consensus for this approach. Ideally, IBD is detected before operation unless the initial presentation is perforation or obstruction necessitating intervention. Appendectomy is performed if the appendix/base of the cecum is not involved with disease. Medical therapy for ulcerative colitis includes steroids and either calcineurin inhibitors or anti-TNFa antibodies, whereas medical therapy for Crohn’s disease includes steroids and thiopurines or methotrexate. Diverticulitis may be cecal or sigmoid in origin (a redundant sigmoid colon may be located in the RLQ); regardless, treatment is identical. Medical therapy consists of bowel rest, intravenous (IV) hydration, and broad-spectrum antibiotics until the patient’s examination improves and WBC returns to normal. If an abscess is present, percutaneous drainage should be performed. If complicated by perforation with peritonitis or colonic obstruction, operative therapy is necessary, typically with segmental resection with or without fecal diversion. Cecal cancer requires a right hemicolectomy and evaluation for metastatic disease. A psoas abscess can often be drained percutaneously and treated with culture-directed antibiotics. Search for an underlying cause, including intravenous drug abuse, primary renal or intestinal pathology, and osteomyelitis, is important. Typhlitis should be considered in neutropenic patients undergoing chemotherapy. A complete blood count (CBC) may show neutropenia, and a CT scan may demonstrate bowel wall edema, pneumatosis of the intestinal wall, and ascites. Management consists of supportive therapy, broad-spectrum antibiotic coverage, and bowel rest, with a potential indication for therapy with granulocyte colony-stimulating factor in patients with concern for systemic infection. Operative management for typhlitis has not yet been standardized. F Patients diagnosed with appendicitis should receive appropriate fluid resuscitation and IV antibiotic coverage targeted at polymicrobial coverage, such as cefoxitin, ertapenem, or ceftriaxone/metronidazole. G Common gynecologic etiologies of RLQ pain include tuboovarian abscesses, pelvic inflammatory disease, ruptured ovarian cysts, ovarian torsion, or an ectopic pregnancy. Pelvic examination and imaging are critical to appropriate diagnosis. H In cases of nonperforated appendicitis or perforated appendicitis without associated abscess, open or laparoscopic appendectomy are accepted techniques. Laparoscopy is preferred in settings where experienced surgeons and appropriate equipment are available and is often chosen if the diagnosis remains in question, if there is concern for pelvic pathology, and in obese patients or patients with medical comorbidities. Nonoperative management of uncomplicated appendicitis with antibiotics is currently being examined; however, the broad applicability of this management remains disputed in the literature.

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Chapter 61  ◆  Right Lower Quadrant Pain  184.e1

Abstract

Keywords

Evaluation of abdominal pain, particularly right lower quadrant pain, is a common surgical conundrum. With a variety of etiologies requiring differing management techniques, accurate diagnosis is imperative.

right lower quadrant pain appendicitis gynecologic pathology

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Chapter 61  ◆  Right Lower Quadrant Pain  185

A History and physical examination • Location, onset, character, duration of pain • Associated local and systemic symptoms • Medical and surgical history • Comorbidities and immunosuppresion

D Unknown etiology

Normal WBC Negative imaging Tolerating diet

Consider discharge Re-evaluate in 24 hrs

Concerning exam Equivocal imaging/labs PO intolerance

Serial abdominal exams Repeat labs/imaging

H

F Appendicitis Acute RLQ pain

Most common etiologies

Non-perforated or peforated w/o abscess

Appendectomy

I

IV antibiotics percutaneous drainage

Perforated w/ abscess or large phlegmon

Appendectomy

G B

Gynecologic etiologies

Laboratory evaluation • CBC • Urinalysis • βHCG

C Imaging options • Pelvic ultrasound • CT scan • MRI

E Less common etiologies

TOA PID Ovarian cyst Ovarian torsion Ectopic pregnancy

Mesenteric adenitis Meckel’s diverticulitis IBD Diverticulitis Cecal cancer Psoas abscess Typhlitis

I

Patients with imaging consistent with perforated appendicitis with an associated large phlegmon or abscess may be managed nonoperatively with IV antibiotics, with percutaneous drainage of abscesses if technically feasible. Alternatively, appendectomy may be appropriate management in the hands of a skilled provider. For patients managed nonoperatively for their appendiceal abscess, there are data to support that patients do not require standard “interval appendectomy” 6 weeks following resolution; these cases should be individualized, and patients over the age of 40 should undergo colonoscopy if appendectomy is not performed. REFERENCES Andersson RE, Petzold MG. Nonsurgical treatment of appendiceal abscess or phlegmon: a systematic review and meta-analysis. Ann Surg. 2007;246(5): 741–748. Di Saverio S, Sibilio A, Giorgini E, et al. The NOTA study (non operative treatment for acute appendicitis): prospective study on the efficacy and safety of antibiotics (amoxicillin and clavulanic acid) for treating patients with right lower quadrant abdominal pain and long-term follow-up of conservatively treated suspected appendicitis. Ann Surg. 2014;260(1): 109–117. Fa-Sioen PRN, Roumen RM, Croiset van Uchelen FA. Complications and management of Meckel’s diverticulum—a review. Eur J Surg. 1999;166: 674–678. Ferzoco LB, Raptopolous V, Silen W. Acute diverticulitis. N Engl J Med. 1998;338:1521–1526. Groebli Y, Bertin D, Morel P. Meckel’s diverticulum in adults: retrospective analysis of 119 cases and historical review. Eur J Surg. 2001;167:518–524. Hindryckx P, Jairath V, D’Haens G. Acute severe ulcerative colitis: from pathophysiology to clinical management. Nat Rev Gastroenterol Hepatol. 2016;13:654–664.

Antibiotics Antibiotics NSAIDs Operative detorsion Methotrexate/OR

Supportive therapy Diverticulectomy/segmental resection Medical therapy unless complicated Medical therapy unless complicated Operative resection Percutaneous or operative drainage Supportive therapy, antibiotics

Ingraham AM, Cohen ME, Bilimoria KY, et al. Comparison of outcomes after laparoscopic versus open appendectomy for acute appendicitis at 222 ACS NSQIP hospitals. Surgery. 2010;148(4):625–635, discussion 635–637. Lipscomb GH, Stovall TG, Ling FW. Nonsurgical treatment of ectopic pregnancy. N Engl J Med. 2000;343:1325–1329. Maxfield MW, Schuster KM, Bokhari J, McGillicuddy EA, Davis KA. Predictive factors for failure of nonoperative management in perforated appendicitis. J Trauma Acute Care Surg. 2014;76(4):976–981. McCutcheon BA, Chang DC, Marcus LP, et al. Long-term outcomes of patients with nonsurgically managed uncomplicated appendicitis. J Am Coll Surg. 2014;218(5):905–913. Morgan C, Tillett T, Braybrooke J, Ajithkumar T. Management of uncommon chemotherapy-induced emergencies. Lancet Oncol. 2011;12(8):806–814. Nagel TC, Sebastian J, Malo JW. Oophoropexy to prevent sequential or recurrent torsion. J Am Assoc Gynecol Laparosc. 1997;4:495–498. Ross J. Pelvic inflammatory disease. BMJ. 2001;322:658–659. Simillis C, Symeonides P, Shorthouse AJ, Tekkis PP. A meta-analysis comparing conservative treatment versus acute appendectomy for complicated appendicitis (abscess or phlegmon). Surgery. 2010;147(6): 818–829. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infections in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Clin Infect Dis. 2010;50(2):133–164. Torres J, Mehandru S, Colombel JF, Peyrin-Biroulet L. Crohn’s disease. Lancet. 2016; published online ahead of print, 1 December 2016. http:// dx.doi.org/10.1016/S0140-6736(16)31711-1. Wilson EB, Cole JC, Nipper ML, Cooney DR, Smith RQ. Computed tomography and ultrasonography in the diagnosis of appendicitis: when are they indicated? Arch Surg. 2001;136:670–674.

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Chapter

62 

VOLVULUS Michelle L. Cowan, MD

A Volvulus, a twisting of the bowel around a fixed point, of either the small or large intestine, often leads to obstruction and/or ischemia, and prompt diagnosis is critical to prevent gangrene, perforation, and/or death. Volvulus often presents with abdominal pain, distention, nausea and/or vomiting, and constipation/obstipation. The duration of symptoms may vary, and symptoms are typically more acute with cecal volvulus versus sigmoid volvulus. Risk factors include a high-fiber diet, chronic constipation, acute or chronic medical illness, and prior abdominal surgery. Sigmoid volvulus is the most common and often affects older males who are institutionalized or have neuropsychiatric disorders. Cecal volvulus often occurs in those of younger age and women, whereas small bowel volvulus is more common in children, although it can still be seen in adults.

performed, water-soluble contrast is preferred to barium to avoid the risk for chemical peritonitis and should not be performed in patients who have evidence of gangrenous bowel, peritonitis, pneumatosis intestinalis, or pneumoperitoneum. D Surgical intervention is recommended for most cases of small bowel obstruction caused by volvulus, with the most common cause being adhesions in adults. After initial nasogastric tube decompression and intravenous fluid resuscitation, surgical exploration involves lysis of adhesions with or without resection of the bowel with anastomosis for any compromised or gangrenous bowel. E Surgical intervention is the standard of care in cecal volvulus. Endoscopic intervention is of limited value. Resection is the standard of care in those who are favorable surgical candidates and those with gangrenous or perforated bowel because the mortality rate for right colectomy is low, 2%, and the complication rate is ~5%. Non-resection techniques may be an alternative in those with viable bowel but who are otherwise unfavorable surgical candidates, with procedures including detorsion alone, detorsion with fixation (cecopexy), or cecostomy tube. However, the choice for these procedures must be weighed with the variable risk for recurrence along with morbidity and mortality.

B Volvulus, a twisting of a redundant segment of bowel around its mesenteric axis, is more common outside of the United States; however, it causes ~3% to 5% of all bowel obstructions in the Western world. In the colon, sigmoid volvulus is the most common (50% to 80%), followed by cecal volvulus (10% to 40%). There are two types of cecal volvulus; one involves twisting of the ileocecal region along its mesentery, and the second is that of a cecal bascule, or anterior cephalad folding of the cecum, which occurs in approximately 10% of patients with cecal volvulus. Up to 10% of cecal volvulus patients are pregnant, and colonic volvulus accounts for a quarter of the cases of colonic obstruction during pregnancy. Small bowel volvulus in children is often the result of congenital malrotation, and colonic volvulus is rare. In adults, small bowel volvulus is commonly caused by adhesive disease followed by a tumor or Meckel’s diverticula.

F In the absence of peritonitis and bowel ischemia, endoscopic decompression is the treatment of choice in sigmoid volvulus, with a success rate of ~70% to 90%. This can be done with either a rigid or flexible scope, and subsequent placement of a rectal tube is recommended to prevent re-torsion and allow for complete decompression and bowel preparation in anticipation of surgery. The mucosa should be carefully examined for viability, and if gangrenous mucosa is noted before decompression, the procedure should be aborted and the patient should be operatively managed. In patients who undergo successful endoscopic decompression as the sole therapy, the recurrence rates are ~40% to 70%; recurrence often occurs soon after discharge, with a recent study demonstrating a recurrence rate of 61% at a median of 31 days. As such, elective resection of the sigmoid colon during the same admission is recommended.

C Because volvulus often presents in older patients with comorbid disease and with symptoms of varying duration, many patients present with significant electrolyte abnormalities and even renal insufficiency caused by dehydration on laboratory work-up. In most instances, abdominal x-rays differentiate between the types of volvulus such that a dilated loop of colon in the right upper quadrant with an “omega” or “bent inner tube” configuration suggests sigmoid volvulus. A dilated loop of colon with central density in the left upper quadrant, or “coffee bean” configuration, is suggestive of cecal volvulus; however, plain films may only demonstrate small bowel dilation and the absence of colonic gas. Plain films may also show pneumoperitoneum. Plain films are diagnostic in only 20% to 70% of cases; thus, if plain films are equivocal, a computed tomography (CT) scan should be performed and is almost always diagnostic. A CT scan may demonstrate other findings, such as a mesenteric whirl sign or ischemic changes of the bowel. A CT scan can also distinguish between organoaxial volvulus of the cecum versus a cecal bascule. Contrast enema is now less commonly used but can be done in the setting of an equivocal diagnosis to demonstrate a tapered point of obstruction, or a “bird’s beak” sign. If

G In patients who present with peritonitis or evidence of bowel ischemia or perforation, endoscopic decompression should be omitted in favor of urgent surgical intervention. Surgery is performed with sigmoid resection and should be performed without detorsion to avoid the release of toxins. H After decompression and before definitive surgical resection, the patient should undergo a full colonoscopy. I

After successful endoscopy, if endoscopy fails, or if peritoneal signs develop, the patient should be managed with sigmoid resection. Depending on the degree of risk, resection with either an end sigmoid colostomy with a rectal stump or a resection with a primary anastomosis is performed. An end colostomy is more commonly done in those with hemodynamic instability and perforated disease. However, recent, limited data suggest no difference in postoperative complications or mortality between the two procedures. Laparoscopy is an option and is often easier after endoscopic decompression when the bowel is less dilated and the patient’s clinical status has improved to tolerate pneumoperitoneum. Recurrence after resection is rare. Alternatives

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Chapter 62  ◆ Volvulus  186.e1

Abstract

Keywords

Volvulus, a twisting of a redundant segment of bowel around its mesenteric axis, is more common outside of the United States however, causes ~3-5% of all bowel obstructions in the western world. This chapter will review the approach and treatment algorithm for volvulus.

sigmoid volvulus cecal volvulus endoscopic decompression

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Chapter 62  ◆ Volvulus  187

D A History and physical Abdominal pain/distention Nausea/vomiting/obstipation Elderly Institutionalized

Surgical intervention - Adhesiolysis - Resection

Small bowel

E Volvulus

Surgical exploration - Resection - Cecopexy - Cecostomy

Cecal

B

Diagnosis Labs Plain films CT scan Contrast enema

F Sigmoid

H Colonoscopy

Endoscopic decompression Fails

C Peritonitis

I Surgical intervention - Resection +/– anastomosis - Total colectomy

G

to resection have been studied, such as extraperitonealization of the sigmoid colon or mesenteric fixation, but they are not currently recommended because of high recurrence rates of ~20% to 40%, with associated morbidity. For patients with sigmoid volvulus in the setting of megacolon or a synchronous cecal, transverse, or splenic flexure volvulus, total abdominal colectomy is the procedure of choice.

Swenson BR, Kwaan MR, Burkart NE, et al. Colonic volvulus: presentation and management in metropolitan Minnesota, United States. Dis Colon Rectum. 2012;55:444–449. Vogel JD, Feingold DL, Stewart DB, et al. Clinical practice guidelines for colon volvulus and acute colonic pseudo-obstruction. Dis Colon Rectum. 2016;59:589–600. Yassaie O, Thompson-Fawcett M, Rossaak J. Management of sigmoid volvulus: is early surgery justifiable. ANZ J Surg. 2013;83:74–78.

REFERENCES Halabi WJ, Jafari MD, Kang CY, et al. Colonic volvulus in the United States: trends, outcomes, and predictors of mortality. Ann Surg. 2014;259:293–301.

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Chapter

63 

DIVERTICULITIS Daine Bennett, MD, and Michelle L. Cowan, MD A Colonic diverticula are false diverticula composed of only mucosal prolapse, which can occur throughout the colon; however, they are most commonly found in the left colon. The prevalence of diverticulosis is increasing and also increases with age, being present in ~70% of people over age 80. Inflammation of these diverticula, called diverticulitis, has a heterogeneous disease presentation comprising both acute and chronic complications. Traditionally, the risk for diverticulosis progressing to diverticulitis was thought to be as high as 20% to 30%; however, this is now thought to be an overestimation, with newer data estimating a risk for only ~5%. Patients with diverticulitis present with classic symptoms of left lower quadrant abdominal pain and tenderness. If recurrent, the pain is often recognizably the same as prior. Patients may also have fever, constipation, or diarrhea. The presence of fecaluria or pneumaturia increases the suspicion of a colovesical fistula. All patients should be asked if they have had a prior colonoscopy. B Laboratory work may demonstrate leukocytosis, and a urinalysis or plain abdominal film can help identify a fistula or pneumoperitoneum and rule out other diagnoses, such as a urinary tract infection or kidney stone. A computed tomography (CT) scan is now used as a standard tool to diagnose and stage diverticulitis, evaluate for possible complications, and rule out other diagnoses. Typical findings will show diverticula with associated inflammation, fat stranding, phlegmon or abscess, extraluminal foci of gas or pneumoperitoneum, fistula, or possible obstruction/stricture. C Diverticulitis can broadly be separated into two categories, uncomplicated and complicated. Complicated diverticulitis with fistula, abscess, obstruction, or perforation is more severe and requires inpatient admission. A phlegmon or small foci of extraluminal air are not considered complicated disease. Initial management for all complicated disease begins with intravenous (IV) fluids, pain control, IV antibiotics, bowel rest, and when needed, total parenteral nutrition (TPN). This has been shown to be effective in up to 91% of patients presenting with complicated diverticulitis, thus avoiding urgent colectomy, which avoids ostomy and decreases perioperative morbidity. D Uncomplicated diverticulitis is limited to signs of inflammation alone, whereas the findings of abscess, pneumoperitoneum, stricture, or fistula are consistent with complicated diverticulitis. Regardless of the severity, antibiotic therapy is typically indicated for all patients with diverticulitis; however, the European AVOD trial recently challenged the need for antibiotics versus fluids and supportive therapy alone in uncomplicated diverticulitis. E Abdominal abscesses up to 3 to 4 cm will often resolve with antibiotics alone. For larger abscesses, image-guided percutaneous drainage may allow patients to avoid colectomy during

initial hospitalization in up to 75% of cases. For those who don’t respond to antibiotics and/or drainage, reimaging to rule out residual abscess should be considered, as should surgical intervention. F Urgent surgery with colectomy is recommended for patients who are toxic-appearing with free perforation resulting in peritonitis. A patient with a fistula, obstruction, or failed percutaneous therapy or those whose pain and bowel function do not improve with medical therapy should undergo semi-urgent surgical intervention. G Antibiotics are still the current standard, and uncomplicated diverticulitis can often be managed in the outpatient setting with oral antibiotics if the patient is able to tolerate oral intake and the pain can be controlled. Antibiotics should provide coverage of both aerobes and anaerobes, such as a fluoroquinolone and metronidazole. Inpatient admission can be offered to those who cannot tolerate oral intake or need more significant pain control while also getting IV antibiotics until discharge. Repeat imaging is used to rule out interval abscess formation or other complication if there is no improvement. Surgery should also be considered if there is no improvement with inpatient admission and medical therapy. H Elective colectomy is generally recommended for patients with complicated diverticulitis after recovering from the acute episode because of estimated higher recurrence rates of ~40%. Colonoscopy should be performed approximately 4 to 6 weeks after resolution of symptoms and before surgery to rule out other diagnoses. I

Surgical decision making, especially in a more urgent situation, should incorporate patient and intraoperative risk factors alongside risk for anastomotic failure with the risk for a permanent ostomy. Options include a resection with a closed rectal stump and an end colostomy versus a resection with a colorectal anastomosis +/– diverting ileostomy; they have been shown to have similar morbidity and mortality at the initial operation, with significantly different reversal rates of approximately 50% versus 90%, respectively. An on-table lavage can be considered, especially in obstructed patients, to help decompress the proximal colon. If a fistula is found, the secondary organ can usually be primarily repaired at the time of the operation. A leak test should be performed on all anastomoses. A combination of oral and mechanical bowel preparation may reduce the risk for surgical site infection and anastomotic leak for elective colectomies. J

Laparoscopic lavage emerged as a potential option for those who have peritonitis or have failed medical therapy as a way of controlling sepsis as opposed to radical surgical resection. However, two recent randomized trials showed an increased reoperation rate with lavage versus resection, with one trial being closed early because of high morbidity with lavage. Thus current guidelines do not recommend operative intervention without colectomy. K Patients with a history of diverticulitis who have not had a recent colonoscopy should undergo colonoscopy 6 to 8 weeks after resolution of symptoms to rule out underlying cancer or inflammatory bowel disease. This is regardless of age.

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Chapter 63  ◆ Diverticulitis  188.e1

Abstract

Keyword

Diverticulitis is a heterogenous disease ranging from mild inflammation to abscess, fistula and either prurulent or feculent peritonitis. Published data over the last several years has helped clarify the natural history of diverticulitis and improve our treatment approach. This chapter will review the most up to date information on how to approach this common but complicated and nuanced disease.

diverticulitis

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Chapter 63  ◆ Diverticulitis  189

H A History and physical Abdominal pain Fever Constipation or diarrhea

E

Elective colectomy

Abscess

C

Failed medical therapy

Complicated

Diverticulitis

F

I

Hartmann’s procedure vs. primary anastomosis

Surgical Management Perforation Fistula/obstruction

Peritoneal lavage

J

B CBC Urinalysis CT scan

Uncomplicated

D

Inpatient vs. Outpatient

G

Colonoscopy

K

Recurrent diverticulitis

Elective colectomy

L The number of episodes of diverticulitis no longer dictates the need for elective colectomy; data show that an increase in elective colectomies has not decreased the rate of emergency operations. The first episode is often the worst, and subsequent episodes mirror the initial presentation. The risk for recurrent episodes is estimated at ~33%, with only approximately 4% to 5% progressing to having a complicated episode. Thus the decision for elective colectomy must be individualized and the risk for operation versus the burden of recurrent disease for the patient weighed. However, patients with chronic renal failure, collagen vascular disease, and immunosuppression are at higher risk for complicated diverticulitis requiring emergency surgery; thus, colectomy should be considered for these patients after the initial episode. REFERENCES

L

Chabok A, Pahlman L, Hjern F, et al. Randomized clinical trial of antibiotics in acute uncomplicated diverticulitis. British Journal of Surgery. 2012;99:532–539. Feingold D, Steele SR, Lee S, et al. Practice parameters for the treatment of sigmoid diverticulitis. Dis Colon Rectum. 2014;57(3):284–294. Li D, Baxter NN, McLeod RS, et al. Evolving practice patterns in the management of acute colonic diverticulitis: a population-based analysis. Dis Colon Rectum. 2014;57(12):1397–1405. Oberkofler CE, Rickenbacher A, Raptis DA, et al. A multicenter randomized clinical trial of primary anastomosis or Hartmann’s procedure for perforated left colonic diverticulitis with purulent or fecal peritonitis. Ann Surg. 2012;256(5):819–826. Schultz JK, Yaqub S, Wallon C, et al. Laparoscopic lavage vs primary resection for acute perforated diverticulitis: the SCANDIV randomized clinical trial. JAMA. 2015;314(13):1364–1375. Vennix S, Musters G, Mulder I, et al. Laparoscopic peritoneal lavage or sigmoidectomy for perforated diverticulitis with purulent peritonitis: a multicentre, parallel-group, randomised, open-label trial. Lancet. 2015;386:1269–1277.

Biondo S, Golda T, Kreisler E, et al. Outpatient versus hospitalization management for uncomplicated diverticulitis: a prospective multicenter randomized clinical trial (DIVER trail). Ann Surg. 2014;259(1):38–44.

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Chapter

64 

LOWER GASTROINTESTINAL BLEEDING Douglas M. Overbey, MD, and John T. Moore, MD A Lower gastrointestinal bleeding (LGIB) was originally defined as bleeding that originates distal to the ligament of Treitz, but newer small bowel enteroscopic modalities have redefined LGIB as distal to the ileocecal valve. Acute LGIB occurs over 3 units of transfused blood or hemodynamic instability) has a reported mortality as high as 21%. The most common etiologies of major lower GI bleeding include diverticulosis (30%), vascular ectasia (10% to 20%), inflammatory bowel disease (9%), polyps (9%), malignancy (8%), and anorectal disease (10%). Minor lower GI bleeding, blood that is only seen with defecation, intermittently, or coming from the surface of the anus, is often because of anorectal pathology. B Clinical information can assist in the differential diagnosis of a lower GI bleed. Painless bleeding is suggestive of diver­ ticulosis, angiodysplasia, hemorrhoids, or neoplasm. Abdominal pain with bleeding suggests ischemic bowel, inflammatory bowel disease, or other forms of colitis. Rectal pain with bleeding suggests an anorectal process such as anal fissure or proctitis. Nonsteroidal anti-inflammatory drug (NSAID) use should also be queried because it proposes an independent risk for LGIB. C Massive lower GI bleeding (severe hematochezia) is a lifethreatening condition. The tenets of management of any GI bleed include (1) resuscitation, (2) localization, and (3) treatment. Minimum requirements for initial resuscitation include two large-bore intravenous (IV) lines, obtaining blood for transfusion, and diagnosing the presence of a coagulopathy. The acuity of the hemorrhage dictates the aggressiveness of the resuscitative measures. Expedient measures to start localizing the source of a lower GI bleed include history; physical, including digital rectal examination; and anoscopy. Nasogastric intubation for gastric lavage with return of bile or emergent esophagogastroduodenoscopy (EGD) is essential to exclude an upper GI source of hemorrhage. Approximately 10% to 15% of patients initially thought to have a lower GI source of hemorrhage are ultimately found to have an upper GI or small bowel source.

D Colonoscopy is generally the test of choice for localization of lower GI bleeding. It provides both diagnostic and therapeutic potential. The diagnostic accuracy of colonoscopy ranges from 45% to 100% and may be improved by a rapid bowel preparation or power irrigation. Endoscopic therapy for a localized bleed includes electrocautery, argon beam coagulation, hemoclips, and injection of epinephrine for an overall hemostasis rate of 50% to 100%, highest within the first 12 hours. Tattoo or anatomic clip placement should be considered to identify the location in case of a re-bleed. Failure to localize the bleed on initial colonoscopy should be followed by EGD (bidirectional endoscopy) or further bowel preparation and repeat colonoscopy. Unlike radiographic examinations, colonoscopy does not require active bleeding during the examination to identify a lesion. E Patients who cannot be stabilized for endoscopy or in whom endoscopy has failed to localize the source should undergo radiographic evaluation if the clinical situation allows. Computed tomography angiography (CTA) provides axial imaging that can show a blush to further localize lower GI bleeding and is generally the initial test of choice. CTA for active GI hemorrhage carries a sensitivity of 79% and specificity of 95%. This can be followed by catheter-directed visceral angiography with the potential for therapeutic intervention. Mesenteric angiography detects bleeding rates as low as 0.5 to 1.5 cc/min. The ability of angiography to localize a lower GI bleed ranges from 40% to 78%. Therapeutic interventions include superselective angiographic coil or gelfoam embolization. Successful halting of the bleed occurs in 60% to 100% of patients, although re-bleeding may occur in 22% to 50% of patients. An alternative imaging modality for slower bleeds involves radiolabeled red blood cell scanning, which can localize bleeds as slow as 0.5 mL/min without therapeutic potential. F Surgery provides definitive treatment of a localized lower GI bleed. Indications for an operation include hemodynamic instability despite aggressive resuscitative efforts, hemorrhage of more than 6 units of blood in 24 hours, or significant rebleeding within a short period of time. If hemodynamic stability allows, localization studies should be performed before an operation to direct a segmental resection. In a hemodynamically unstable patient or in a bleeding patient in whom no bleeding site is located at surgery, a subtotal colectomy is the procedure of choice after ruling out anorectal pathology. REFERENCES ASGE Clinical Practice Guideline. The role of endoscopy in the patient with lower GI bleeding. Gastrointest Endosc. 2014;79(6):875–885. Kennedy DW, Laing CJ, et al. Detection of active gastrointestinal hemorrhage with CT angiography: a 4(1/2)-year retrospective review. J Vasc Interv Radiol. 2010;21(6):848–855. Lhewa DY, Strate LL. Pros and cons of colonoscopy in management of acute lower gastrointestinal bleeding. World J Gastroenterol. 2012;18(11): 1185–1190. Strate LL, Gralnek IM. ACG clinical guideline: management of patients with acute lower gastrointestinal bleeding. Am J Gastroenterol. 2016;111(4): 459–474.

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Chapter 64  ◆  Lower Gastrointestinal Bleeding  190.e1

Abstract

Keywords

This chapter summarizes the initial management of a patient presenting with a lower gastrointestinal bleed.

lower gastrointestinal (GI) bleed hemorrhage hematochezia

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Chapter 64  ◆  Lower Gastrointestinal Bleeding  191

A H&P Anorectal pain Abdominal pain Changed bowel habits Fever Color of blood Prior bleeds Anticoagulants NSAIDs Chronic bowel ailments

B Lower GI bleed

Lab Hct Platelets PT/PTT/TEG Type and crossmatch

Observe UGIB algorithm Subtotal colectomy Blood from NGT LGIB in unstable patient

C Resuscitate NGT lavage +/− transfusion Digital rectal exam/anoscopy

Anorectal pathology

No blood from NGT No anorectal pathology

LGIB in stable patient

Unable to localize bleed

E

Mesenteric angiography or tagged red blood cell scan

CTA abdomen and pelvis Cannot tolerate 4 hr rapid prep or sedation

Localization of bleeding

Angioembolization

F Segmental colon resection

D Re-bleed

Colonoscopy Treat locally

Subtotal colectomy

Endoscopic treatment

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Chapter

65 

ULCERATIVE COLITIS Brandon C. Chapman, MD, and Jon D. Vogel, MD

who do not respond adequately to 3 to 4 days of steroid treatment. H Ulcerative colitis, of mild to moderate severity, is treated with medications including steroids (to induce remission) and a variety of anti-inflammatory medications, including 5-aminosalicylates, immunomodulators (e.g., azathioprine), anti-TNF alfa drugs (e.g., infliximab, adalimumab), and the anti-integrin vedolizumab. I

A Ulcerative colitis usually presents with bloody diarrhea, fecal urgency, and tenesmus. The differential diagnosis includes Clostridium difficile colitis, other infectious colitides, Crohn’s disease, radiation proctitis, and colorectal polyp or cancer. B Endoscopic evaluation of the rectum, colon, and ileum with biopsies will help distinguish ulcerative colitis from other causes of proctocolitis. Ulcerative colitis begins in the rectum and extends proximally in a continuous distribution. The “skip areas” of normal mucosa, deep linear ulcers, and patchy distribution of mucosal inflammation, characteristic of Crohn’s disease, are absent in untreated ulcerative colitis. Histologic assessment may reveal acute or chronic inflammation consistent with ulcerative colitis but not granulomas, which are suggestive of Crohn’s disease. C Imaging studies such as computed tomography (CT) or magnetic resonance (MR) enterography provide little in the assessment of ulcerative colitis but may be used to help distinguish Crohn’s disease from ulcerative colitis. Plain abdominal radiographs are used with acute presentations of ulcerative colitis to exclude megacolon or pneumoperitoneum. D Severe acute or “toxic” colitis is an emergency presentation of ulcerative colitis that presents with increased stool frequency, bloody stool, fecal urgency, tenesmus, abdominal pain, and fever. Tachycardia, abdominal distention and tenderness, leukocytosis, anemia, and elevated serum C-reactive protein are also common findings in patients with severe acute colitis. E Evaluation and treatment of severe acute ulcerative colitis includes plain radiographs of the abdomen to exclude megacolon (transverse colon diameter ≥ 6 cm) or pneumoperitoneum suggestive of colon perforation. Concurrent Clostridium difficile and/or cytomegalovirus (CMV) colitis should be determined. Careful flexible sigmoidoscopy may be performed to aid diagnosis as needed. F Ulcerative colitis is a risk factor for colorectal cancer. Clinical guidelines support annual surveillance colonoscopy beginning 8 to 10 years after the colitis diagnosis. Random or chromoendoscopy-guided biopsies are performed to detect flat dysplasia. In most cases, raised mucosal lesions (polypoid or non-polypoid) should be endoscopically excised or biopsied when excision is not possible or not safe. G Initial treatment of severe acute ulcerative colitis is with intravenous steroid (e.g., methylprednisone 30 mg every 12 hours) and supportive care. Venous thromboembolism prophylaxis is also advised. Infliximab is considered for patients

Total abdominal colectomy with ileostomy is indicated for severe acute colitis refractory to medical therapy or complicated by persistent or progressive megacolon, colonic perforation, or hemorrhage. J

Total proctocolectomy, with ileal pouch anal anastomosis or end ileostomy, is generally recommended for confirmed biopsy results of flat high-grade dysplasia or cancer. K Completion proctectomy with J-pouch ileoanal anastomosis (IPAA) or end ileostomy may be offered to patients with prior severe acute colitis or other emergent presentation of ulcerative colitis who previously underwent urgent total abdominal colectomy. Most often, a defunctioning ileostomy is created when an IPAA is made. L Proctocolectomy with J-pouch ileoanal anastomosis is indicated for mild to moderate ulcerative colitis that cannot be adequately and safely controlled with medical therapy and when ulcerative colitis is complicated by dysplasia or cancer. The J-pouch ileoanal anastomosis is most often performed with a double-stapling technique that leaves a small “cuff ” of rectal mucosa in place. Alternatively, complete excision of the rectal mucosa with sutured pouch-anal anastomosis may be performed. The stapled technique is associated with better functional outcomes. M End ileostomy or continent ileostomy (Kock pouch) are alternatives to ileal J-pouch anal anastomosis that may be considered in some patients (e.g., patients with impaired anal sphincter function). N Total abdominal colectomy with ileorectal anastomosis is an alternative to ileal pouch anal anastomosis or end ileostomy that may be considered in extraordinary cases of ulcerative colitis in which the rectum has been spared of severe inflammation or other pathology. O Pouchitis is an inflammatory condition of the ileal J pouch that presents with increased stool frequency, blood in the stool, pelvic pain, and low-grade fever. Treatment of pouchitis begins with a 10-day course of antibiotics. Occasionally, progressive or chronic pouchitis necessitates escalation of medical therapy. REFERENCES da Luz Moreira A, Kiran RP, Lavery I. Clinical outcomes of ileorectal anastomosis for ulcerative colitis. Br J Surg. 2010;97(1):65–69. Danese S, Fiocchi C. Ulcerative colitis. N Engl J Med. 2011;365:1713–1725. Farraye FA, Odze RD, Eaden J, et al. AGA medical position statement on the diagnosis and management of colorectal neoplasia in inflammatory bowel disease. Gastroenterology. 2010;138:738. Ross H, Steele SR, Varma M, et al. Practice parameters for the surgical treatment of ulcerative colitis. Dis Colon Rectum. 2014;57(1):5–22.

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Chapter 65  ◆  Ulcerative Colitis  192.e1

Abstract

Keywords

Ulcerative colitis is a chronic inflammatory condition of the large intestine that is characterized by relapsing and remitting episodes of symptomatic mucosal inflammation. This chapter reviews the diagnostic work-up and surgical management of patients with ulcerative colitis.

ulcerative colitis inflammatory bowel disease

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Chapter 65  ◆  Ulcerative Colitis  193 Perforation Severe

Uncontrollable hemorrhage

G

A History and physical Bloody diarrhea Fecal urgency Tenesmus

NPO Steroids Antibiotics TPN Infliximab

Toxic colitis

I

K

Total or near-total abdominal colectomy with ileostomy

Completion proctectomy with J-pouch ileoanal anastomosis

Persistent

H

B ULCERATIVE COLITIS

5-aminosalicylates Steroids Immunomodulators Anti-TNF alpha agents Anti-integrin

Mildmoderate

O

J-pouch ileoanal anastomosis

C D E Workup CMV/C. difficile assays Plain radiographs Endoscopy ±CT Enterography ±MRI Enterography

L

F Chronic

Malignancy

J Total proctocolectomy

N Total abdominal colectomy with ileorectal anastomosis

M End ileostomy or continent ileostomy (Kock pouch)

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Chapter

66 

ISCHEMIC COLITIS Chady Atallah, MD, and Jonathan E. Efron, MD INTRODUCTION Ischemic colitis can present with a wide range of severity, from a mild, self-limiting form to severe colitis and gangrene. It occurs most predominantly in elderly patients. High-risk populations include patients undergoing surgery where the inferior mesenteric artery (IMA) is ligated (abdominal or aortic surgery) and patients with low-flow states (septic or cardiogenic shock). Of patients diagnosed with ischemic colitis, 20% will require surgical intervention, whereas the rest can be successfully treated with conservative management. Isolated right-sided ischemic colitis tends to have worse outcomes. A The clinical presentation is usually nonspecific, with the most common symptoms being abdominal pain and cramping, hematochezia, and tenesmus. Only 50% of patients will have all three signs, requiring clinicians to have a high index of suspicion. Other symptoms include nausea and vomiting, nonbloody diarrhea, and fever. Medical history allows clinicians to identify patients at risk for developing ischemic colitis. This should include prior or recent abdominal and aortic surgeries, including endovascular procedures; cardiovascular risk factors; and a history of hypercoagulable state, metabolic and rheumatoid diseases, and certain drugs (constipation-inducing medications, oral contraceptives, serotoninergics, cocaine). It is important to distinguish patients with ischemic colitis from patients with acute mesenteric ischemia who present with acute-onset abdominal pain that is out of proportion to the physical examination. Those patients require immediate evaluation with computed tomography (CT) arteriography and should undergo urgent surgical intervention. Furthermore, a minority of patients with ischemic colitis will present with signs of perforation, generalized peritonitis, and sepsis. These patients should also undergo immediate laparotomy and segmental colonic resection and diversion. B Regardless of how severe the colitis is, all patients with suspected colonic ischemia should receive aggressive fluid resuscitation and broad-spectrum antibiotics. It is believed that in moderate to severe cases with transmural ischemia, bacterial translocation can occur and cause bacteremia and sepsis, and therefore patients should get aerobic and anaerobic antimicrobial coverage. Narcotics should be used with caution because they can cause severe constipation, making the colitis worse, and may also interfere with serial abdominal examinations, causing them to be unreliable and mask signs of complications like perforation.

C When there are no signs of peritonitis, patients should undergo a thorough work-up to establish the proper diagnosis. Initial laboratory evaluation can show nonspecific abnormal values like leukocytosis. Severe cases can have signs of metabolic acidosis with elevated lactate and lactate dehydrogenase (LDH) and elevated blood urea nitrogen (BUN) and creatinine (specifically with low-flow states). Plain film radiograph of the abdomen is nonspecific and most commonly shows “thumbprinting” and colonic dilation. It can also show pneumoperitoneum in cases of perforation. A CT scan of the abdomen with intravenous and oral contrast is very commonly performed and usually shows bowel thickening and peri-colonic fat stranding in a segmental distribution. In more severe cases of colonic ischemia, pneumatosis and portal venous gas can be seen, which warrants surgical exploration. Magnetic resonance imaging (MRI) does not yield more information than a CT scan but can be useful in patients with kidney failure. D After the initial resuscitation and the initiation of intravenous antibiotics, acute surgical exploration is indicated for patients with peritonitis. This is made through a midline incision, with inspection and evaluation of the small and large bowel. All segments of ischemic colon should be anatomically resected, and diversion with an end colostomy or ileostomy should be performed. Resection margins should be wide enough to ensure healthy tissue because the margins’ perfusion may be difficult to assess intraoperatively. In case of dusky bowel with questionable viability, a temporary closure with a planned second look 24 hours later is advised. Primary anastomosis should not be performed in the acute setting. E The gold standard for the diagnosis of ischemic colitis is flexible sigmoidoscopy or colonoscopy. It should be performed within 24 to 48 hours of clinical presentation. Mild colitis presents with mucosal edema and erythema, petechial hemorrhage, and minimal ulceration, whereas severe cases have dusky mucosa, hemorrhagic ulceration, or frank necrosis. The colon is affected in a segmental manner, with the watershed areas (right colon, splenic flexure, and recto-sigmoid junction) being the most commonly affected. Patients without peritonitis can be managed with intravenous hydration, antibiotics, and bowel rest until all of the work-up is completed. If symptoms do not improve within 2 weeks with supportive care, exploration may be warranted, and segmental resections may be performed. Long-term complications from ischemic colitis include colonic strictures that may require surgical resection of the affected segments. After careful assessment of the remaining colon margins, primary anastomosis in these situations is acceptable. In conclusion, the management of ischemic colitis is nonsurgical in the majority of patients and includes intravenous hydration, antibiotics, and bowel rest. Urgent exploration is required for patients with peritonitis. Segmental resection is also needed for patients with nonresolution of symptoms or with long-term complications of their disease. A high index of suspicion should always be maintained in high-risk populations.

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Chapter 66  ◆  Ischemic Colitis  194.e1

Abstract

Keyword

This chapter outlines the etiology of ischemic colitis and proposes a management algorithm based on the patient’s clinical condition.

ischemic colitis

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Chapter 66  ◆  Ischemic Colitis  195 Stricture

A RESOLUTION

HISTORY AND PHYSICAL - Abdominal - Pain/cramping - Tenesmus - Hematochezia - Low grade fever, nausea, vomiting

E Colonic wall thickening Peri-colonic fat stranding

Recent abdominal or aortic surgery Low flow state: - Septic shock - Cardiogenic shock

Ischemic colitis

Labs: - CBC - ABG, lactate, LDH - BUN, Cr

C B

CT scan with IV and PO contrast

No peritonitis

Supportive measures IV hydration IV antibiotics Bowel rest Analgesics

Portal venous gas Pneumatosis Pneumoperitoneum

D Peritonitis

Mucosal edema, erythema Petechial hemorrhage

SUPPORTIVE MEASURES Continued pain Continued bleeding Recurrent sepsis

Flexible sigmoidoscopy Colonoscopy Severe hemorrhagic ulceration Frank necrosis

Repeat CT/scope

SURGICAL MANAGEMENT Segmental resection, wide margins +/– Temporary closure and second look End ileostomy or colostomy +/– Primary anastomosis (if elective)

+/– Abdominal X-ray

REFERENCES Brandt LJ, Feuerstadt P, Longstreth GF, et al. ACG clinical guideline: epidemiology, risk factors, patterns of presentation, diagnosis, and management of colon ischemia (CI). Am J Gastroenterol. 2015;110:18–44. Genstorfer J, Schafer J, Kettelhack C, et al. Surgery for ischemic colitis: outcome and risk factors for in-hospital mortality. Int J Colorectal Dis. 2014;29(4):493–503.

Nagata N, Niikura R, Aoki T, et al. Natural history of outpatient-onset ischemic colitis compared with other lower gastrointestinal bleeding: a long-term cohort study. Int J Colorectal Dis. 2015;30(2):243–249. O’Neill S, Yalamarthi S. Systematic review of the management of ischaemic colitis. Colorectal Dis. 2012;14:751–763. Sun D, Wang C, Yang L, et al. The predictors of the severity of ischaemic colitis: a systematic review of 2823 patients from 22 studies. Colorectal Dis. 2016;18(10):949–958.

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Chapter

67 

TOXIC MEGACOLON Lauren Steward, MD, and Michelle L. Cowan, MD

A Patients with acute colitis often present with abdominal pain, bloody diarrhea, and general malaise. Most of those who present with or progress to toxic megacolon often have signs of systemic toxicity, including fever, tachycardia, hypotension, or altered mental status. On physical examination, the patient with toxic megacolon will likely have abdominal tenderness with or without peritonitis. B Toxic megacolon is the final and potentially lethal complication of a number of different colonic processes. Characterized by nonobstructive colonic dilatation coupled with systemic toxicity, the term is a misnomer because severe toxicity can happen without dilation, “toxic colitis.” By definition, megacolon is a transverse colon diameter > 6 cm or a cecal diameter > 9 cm. One must search for an underlying cause, and given the diverse etiology of toxic megacolon, it is important to obtain a clear history of present illness and complete a thorough physical examination. Although it is most often associated with a complication of inflammatory bowel disease (IBD), it can be associated with other causes of colitis, including Clostridium difficile (C. dif) colitis, infectious colitis such as Escherichia coli, cytomegalovirus (CMV), or parasite infections as well as diverticulitis, ischemic colitis, or drug-induced colitis. C The work-up begins with laboratory evaluations, which may reveal significant electrolyte abnormalities, including hypo- or hypernatremia, hypokalemia, alkalosis resulting from contraction alkalosis, or acidosis caused by sepsis. A complete blood count (CBC) may demonstrate leukocytosis and anemia. Hypoalbuminemia may signify overall chronic inflammation and malnutrition because of ongoing illness such as in IBD. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are markers of inflammation and likely to be elevated but nonspecific. Stool samples should be sent for culture, ova, and parasites to rule out infectious etiology. CMV colitis can only be ruled out with biopsy by flexible sigmoidoscopy, which should be performed in all IBD patients and those with a clinical suspicion; however, full colonoscopy is not routinely advised. Plain films may reveal a dilated colon with multiple air–fluid levels. A computed tomography (CT) scan is not routinely necessary but may be helpful identifying complications of toxic megacolon including perforation or abscess. True toxic megacolon guidelines for clinical diagnostic criteria are as follows: (1) radiographic evidence of colonic dilatation, transverse colon diameter > 6 cm or cecum > 9 cm; (2) three of the following clinical signs: temperature > 38° C, heart rate > 120 bpm, white blood cell count > 10.5, and/or anemia requiring transfusion; and (3) one of the following: altered mental status, dehydration, electrolyte disturbances, and/or hypotension.

D Nonoperative therapy for toxic megacolon and toxic colitis should be coupled with serial laboratory results and serial examinations so as not to delay operative intervention should the clinical situation deteriorate. The initial treatment for toxic colitis or megacolon is the same for all and ideally should begin concomitant with the work-up to avoid delay and worsening sepsis. This begins with full bowel rest with nothing by mouth, a nasogastric tube to decompress the bowel, and broad-spectrum antibiotics. Patients with IBD-related toxic megacolon should be started on intravenous (IV) steroids. Those with C. dif infection should be started on oral vancomycin given their clinical toxicity, with discontinuation of any offending agents. Antidiarrheal agents should be avoided. After resuscitation, a decision is made whether to treat with aggressive nonoperative management or proceed to the operating room. Medical therapy can continue if the patient demonstrates improvement in the initial presentation, such as reversal of fever, leukocytosis, tachycardia, or abdominal pain, as well as improvement in the bloody diarrhea. With improvement, patients can be transitioned to oral therapies with discharge and outpatient follow-up. The decision to operate should be made for patients who deteriorate despite medical therapy. Some patients will improve only partially with smoldering disease or will plateau, thus presenting a surgical dilemma. Reassessment at approximately 48 hours is important to help assess the patient’s ultimate ability to respond to nonoperative therapy alone. For IBD patients, this plateau can provide an opportunity to discuss the addition of cyclosporine or antibody-based therapy. E Absolute indications for surgery include continued hemodynamic instability, uncontrolled sepsis, diffuse peritonitis, pneumoperitoneum, and major hemorrhage. Relative indications include those who don’t respond to nonoperative therapy after a 48-hour reassessment or worsening signs or symptoms during this period. F Fecal microbiota transplantation is safe and effective for refractory or recurrent C. dif infection and can be considered in those with no response or a partial response to medical therapy as long as they are clinically stable and without progression of disease. G The operation of choice for patients with toxic megacolon is almost always a subtotal colectomy and end ileostomy regardless of underlying etiology. Often the rectal stump can be closed and remain inside the abdomen even if involved in the underlying disease, especially if length is needed at the second, reversal operation. However, if there is concern about the rectal stump staple line, the closed stump can be exteriorized at the level of the fascia, typically at the inferior edge of the midline wound. This prevents pelvic sepsis and results in a surgical site infection (SSI) if dehiscence of the rectal stump staple line occurs. Only rarely is a total proctocolectomy performed, even in IBD, because the pelvic dissection has less morbidity if done at a separate operation when the patient is healthier. Simple diversion should be avoided because this does not remove the underlying cause of toxicity and is associated with high rates of failure. H Patients who recover with nonoperative therapy should undergo colonoscopy approximately 4 to 6 weeks after resolution of symptoms to confirm endoscopic remission and identify possible causes of underlying etiology.

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Chapter 67  ◆  Toxic Megacolon  196.e1

Abstract

Keywords

Toxic megacolon is the final and potentially lethal complication of a number of different colonic processes. Given the diverse etiology of toxic megacolon, one must search for an underlying cause and understand the various management options indicated for each cause. This review provides an algorithm to streamline the evaluation and treatment of toxic megacolon.

toxic megacolon toxic colitis ulcerative colitis Clostridium difficile

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Chapter 67  ◆  Toxic Megacolon  197

A

G Operative intervention - Subtotal colectomy with end ileostomy

History & physical exam Pain Fever Diarrhea Abdominal distention and tenderness

E Indications for surgery

B Toxic megacolon Failure

F Fecal

microbiota transplantation

D

C

Failure

Diffuse peritonitis Pneumoperitoneum Major hemorrhage Uncontrolled sepsis

Non-operative therapy - ICU admission - Bowel rest with nasogastric tube - Broad-spectrum antibiotics OR oral vancomycin for C. difficile infection - Serial labs and abdominal exams

Labs Imaging Stool studies Sigmoidoscopy

REFERENCES Drekonja D, Reich J, Gezahegn S, et al. Fecal microbiota transplantation for Clostridium difficile infection: a systematic review. Ann Intern Med. 2015;162(9):630–638.

H Colonoscopy

Kaiser AM, Hogen R, Bordeianou L, et al. Clostridium difficile infection from a surgical perspective. J Gastrointest Surg. 2015;19(7):1363–1377. Ross H, Steele S, Varma M, et al. Practice parameters for the surgical treatment of ulcerative colitis. Dis Colon Rectum. 2014;57:5–22.

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Chapter

68 

C. DIF COLITIS Juliane Y. Cruz, MD, and Howard S. Kaufman, MD A Clostridium difficile infection (CDI) is one of the most common nosocomial infections. The bacterium is a grampositive anaerobic bacillus that colonizes the intestinal tract after disruption of the normal gut flora. Fluoroquinolones are the most likely preceding antibiotic to cause CDI. Cephalosporins, clindamycin, ampicillin, and amoxicillin are also commonly associated with CDI. Risk factors include advanced age, surgery, immunosuppressive medications, HIV, and chemotherapy. Surgical patients account for about half of the infections. In all hospitalized patients with confirmed CDI, contact precautions should be instituted. The spore form of C. difficile is resistant to alcohol. The spread of CDI can be limited by health-care workers with routine hand washing, the use of gloves, and the use of patientdesignated stethoscopes. B The gold standard for diagnosis of CDI is toxigenic stool culture or a cell cytotoxicity assay that detects toxins A or B. Both tests take 2 days for results. An enzyme-linked immunosorbent assay (ELISA) can also detect toxin A or B and is most commonly used to obtain a faster result; however, this test is less sensitive. More recently, an immunoassay for an enzyme produced by the bacteria called glutamate dehydrogenase has been about 90% sensitive in detecting CDI. It can be used to screen patients while waiting for a stool culture or cell cytotoxicity assay to result. Additional studies that can be useful in diagnosis include abdominal x-rays, computed tomography (CT) scan, and colonoscopy. X-ray can show edema of the colon, thumbprinting, haustral thickening, ileus, or megacolon. A CT scan can be useful in detecting the extent of colitis and perforation or megacolon. The “accordion sign” reveals alternating highlighting of oral contrast in the colonic lumen among a severely edematous mucosal wall. Colonoscopy may reveal pseudomembranes. Sigmoidoscopy is generally not preferred because about one-third of cases are limited to the right colon. C In mild to moderate CDI, symptoms may include watery diarrhea (3 to 10 stools per day) and abdominal pain/ cramping in the setting of known antibiotic therapy currently or within the previous 2 months. D In moderate to severe CDI, signs and symptoms can additionally include abdominal distention, fever, and leukocytosis. An abdominal examination may also show peritoneal signs. E In mild to moderate cases of CDI, initial therapy consists of oral vancomycin (125 mg 4× daily for 10 days) or oral metronidazole (500 mg tablet 3× daily for 10 days) if vancomycin unavailable.

F Severe CDI can progress to fulminant colitis when the following are present: hypotension requiring vasopressor support, toxic megacolon, colonic perforation or ischemia, and lack of response to medical therapy after 48 hours. G In severe CDI, the preferred treatment is oral vancomycin (125 mg 4× daily for 10 to 14 days) or fidaxomicin (200 mg 2× daily for 10 days). H Intravenous (IV) metronidazole with or without vancomycin enemas can also be given to patients unable to tolerate enteral antibiotics. I

Recurrence is defined as a repeat episode of CDI within 8 weeks of previous successful treatment after clinically apparent resolution. J

Initial recurrence (with identical symptoms) can be treated with the initial therapy.

K A repeat recurrence can be treated with oral vancomycin for 10 to 14 days or a pulsed vancomycin regimen. L Fidaxomicin can be used in recurrence. It is equivalently effective in treatment and has a decreased recurrence rate when compared with vancomycin; however, it is far more expensive. M Fecal microbiota transplant (FMT) is the administration of donor stool directly to the gastrointestinal (GI) tract through a nasogastric tube, upper/lower endoscopy, or enema. Recent trials have demonstrated resolution rates of 87% to 92%. FMT use is currently limited to >3 recurrences unresponsive to antibiotic therapy and fulminant colitis unresponsive to 48 hours of therapy. N Total abdominal colectomy and end ileostomy is the currently accepted surgical intervention in cases of severe or fulminant CDI. Segmental colectomies have traditionally been associated with lower survival rates than total abdominal colectomy. Diverting loop ileostomy and colonic lavage with vancomycin pushes and polyethylene glycol solution could potentially allow for colonic preservation. This procedure remains experimental. REFERENCES Bagdasarian N, Rao K, Malani P. Diagnosis and treatment of Clostridium difficile in adults. JAMA. 2015;313:398–408. Kassam Z, Lee C, et al. Fecal microbiota transplantation for Clostridium difficile infection: a systematic review and meta-analysis. Am J Gastroenterol. 2013;108:500–508. McDonald LC, Gerding DN, Johnson S, et al. Clinical Practice Guidelines for Clostridium difficile infection in adults and children: 2017 Update by the infection diseases society of America (IDSA) and society for Healthcare Epidemiology of America (SHEA). Clin Infec Dis. 2018;66(7):e1–e48. Stanley JD, Burns PR. Clostridium difficile and the surgeon. Am Surg. 2010;76:235–244. Steele SR, McCormick J, Melton GB, et al. Practice parameters for the management of Clostridium difficile infection. Dis Colon Rectum. 2015;58:10–24. Surawicz CM, Brandt LJ, et al. Guidelines for diagnosis, treatment, and prevent of Clostridium difficile infections. Am J Gastroenterol. 2013;108:478–498.

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Chapter 68  ◆  Colitis  198.e1

Abstract

Keywords

This chapter contains the current medical and surgical treatment of Clostridium difficile colitis. The treatment options for mild, moderate, severe, fulminant, and recurrent Clostridium difficile colitis are described. The laboratory and imaging workup for Clostridium difficile colitis is also included in this chapter.

clostridium difficile infection colitis diarrhea megacolon

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Chapter 68  ◆  C. dif Colitis  199

K History and physical exam - Diarrhea - Recent antibiotic use - Abdominal pain

I

J

Recurrent

Repeat initial treatment

PO vancomycin/ pulsed vancomycin Fidaxomicin

M FMT

L Fulminant

PO vancomycin

No improvement after 48 hours

F C. dif colitis

Severe

A

B Labs - CCA/ELISA - Stool culture/PCR/ EIA - Abdominal XR - CT - Colonoscopy

D

G

PO vancomycin or fidaxomicin

PO vancomycin or PO metronidazole

Moderate

E Mild

C

PO vancomycin or PO metronidazole

Ileus

H

IV metronidazole +/– vancomycin enemas

No improvement after 48 hours and megacolon/ perforation/ ischemia

N Total abdominal colectomy and end ileostomy

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Chapter

69 

LARGE BOWEL OBSTRUCTION Michael Radomski, MD, and Ryan A. Lawless, MD A The history and physical examination are the mainstays of initial investigation in those patients with large bowel obstruction. Peritoneal findings prompt urgent surgical invention. Recent hospitalization, antibiotic or narcotic use, and orthopedic surgery often lead to functional obstructions. Hematochezia or previous findings of diverticular disease are concerning for diverticulitis, diverticular stricture, or malignancy. B Lactate and base deficit are used as markers of resuscitation. Elevated values that fail to correct with aggressive resuscitation are concerning for ongoing ischemia. Leukocytosis and bandemia are also concerning for a perforated viscus. C Abdominal series radiographs include an upright chest and supine and upright abdominal radiographs and can diagnose free air, volvulus (both cecal and sigmoid), acute colonic pseudoobstruction, and constipation. Adjunctive imaging with computed tomography (CT) scan is often used, which can help diagnose the point of obstruction. Concerning findings include cecal diameter > 12 cm, pneumatosis, and massive diffuse colonic dilation with thickening. which can be seen in toxic megacolon. A CT scan may show a concerning area of obstruction with no definitive lesion; in these patients, contrast-enhanced enemas can aid in diagnosis. D Patients will often present with hypovolemia from fluid sequestration and electrolyte abnormalities. These should be corrected, and fluid resuscitation should be done with a balanced salt solution. Antibiotics should be initiated for infectious etiologies and patients with concern for perforation or shock. E All causes of mechanical obstruction must be ruled out before attributing the obstruction to a functional cause. Exacerbations of inflammatory bowel disease and diverticulitis can present both as a functional obstruction and as a mechanical obstruction. Clinical deterioration, peritonitis, and clinical signs of perforation can occur at virtually every step of the work-up for all conditions. If this occurs, patients should undergo emergent surgical treatment. F The extent of resection and decision for reconstruction is often determined intraoperatively and is dependent on the patient’s clinical status; the status of the colon, including thickening, caliber, and contamination; and concern for further ischemia. Primary anastomosis is widely accepted in the properly selected patient. Diverting ileostomy can provide anastomotic protection in tenuous cases. G Management of patients with pneumatosis can be difficult. Radiographic findings of pneumatosis without peritonitis, acidemia, or free air can be observed with close surgical follow-up.

Benign causes include recent colonoscopy, chemotherapy, and malignancy. There is a low threshold for surgical investigation and intervention. H Colo-colonic intussusception is a rare entity but is associated with a lead point in 90% of cases. Most commonly, the lead point is adenocarcinoma. Patients with spontaneous reduction and resolution of symptoms should undergo colonoscopy. I

Patients with malignant large bowel obstructions can be treated initially with endoscopic stenting as either a bridge to surgical resection or for palliation. Stents for left-sided obstruction are widely accepted; however, there is debate over the utility of stenting right-sided lesions because they are believed to have a higher failure rate and are more difficult to place. Stenting of obstructions 5 cm from the dentate is relatively contraindicated because it can lead to tenesmus and pain. Distal lesions can be palliated or temporized with a loop colostomy in patients who are not candidates for oncologic resection. Right-sided lesions can be treated with right hemicolectomy. J

Inflammatory bowel disease can cause both functional and mechanical obstructions. Acute exacerbations usually lead to functional obstructions in the acute setting. This can lead to toxic megacolon and perforation requiring emergent surgery. Patients with acute exacerbations should be made NPO and treated medically with immunomodulating medications. Recurrent exacerbations can lead to colonic obstruction via stricture formation. Colon strictures occur in approximately 10% of patients with Crohn’s disease. K Acute exacerbations of diverticulitis can often present with pain, bloating, fever, and leukocytosis. Initial medical management with NPO, intravenous (IV) fluids, and the appropriate use of antibiotics allows for resolution in most patients. Complicated disease or patients with a nonresolving clinical course should be considered for surgical resection of the affected segment of colon. L Acute colonic pseudo-obstruction is a colonic ileus characterized by acute colonic dilation, typically in hospitalized or institutionalized patients. Initial management should be conservative and consist of NPO, nasogastric (NG) decompression, optimization of volume and electrolytes, treatment of underlying disease process, minimization of narcotics, serial abdominal examinations, serial abdominal radiographs, and ambulation. It is imperative to rule out distal obstruction before attempts at decompression. This can usually be done with a CT scan with rectal and IV contrast. Cecal diameter greater than 12 cm is concerning for impending perforation. M Nonsurgical detorsion can be done via multiple modalities, including rigid sigmoidoscopy, flexible sigmoidoscopy, or colonoscopy. Leaving a rectal tube to prevent recurrence is controversial. N Debilitated patients with viable bowel may benefit from cecopexy or a cecostomy; however, recurrence rates are as high as 28%. Right hemicolectomy is the preferred treatment in patients who can tolerate an operation. As in sigmoid volvulus, if necrotic bowel is encountered upon entry, detorsion of the volvulus is contraindicated.

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Chapter 69  ◆  Large Bowel Obstruction  200.e1

Abstract

Keywords

Large bowel obstructions can be caused by multiple disease processes, both intrinsic and extrinsic to the bowel. This algorithm covers this vast array of etiologies and the surgical management of large bowel obstructions.

large bowel obstruction colonic obstruction pseudo-obstruction

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A

D

NPO/NGT Volume resuscitation Electrolyte replacement Appropriate antibiotics

B

Abdominal series X-ray CT scan Contrast enema

C

Labs and imaging CBC and differential Metabolic panel Hemoccult Lactate Base deficit

Large bowel obstruction

History and physical examination Distention/constipation Nausea/vomiting Pain/peritonitis Hematochezia Fever/sepsis/shock Narcotic use Antibiotic use Electrolyte abnormalities Surgical history Previous colonoscopic findings

Functional

Mechanical

E

J

Medical therapy

Fecal impaction

U

Surgical decompression

Colonic inertia

S

Pelvic floor dysfunction

Medical therapy

Neostigmine challenge Q Colonoscopic decompression

Anorectal manometry Colonic transit studies

P

Manual disimpaction

Endoscopic dilation

T

See colorectal cancer

Surgical resection

Medical treatment

Nonresolution Stricture Fistula H/o abscess/peforation Immunocompromised

Colonoscopy

O

Surgical resection vs. diversion

Endoscopic biopsy +/– stent

Acute colonic pseudo-obstruction

L

Constipation

Diverticulitis

K

Inflammatory bowel disease

Mass

I

R Operative intervention

Surgical resection

Surgical resection vs. Cecopexy/cecostomy

N

Nonsurgical detorsion

Cecal volvulus/bascule

Sigmoid volvulus

M

Recurrent/chronic symptoms Nonresolution

Intussusception

H

Reduction and surgical correction

Hernia

Emergent surgical treatment Peritonitis Ischemia Shock F Toxic megacolon Free air Pneumatosis G

V

Subtotal colectomy

Botulinum toxin

Surgical resection

Chapter 69  ◆  Large Bowel Obstruction  201

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202  Part V  ◆  Alimentary Tract O Newly diagnosed colonic strictures must be evaluated for underlying malignancy because the incidence of colon cancer in Crohn’s disease ranges from 2% to 7%. P Severe refractory constipation can be further evaluated by colonic transit studies. Anorectal manometry can be used to assess pelvic floor dysfunction. Q Patients who fail initial management or have increasing distention on abdominal radiographs should undergo a neostigmine challenge. This must be done in a monitored setting because of the risks of bradycardia. R If necrotic bowel is encountered upon entry, detorsion of the volvulus is contraindicated. Options for surgical resection are based on the clinical status of the patient. In debilitated or hemodynamically unstable patients, a Hartmann’s procedure should be done. Stable patients are candidates for sigmoidectomy with primary anastomosis. S Botulinum toxin injected into the puborectalis muscle can be used to treat pelvic floor dysfunction. Patients with severe disabling symptoms, slow colonic transit, and no pelvic floor dysfunction are candidates for subtotal colectomy with ileorectal anastomosis. T Endoscopic dilation is widely used for colonic strictures in inflammatory bowel disease. Repeated dilations can be done. Strictures less than 4 cm are associated with better surgery-free long-term outcomes. Segmental surgical resection is reserved for those patients who have failed all other modalities.

U Medical therapy is the mainstay of treatment in patients with constipation. Dietary modification, minimization of narcotics and constipating medications, and the use of bulkforming laxatives are sufficient to treat most cases. Biofeedback behavioral modifications can also be used in patients with pelvic floor dysfunction. Refractory constipation can be treated with more aggressive pharmacotherapy. V In the absence of perforation, surgery should be reserved for those patients who have failed multiple rounds of decompression, either with neostigmine or serial colonoscopies. Surgical options include cecostomy tube placement and subtotal colectomy. REFERENCES Guzman AR, Wehkamp J, Kirschniak A. Endoscopic balloon dilation of Crohn’s-associated intestinal strictures: high patient satisfaction and long-term efficacy. United European Gastroenterol J. 2016;4(6): 794–799. Ho LM, Paulson EK, Thompson WM. Pneumatosis intestinalis in the adult: benign to life-threatening causes. AJR Am J Roentgenol. 2007;188: 1604–1613. Honjo H, Mike M, Kusanagi H, Kano N. Adult intussusception: a retrospective review. World J Surg. 2015;39(1):134–138. Kim EJ, Yoon JK. Stents for colorectal obstruction: past, present, and future. World J Gastroenterol. 2016;22(2):842–852. Liu LW. Chronic constipation: current treatment options. Can J Gastroenterol. 2011;25(B):22B–28B. Maloney N, Vargas HD. Acute intestinal pseudo-obstruction (Ogilvie’s syndrome). Clin Colon Rectal Surg. 2005;18(2):96–101. Mills S, Stamos MJ. Colonic Crohn’s disease. Clin Colon Rectal Surg. 2007;20(4):309–313.

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Chapter

70 

RECTAL PROLAPSE Susan L. Gearhart, MD, MEHP

A Rectal prolapse affects less than 1% of the population, and the frequency is higher in women and in the elderly. Risk factors include multiparity, constipation/straining, and psychiatric comorbidities. Common symptoms at presentation include bleeding (~100%), fecal incontinence (~50% to 75%), constipation (~25%), and urinary incontinence (~40%). On examination, external full-thickness rectal prolapse is diagnosed by the presentation of the entire circular circumference of the rectum protruding through the anal verge. Prolapse generally is reproduced with straining, but on occasion, the prolapse can be nonreducible. In this case, one should consider a more urgent intervention to prevent damage to the rectum or the anal sphincter muscles. One technique for reducing a prolapse is to sprinkle sugar on the prolapsed mucosa and apply a gentle squeeze to remove the edema from the rectum, allowing it to be reduced. B Because rectal prolapse is more common in the elderly, thorough preoperative evaluation with a comprehensive geriatric assessment (CGA) should be considered in the frail. Common conditions that can be associated with rectal prolapse include anemia, hypothyroidism, liver failure with ascites, and malnutrition. If possible, the patient should be optimized. However, recent reports have indicated that frail patients do well with interventions to correct their rectal prolapse. If a patient is found to be anemic and has not had a recent colonoscopy, this should be performed with attention to the rectosigmoid. Solitary rectal ulcers can be found in the anterior rectum in 10% to 15% of patients with prolapse. C Symptoms of fecal incontinence in patients with rectal prolapse are thought to be secondary to the increase in rectal pressure as a result of the rectal intussusception in combination with weakened sphincter muscles. Anorectal manometry (ARM) with pudendal nerve testing can be performed and provides prognostic significance. Up to 80% of patients with fecal incontinence and rectal prolapse will have improvement in their symptoms of incontinence once the prolapse is fixed. However, the presence of prolonged pudendal nerve latency is seen more commonly in patients who do not achieve improvements in their incontinence symptoms. D Pelvic organ prolapse (POP) is defined as the descent of the anterior or posterior vaginal wall, uterus, cervix, or apex of the vagina (s/p hysterectomy) toward the vaginal introitus (hymen). There are four stages indicating the amount or prolapse seen. If POP is observed on examination of the patient with rectal prolapse, additional imaging and a referral to urogynecology should be considered. Magnetic resonance (MR) defecography will often demonstrate disorders of the anterior compartment, which may be addressed at the same time as the rectal prolapse. The finding of POP is associated with higher rates of recurrence after surgery for rectal prolapse.

E Constipation is a common condition contributing to rectal prolapse, and efforts should be made to improve these symptoms before repair, or postoperative straining may lead to early recurrence of the prolapse. Dietary modifications with an increase in water and fiber consumption are a common intervention that can improve constipation. A referral to gastroenterology should also be considered. Anorectal manometry (ARM) may identify the pattern of obstructed defecation syndrome (ODS). If ODS is found, a referral for pelvic floor physical therapy should be made either before surgery or after surgery depending on the severity of the prolapse. F The surgical approach to rectal prolapse in patients with fecal incontinence favors the abdominal approach. Recent reports have indicated that there is less improvement in symptoms of fecal incontinence with the perineal approach. Common abdominal approaches for rectal prolapse and fecal incontinence include the robotic or laparoscopic ventral rectopexy (R/LVR) with mesh or a posterior dissection. The use of robotic or laparoscopic techniques has shown equivalent outcomes. R/LVP is associated with a 60% to 80% improvement in fecal incontinence symptoms and a recurrence rate of 15% at 10 years. Posterior repair with suture rectopexy alone is associated with an increased risk for recurrence (30% at 10 years). Although resection of the redundant sigmoid colon combined with a posterior dissection improves long-term recurrence rates, there is an association with increased postoperative symptoms of fecal incontinence. Because of the notable improvements in symptoms of fecal incontinence, an isolated procedure for fecal incontinence should not be performed at the same time as the prolapse is repaired. If symptoms of incontinence persist after repair, placement of sacral neurostimulator is associated with significant improvements in symptoms of fecal incontinence and quality of life. G The perineal approach to rectal prolapse that is most commonly performed is the Altemeier procedure. This procedure involves a full-thickness resection of the prolapsed rectum and a coloanal anastomosis. However, recurrence rates can be as high as 30% at 2 years. If a levatorplasty is performed, recurrence rates are lower (20%). This procedure is generally reserved for frail elderly patients with limited mobility and a short life expectancy. A second perineal procedure, the Delorme procedure, is appropriate for patients with a short segment (90%), with relatively low recurrence. Surgeons treating pilonidal disease clearly have a number of options within their armamentarium. In the setting of an acute abscess, a simple incision and drainage off-midline is the most reasonable option. For complex or recurrent disease, a more sophisticated approach is in order. The reality is that there is little direct comparative data comparing complex procedures for the disease. Reported outcomes likely reflect patient selection and technical precision more than an inherent benefit of one procedure over another. Furthermore, long-term follow-up data suggest that overall recurrence rates after primary and secondary surgery have been significantly underestimated across all procedures, with the actual number being closer to 22%. Until randomized controlled studies follow patients out beyond 5 years, the “ideal” management will be unclear. Sound decision making and the ability to master three or four surgical techniques far outweigh any of the imperfect data that exist to support one procedure over another.

REFERENCES Armstrong JH, Barcia PJ. Pilonidal sinus disease. The conservative approach. Arch Surg. 1994;129:914–917. Bolandparvaz S, Moghadam DP, Salahi R, et al. Evaluation of the risk factors of pilonidal sinus: a single center experience. Turk J Gastroenterol. 2012;23:535–537. Can MF, Sevinc MM, Hancerliogullari O, et al. Multicenter prospective randomized trial comparing modified Limberg flap transposition and Karydakis flap reconstruction in patients with sacrococcygeal pilonidal disease. Am J Surg. 2010;200:318–327. Can MF, Sevinc MM, Yilmaz M. Comparison of Karydakis flap reconstruction versus primary midline closure in sacrococcygeal pilonidal disease: results of 200 military service members. Surg Today. 2009;39:580–586. Dogru O, Camci C, Aygen E, et al. Pilonidal sinus treated with crystallized phenol: an eight-year experience. Dis Colon Rectum. 2004;47:1934–1938. Doll D, Matevossian E, Wietelmann K, et al. Family history of pilonidal sinus predisposes to earlier onset of disease and a 50% long-term recurrence rate. Dis Colon Rectum. 2009;52:1610–1615. Ghnnam WM, Hafez DM. Laser hair removal as adjunct to surgery for pilonidal sinus: our initial experience. J Cutan Aesthet Surg. 2011;4: 192–195. Lorant T, Ribbe I, Mahteme H, et al. Sinus excision and primary closure versus laying open in pilonidal disease: a prospective randomized trial. Dis Colon Rectum. 2011;54:300–305. Milone M, Musella M, Di Sardo Spiezio A, et al. Video-assisted ablation of pilonidal sinus: a new minimally invasive treatment—a pilot study. Surgery. 2014;155:562–566. Nursal TZ, Ezer A, Calişkan K, et al. Prospective randomized controlled trial comparing v-y advancement flap with primary suture methods in pilonidal disease. Am J Surg. 2010;199:170–177.

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Chapter

76 

ANAL FISSURE Patrick T. Hangge, MD, and Tonia M. Young-Fadok, MD, MS, FACS, FASCRS

A An anal fissure is a disruption of the sensate anoderm lining the distal anal canal. This very common condition may occur after a large, hard bowel movement or, conversely, may be associated with a bout of diarrhea. Most fissures are acute, heal within several days, and never come to medical attention. Increased resting anal pressure, attributed to spasm of the internal sphincter, may result in chronic anal fissure. The condition is frequently attributed to hemorrhoids by both patients and primary care providers. The hallmark symptom is pain during and after defecation. The pain may last minutes with acute fissures but hours in the chronic setting, leading to avoidance of defecation. Rectal bleeding is common, typically consisting of small quantities of red blood noted on the toilet tissue (“wipe bleeding”). B The typical patient is a young adult, and both genders are equally affected. The history suggests the diagnosis (i.e., pain and bleeding with defecation), which is confirmed by physical examination. The key for a successful examination is slow, gentle distraction of the perianal skin by opposing traction with the thumbs. The vast majority of fissures will be in the posterior midline (25% of women have anterior fissures compared with 8% of men, and 3% of patients have both anterior and posterior fissures). A sentinel skin tag at the anal verge is an additional clue. Once the fissure is seen, instrumentation should be avoided because any attempt at digital examination or endoscopy is painful and not well tolerated. Such elements of the physical examination can be performed when the fissure has healed. Further tests, such as colonoscopy to evaluate bleeding, should also be deferred until the symptoms have resolved. When the diagnosis is in doubt because of pain precluding an adequate evaluation, examination under anesthesia will rule out an occult perianal abscess. C An acute anal fissure has been present for less than 8 weeks and has the appearance of a simple tear of the distal anoderm. Acute fissures usually heal with standard conservative measures (see F). D A chronic anal fissure may show heaping of the fissure edges, granulation tissue, and exposed fibers of the internal anal sphincter (IAS) muscle. A sentinel skin tag is often present at the distal end of the fissure, and a hypertrophied anal papilla may be seen at the proximal point. E Fissures that are off the midline, are multiple, or are painless, and those that fail to heal, require further evaluation. These should be examined under anesthesia with biopsies and cultures because this presentation may exist with Crohn’s disease, anal carcinoma, lymphoma, HIV or AIDS, tuberculosis, syphilis, or melanoma.

F Almost half of patients with acute fissures heal with no intervention or respond to increased oral fluid intake, fiber supplementation, stool softeners, Sitz baths, and topical analgesics. Sitz baths plus bulking agents, with or without topical anesthetics, plus use of 2% hydrocortisone, result in approximately 85% healing of acute fissures. G Pharmacologic intervention is aimed at reduction of sphincter tone, without the permanent dysfunction that can result from surgical approaches. H Lateral internal sphincterotomy (LIS) is associated with healing rates of 95% to 100% and confirmed by multiple randomized trials to be superior to conservative therapy. A majority of patients retain continence and preserve their quality of life after LIS. Therefore it is appropriate to proceed directly to LIS if pain is severe or intolerable, even without confirmed failure of pharmacologic treatment. Lateral sphincterotomy is performed to avoid the potential “keyhole deformity” associated with midline sphincterotomy—a groove that allows the loss of flatus or liquid stool. Reported rates of incontinence vary widely from 8% to 30%, probably reflecting the greater extent of IAS division in older studies plus subtle yet clinically unimportant changes that may be detected on questionnaires. LIS corresponding to the length of the fissure, as compared with traditional LIS extending to the dentate line, results in equivalent-to-worse healing rates with less incontinence (grade 2B). Anal dilation is condemned. Almost no studies are standardized, and there is a high risk for dilation causing incontinence. I

Although many acute fissures heal spontaneously, some become chronic. Ambulatory manometry in the latter group has demonstrated sustained resting hypertonia with rare episodes of spontaneous IAS relaxation. Cadaveric studies show a reduction of vascularity in the normal posterior midline of the anal canal in 85% of individuals. Anodermal perfusion is dependent on arterioles that cross the IAS, so high anal pressures may reduce perfusion pressure to the posterior midline and prevent healing. J

Nitric oxide is the primary nonadrenergic, noncholinergic neurotransmitter in the IAS and results in IAS relaxation. Exogenous nitrates release nitric oxide. Topical 0.2% glyceryl trinitrate or nitroglycerin (GTN) results in decreased anal pressure and can be used as first-line therapy in the treatment of anal fissure (grade 1A). Randomized trials show healing rates of 50% to 70% but recurrence rates near 50%. Headache is the most common side effect in half to two-thirds of patients. In a randomized trial, GTN resulted in healing in less than 30% compared with 90% of patients undergoing LIS. K Increased cellular calcium levels mediate contraction of the IAS, so calcium channel blockers (CCBs) reduce IAS tone. Nifedipine gel (0.2%) and diltiazem gel (2%) result in healing of 65% to 95% of chronic anal fissures in randomized trials. Results of topical therapy with calcium channel blockers are similar to those of topical nitrates, without the side effect of headaches, and this approach can be used as first-line therapy (grade 1A). L Botulinum toxin (BT) prevents nerve impulses by inhibiting acetylcholine release from presynaptic nerve terminals. BT has similar results to topical therapies as a first-line treatment,

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Chapter 76  ◆  Anal Fissure  224.e1

Abstract

Keywords

An anal fissure is a disruption of the anoderm. It causes pain with bowel movements and usually occurs in the young adults. They can be classified as acute, chronic and atypical. Most heal without intervention. Pharmacologic intervention is aimed at reduction of sphincter tone. Lateral internal sphincterotomy leads to healing in 95-100%.

anal fissure lateral internal sphincterotomy nitroglycerin nifedipine botulinum

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Chapter 76  ◆  Anal Fissure  225

F Conservative therapy History A Duration Pain with BM Wipe bleeding

D ANAL FISSURE

Chronic

E Atypical

I Chronic fissure

J

C Acute

Heal

G Pharmacologic therapy

H

Nitroglycerin

K

Heal

Repeat M pharmacologic therapy

Nifedipine

L

Botulinum toxin

Lateral internal sphincterotomy

Physical examination B Inspection EUA Defer endoscopy until healed

Fail

N

Good tone

LIS

Poor tone

Advancement flap

O

and small retrospective studies have demonstrated modest improvement in healing for BT use as second-line therapy (grade 1C). Recent meta-analyses and randomized controlled studies also show equivalent healing rates among BT and topical therapies, ranging widely from 18% to 71%. Published techniques usually involve injection on either side of the fissure, directly into the internal sphincter or in the intersphincteric space. Commonly, 20 to 60 units are injected, although anywhere from 10 to 100 units have been used in the literature.

O In patients with fissures who also have low sphincter tone (e.g., elderly patients, postpartum women, inflammatory bowel disease [IBD] patients, or patients with prior anorectal operations), LIS is not recommended because of increased risk for incontinence. In these cases, an anal or rectal advancement flap can aid healing. Success with rotational, V-Y, and island flaps has been described.

M Randomized trials of GTN, CCB, and BT have suggested further healing in patients who have been given an additional trial of therapy. Further pharmacologic therapy may thus be justified if patients have mild to moderate symptoms only and wish to avoid operative intervention.

Berry SM, Barish CF, Bhandari R, et al. Nitroglycerin 0.4% ointment vs placebo in the treatment of pain resulting from chronic anal fissure: a randomized, double-blind, placebo-controlled study. BMC Gastroenterol. 2013;13:106. Cross KLR, Massey EJD, Fowler AL, Monson JRT. The management of anal fissure: ACPGBI position statement. Colorectal Dis. 2008;10:1–7. Hananel N, Gordon PH. Re-examination of clinical manifestations and response to therapy of fissure-in-ano. Dis Colon Rectum. 1997;40:229–233. Nelson R. Non-surgical therapy for anal fissure. Cochrane Database Syst Rev. 2006;(4):CD003431. Sajid MS, Whitehouse PA, Sains P, Baig MK. Systematic review of the use of topical diltiazem compared with glyceryltrinitrate for the nonoperative management of chronic anal fissure. Colorectal Dis. 2013;15:19–26. Stewart DB Sr, Gaertner W, Glasgow S, et al. Clinical practice guideline for the management of anal fissures. Dis Colon Rectum. 2017;60:7–14.

N LIS is the procedure of choice in chronic fissure patients without any underlying fecal incontinence (grade 1A). In this select group, surgery may be offered with or without documented failure of pharmacologic therapy. A thorough discussion of the potential, albeit small, risk for altered continence after LIS is warranted preoperatively.

REFERENCES

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Chapter

77 

GROIN HERNIA Alexander P. Nagle, MD, and Kenric M. Murayama, MD A The history often includes an intermittent bulge and/or a dull sensation in the groin. The symptoms are often worse with heavy lifting, straining, or exercise. A history of heavy lifting is important, in both the planning for postoperative disability and the consideration for long-term recurrence rates. The history should also include questions about chronic coughing, straining to defecate, and difficulties with urination. These symptoms may reveal an underlying pathology (benign prostatic hyperplasia [BPH] or prostate, colon, and lung cancer). Preoperative urinary dysfunction also indicates an increased risk for postoperative urinary retention. The examination consists of observing the groin area for evidence of a bulge while the patient coughs. This is repeated with the examiner’s index finger invaginated into the external ring—palpation of a bulge or a significant pressure impulse denotes a hernia. If the hernia is incarcerated, the physical examination should note any signs of strangulation, such as fever, tenderness, and erythema. B Of groin hernias, 97% are inguinal, and 3% are femoral. The male-to-female ratio is 9 : 1. The most common type of inguinal hernia is an indirect hernia in both sexes. Femoral hernias are more common in women. Inguinal hernias are bilateral in 20% of cases. The lifetime risk for developing an inguinal hernia is about 10%. Groin hernias have a pronounced adverse economic impact, considering the cost of the operation and hospital stay plus the incapacity and lost working hours. C In patients who report symptoms but do not have a palpable defect, an ultrasound may be helpful. An ultrasound of the inguinal area with the patient in the supine and upright positions, and with the Valsalva maneuver, has a reported diagnostic sensitivity and specificity of greater than 90%. However, ultrasound is highly operator dependent. D Symptomatic reducible hernias should undergo elective repair. Traditionally, the risk for incarceration was thought to be high; thus, even patients with minimal symptoms had repair to prevent hernia complications. However, several randomized clinical trials comparing elective repair to watchful waiting found a very low risk for incarceration. Long-term results show that a high number of initially minimally symptomatic patients develop symptoms over time and have repair. Thus most patients should have elective repair unless the surgical risk is high. E If the patient has an incarcerated inguinal hernia and strangulation is not suspected, an attempt at reduction by using sedation, Trendelenburg’s positioning, and gentle sustained pressure over the groin mass is appropriate. Vigorous repetitive attempts at reducing an incarcerated hernia are ill advised and may produce “reduction en masse,” wherein the entire hernia sac and its contents are reduced so that even though the external bulge is gone, the incarceration within the sac remains. If there

are any indications of strangulation (fever, erythema, pain, leukocytosis, bowel obstruction, or peritonitis), reduction should not be attempted. F A strangulated hernia implies that the vascular supply to the contents of the hernia is compromised. A strangulated inguinal hernia is a surgical emergency. The patient should be prepared with intravenous (IV) hydration, a nasogastric tube, correction of electrolytes, and IV antibiotics. G Most elective inguinal hernia repairs can be done on an outpatient basis. Recurrence rates for groin hernias range from 1% to 10%. With the many techniques available, treatment should be individualized. Excellent results with very low recurrence rates have been reported for both open and laparoscopic techniques. There has been a trend toward using prosthetic mesh because of the “tension-free” nature of the repair. Although there is controversy regarding laparoscopic repair for unilateral, newly diagnosed hernias, it seems ideally suited for recurrent and/or bilateral hernias. Recurrent hernias repaired without mesh have a higher rate of recurrence; therefore, these cases are best managed using mesh, either via an open or a laparoscopic approach. H When operating for an incarcerated or possible strangulated hernia, most surgeons would use the standard anterior inguinal incision. The hernia sac is dissected and then opened under direct vision. It is important to control the base of the hernia sac to prevent dropping of the contents into the abdominal cavity before adequate inspection. If necessary, it may be possible to do a bowel resection and anastomosis through the inguinal incision. There should be a low threshold to convert to a midline incision if the bowel cannot be adequately inspected. If the bowel is ischemic or a bowel resection is performed, mesh should not be used because of the high risk for infection. If the defect is too large to close primarily, then a piece of absorbable or biological (small intestine submucosa) mesh may be used to repair the hernia defect. An alternative technique is an open preperitoneal (posterior) approach. This has the advantage of being able to convert to a laparotomy without a separate incision. I

Laparoscopic inguinal herniorrhaphy has the following potential advantages: (1) less postoperative pain, (2) reduced recovery time, (3) easier repair of a recurrent hernia because the repair is performed in a tissue plane that has not been dissected previously, (4) the ability to treat bilateral hernias, (5) the performance of a simultaneous diagnostic laparoscopy, and (6) improved cosmesis. The earlier return to full activity is an important socioeconomic factor because the decrease in the time away from work could potentially offset the higher operative costs. The laparoscopic repair might have a lower recurrence rate because of the mechanical advantage gained by placing the mesh on the “inside” of the abdominal wall musculature. The main arguments against laparoscopic inguinal hernia are that (1) conventional inguinal hernia repair is an effective operation performed as an outpatient procedure with low morbidity and mortality, (2) it requires general anesthesia, (3) it is more expensive, and (4) it requires mesh. Some abdominal incisions or treatments (prostatectomy, prostate external radiation therapy [XRT]) preclude adequate or safe laparoscopic dissection. The type of laparoscopic approach—transabdominal preperitoneal (TAPP) or totally extraperitoneal (TEP)—depends mainly on the surgeon’s preference and level of experience.

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Chapter 77  ◆  Groin Hernia  226.e1

Abstract

Keywords

Inguinal (groin) hernias are one of the most common operations done and the addition of the laparoscopic approach has expanded options for patients. A rational approach to repair choices is critical in providing patients with the best treatment options and with consideration of the status of the hernia at the time of surgery.

inguinal hernia groin hernia management and repair of groin hernias

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Chapter 77  ◆  Groin Hernia  227 J

The TAPP approach involves a transperitoneal approach to the inguinal region. The peritoneum is incised, and a peritoneal flap is created. Once the preperitoneal space is entered, the dissection and conduct of the operation are similar to the TEP. After the mesh is placed, it is then covered by the peritoneal flap. The disadvantage of a TAPP is that it requires entrance into the peritoneal cavity and exposes the patient to potential intraabdominal injury and late adhesion formation. K The TEP repair stays completely extraperitoneal. A specialized balloon is passed along the posterior rectus sheath down to the pubis symphysis. The balloon is then used to dissect the preperitoneal space, exposing the entire myopectineal orifice. The cord is skeletonized, the hernia sac is reduced, and mesh is used to cover the defect. Medially, the mesh is tacked to Cooper’s ligament. Laterally, the mesh is tacked to the lateral aspect of the transversus abdominis aponeurosis and to the iliopubic tract. Tacks should not be placed below the lateral iliopubic tract to avoid injury to the genitofemoral and the lateral femoral cutaneous nerves. The other anatomic landmark of great importance is the “triangle of doom.” This triangle is bordered laterally by the spermatic vessels and medially by the vas deferens; located within this triangle are the external iliac artery and vein and the femoral nerve. L The open anterior approach is still the gold standard against which other techniques must be measured. Most hernias can be treated by using local anesthesia in an outpatient setting at a low cost. Excellent results with very low recurrence rates have been reported for both primary repairs without mesh and for repairs using mesh. The advantage of a mesh repair is that it provides a tension-free repair. In cases of a large defect, attenuated tissue, or recurrence, a mesh repair is favorable. Although there has been a trend toward an increased use of mesh, there

is a slight risk for mesh erosion and infection, which must be considered. M The open preperitoneal (posterior) approach has been advocated by Nyhus and Stoppa. For unilateral hernias, it uses a horizontal skin incision in the right or left lower quadrant above the traditional incision used for an anterior repair. For bilateral hernias, a subumbilical midline or Pfannenstiel incision is used. The preperitoneal space is created, and the entire myopectineal orifice is exposed. Direct, indirect, and femoral hernias can all be repaired via this approach. Modifications using prosthetic material have become more popular, particularly for recurrent or bilateral hernias. The Stoppa technique uses a giant prosthetic mesh that extends far beyond the myopectineal orifice and envelops the visceral sac. In cases of recurrent or re-recurrent hernia, this approach avoids dissection in scar tissue. N Excellent results have been reported for hernias repaired primarily (without mesh). The technique involves opening the external oblique and freeing the spermatic cord. The hernia sac is dissected and usually ligated. Common repairs include the Bassini, the McVay, and the Shouldice. The Bassini repair and its modifications are accomplished by suturing the conjoined tendon of the transversus abdominis and the internal oblique muscles to Poupart’s ligament. The McVay repair pulls the floor of the inguinal canal laterally and attaches it to Cooper’s ligament under the inguinal ligament. The Shouldice repair uses a multilayer, imbricated repair of the inguinal canal floor with running sutures. O Many surgeons routinely use mesh in an effort to reduce tension and recurrence. The mesh incites the formation of scar tissue to further increase tensile strength beyond that provided by the mesh alone. The Lichtenstein repair uses a segment of

History and physical examination Bulge Palpable mass Pain Fever A Erythema

D Reducible

J I Laparoscopic repair

TAPP

K TEP

G Elective surgical repair

N L

B Inguinal hernia

E

Urgent repair

Incarcerated

H Emergent repair

C

Lab CBC U/S

No mesh

Anterior

O

Open repair

Mesh

M Posterior

F Strangulated

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228  Part V  ◆  Alimentary Tract prosthetic mesh sutured medially to the pubic tubercle, inferiorly to Poupart’s ligament, and superiorly to the conjoined tendon. Laterally the mesh is split and wrapped around the spermatic cord, and the tails are sutured together. The use of the mesh “plug” as described by Rutkow has gained popularity because it is relatively simple and fast, and it requires only minimal dissection. The mesh plug is placed in the internal ring or onto the inguinal floor and secured with interrupted sutures. A second piece of mesh is placed on the inguinal canal from the pubic tubercle to above the internal ring. The onlay mesh may or may not be secured with sutures. The onlay mesh is intended to strengthen the direct space in an indirect repair and the area of the internal ring in a direct repair. The onlay piece of mesh is

meant to serve as a form of prophylaxis against future herniation by creating further tissue ingrowth. REFERENCES Felix EL, Michas CAA, Gonzalez MH. Laparoscopic hernioplasty: TAPP vs TEP. Surg Endosc. 1995;9:984–989. Fitzgibbons RJ Jr, Camps J, Cornet DA, et al. Laparoscopic inguinal herniorrhaphy: result of a multicenter trial. Ann Surg. 1995;221:3–13. Lichtenstein IL, et al. The tension-free hernioplasty. Am J Surg. 1989;157: 188. Phillips EH, Arregui M, Carroll BJ, et al. Incidence of complications following laparoscopic hernioplasty. Surg Endosc. 1995;9:16–21. Stoppa RE. The preperitoneal approach and prosthetic repair of groin hernias. In: Nyhus LM, Condon RE, eds. Hernia. 4th ed. Philadelphia: JB Lippincott; 1995:188–206.

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Chapter

78 

VENTRAL HERNIA Paul Nobert Montero, MD, FACS, and Krzysztof Wikiel, MD

A Ventral hernia occurs in up to 20% of laparotomy incisions or can occur primarily (mostly in the epigastrium). Variables, including approach, materials, and patient factors, result in a dearth of data to guide optimal repair, particularly given the time-dependent endpoints of recurrence or infection. Surgeon preference of technique and materials guide the surgical approach, which must be individualized to the patient. B Indications for emergent ventral hernia repair include incarceration with obstruction, strangulation (incarcerated tissue with ischemia), or extreme/unrelenting pain. Minimally invasive surgical (MIS) approaches for emergent hernia repair are gaining favor among surgeons with the appropriate skill set, particularly for hernias with incarcerated omentum. Associated bowel obstruction is a relative contraindication for an MIS approach. C Elective ventral hernia repair allows for preoperative optimization. Key aspects of optimization include glucose control (Hgb A1c < 8, preferably < 7.3), tobacco cessation (>4 weeks), and weight loss in patients with obesity (body mass index [BMI] < 40, preferably < 35 but individualized to patient and defect size). D A clean case involves no contamination, including concomitant procedures such as cholecystectomy. E Contamination can result from violation of the gastrointestinal (GI) tract, infection present at the time of operation, stoma status, or a break in sterility. F The minimally invasive approach to ventral hernia repair, which includes standard laparoscopic or robotic-assisted techniques, offers several advantages, including shorter hospital stay, decreased infection, and reduced overall complication rate. Recurrence rates are comparable. However, the laparoscopic approach may result in a higher incidence of seroma formation, requires a barrier mesh and associated fixation, and is often unable to restore functional abdominal wall anatomy (recreation of linea alba). Robotic repair facilitates fascial re-approximation and affords the ability to fixate mesh in a potentially less painful manner. Additionally, the hernia sac can often be removed

robotically, seroma incidence may be decreased, and a preperitoneal, non-barrier mesh placement is feasible with a robotic approach. Generally, MIS techniques are better applied in smaller defects ( 5 cm, with a serum bilirubin < 3 mg/dL. Other options are systemic chemotherapy, percutaneous ethanol injections, and microwave ablation. O Systemic therapy, including chemotherapy, had been largely abandoned in the management of HCC because of its limited effectiveness. In 2008 a multicenter phase III double-blind randomized controlled trial demonstrated that sorafenib, an oral multikinase VEGF inhibitor, conferred a 3-month survival advantage to patients with advanced HCC. It is increasingly widely used, often in conjunction with other liver-targeted therapies.

Presentation and Risk Factors

L

B Viral hepatitis C Ethnicity

Other risk factors

Screening

D No

F

A Hepatocellular Carcinoma

Staging

K

Not Transplant Candidate Co-morbid factors > 4 lesions Gross vascular invasion LN (+) or Metastasis

V

Workup

E

Presentation

U

Yes Resection candidate

O

Systemic Therapy

P

EtOH Injection

Q

RFA Single lesion < 5 cm Child’s A/B

R N

S T

Resection Non-Cirrhotic/ Child’s A No metastasis

Microwave Ablation TACE Multi-focal > 5 cm Child’s A/B/C Bili < 3 90 Yttrium

No Transplant candidate

M Diagnosis Ultrasound

G

CT scan or MRI Tumor markers Nuclear imaging

H I J

Palliative Care

Yes

Liver Transplant Evaluation Milan Criteria: 1 lesion < 5 cm 3 lesions < 3 cm No gross vascular invasion No metastasis

LDLT Suitable donor

Z

W

Liver Transplant DDLT MELD score UNOS wait list

X

Y Bridge therapy RFA/TACE/ 90Yttrium/EtOH

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250  Part VI  ◆ Oncology P Injection of 99.5% ethanol (ETOH) into an HCC of less than 5 cm in diameter by either a percutaneous or open operative approach leads to the ablation of tumor foci in many cases. Despite its low-side-effect profile and reported effectiveness, the recurrence rate at 5 years is greater than 80%. Multiple treatments are usually required because of the tumor’s propensity for recurrence. Q RFA involves ultrasound-guided placement of an electrode into the center of a tumor by an open operative, laparoscopic, or percutaneous technique. The electrode is connected to a radiofrequency generator that heats the probe and results in coagulative necrosis of the tumor. Candidates for RFA include Child’s A or B patients with a solitary lesion < 5 cm. RFA can be used as primary therapy in cirrhotic patients who are not candidates for resection or as bridging therapy in patients who are awaiting transplantation. R Microwave ablation causes local tissue hyperthermia by dielectric hysteresis. It is gaining in popularity because of some studies that show increased efficacy and shorter ablation times compared with RFA. S Various embolization techniques have been undertaken for the treatment of HCC using polyvinyl-chloride alcohol particles, gelatin particles, ivalon, Gelfoam, or Lipiodol, either alone or in combination with chemotherapeutic agents (cisplatin, Adriamycin, or mitomycin-C). Embolization acts by causing ischemic necrosis of the tumor. Drug-eluting beads TACE provides the advantage of occluding the feeding vessel while doxorubicin is being progressively released. Chemoembolization can be used as neoadjuvant therapy to downsize tumor burden prior to resection, as a palliative treatment in patients with unresectable lesions, or as bridge therapy in patients awaiting transplantation. It is now considered the standard of care of patients with intermediate-stage HCC without vascular invasion or metastases and is especially useful for large and multifocal disease. Its use is limited by liver function, and there is a risk for liver failure if employed when bilirubin levels exceed 3 mg/dL. T Selective internal radiation therapy with 90-Yttrium microspheres involves the injection of radiation microspheres into the hepatic artery and has shown reasonable objective response rates, with a decrease in both serum tumor markers and tumor burden on CT scan. This form of radiation is better tolerated by nontumorous tissue than traditional external beam radiotherapy. Repeated treatments can be given to residual or recurrent tumors in patients with nonresectable HCC. Objective response is measured by following serum AFP levels and serial CT findings. U Prior to liver resection for HCC, routine preoperative evaluation includes serum AFP determination, liver function tests (alanine aminotransferase [ALT], aspartate transaminase [AST], total bilirubin, prothrombin time [PT], partial thromboplastin time [PTT]), cross-sectional imaging of the abdomen, and appropriate cardiac and pulmonary clearance. Evaluation of the functional liver remnant must be considered to avoid small-for-size syndrome and liver failure postoperatively. Methods such as the galactose tolerance and indocyanine green (ICG) tests can be employed, and preoperative adjuncts such as portal vein embolization can be considered.

V The ideal candidate for resection is a non-cirrhotic or Child’s A patient with a single lesion and no metastasis. The Makuuchi selection criteria rely on ascites, serum bilirubin, and ICG retention rate to determine candidacy for liver resection for HCC, and patients are considered good candidates if they have no ascites and a serum bilirubin of ≤ 2 mg/dL.15 Unfortunately, only 10% to 37% of patients with HCC are eligible to undergo resection at the time of diagnosis.16 Overall, improved outcomes have been observed in cases of single and small tumors, absence of vascular invasion, absence of cirrhosis, negative node involvement, absence of metastases, negative resection margins, and fibrolamellar types. In high-volume centers, the 90-day mortality of liver resections is expected to be less than 4%.17 Surgical resection of HCC has reported 5-year survival rates of 50% to 70%, although recurrence rates at 5 years are reported at around 70%.18 It is well documented that the greatest risk factor for the development of a second HCC in the liver is a previous diagnosis of HCC. Data suggest that this risk is up to 40% at 2 years for patients with a single initial lesion. Other advances in liver resection for HCC include the increased use of minimally invasive techniques, including laparoscopy and robotics, which have been reported to have good results. W Living-donor liver transplantation (LDLT) is also an alternative for patients with HCC in the setting of cirrhosis. LDLT was first offered in Asia, where cadaver liver donation is rare, but LDLT has gained acceptance in the United States and is offered by many transplant centers. There was a suggestion at one time that the recurrence rates of HCC were higher after LDLT compared with deceased-donor liver transplantation (DDLT), but this has been largely disproven. X In February 2002, the Model for End-Stage Liver Disease (MELD) scoring system was implemented in the United States to allocate the scarce liver organ donors. The MELD system ranks patients with cirrhosis based on their risk for death. The MELD priority score (6 to 40 points) is calculated from a formula that takes into account serum total bilirubin, international normalized ratio (INR), and serum creatinine. Recognizing that early-stage HCC patients have a limited window to receive a potentially curative liver transplant, additional MELD priority points are assigned to patients with stage II HCC (28 points), which currently occurs 6 months after listing. The United Network of Organ Sharing (UNOS) has also adopted the Milan criteria to determine transplantation candidacy for HCC patients. Y A variety of nonsurgical therapies can be employed in the neoadjuvant setting for patients awaiting DDLT and are colloquially known as bridge therapies. RFA, TACE, 90-Yttrium, and ETOH injection can all be used once the patient is placed on the UNOS list with an initial MELD score to slow disease progression and compensate for the increased waiting time. These therapies have been used to help maintain eligibility for those transplant candidates with progressive disease and have also been used to downstage patients who initially present with HCC tumors outside of Milan criteria. Patients who are downstaged and then transplanted do not appear to have worse outcomes than those who are transplanted upfront. Z Liver transplantation for HCC results in 1- and 5-year survival rates ranging from 42% to 71% and from 20% to 45%, respectively, which are comparable to those for patients

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Chapter 83  ◆  Hepatocellular Carcinoma  251 transplanted without malignancy. Improved outcomes have been reported with incidentally discovered HCC and fibrolamellar variants. Despite this, prolonged waiting times and the lack of readily available organs have led to the progression of tumors to the extent that many potential recipients become noneligible candidates for transplantation. REFERENCES Andreou A, Vauthey JN, Cherqui D, et al. Improved long-term survival after major resection for hepatocellular carcinoma: a multicenter analysis based on a new definition of major hepatectomy. J Gastrointest Surg. 2013;17(1): 66–77. Bellissimo F, Pinzone MR, Cacopardo B, Nunnari G. Diagnostic and therapeutic management of hepatocellular carcinoma. World J Gastroenterol. 2015;21(42):12003–12021.

Bruix J, Reig M, Sherman M. Evidence-based diagnosis, staging, and treatment of patients with hepatocellular carcinoma. Gastroenterology. 2016;150(4):835–853. Dageforde LA, Fowler KJ, Chapman WC. Liver transplantation for hepatocellular carcinoma: current update on treatment and allocation. Curr Opin Organ Transplant. 2017;22:128–134. Heckman JT, Devera MB, Marsh JW, et al. Bridging locoregional therapy for hepatocellular carcinoma prior to liver transplantation. Ann Surg Oncol. 2008;15:3169–3177. Llovet JM, Ricci S, Mazzaferro V, et al. Sorafenib in advanced hepatocellular carcinoma. N Engl J Med. 2008;359(4):378–390. Reddy SK, Steel JL, Chen HW, et al. Outcomes of curative treatment for hepatocellular cancer in nonalcoholic steatohepatitis versus hepatitis C and alcoholic liver disease. Hepatology. 2012;55:1809–1819. Tohme S, Geller DA, Cardinal JS, et al. Radiofrequency ablation compared to resection in early-stage hepatocellular carcinoma. HPB (Oxford). 2013;15:210–217.

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Chapter

84 

GALLBLADDER CARCINOMA Aaron Lewis, MD, and Yuman Fong, MD

A Gallbladder cancer (GBC) is an uncommon cancer, with fewer than 5000 cases diagnosed each year in the United States. The incidence varies significantly by regions in the world, with the highest incidence found in the indigenous populations of the Andes Mountains, northeastern Europeans, and Israelis. It oftentimes is an incurable disease with a poor prognosis because of the frequently late presentation. Systemic therapies, generally speaking, are ineffective. When appropriate, surgery may be efficacious in treating localized disease. B Risk factors for GBC include gallstones, porcelain gallbladder, gallbladder polyps, primary sclerosing cholangitis, chronic infections, congenital biliary atresia, anatomic variations of the pancreatobiliary ducts, medications, obesity, diabetes, and exposure to carcinogens. Cholelithiasis occurs in 75% to 90% of patients with gallbladder cancer in comparison to a 0.3% to 3% incidence of gallstones in the general population; however, it is difficult to determine a true cause-and-effect relationship. Porcelain gallbladder is associated with calcification from longstanding inflammation. The risk for GBC is likely lower than historically thought, with more recent estimates of 10 ≤2 >2, ≤5 >5, ≤10 >10

None Very Low Low Moderate None Moderate High High

None Low Moderate High High High High High

None Low Insufficient Data High Insufficient Data High Insufficient Data High

None Low Insufficient Data High High High Insufficient Data High

>5/50 per HPF

Adapted from the 2010 National Comprehensive Cancer Network. “Update on the Management of Patients with Gastrointestinal Stromal Tumors.”

Surveillance

A

F

Clinical presentation, history and physical

Localized

G

K

I Pathology review and risk stratification

Surgery Re-image

H D Pathology review, molecular marker determination

GIST

B

J

Neoadjuvent therapy

E

Adjuvant therapy

Staging

K Surveillance

Not a GIST

C Workup, imaging, endoscopy and/or biopsy

Follow appropriate treatment for diagnosis

Recurrence or evidence of metastatic disease

L

Metastatic

Tyrosine kinase inhibitors (TKIs)

M

Re-image

Resectable Determine Selective resectability resection Not resectable Continue medical management

J

Adjuvant therapy is recommended for patients with high-risk tumor features (high mitotic index and larger, nongastric tumors). Several large studies have demonstrated a significant improvement in recurrence-free survival for patients treated with adjuvant imatinib. Patients without mutations that would be targeted by imatinib (wild-type) do not appear to have the same benefit from imatinib, but other tyrosine kinase inhibitors such as sunitinib may have more promise. Adjuvant treatment with imatinib for 3 years was associated with a relapse-free survival and overall survival advantage in a randomized trial compared with 1 year of therapy in high-risk patients, and therefore the

current recommendations are 3 years of treatment in this group. In the low-risk group, risk–benefit analysis suggests that adjuvant therapy should not be used. K The optimal surveillance schedules are not known. For high-risk patients, some institutions follow their patients with an abdominal CT scan or magnetic resonance imaging (MRI) every 3 to 6 months for 3 years during adjuvant therapy. Upon cessation of adjuvant therapy, these patients are then followed every 3 to 6 months for 2 years, then every 6 months until 5 years from the end of adjuvant therapy, and finally annually

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258  Part VI  ◆ Oncology thereafter. For low-risk patients, the usefulness of a routine follow-up is not known. Very low-risk patients likely do not require routine follow-up. L Metastatic disease and tumor recurrence are indications for therapy with imatinib or other tyrosine kinase inhibitors. If the initial work-up shows metastatic disease, imatinib is the first choice of therapy, with re-staging and possible surgical resection in the future. However, in some situations, upfront surgical intervention may be indicated, such as hollow organ perforation, intraabdominal hemorrhage, or obstruction secondary to tumor. In the case of recurrent tumors, the location, size, and symptoms will determine the course of action. Similar to a primary tumor, if the tumor is localized, primary surgical resection may be indicated. However, if the disease is diffuse, medical therapy should be initiated, with possible selected resection at a later date depending on the tumor response and patient symptoms. M If a patient is undergoing imatinib therapy for recurrent or metastatic disease, reimaging is performed to determine response to therapy. Some retrospective data have suggested that select patients with focal progression may benefit from selective debulking of drug-resistant areas. If patients have global imatinib

resistance, increasing doses or different tyrosine kinase inhibitors may be used. In other cases, palliative operations to treat the symptoms of the tumor (perforation, bleeding, or obstruction) may be undertaken. REFERENCES Bamboat ZM, Dematteo RP. Updates on the management of gastrointestinal stromal tumors. Surg Oncol Clin N Am. 2012;21(2):301–316. Chok AY, Goh BKP, Koh YX, et al. Validation of the MSKCC gastrointestinal stromal tumor nomogram and comparison with other prognostication systems: single-institution experience with 289 patients. Ann Surg Oncol. 2015;22(11):3597–3605. Demetri GD, et al. NCCN task force report: update on the management of patients with gastrointestinal stromal tumors. J Natl Compr Canc Netw. 2010;8(S2):S1–S41. Joensuu H, DeMatteo RP. The management of gastrointestinal stromal tumors: a model for targeted and multidisciplinary therapy of malignancy. Annu Rev Med. 2012;63:247–258. Joensuu H, Eriksson M, Sundby Hall K, et al. One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. JAMA. 2012;307:1265–1272. Raut CP, Posner M, Desai J, et al. Surgical management of advanced gastrointestinal stromal tumors after treatment with targeted systemic therapy using kinase inhibitors. J Clin Oncol. 2006;24(15):2325– 2331. The ESMO/European Sarcoma Network Working Group. Gastrointestinal stromal tumours: ESMO clinical practice guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2014;25(suppl 3):Iii21–ii26.

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Chapter

86 

PANCREATIC NEUROENDOCRINE TUMORS Robert J. Torphy, MD, and Barish H. Edil, MD A Pancreatic neuroendocrine tumors (pNETs) are unique in their ability to secrete biologically active gastrointestinal hormones, resulting in distinct clinical syndromes associated with the production of insulin, gastrin, vasoactive intestinal peptide (VIP), glucagon, or somatostatin. However, the large majority (50% to 75%) of pNETs are nonfunctional. pNETs can also be characterized by their sporadic or syndromal presentation. Although most pNETs are sporadic, several inherited disorders predispose patients to developing pNETs, including multiple endocrine neoplasia type 1 (MEN1), Von Hippel–Lindau disease (VHL), neurofibromatosis 1 (NF1), and tuberous sclerosis (TS). With these syndromes, the lifetime incidence of pNET is 80% to 100% in MEN1, 20% in VHL, 10% in NF1, and about 1% in TS. It is important to understand and recognize these unique presentations to help guide the patient toward the appropriate genetic counseling. Furthermore, these tumors tend to behave more indolently, and a syndromic presentation may affect further work-up and management. B pNETs are rare neoplasms arising from pluripotent pancreatic stems cells. These neoplasms represent only 1% to 2% of pancreatic neoplasms, with an incidence in population studies of less than 1 per 100,000 persons per year and a prevalence in autopsy studies ranging from 0.8% to 10%. pNETs typically present in three ways: upon work-up of a clinical syndrome associated with a functional tumor, after presenting with symptoms of mass effect, or identified incidentally on imaging. A thorough history and physical examination is an important first step to stratify patients by their likelihood of having a functional or nonfunctional pNET and to determine if they have a family history suspicious for a syndromic presentation. C The most common functional pNET is an insulinoma, representing 30% to 45% of pNETs. These tumors secrete insulin and present with symptomatic hypoglycemia. Biochemical evaluation for insulinomas is targeted at identifying the Whipple triad: hypoglycemic symptoms during fasting or activity, low glucose levels (200 pg/mL above baseline). Importantly, these tests should not be performed while a patient is on a proton pump inhibitor. E VIPomas ( 5 to 10 cm, abutment of neurovascular structures or joint/ bone), radiation therapy should be considered as an adjunct to radical limb-sparing resection, with the goal of improving local disease control. When considering radiation, it is important to weigh the following factors: (1) risk for local recurrence (highest in non-lipomatous histology, positive/close margin, high grade,

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Chapter 106  ◆  Soft Tissue Masses of the Extremities  322.e1

Abstract

Keywords

Optimal management of extremity soft tissue masses requires an understanding of soft tissue sarcoma biology. The goal of the clinical evaluation is to discern local signs and symptoms concerning for malignancy as well as any relevant predisposing factors. Further evaluation proceeds based on the degree of suspicion of malignancy. Small masses without concerning clinical features are likely benign and can be observed. Masses that are larger than 5 cm, symptomatic, or growing warrant further investigation with a biopsy and imaging to establish key tumor factors (i.e., histologic subtype, grade, size, proximity to critical structures) that predict outcome and determine management. Radical resection versus multimodal or nonoperative treatment is dictated by anatomic and biologic resectability. Details of a systematic approach are described herein.

sarcoma desmoid liposarcoma leiomyosarcoma myxofibrosarcoma

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Chapter 106  ◆  Soft Tissue Masses of the Extremities  323 TABLE 106.1  Common benign and malignant soft tissue neoplasms Clinical Behavior

Histologic Subtype

Cell of Origin

Benign

Desmoid fibromatosis Atypical lipomatous tumor Liposarcoma (round cell, pleomorphic, dedifferentiated, myxoid subtypes) Undifferentiated pleomorphic sarcoma Synovial sarcoma Myxofibrosarcoma Leiomyosarcoma Fibrosarcoma Malignant peripheral nerve sheath tumor Solitary fibrous tumor Rhabdomyosarcoma Angiosarcoma Epithelioid sarcoma Ewing sarcoma

Fibroblast/myofibroblast Adipocyte Adipocyte Unknown Unknown Fibroblast/myofibroblast Smooth muscle Fibroblast Schwann/perineurium Fibroblast/myofibroblast Skeletal muscle Endothelial Unknown Primitive neuroectoderm

Malignant

A History: • Local symptoms (pain, neuropathy, swelling) • Rapid growth • Predisposing or non-neoplastic condition

Physical exam: • Size • Site (depth/mobility, proximity to joint, neurovascular structures) • Distal neurovascular status • Consistency • Signs of predisposing or non-neoplastic condition

Observe (remove if symptoms)

D

5 cm, suspicion of neoplasm

C Benign or malignant?

• CXR Malignant

MRI

Low

Resectability

Extremity soft tissue mass

Observe

Grade

B

older age, size > 5 cm); (2) estimated benefit of radiation (10% to 20% absolute risk reduction of local recurrence); (3) toxicity of radiation (joint fibrosis, edema, two-fold incidence of wound complications in lower extremity if given preoperatively); (4) salvage options (e.g., additional surgery) if tumor recurs locally.

High • Chest CT • Histologyspecific imaging

High-Risk Biology Systemic chemotherapy should be considered in addition to resection for a localized extremity sarcoma at high risk for occult metastatic disease (i.e., large size > 5 to 10 cm, high grade, high-risk histology, including Ewing sarcoma, angiosarcoma,

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324  Part VI  ◆ Oncology undifferentiated pleomorphic sarcoma, synovial sarcoma, and round cell or pleomorphic liposarcoma). Common regimens include Adriamycin plus ifosfamide and gemcitabine plus docetaxel. In a large meta-analysis, adjuvant chemotherapy was associated with a modest 6% survival benefit. Nomograms based on tumor grade, subtype, size, and age can be used to identify patients at high risk for sarcoma-specific death who may benefit from adjuvant chemotherapy. For an extremity sarcoma with oligometastatic disease amenable to resection, the recommended management includes resection of both the primary tumor and metastases, with consideration of neoadjuvant or adjuvant chemotherapy based on histology-specific risk for recurrence and response to chemotherapy. Predictors of increased survival in this setting include longer time to first metastasis, lower number of metastases, no extrapulmonary disease, histologic subtype (e.g., leiomyosarcoma), primary tumor size < 10 cm, and minimally invasive resection.

Unresectable Irresectability is defined by anatomic, biological, and patientspecific factors. For localized tumors invading critical neurovascular structures that are not amenable to limb-sparing resection, treatment options include nonoperative treatment (i.e., systemic chemotherapy and/or radiation followed by reassessment of resectability), amputation, or consideration of regional chemotherapy with TNF-alpha– and melphalan-based isolated limb perfusion, which is associated with over 80% limb salvage but currently only available in Europe. Numerous or multifocal metastases

with short disease-free interval or synchronous presentation of metastatic and primary disease portend poor survival and minimal chance for cure. Such tumors should be managed nonoperatively with systemic chemotherapy, possible radiation, and scheduled multidisciplinary reassessment. In the setting of marked tumor response, palliative resection can be considered to prolong disease control. Finally, severe patient comorbidities or poor functional status may warrant nonoperative management and ongoing multidisciplinary reassessment. REFERENCES Brennan MF, Antonescu CR, Alektiar KM. Management of Soft Tissue Sarcoma. 2nd ed. S.l.: Springer International Publishing; 2016. Cahlon O, Brennan MF, Jia X, et al. A postoperative nomogram for local recurrence risk in extremity soft tissue sarcomas after limb-sparing surgery without adjuvant radiation. Ann Surg. 2012;255(2):343–347. Chudgar NP, Brennan MF, Munhoz RR, et al. Pulmonary metastasectomy with therapeutic intent for soft-tissue sarcoma. J Thorac Cardiovasc Surg. 2017;154(1):319–330. Crago AM, Denton B, Salas S, et al. A prognostic nomogram for prediction of recurrence in desmoid fibromatosis. Ann Surg. 2013;258(2):347–353. Kattan MW, Leung DH, Brennan MF. Postoperative nomogram for 12-year sarcoma-specific death. J Clin Oncol. 2002;20(3):791–796. O’Sullivan B, Davis AM, Turcotte R, et al. Preoperative versus postoperative radiotherapy in soft-tissue sarcoma of the limbs: a randomised trial. Lancet. 2002;359(9325):2235–2241. Pervaiz N, Colterjohn N, Farrokhyar F, et al. A systematic meta-analysis of randomized controlled trials of adjuvant chemotherapy for localized resectable soft-tissue sarcoma. Cancer. 2008;113(3):573–581. Pisters PW, Harrison LB, Leung DH, et al. Long-term results of a prospective randomized trial of adjuvant brachytherapy in soft tissue sarcoma. J Clin Oncol. 1996;14(3):859–868.

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Chapter

107 

should only be considered if the cytologic diagnosis is questionable.

CUTANEOUS MELANOMA

H Stage IV melanoma has historically had a poor prognosis, especially those with multiple distant metastases. However, survival rates have dramatically improved with the new targeted agents and immunotherapy anti-PD-1 and CTLA-4 inhibitors.

Charles M. Balch, MD, and Rene Gonzalez, MD

I

A The risk for developing melanoma increases with a family history of the disease, excess sun exposure, and a change in the size or appearance of a skin lesion. Pigmented skin changes are evaluated by the ABCDE system for asymmetry, irregular border, variegation of color, diameter ≥ 6 mm, and elevation. B Routine studies such as complete blood count (CBC), chest radiograph, and liver function tests (LFTs) are performed routinely but are of unproven value. An elevated LDH is of prognostic value for metastases. Imaging studies are helpful only if distant metastatic disease is suspected. C Early detection and treatment of primary melanoma improve prognosis. Lesions ≤ 1 cm diameter should be excised for biopsy. Incisional biopsy is used only for larger lesions, usually using a 6-mm punch biopsy instrument. Shave biopsy is discouraged when melanoma is suspected because prognosis and survival are closely linked to tumor thickness. Further, this full-thickness biopsy information is used to make recommendations for sentinel lymph node biopsy and for consideration of adjuvant therapy. D In patients who are clinically node negative, measuring tumor thickness and the presence or absence of surface ulceration are the most important predictive factors used for staging and decisions about surgical management. The American Joint Committee on Cancer (AJCC) melanoma staging (8th edition) was recently implemented and emphasizes tumor thickness, ulceration, whether the detection of nodal metastases was clinically evident or clinically occult (detected by the sentinel node biopsy), and the number of lymph node metastases. E Complete surgical excision is the cornerstone of surgical treatment. Current recommendations for adequate margins by the thickness of the lesion are as follows: 0.5 cm for melanoma in situ; 1.0 cm for 0.1- to 1-mm melanoma; 1 to 2 cm for 1- to 2-mm melanomas; and 2 cm for lesions > 2 mm thick. F A sentinel lymph node biopsy (SLNB) should be performed for all melanomas >1.00 mm thick and in some high-risk thin (T1b) melanomas. SLNB predicts the involvement of regional nodes with melanoma and correlates strongly with survival. It must be performed before the wide local excision (WLE) of the primary lesion. SLNB can be used with radionuclide lymphatic mapping to facilitate location of the sentinel node. If the sentinel node shows no evidence of disease, there is a less than 5% percent chance that any regional nodes contain melanoma. G A palpable regional lymph node should first be investigated with fine-needle aspiration (FNA) biopsy; an open biopsy

If the sentinel node does have metastases, a complete lymph node dissection is often considered for staging and regional disease control. However, a recent study did not demonstrate a survival benefit, although it showed improved regional disease control and added staging value. Patients with micrometastases (measuring less than 1 to 2 mm) can be considered for no further surgery with careful follow-up with serial ultrasound examination of their regional nodes. J

For patients presenting with larger-volume micrometastases after SLNB and for those presenting with clinically palpable metastases, a regional lymph node dissection is appropriate for staging and regional disease control. Limited node dissection is not indicated because of the risk for recurrent regional disease. K Occasionally, patients with a solitary metastasis may have a durable remission after surgical excision. Candidates for surgery may have skin, lymphatic, pulmonary, cerebral, or small bowel lesions. Stereotactic radiosurgery is useful palliation for cerebral metastases. Radiation therapy to bony metastases and masses causing vascular or neurologic compression or pain can also be palliative. Such patients should also be considered for targeted therapy or immunotherapy. L For systemic therapy in advanced disease, the two major options are immunotherapy (single-agent anti-PD-1 or combination ipilimumab + nivolumab) and, for patients with a BRAF mutation, also combination BRAF + MEK inhibition. The selection of treatment is based on the presence or absence of a BRAF mutation, performance status, comorbidities, the need for a rapid response, local experience, and other factors. The consensus among experts seems to be tilting toward immunotherapy. Talimogene laherparepvec is a genetically modified oncolytic viral therapy approved by the Food and Drug Administration (FDA) in 2015 for the local treatment of unresectable injectable lesions in patients with melanoma. However, its use has been overshadowed by the rapid progress of other systemic agents. M The checkpoint inhibitor anti-PD1 or a combination of BRAF and MEK inhibitors in patients with BRAF mutations have been approved as an adjuvant therapy for Stage III and resected Stage IV patients, with significant improvement in survival. N There is little evidence that follow-up improves outcome. However, this may be changing with the advent of effective systemic treatment. Examination includes palpation for local recurrence, in-transit metastases, and lymph nodes. The skin is inspected for new primaries and other skin cancers. A reasonable schedule for follow-up is every 3 to 4 months for 2 years, every 6 months for 3 years, and then yearly. A chest x-ray is obtained annually because the lungs are the most frequent site of visceral recurrence.

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Chapter 107  ◆  Cutaneous Melanoma  326.e1

Abstract

Keywords

The management of cutaneous melanoma is becoming more complex on the one hand, but decisions are now based more on evidence from clinical trials. The decision algorithm in this chapter is based on the results of contemporary clinical trials, the updated melanoma staging criteria and peer-reviewed melanoma guidelines from NCCN and ASCO. The availability of new systemic agents –both targeted therapies for patients with bRAF mutation metastases) and checkpoint inhibitors (anti-PD1, anti-PDL1 and anti-CTLA4 drugs) should be incorporated into the management of melanoma patients with both Stage III (as adjuvant therapy) and Stage IV melanoma.

melanoma surgical treatment lymphadenectomy targeted therapy immunotherapy

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Chapter 107  ◆  Cutaneous Melanoma  327

A History and Physical Family history Sun exposure Increasing size ABCDE system Regional Lymph nodes

E T 1.0 cm

M AUS/FLUS

N

Monitor Repeat FNA

Q

Molecular testing

SFN

O Suspicious

P

Tx

R

Malignant

O Cytologic features suspicious for papillary carcinoma include a highly cellular aspirate with scant colloid, papillary structures, cellular pleomorphism and overlapping, nuclear inclusion bodies, and intranuclear grooves. The risk for malignancy is 60% to 75%. Molecular testing is not done routinely and only if it would change surgical management. Atypical spindle-shaped cells on FNA should raise suspicion of medullary thyroid carcinoma (MTC). A calcitonin level should be obtained before thyroidectomy is undertaken. Patients with MTC require total thyroidectomy and central neck and ipsilateral modified neck dissection. Contralateral modified neck dissection may also be necessary.

multiple nodules, molecular testing, patient preference, family history of cancer, or history of radiation exposure. For patients with thyroid cancer > 4 cm, gross extrathyroidal extension, clinically apparent positive lymph nodes, or metastasis to distant sites, total thyroidectomy is the procedure of choice. A lobectomy is appropriate for patients with cancer of 1 to 4 cm, no extrathyroidal extension, and no apparent positive lymph nodes or distant metastasis. Therapeutic central neck dissection is performed for patients with clinically apparent node metastasis, and prophylactic dissection should be considered if the patient has an advanced primary tumor or is to have a therapeutic lateral node dissection.

P The rate of false-positive FNA of malignancy is as low as 1%. Patients should undergo surgery unless they are very high risk because of comorbidity or have a short life expectancy.

REFERENCES

Q Molecular testing is classified by use as a rule-out or rule-in test. Further molecular markers may influence surgical decision making. Performance of the specific test is influenced by the pretest probability of malignancy according to the Bethesda classification. A panel testing mRNA expression for 167 gene expression classifier (GEC) is used as a rule-out test because of a high negative predictive value (93%) in a prospective multicenter trial. However, the GEC has low specificity (45% to 50%), so it is unable to rule in cancer in indeterminate nodules. Mutational testing for a panel of gene mutations (BRAF RAS RET/PTC, PAX8/PPARg) is useful as a rule-in test with high specificity and positive predictive value. However, the test does not have the sensitivity to effectively rule out cancer. Next-generation sequencing may have better sensitivity. Nodules that have benign results on molecular testing should be monitored, whereas positive results would suggest thyroidectomy. R Thyroid lobectomy is the procedure of choice for a solitary nodule with indeterminate cytology. Total thyroidectomy may be appropriate based on sonographic high-risk features,

Alexander EK, Kennedy GC, Baloch ZW, et al. Preoperative diagnosis of benign thyroid nodules with indeterminate cytology. N Engl J Med. 2012;367:705–715. Carty SE, Cooper DS, Doherty GM, et al. Consensus statement on the terminology and classification of central neck dissection for thyroid cancer. Thyroid. 2009;19:1153–1158. Cibas ES, Ali SZ. The Bethesda system for reporting thyroid cytopathology. Thyroid. 2009;19:1159–1165. Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association management guidelines for adult patients with thyroid nodules and differentiated thyroid cancer: the American Thyroid Association guidelines task force on thyroid nodules and differentiated thyroid cancer. Thyroid. 2016;26:1–133. Nikiforov YE, Carty SE, Chiosea SI, et al. Highly accurate diagnosis of cancer in thyroid nodules with follicular neoplasm/suspicious for a follicular neoplasm cytology by thyroseq v2 next-generation sequencing assay. Cancer. 2014;120:3627–3634. Nishino M. Molecular cytopathology for thyroid nodules: a review of methodology and test performance. Cancer Cytopathol. 2016;124:14–27. Wells SA Jr, Asa SL, Dralle H, et al. Revised American Thyroid Association guidelines for the management of medullary thyroid carcinoma. Thyroid. 2015;25:567–610. Yeh MW, Bauer AJ, Bernet VA, et al. American Thyroid Association statement on preoperative imaging for thyroid cancer surgery. Thyroid. 2015;25:3–14. Yip L, Sosa JA. Molecular-directed treatment of differentiated thyroid cancer: advances in diagnosis and treatment. JAMA Surg. 2016;151: 663–670.

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Chapter

111 

WELLDIFFERENTIATED THYROID CANCER Josefina C. Farra, MD, and John I. Lew, MD A Thyroid nodules are commonly found among the general population. Palpable thyroid nodules are prevalent in approximately 5% of adults in the United States. Nonpalpable thyroid nodules can be detected by ultrasound (US) in 19% to 68% of the population. The clinical relevance of thyroid nodules is determined by the risk for malignancy. Between 7% and 15% of thyroid nodules have underlying malignancy discovered on final pathology after surgical excision. B Family history of thyroid cancer is a known risk factor for thyroid malignancy. There is a known association for increased risk for development of well-differentiated thyroid cancer (WDTC) in patients with a positive family history of thyroid cancer. Familial tumors may account for 5% to 15% of differentiated thyroid carcinoma. Having a first-degree relative with thyroid cancer has been associated with up to a 10-fold increase in risk. C History of significant radiation exposure increases the risk for thyroid cancer. The relationship between malignancy and nontherapeutic or childhood exposure to radiation has been well established. The risk for cancer increases proportionally with higher doses of radiation exposure, and excess risk persists for 30 years after exposure. Additionally, cancer risk decreases with increased age at exposure. D Thyroid ultrasound (US) should be performed in all patients with a suspected thyroid nodule. Additionally, cervical lymph nodes should be imaged. US can evaluate the general architecture of the thyroid gland and characterize all thyroid nodules. Nodule size is reported in three dimensions, and location within the thyroid gland is specified. Features of thyroid nodules are described: composition (solid, cystic, spongiform), echogenicity, margins, presence and type of calcifications, and shape. US features associated with increased risk for thyroid cancer include solid composition, hypoechogenicity, irregular margins, microcalcifications, and shape taller rather than wider. Presence or absence of these features can determine the risk for malignancy and, when considered with nodule size, can help determine the decision to proceed with fine-needle aspiration of a thyroid nodule. E Fine-needle aspiration (FNA) is performed in thyroid nodules ≥ 1 cm with intermediate- or high-suspicion ultrasonographic patterns. FNA cytology is reported using the Bethesda System for Reporting Thyroid Cytopathology (BSRTC), which defines six diagnostic categories, with an estimated risk for malignancy for each category: (i) nondiagnostic/unsatisfactory, (ii) benign, (iii) atypia of undetermined significance/follicular

lesion of undetermined significance (AUS/FLUS), (iv) follicular neoplasm/suspicious for follicular neoplasm (FN/SFN), (v) suspicious for malignancy, (vi) malignant. Molecular testing of FNA samples is used to aid in the diagnostic accuracy of indeterminate cytology (AUS/FLUS/FN) and to assist in planning the extent of thyroid surgery. F Cross-sectional imaging with a computed tomography (CT) scan of the neck is recommended for patients with clinical suspicion of advanced thyroid cancer to evaluate the extent of primary tumor invasion and lymph node involvement. G Appropriate history and evaluation should be undertaken to determine possible laryngeal nerve dysfunction and vocal cord paresis in the work-up of patients with thyroid cancer. Voice abnormalities or changes, dysphagia, airway symptoms, or prior operations in the neck or chest increase the risk for nerve injury. These patients should undergo a preoperative laryngeal examination to determine vocal cord function before undergoing thyroid surgery. H WDTC arises from thyroid follicular epithelial cells. WDTC includes papillary thyroid cancer, follicular thyroid cancer, and Hürthle cell cancer, which account for the majority of thyroid malignancies. Papillary thyroid cancer (PTC) makes up about 85% of cases. The main diagnostic features of PTC are its nuclear changes that include subtle irregularities in the nuclear contour and size, deep nuclear grooves, and pseudo-inclusions resulting from cytoplasmic invaginations. Follicular thyroid cancer (FTC) and Hürthle cell cancer (HCC) make up about 12% of cases. FTC is determined microscopically through the identification of capsular or vascular invasion. HCC is considered a subtype of FTC and is characterized by the presence of oncocytes rich in mitochondria (Hürthle cells). I

The operative approach for patients with known WDTC by FNA is determined by the size and clinical features of the thyroid cancer. Previously, patients with WDTC > 1 cm with or without evidence of locoregional spread underwent total thyroidectomy. Recent data have led to revised operative recommendations. Patients with thyroid cancer > 4 cm or any size thyroid cancer with gross extrathyroidal extension or clinically apparent metastasis to lymph nodes should undergo total thyroidectomy with central lymph node dissection. Patients with thyroid cancer > 1 cm and < 4 cm without extrathyroidal extension and clinically apparent lymph nodes may undergo either total thyroidectomy or thyroid lobectomy with isthmusectomy as the initial procedure (decision to be made by treatment team based on follow-up plan and patient preference). Patients with thyroid cancer < 1 cm without extrathyroidal extension and clinically apparent lymph nodes should undergo thyroid lobectomy with isthmusectomy. J

Any patient with biopsy-proven metastatic lateral cervical lymph nodes should undergo modified radical neck dissection, which includes removal of all ipsilateral cervical lymph node groups from levels II through V. The internal jugular vein, sternocleidomastoid muscle, and spinal accessory nerve are preserved. K Early postoperative surveillance and therapeutic management decisions are based on risk stratification for predicting the

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Chapter 111  ◆  Well-Differentiated Thyroid Cancer   336.e1

Abstract

Keywords

Thyroid nodules are commonly found among the general population. Between 7% and 15% of thyroid nodules have underlying malignancy discovered on final pathology after surgical excision. Thyroid ultrasound (US) should be performed in all patients with a suspected thyroid nodule. US features associated with increased risk for thyroid cancer include solid composition, hypoechogenicity, irregular margins, microcalcifications, and shape taller rather than wider. Fine-needle aspiration (FNA) is performed in thyroid nodules ≥ 1 cm with intermediate- or high-suspicion ultrasonographic patterns. The operative approach for patients with known well-differentiated thyroid cancer (WDTC) by FNA is determined by the size and clinical features of the thyroid cancer. Patients with thyroid cancer > 4 cm or any size thyroid cancer with gross extrathyroidal extension or clinically apparent metastasis to lymph nodes should undergo total thyroidectomy with central lymph node dissection. Patients with thyroid cancer > 1 cm and < 4 cm without extrathyroidal extension and clinically apparent lymph nodes may undergo either total thyroidectomy or thyroid lobectomy with isthmusectomy as the initial procedure (decision to be made by treatment team based on follow-up plan and patient preference). Patients with thyroid cancer < 1 cm without extrathyroidal extension and clinically apparent lymph nodes should undergo thyroid lobectomy with isthmusectomy.

well-differentiated thyroid cancer papillary thyroid cancer follicular thyroid cancer fine-needle aspiration

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Chapter 111  ◆  Well-Differentiated Thyroid Cancer   337 History and physical exam Thyroid nodule A Palpable lymph nodes Family history thyroid cancer Head/neck radiation history

B C

Operative approach Thyroid cancer >4 cm or any size with gross extrathyroidal extension or clinically apparent metastasis to lymph nodes

I Total thyroidectomy with central lymph node dissection

Any biopsy proven metastatic lateral cervical lymph nodes WELL-DIFFERENTIATED THYROID CANCER Papillary thyroid cancer Follicular thyroid cancer Hürthle cell cancer

H

J

ATA low risk

Modified radical neck dissection

K

Thyroid cancer >1 cm and 200 pg/mL. G Total thyroidectomy, central neck dissection, and dissection of the involved neck compartment are the treatments of choice for patients with a Ctn level < 500 pg/mL and evidence of lymph node involvement. Prophylactic contralateral lateral neck compartment dissection might be considered if the Ctn level is >200 pg/mL. H Imaging evaluation for distant metastatic disease should be obtained in patients with extensive neck disease and signs or symptoms of regional or distant metastases and in all patients with a serum Ctn level greater than 500 pg/mL. This should consist of a contrast computed tomography (CT) scan of the neck and chest, a three-phase contrast-enhanced multidetector CT or contrast-enhanced magnetic resonance imaging (MRI) of the liver, and bone scintigraphy and axial MRI to evaluate for bone metastases. I

No evidence of metastatic disease and a serum Ctn level greater than 500 pg/mL dictates a total thyroidectomy and central neck dissection. The management of the lateral neck is based on ultrasound results, and one should consider prophylactic contralateral or bilateral lateral neck compartment dissection in this group of patients. External beam radiotherapy (EBRT) to the neck should be considered if there is residual MTC, if extensive nodal disease was encountered, or if there was extension of MTC beyond the thyroid gland. J

Presence of metastatic disease mandates palliative surgery with the intent to improve symptoms and reduce tumor burden but preserve function (speech, swallowing, shoulder mobility, parathyroid function) and minimize morbidity. Regional disease can be treated with directed therapies such as EBRT, radiofrequency ablation (RFA), cryoablation, or embolization. In patients with significant tumor burden and/or disease progression, systemic agents such as tyrosine kinase inhibitors (vandetanib

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Chapter 112  ◆  Medullary Thyroid Carcinoma  338.e1

Abstract

Keyword

Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor that is derived from the parafollicular C-cells (calcitonin-producing cells) of the thyroid gland. It accounts for approximately 4% of all thyroid cancers in the United States. The majority of MTCs are sporadic, and about 25% are hereditary, as part of the multiple endocrine neoplasias (MEN2A or MEN2B) or familial MTC (FMTC). The only curative treatment for MTC, sporadic or hereditary, is complete surgical resection.

medullary thyroid cancer

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Chapter 112  ◆  Medullary Thyroid Carcinoma  339

A

No LN Neck US

History Family history Physical exam

Ctn < 500 pg/mL

C Serum Ctn Serum CEA Neck ultrasound

Yes LN Neck US

E

F

Total thyroidectomy + central neck dissection - Ctn > 20 pg/mL: +/– ipsilateral lateral neck dissection - Ctn > 200 pg/mL: +/– bilateral lateral neck dissection

G

Total thyroidectomy + central neck dissection + involved lateral neck dissection Ctn > 200 pg/mL: +/– bilateral lateral neck dissection

I Total thyroidectomy + central neck dissection + bilateral lateral neck dissection

H

MTC

Ctn > 500 pg/mL

Evaluation for distant mets: - CT neck and chest - Triple-phase contrastenhanced CT or MRI liver - Bone scintigraphy and axial MRI

J Thyroidectomy

FNA biopsy

D

B

DNA analysis

Evaluate for Pheo

Adrenalectomy first

Evaluate for HPT

Parathyroidectomy at time of thyroidectomy

RET positive

+/– EBRT to neck if: - Residual MTC - Extensive nodal disease - ETE

Treat regional disease Systemic therapy with TKI vs clinical trial

MTC (medullary thyroid cancer); FNA (fine needle aspiration); Ctn (calcitonin); CEA (carcinoembryonic antigen); LN (lymph nodes); US (ultrasound); mets (metastases); pheo (pheochromocytoma); HPT (hyperparathyroidism); TKI (tyrosine kinase inhibitors)

or cabozantinib) should be considered. These agents have been shown to provide high rates of disease control and improve progression-free survival. Cytotoxic chemotherapeutic agents are not recommended as first-line therapy because they have not been shown to be effective in treating MTC. REFERENCES Chen H, Sippel RS, O’Dorisio MS, et al. The North American Neuroendocrine Tumor Society consensus guideline for the diagnosis and management of neuroendocrine tumors: pheochromocytoma, paraganglioma, and medullary thyroid cancer. Pancreas. 2010;39(6): 775–783.

Hadoux J, Pacini F, Tuttle RM, et al. Management of advance medullary thyroid cancer. Lancet Diabetes Endocrinol. 2016;4:64–71. Kim BH, Kim IJ. Recent updates on the management of medullary thyroid carcinoma. Endocrinol Metab (Seoul). 2016;31(3):392–399. Konstantinidis A, Stang M, Roman SA, Sosa JA. Surgical management of medullary thyroid carcinoma. Updates Surg. 2017;69(2):151–160. Randle RW, Balentine CJ, Leverson GE, et al. Trends in the presentation, treatment, and survival of patients with medullary thyroid cancer over the past 30 years. Surgery. 2017;161(1):137–146. Wells SA, Asa SL, Dralle H, et al. Revised American Thyroid Association guidelines for the management of medullary thyroid carcinoma. Thyroid. 2015;25(6):567–610.

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Chapter

113 

HYPERCALCEMIA AND HYPERPARATHYROIDISM Oliver Fackelmayer, MD, and Christopher D. Raeburn, MD A The combination of an elevated or high normal calcium level and inappropriately elevated parathyroid hormone (PTH) level (on two separate occasions) confirms the diagnosis of primary hyperparathyroidism (PHPT). The advent of automated serum analyzers in the 1970s significantly increased the prevalence of PHPT because of increased recognition; however, an earlier diagnosis in most patients has decreased the incidence of severe complications. The incidence of PHPT increases with age, is 2 to 3 times higher in women compared with men, and is reported to be as high as 1% in postmenopausal women. Not all patients with PHPT require treatment. A thorough history and physical examination are important to determine whether operative or nonoperative management is most appropriate. B The diagnosis of hypercalcemia should be confirmed by either an ionized calcium or an albumin-corrected calcium level (corrected calcium = serum calcium + 0.8 [4.0 – albumin]). Once confirmed, hypercalcemia should be further evaluated with a PTH level. A low PTH level should prompt evaluation for other causes of hypercalcemia, such as malignancy, sarcoidosis/ granulomatous diseases, vitamin D intoxication, or multiple myeloma. A thorough history and physical will often reveal associated signs and symptoms suggestive of these other causes. If parathyroid function is normal, PTH levels should be suppressed as serum calcium levels increase. Thus a PTH level that is mid-normal to mildly elevated in the setting of hypercalcemia is inappropriate and usually indicates PHPT. However, in this scenario, a 24-hour urinary calcium and creatinine should be obtained to evaluate for familial hypocalciuric hypercalcemia (FHH). Normal or elevated urinary calcium levels confirm PHPT. If urinary calcium levels are less than 100 mg/24 hr or the calcium-to-creatinine clearance ratio is less than 0.01 (in the absence of thiazide diuretics and/or vitamin D deficiency), then genetic testing should be considered to exclude FHH because this rare entity requires no treatment. C Classic symptoms of PHPT are most commonly because of kidney stones or bone disease. Surgery is clearly indicated for PHPT patients with kidney stones (15% to 20%) or pathologic fractures from severe bone disease (5%). Parathyroid crisis (1% to 2%) is a much less common presentation of PHPT and typically is associated with severe central nervous system dysfunction because of severe hypercalcemia (>15 mg/dL). After medical correction of hypercalcemia (intravenous fluid, diuretics, bisphosphonates, calcitonin), surgery should be performed promptly.

D Most patients with PHPT do not have classic symptoms and are termed “asymptomatic.” Several organizations have published guidelines for the management of PHPT in asymptomatic patients. These guidelines recommend surgery for the presence of any one or more of the following criteria: (1) age less than 50, (2) serum calcium more than 1 mg/dL over the upper limit of normal, (3) creatinine clearance below 60, (4) osteoporosis (T-score < –2.5 on bone densitometry), (5) 24-hr urinary calcium over 400 mg, (6) radiographic imaging showing occult vertebral fracture or nephrolithiasis/nephrocalcinosis, (7) patient is unable/unwilling to undergo surveillance testing. E For patients who do not meet any of these criteria, the guidelines state that either surgery or surveillance is reasonable and safe. Although these guidelines are for the management of asymptomatic PHPT, myriad subjective symptoms are commonly attributed to PHPT, such as fatigue, weakness, musculoskeletal aches/pains, depressed/labile mood, abdominal pain, constipation, and trouble concentrating. Because of the subjectivity of these symptoms and variability in postoperative symptom resolution, the guidelines do not include them in the criteria for surgical indication. However, patients with many of these subjective symptoms but who do not meet guideline criteria may prefer surgery in hopes that their symptoms will improve after surgery. F A traditional parathyroidectomy entails a four-gland exploration and is still performed routinely by some experienced parathyroid surgeons; however, because a single parathyroid adenoma is the cause of PHPT in 80% to 85%, a focused or minimally invasive procedure is now commonly performed. This requires accurate preoperative imaging to localize the adenoma. It is important to understand that imaging has no utility in making the diagnosis of PHPT or in determining whether surgery is indicated. Preoperative imaging is used purely to facilitate the surgery, and patients with negative imaging are still can­ didates for surgery. Ultrasonography, technetium Tc99m sestamibi, and 4D CT scans are the most commonly used modalities; the accuracy of each varies widely between different institutions, but, on average, they have sensitivities of 70% to 90% and specificities of 90%. Many experts recommend ultrasound in all patients before parathyroidectomy because of its cost-effectiveness, lack of radiation exposure, and ability to detect concomitant thyroid pathology, which is present in up to 50% of PHPT patients. G Surgery is the only effective treatment of PHPT and is more cost-effective than surveillance or pharmacologic therapy. Although medical treatment with cinacalcet may decrease PTH and calcium values, it does not mitigate the end-organ effects of PHPT, is commonly associated with gastrointestinal (GI) side effects, is quite expensive, and is not indicated for patients who are surgical candidates. Surveillance testing for those patients with PHPT who do not undergo surgery should include annual serum calcium/creatinine and bone density assessment every 1 to 2 years. Patients should also be recommended to stay hydrated and avoid vitamin D deficiency. H Positive localization on preoperative imaging permits focused or minimally invasive parathyroidectomy. Rapid intraoperative PTH assay should be used to measure PTH at 10 minutes after removal of the adenoma. A decrease of 50% or more from baseline is consistent with cure. The success of this approach is

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Chapter 113  ◆  Hypercalcemia and Hyperparathyroidism  340.e1

Abstract

Keywords

Primary hyperparathyroidism (PHPT) is a common cause of hypercalcemia, and parathyroidectomy is clearly indicated for patients with classic symptoms. There are consensus guidelines to help guide the management of asymptomatic PHPT. Most patients with PHPT have a single adenoma that, if localized on preoperative imaging, can be removed by a minimally invasive parathyroidectomy using intraoperative parathyroid hormone (PTH) assay to confirm cure. A conventional four-gland exploration is used when the adenoma is not able to be localized preoperatively. Both procedures are safe and have a high success rate (95%).

hyperparathyroidism hypercalcemia parathyroidectomy

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Chapter 113  ◆  Hypercalcemia and Hyperparathyroidism  341 excellent (95% or more) and equivalent to traditional four-gland exploration. If the PTH does not decrease appropriately after removing an abnormal parathyroid, then a four-gland exploration is required because the patient likely has multi-glandular disease.

to avoid missing the second adenoma and resultant persistent PHPT.

In patients with primary HPT, 85% have a single adenoma, which, when excised, cures the patient. Routine biopsy of normal parathyroids and/or a frozen section of a typical parathyroid adenoma is unnecessary in most cases.

L Of parathyroids, 90% are located within 1 to 2 cm of the intersection of the recurrent laryngeal nerve and inferior thyroid artery, with the majority of superior glands being superior and posterior to this point and the inferior glands being inferior and anterior to this point. Superior glands are commonly found just deep to the visceral fascia but are rarely deep to the thyroid capsule itself. After incision of the visceral fascia, these glands can be easily identified and extruded. As a superior adenoma enlarges, it sometimes will descend down into the paraesophageal space. The location of the inferior parathyroids is more variable, but the majority can be found adhered to the inferior pole of the thyroid or in the superior aspect of the thyrothymic ligament. Less commonly, they can be in the mediastinal portion of the thymus, intrathyroidal, or undescended within the carotid sheath, usually near the carotid bifurcation. In the event that the fourth gland cannot be located, frozen-section confirmation of suspected parathyroids should be performed before closure.

K Double adenomas are not very common but increase in incidence with patient age. Either intraoperative PTH measurement or identification of all four parathyroids is required

M If all four parathyroids are enlarged (5% to 10%), a 3.5-gland excision should be performed. A remnant of approximately 25 mg can be left in situ if not devascularized. If the remnant

I

A traditional four-gland exploration is the procedure of choice for the 15% to 20% of patients in whom preoperative imaging fails to localize an abnormal gland or when an intraoperative PTH measurement is not available. This time-tested procedure has a high success rate (95%) and low complication rate and can still be performed via a small incision and on an outpatient basis. All four parathyroids must be identified and the abnormal gland(s) removed. When available, intraoperative PTH monitoring can be used to further confirm the success of the operation. J

A

H

History and physical examination Family history Fatigue Musculoskeletal pains Depressed/labile mood Abdominal pains/constipation Kidney stones Pathologic fractures

F Preoperative imaging

C

Classic symptoms

Hypercalcemia/primary hyperparathyroidism

Labs PTH/calcium x 2 Creatinine Vitamin D-25OH 24-hr urine calcium

B

D

Localized

Minimally invasive parathyroidectomy

Not localized

Bilateral neck exploration

Asymptomatic

Either surgery or observation both appropriate (patient choice)

3 normal (3%) Missing fourth 4 enlarged (5-10%) Supernumerary

Criteria not met

Excise adenoma

K L M N

G Surveillance testing Annual calcium and creatinine Bone density every 1-2 years

No

J

2 enlarged 2 normal (3-10%)

Consider consensus guidelines

Yes

I

1 enlarged 3 normal (85%)

Criteria met

E

Excise adenoma Appropriate PTH drop

Known familial

Excise adenomas Cervical thymectomy Explore carotid sheath Consider thyroid lobectomy Excise 3.5 glands 25 mg remnant Cervical thymectomy

MEN 1 MEN 2a

Parathyroid carcinoma (5 to 10 times upper limit of normal), and/or the parathyroid tumor is locally invasive to surrounding structures, in which case, en bloc resection of the tumor and surrounding structures should be performed. This should include the ipsilateral thyroid and central neck nodes and may require sacrifice of the recurrent nerve if involved. P Persistent postoperative hypercalcemia, or recurrence of hypercalcemia after parathyroidectomy, should be addressed

by first confirming the diagnosis. Before attempts at reoperation, the severity of disease should be graded to weigh against the risks of reoperation. All operative and pathology reports should be meticulously reviewed to delineate exactly which glands have been identified and/or excised. In cases of persistent/recurrent HPT, accurate localization of the abnormal parathyroid is paramount to reoperative success. Sestamibi scanning (preferably with I123 and SPECT imaging), CT neck and chest (preferably with “4D” contrast enhancement), and neck ultrasound may all be necessary; when possible, the abnormal gland should be localized by two different imaging modalities. In rare cases, parathyroid venous sampling by an experienced interventional radiologist may be necessary to localize the abnormal parathyroid. REFERENCES Ambrogini E, Cetani F, Cianferotti L, et al. Surgery or surveillance for mild asymptomatic primary hyperparathyroidism: a prospective, randomized clinical trial. J Clin Endocrinol Metab. 2007;92(8):3114–3121. [Epub 2007 May 29]. Khan AA, Hanley DA, Rizzoli R, et al. Primary hyperparathyroidism: review and recommendations on evaluation, diagnosis, and management. A Canadian and international consensus. Osteoporos Int. 2017;28(1):1–19. doi:10.1007/s00198-016-3716-2. [Epub 2016 Sep 9]. Silverberg SJ, Clarke BL, Peacock M, et al. Current issues in the presentation of asymptomatic primary hyperparathyroidism: Proceedings of the Fourth International Workshop. J Clin Endocrinol Metab. 2014;99(10): 3580–3594. doi:10.1210/jc.2014-1415. [Epub 2014 Aug 27]. Udelsman R, Åkerström G, Biagini C, et al. The surgical management of asymptomatic primary hyperparathyroidism: Proceedings of the Fourth International Workshop. J Clin Endocrinol Metab. 2014;99(10):3595–3606. doi:10.1210/jc.2014-2000. [Epub 2014 Aug 27]. Wilhelm SM, Wang TS, Ruan DT, et al. The American Association of Endocrine Surgeons guidelines for definitive management of primary hyperparathyroidism. JAMA Surg. 2016;151(10):959–968. doi:10.1001/ jamasurg.2016.2310.

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Chapter

114 

HYPOGLYCEMIA AND INSULINOMA Alan P. B. Dackiw, MD, PhD, MBA, FACS

A Insulinomas are the most common of the islet cell tumors but remain rare, having an incidence of approximately four cases per 1 million patient-years. Sixty percent of patients are female, the median age of presentation is in the fourth or fifth decade of life, and essentially all tumors are intrapancreatic. Approximately 90% are solitary, 6% are malignant, and 8% may be associated with multiple endocrine neoplasia syndrome type 1 syndrome (MEN1). Approximately 90% of patients are cured with initial surgery. Recurrence rates of up to 20% have been seen in MEN1 patients. Symptoms of hypoglycemia begin at plasma glucose levels of approximately 55 mg/dL, and the more specific symptoms of neurocognitive impairment begin at 50 mg/dL. The symptoms of hypoglycemia may be characterized as either autonomic, such as sweating, tremor, anxiety, palpitations, and nausea, or as neuroglycopenic, with confusion, dizziness, headache, and what may appear as stroke-like symptoms, with difficulty speaking and thinking. Symptoms are most often associated with fasting and exercise, often occurring early in the morning from fasting overnight. On occasion, symptoms may occur postprandially, although postprandial symptoms are more often suggestive of noninsulinoma pancreatogenous hyperinsulinemia syndrome (NIPHS). Symptoms of hypoglycemia associated with documented plasma glucose levels less than 50 mg/dL with relief of symptoms by the correction of the low glucose levels, often referred to as “Whipple’s triad,” necessitate further evaluation. It is also important to rule out other medical causes of hypoglycemia, including drugs, systemic disease (hepatic, renal, cardiac, sepsis), and autoimmune disease. Close consultation and multidisciplinary care with colleagues in medical endocrinology in the management of these patients in addition to diabetic patients who may experience hypoglycemia is of critical importance. A family history of endocrine neoplasia raises suspicion for MEN1. B It is an important principle that biochemical confirmation of disease be done before any imaging studies. Hyperinsulinism must be confirmed biochemically, and factitious hypoglycemia must be ruled out. The supervised 72-hour fast is the gold standard for diagnosis, although 72 hours is rarely necessary to make the diagnosis, with most patients developing symptoms in the first 24 to 48 hours. A positive fast consists of fasting hypoglycemia (plasma glucose < 45 mg/dL) and concomitant hyperinsulinemia. Plasma C-peptide levels (>200 pmol/L) and measured plasma proinsulin levels confirm endogenous hyperinsulinism versus a factitious cause. Assays for first- and secondgeneration plasma sulfonylureas are obtained at the completion of the fast, also ruling out a factitious cause. Insulin surrogates may also be measured at the conclusion of a fast because βOH butyrate levels will be low ( 2; atrophic gastritis, renal failure, postvagotomy, anti-secretory therapy with proton pump inhibitors [PPIs], and high-dose histamine H-2 receptor blockers) excludes ZES. Other causes of hypergastrinemia such as short bowel syndrome, gastric outlet obstruction, and retained gastric antrum can be ruled out by a careful medical history. An FSG level of more than 1000 pg/mL (10 times the upper limit of normal) along with basal acid output (BAO) above 15 mEq/H is usually diagnostic of gastrinoma, and an FSG level of more than 1,500 pg/ mL is suggestive of metastatic disease. Two-thirds of gastrinoma patients have an FSG level of less than 1000 pg/mL, and provocative confirmatory testing may be necessary in this clinical scenario. Previously, a ratio of BAO to maximum acid output (MAO) of greater than 0.7 or an increase in MAO (more than 48 mEq/h in men and more than 30 mEq/h in women) with stimulation supported the diagnosis of ZES. MAO measurement requires subcutaneous pentagastrin, which is no longer available in the United States, or secretin stimulation. In most patients, to clearly diagnose ZES, gastric acid secretion or pH should be performed after cessation of PPI. PPI withdrawal should only be done if the result will change management and if it is done at an experienced center. A safe method of withdrawing PPIs involves stopping the PPI 1 to 2 weeks before the tests and starting highdose ranitidine (600 mg orally every 6 hours). Ranitidine is stopped 30 hours before the tests, and antacids may be used as needed until midnight before the tests. All patients should be screened for primary hyperparathyroidism and prolactinomas by measuring serum calcium and PTH and prolactin to exclude MEN1. In patients with MEN1, ZES may be the first manifestation in approximately 50% of patients before primary hyperparathyroidism is diagnosed. In patients who have clinical features of Cushing’s syndrome or an adrenal mass, a 24-hour urinary cortisol level, serum adrenocorticotropic hormone (ACTH), and low-dose dexamethasone suppression test should be considered. D The hypersecretion of acid can now be controlled in almost every patient by the administration of PPIs (gastric H/ K+–ATPase), and it is extremely rare for patients to die from acid-related complications. Standard doses of oral PPIs are begun and titrated to control acid secretion. The average dosage of omeprazole is 65 mg/day. Vitamin B12 deficiency can occur in 6% of ZES patients treated with PPIs, and serum B12 levels should be evaluated periodically. Patients should also be monitored for osteoporosis and hypomagnesemia because they have been associated with long-term PPI use. E Imaging is necessary for the evaluation of metastatic disease and for assessing resectability when indicated. Pancreatic and duodenal tumors are small, and the latter arise from the submucosal layers, which makes their detection difficult on anatomical imaging and endoscopy. A thin-slice computed tomography (CT) scan of the abdomen and pelvis should be performed to identify primary tumor, regional lymph node metastases, and liver metastases. NETs classically appear as hyperenhancing lesions during arterial and portal venous phases. Magnetic resonance imaging (MRI) is complementary to CT scanning and is most helpful for detecting liver and/or bone metastases. Somatostatin receptor scintigraphy with single-photon emission computerized tomography (SPECT), which has a sensitivity of 78% to 86%, has been used and is useful in staging

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Chapter 115  ◆  Zollinger-Ellison Syndrome  348.e1

Abstract

Keywords

Gastrinoma is a neuroendocrine tumor (NET) that secretes gastrin and may occur as a sporadic or inherited disease (as part of multiple endocrine neoplasia type 1 [MEN1]). Virtually all medical complications associated with the elevated gastrin serum levels can be treated medically using proton pump inhibitors. All patients with sporadic gastrinomas should have the tumor resected if possible, and most patients with MEN1-associated gastrinoma should have medical therapy unless they develop metastasis or locally invasive tumors. Preoperative localization studies should include thin-cut computed tomography (CT) scan, endoscopy, endoscopic ultrasound, and 68-gallium DOTA peptide analogs to properly localize and stage the patient. Even if all localizing studies are negative and a patient has biochemical evidence of a sporadic gastrinoma, surgical exploration with a duodenotomy and intraoperative ultrasound of the pancreas and bimanual palpation localizes most lesions. Surgical treatment for sporadic gastrinoma is associated with improved survival. Patients with isolated liver metastasis may benefit from hepatectomy or local ablative procedures or embolization. Patients with widely metastatic or unresectable gastrinoma may be treated with somatostatin analogs, targeted agents such as sunitinib and everolimus, and/or peptide receptor radionucleotide therapy; all of these treatments have been associated with prolonged progression-free survival.

gastrinoma neuroendocrine tumor surgery gastrin proton pump inhibitor computed tomography (CT) scan endoscopy endoscopic ultrasound 68-gallium DOTA imaging somatostatin analog sunitinib everolimus peptide receptor radionuclide therapy

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Chapter 115  ◆  Zollinger-Ellison Syndrome  349 NETs, but recent studies have demonstrated that imaging with positron emission tomography CT (PET/CT) using 68 galliumlabeled high affinity DOTA peptides (DOTATATE, DOTANOC, DOTATOC) has the highest sensitivity (93%) and specificity (91%) for localizing NETs. Endoscopic ultrasound may detect a pancreatic primary tumor or regional lymphadenopathy, but it is not useful for detecting small duodenal primary tumors. Selective arteriography and hepatic vein sampling are invasive and should be used only if all other tests are negative. In patients who have advanced disease where a high-grade gastrinoma is suspected or is consistent with Grade 3 NET from biopsy samples, 18F FDG PET/CT should be considered because these tumors are less avid on somatostatin receptor scintigraphy but are positive on FDG PET/CT (flip-flop phenomenon—poorly differentiated and high-grade NET have decreased somatostatin receptor expression and increased glucose metabolism). F Patients with sporadic gastrinoma should have surgical treatment. If there is locoregional disease, patients should undergo surgical exploration and resection of the primary tumor

with therapeutic/prophylactic lymphadenectomy. Surgical treatment is associated with a high biochemical cure rate and improves the overall survival of patients with sporadic ZES. Even when the preoperative anatomic/functional/endoscopic localizing studies are negative, patients with sporadic gastrinoma should undergo surgical exploration because the tumor is commonly localized in the duodenum or pancreas at the time of surgical exploration. Intraoperative use of a gamma-detection probe for radio-guided localization and surgical resection of gastrinoma using a 68 gallium-labeled high-affinity DOTA peptide have been shown to be feasible and may result in improved long-term patient outcome. G Surgical treatment of patients with MEN1-associated nonmetastatic gastrinoma is not indicated because PPI effectively controls acid hypersecretion, and a biochemical cure is rarely achieved with surgical resection. Patients with MEN1associated metastatic disease or who are suspected of having metastatic disease or a locally invasive tumor should have surgical resection if the tumor sites are resectable. In patients with MEN1,

J Targeted therapy Liver-directed therapy Chemotherapy

A Clinical presentation • Refractory peptic ulcer disease • Diarrhea • Family history of MEN1

Unresectable liver metastases Distant metastases

E

Sporadic

CT scan/MRI 68-Gallium DOTA PET/CT scan Other (18F FDG PET)

Consideration for surgery

K

Resectable liver metastases

Surveillance

Excision

B ZOLLINGER-ELLISON SYNDROME

I

F

Potentially resectable Gastrinoma identified

Medical therapy initiated

D

H MEN1

C Biochemical testing • Fasting serum gastrin • Gastric pH measurement • Provocative stimulation • Calcium • Intact PTH • Prolactin • 24-hour urinary cortisol level, serum ACTH, and low dexamethasone suppression test in patients with features of Cushing’s syndrome or an adrenal mass

Laparotomy

E

Consideration for surgery

CT scan/MRI 68-Gallium DOTA PET/CT scan Other (18F FDG PET)

G

≥2 cm or resectable metastasis

No tumor identified continue medical therapy and surveillance

K

Continued medical therapy and surveillance for metastases K

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350  Part VII  ◆ Endocrine gastrinomas are frequently small (thus undetectable by localization imaging) and multiple. Moreover, gastrinomas may be associated with nonfunctioning pancreatic NETs that are detected at exploration. In the past, some surgeons advocated aggressive resection of localized gastrinomas in patients with MEN1, but it was virtually impossible to achieve a biochemical cure, and more than 95% of patients relapsed within 3 years of surgery. Thompson and colleagues (1993) had advocated duodenotomy and removal of mucosal tumors, pancreatic head tumor enucleation, peripancreatic lymph node dissection, and distal pancreatectomy. Eugastrinemia and failure to stimulate with secretin were achieved in approximately 33% of patients using this approach, but there was no association with longer survival. Considering the morbidity associated with surgical intervention, and given the excellent long-term survival rate in patients with MEN1-associated localized gastrinoma, most centers, including ours, favor active surveillance in patients unless the growth of the primary tumor in the duodenum or pancreatic NETs is equal to or greater than 2 cm or if sites of questionable metastatic disease develop. H Sporadic gastrinoma resection is associated with a decrease in the incidence of subsequent liver metastases and higher long-term survival. Long-term survival after gastrinoma resection is excellent, and when deaths from other causes are excluded, 5- and 10-year survival rates are 100% and 95%, respectively. Primary tumors are usually identified in the gastrinoma triangle. Adequate exploration includes complete mobilization of the pancreas, bimanual palpation, and intraoperative ultrasound of the pancreas and liver. Evaluation of the duodenum may be facilitated by endoscopy with transillumination, and a 3-cm longitudinal duodenotomy at the junction of the first and second portions of the duodenum should be done to inspect and palpate the duodenum. Surgical resection can usually be accomplished by enucleation, but formal resection may be required for larger tumors or tumors that are locally invasive through the bowel wall. The regional lymph node basin should be resected. If a complete resection can be achieved, nonanatomic liver resection, radiofrequency, or cryoablation of liver metastases is indicated. There exist limited data on the feasibility and outcome of using minimally invasive surgical approaches because manual palpation is an essential component of surgical exploration for gastrinomas (approximately 30% of the tumors are not detected with standard radiological localization techniques preoperatively). Given the effectiveness of medical therapy for acid control, parietal cell vagotomy is not necessary. Other acid-reducing surgical procedures are also no longer used because of the effectiveness of PPI therapy. Total gastrectomy is rarely indicated in patients with ZES. Indications for total gastrectomy include failure of previous ulcer surgery or medical therapy or complications of previous gastric surgery, such as gastrojejunal-colic fistula. The presence of severe gastroesophageal reflux disease with stricture formation is challenging and may necessitate anti-reflux surgery or total gastrectomy. I

It is unclear if treatment of NET liver metastasis (NETLM) in patients with ZES effects patient survival and results in a long-term cure. Although there are limited data specifically focused on ZES-associated NETLM treatment outcomes, there have been several studies in NETLM composed of a heterogeneous group. In a large, multi-institutional study (n = 339) of patients

undergoing liver surgery for NETLM, the recurrence rates were 94% at 5 years and 99% at 10 years. On the other hand, in a recent multi-institutional study (n = 376) evaluating cure rates in NETLM, the following variables were independently associated with a cure: (1) liver involvement of 1 cm in diameter that is discovered at the time of an imaging procedure performed for an otherwise unrelated clinical indication. Autopsy series reveal an incidence of 6% in patients who have no evidence of adrenal disease before death. Abdominal computed tomography (CT) identifies clinically inapparent adrenal tumors in 0.2% to 7% of studies, and prevalence increases with age. B The majority of incidentalomas (80%) are benign and nonfunctioning. However, it is incumbent upon the clinician to assess whether the mass is hormonally active and/or malignant. The initial evaluation of the clinically silent adrenal tumor should include a history and physical examination for signs and symptoms suggestive of glucocorticoid, mineralocorticoid, catecholamine or sex hormone excess. C Primary adrenal malignancy is found in 5% of patients in whom an incidental adrenal mass is identified. Unexplained weight loss, abdominal pain, abdominal fullness, and fever are common symptoms of malignancy, but most patients with small tumors will be asymptomatic. Virilization is common in patients with adrenocortical carcinoma (ACC), but patients may occasionally present with feminization or hyperaldosteronism. In addition, a prior history of malignancy, particularly lung cancer, colorectal cancer, renal cell carcinoma, melanoma, or lymphoma, should increase suspicion for an adrenal metastatic lesion. D All patients with an adrenal incidentaloma must be tested for evidence of hypercortisolism, hyperaldosteronism, and pheochromocytoma. Subclinical Cushing’s syndrome (SCS) is the most common abnormality associated with functional lesions and is found in 5% to 10% of cases. E Hypercortisolism is associated with increased risk for cardiovascular, metabolic, and psychiatric diseases and with adrenal insufficiency after adrenalectomy. The best screening test for the diagnosis of occult hypercortisolism is the 1-mg overnight dexamethasone suppression test. A serum cortisol level above 5 µg/dL is considered abnormal. The additional finding of either high late-night salivary cortisol or elevated 24-hour urine free cortisol is considered confirmatory. Confirmation of autonomous cortisol hypersecretion can also be obtained with a 2-day low-dose or high-dose dexamethasone suppression test. Lack of dexamethasone suppression and a low adrenocorticotropic hormone (ACTH) level support the diagnosis of a cortisolproducing adrenal adenoma. In patients with suspected

cortisol-producing ACC, clinicians may also test for sex steroids and steroid precursors, including androstenedione, testosterone, and dehydroepiandrosterone sulfate (DHEA-S). For patients with sequelae of Cushing’s syndrome, including hypertension, abnormal glucose tolerance, and osteoporosis, adrenalectomy is recommended; for those with SCS, the long-term benefits of adrenalectomy are unknown, and surgery remains controversial. F The second most common functioning incidentalomas are pheochromocytomas, which represent about 5% of cases. Elevated plasma-free metanephrine and normetanephrine levels are the most sensitive test for pheochromocytoma; 24-hour total urinary metanephrine and fractionated catecholamines also suggest the diagnosis but have a higher false-negative rate. Use of tricyclic antidepressants, decongestants, amphetamines, reserpine, and phenoxybenzamine should be discontinued to eliminate the possibility of a false-positive result. Associated familial syndromes are present in about 25% of cases, so genetic counseling and testing for an RET mutation, mutations in the VHL gene, and subunits of the succinate dehydrogenase genes are recommended. All patients with pheochromocytoma should undergo adrenalectomy only after adequate α-adrenergic blockade. G Aldosteronomas account for 1% of incidentalomas. Classically, screening for this rare diagnosis has included measurement of patient blood pressure and serum potassium only. However, at least 20% of patients with hyperaldosteronism have normal serum potassium. The best screening test in patients with an adrenal incidentaloma and hypertension is a measurement of ambulatory morning plasma aldosterone concentration (ng/ dL) to plasma renin activity (ng/mL per hr) ratio (PAC/PRA ratio). A PAC/PRA ratio > 20 and a plasma aldosterone level > 15 ng/dL are diagnostic of hyperaldosteronism. Patients need to discontinue spironolactone for 6 weeks before testing. A confirmatory test may include measurement of 24-hour urinary aldosterone secretion with oral salt loading or saline infusion; persistently elevated urinary aldosterone and renin levels characterize hyperaldosteronism. Patients with confirmation of hyperaldosteronism and a unilateral adrenal mass should be considered for adrenalectomy and are generally good candidates for the laparoscopic approach. However, adrenal venous sampling is recommended in patients over 40 years old to document a unilateral source of aldosterone excess and to rule out bilateral adrenocortical micro- or macrohyperplasia. H Phenotypic descriptions of benign and malignant adrenal masses have emerged. Computed tomography (CT) is the primary adrenal imaging modality, and evaluation of adrenal lesions depends on morphology and density, measured in Hounsfield units (HU). Adrenal adenomas have low attenuation (18 HU) and have characteristic irregular borders with a heterogeneous appearance. They may also exhibit evidence of invasion into surrounding structures. After contrast administration, they typically have less than 50% washout on delayed images.

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Chapter 116  ◆  Adrenal Incidentaloma  352.e1

Abstract

Keyword

An adrenal incidentaloma is defined as an adrenal mass discovered at the time of an imaging procedure performed for an unrelated clinical indication. The majority are benign and nonfunctioning. Primary malignancy is rare. All patient must be tested for functional tumors which should be removed. Tumors worrisome for malignancy should be resected. Small benign nonfunctioning tumors, observation is the best management.

adrenal incidentaloma

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Chapter 116  ◆  Adrenal Incidentaloma  353 J

Fine-needle aspiration biopsy (FNA) is very rarely used in the evaluation of a patient with an adrenal incidentaloma. It should only be considered in those cases in which the diagnosis would otherwise alter clinical management. A hormonal evaluation is essential, even in patients with a previous history of cancer, because percutaneous biopsy of an undiagnosed pheochromocytoma may be associated with hypertensive crisis, hemorrhage, and/or death. Routine FNA is not recommended in the evaluation of patients with an incidentaloma because FNA of adrenal masses carries a significant risk for complications, and cytologic analysis will not distinguish among primary adrenal tumors.

classic teaching suggests that the risk for adrenal carcinoma is significantly associated with increasing mass size, imaging characteristics are more reliable for determining the risk for malignancy. The presence of a radiographic phenotype worrisome for malignancy is a stronger indication for adrenalectomy. All patients with unilateral adrenal masses that are functional, are increasing in size, or exhibit concerning radiologic features should be considered for adrenalectomy by either an open laparoscopic or retroperitoneoscopic approach. Minimally invasive adrenalectomy has the advantages of shortened recovery time and decreased postoperative pain. Preoperative suspicion of adrenal carcinoma is considered a relative contraindication for laparoscopic or retroperitoneoscopic adrenalectomy. Adrenalectomy for isolated metastasis from a nonadrenal primary has been reported in individual cases, but there is no evidence that adrenal metastasectomy improves patient survival.

K Pheochromocytomas also exhibit a characteristic radiologic phenotype. They usually enhance greater than 100 HU, exhibiting what is commonly referred to as a “lightbulb” appearance on contrast-enhanced images. They have washout of greater than 50% on delayed images. On magnetic resonance imaging (MRI), they also exhibit a characteristically bright signal on T2-weighted images. In cases of biochemical evidence of pheochromocytoma without CT or MRI localization, iodine-123 metaiodobenzylguanidine scintigraphy may be done to localize the lesion, which may be extra-adrenal (paraganglioma).

M In patients with nonfunctional unilateral masses and clearly benign radiologic features, observation is the best management option. Most centers recommend follow-up imaging with CT or MRI 3 to 6 months after diagnosis, followed by repeat annual imaging and biochemical testing for 5 years thereafter. An interval increase in tumor size of 1 cm or greater, a change in radiologic appearance suggestive of malignancy, or evidence of hormonal function should be treated with adrenalectomy. Although rare, there is some evidence that incidentalomas require long-term follow-up because they can grow in size or become functional. The most common hormonally active lesion in patients with previously inactive adenomas is SCS.

L In the absence of abnormal hormone production or worrisome radiologic features, recommendations for adrenalectomy for incidentalomas are based on the size of the lesion or its growth over time. The majority of adrenal incidentalomas less than 4 cm in diameter are benign adenomas, and adrenal carcinomas smaller than 4 cm have rarely been reported. Although

E

B, C

History and Exam Signs/symptoms of Cushing’s syndrome Feminization or virilization Paroxysmal symptoms Hypertension History of malignancy

1-mg dexamethasone suppression study

Cortisol-producing adenoma

F Functional

Plasma free metanephrines/ normetanephrines

K Pheochromocytoma

L Adrenalectomy

G A

Adrenal Incidentaloma

D

Hormonal evaluation

Plasma aldosterone concentration (PAC)/ plasma renin activity (PRA)

H Benign CT/MRI Lipid content Borders Washout B, C Labs Hypokalemia, hypernatremia Hyperglycemia

Nonfunctional

Primary hyperaldosteronism

Observation CT 3-6 and 12 months Yearly biochemical evaluation No change

Continued observation Yearly CT/biochemical evaluation

M

I

Malignant

Adrenalectomy FNA

Metastatic

L

Adrenalectomy for change in CT findings or functionality

J L

Systemic therapy Adrenalectomy

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354  Part VII  ◆ Endocrine REFERENCES Azoury S, Nagarajan N, et al. Computed tomography in the management of adrenal tumors: does size still matter? J Comput Assist Tomogr. 2017. Comlekci A, Yener S, et al. Adrenal incidentaloma, clinical, metabolic, follow-up aspects: single centre experience. Endocrine. 2010;37(1):40–46. Fassnacht M, Wiebke A, et al. Management of adrenal incidentalomas: European Society of Endocrinology clinical practice guideline in collaboration with the European network for the study of adrenal tumors. Eur J Endocrinol. 2016;175(2):G1–G34. Grumbach MM, Biller BM, et al. Management of the clinically inapparent adrenal mass (“incidentaloma”). Ann Intern Med. 2003;138:424–429.

Kapoor A, Morris T, et al. Guidelines for the management of the incidentally discovered adrenal mass. Can Urol Assoc J. 2011;5(4):241–247. Nieman L. Approach to the patient with an adrenal incidentaloma. J Clin Endocrinol Metab. 2010;95(9):4106–4113. Young WF. The incidentally discovered adrenal mass. N Engl J Med. 2007;356: 601–610. Zeiger MA, Thompson GB, et al. AACE/AAES medical guidelines for the management of adrenal incidentalomas. Endocr Pract. 2009;15(5): 450–453.

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Chapter

117 

PHEOCHROMOCYTOMA Travis J. McKenzie, MD, and David R. Farley, MD A Pheochromocytoma, “the great mimic,” may generate signs and symptoms compatible with many other diseases (e.g., hyperthyroidism, diabetes mellitus, mental illness, eclampsia of pregnancy, or gram-negative sepsis). Although hypertension remains the most prominent sign in patients with pheochromocytoma, owing to the sheer rarity of this disorder (incidence, 1 : 100,000 Americans, or 0.1% of all hypertensive patients), most patients with hypertension and associated complaints of headaches, palpitations, and flushing likely do not have a pheochromocytoma. The onus, therefore, lies with the physician to consider and rule out this rare disorder because untreated pheochromocytoma may manifest potentially lethal consequences. B Modern radiologic studies (computed tomography [CT] or magnetic resonance imaging [MRI]) performed for other reasons may identify an incidental adrenal neoplasm. It is imperative to clinically and biochemically investigate all such adrenal incidentalomas to rule out pheochromocytoma. Approximately 3% of incidentalomas are pheochromocytoma. Approximately half of patients with incidentally discovered pheochromocytoma may have no clinical history of the classic manifestations of catecholamine excess, and therefore, an unremarkable history cannot exclude pheochromocytoma. C Occasionally the suspicion of pheochromocytoma surfaces during medical intervention (e.g., hemodynamic instability during angiography, childbirth, or surgical intervention). Immediate blood pressure control during the untoward event is imperative, as is prompt completion or termination of the procedure. Thereafter, the diagnosis of pheochromocytoma must be excluded. Unfortunately, as many as 800 Americans may die every year from unsuspected pheochromocytomas. D Modern abdominopelvic CT and MRI accurately identify most adrenal neoplasms. Adrenal-directed CT, which includes thin-section (3-mm), noncontrast enhanced imaging to evaluate density, and delayed phase after venous contrast enhancement offer invaluable information that can further suggest a diagnosis of pheochromocytoma versus cortical adenoma. Ninety-eight percent of catecholamine-secreting tumors are intraabdominal; 90% lie within the adrenal gland(s). Equivocal CT or familial syndromes (e.g., multiple endocrine neoplasia [MEN2], neuro­ fibromatosis type 1 [NF1], or von Hippel-Lindau [VHL]) should prompt consideration of obtaining 123I-meta-iodobenzylguanidine (MIBG) scintigraphy or MRI. E Whether paroxysmal (about 45%) or sustained (about 50%), most hypertensive patients with pheochromocytomas se­crete excessive catecholamines. Measurement of 24hour urinary fractionated catecholamines (i.e., epinephrine, nor­epinephrine, and dopamine) and metanephrine identifies this disorder in more than 98% of patients, even including those

without overt symptoms and signs of a pheochromocytoma. Measurement of fractionated plasma metanephrine is highly sensitive (around 99%) but lacks specificity (85%) when compared with the combination of 24-hour urinary total metanephrine and catecholamines. When biochemical testing is positive, potential causes of false-positive results, such as medications (e.g., tricyclic antidepressants, levodopa, or drugs containing catecholamines) or clinical situations (e.g., physical stress or withdrawal from clonidine or other drugs), should be considered. Most patients diagnosed with pheochromocytoma or paraganglioma should undergo genetic counseling and screening for familial predis­position, including MEN2, VHL, NF1, and hereditary pheochromocytoma/paraganglioma (SDH). F Patients with imaging evidence of an adrenal neoplasm, biochemical evidence of catecholamine or metanephrine excess on 24-hour urine or plasma studies, and who are fit to tolerate general anesthesia warrant resection. Perioperative pharmacologic therapy lowers morbidity and mortality by minimizing intraoperative hemodynamic instability. A variety of regimens (e.g., prazosin, calcium channel blockers, and labetalol) have been used successfully. The authors’ preference is for 7 to 10 days of outpatient nonselective α-adrenergic receptor blockade (phenoxybenzamine, 10 to 40 mg PO twice daily, titrated to normal blood pressure, resolution of spells, and onset of nasal congestion and mild orthostatic hypotension) with additional β-blockade as needed over the last 3 preoperative days to minimize tachyarrhythmias (propranolol, 10 mg PO four times daily). Although α- and β-adrenergic blockade along with salt loading and repletion of intravascular volume is useful, meticulous surgical technique and an experienced anesthesiologist are essential to safe operative intervention. G Laparoscopic or retroperitoneoscopic unilateral or bilateral adrenalectomy is safe and efficacious and offers significant advantages over open adrenalectomy. Open operation is logical if the adrenal lesion is >10 cm or is likely to be malignant. Retroperitoneoscopic adrenalectomy offers the advantage of avoiding troublesome adhesions in the setting of previous upper abdominal surgery. Identification of previously unsuspected metastatic disease is uncommon, but palliative resection, if safely accomplished, is beneficial. Although metastatic tumors respond poorly to radiation or chemotherapy, limited palliation with resection, radiation therapy (bony metastases), therapeutic 131I MIBG, cytotoxic chemotherapy, or radiofrequency ablation has been reported. The mainstay of treatment in such patients is control of hypertension with long-term α-adrenergic blockade. H Prevention of profound catecholamine-induced hypertension may be prevented by early adrenal vein ligation. This advantage must be balanced by the possibility of intratumoral hypertension/venous congestion that may precipitate troublesome bleeding. Judicious use of intravenous fluids and sodium nitroprusside can be used as indicated. Continuous arterial pressure monitoring and excellent venous access with large-bore peripheral intravenous (IV) lines are essential. Central venous access for pressure monitoring and vasopressor infusion is used as needed. I

Minimally invasive adrenalectomy for pheochromocytoma is both safe and effective. Morbidity is uncommon (7 cm) benign tumors require good surgical decision making about access ports, patient positioning, mobilization, CO2 insufflation space, and surgeon experience.

bilateral adrenalectomy may help palliate the patient with cortisol excess. Inhibitors of cortisol production are used for palliation but are less successful in the setting of ectopic ACTH because of more potent adrenal stimulation from higher ACTH levels. Octreotide inhibits ACTH secretion and has been used with moderate success to decrease cortisol levels from disseminated tumors.

L Suspicion for ACC should increase with masses > 6 cm, heterogeneous or necrotic masses, attenuation >10 Hounsfield units, or if there is radiographic evidence of local invasion or distant disease. Nearly 50% of these are hormonally active, most often presenting with cortisol excess. These malignant tumors are extremely aggressive, and as many as 50% are identified at an advanced stage.

O Surgical resection remains the mainstay of therapy for ACC, particularly stage I to III disease. An open approach is used for en bloc excision, node dissection, and possible vascular reconstruction and to identify locoregional metastases. Risks of laparoscopic surgery for primary adrenal malignancy include seeding at the port site, tumor fracture, and incomplete resection leading to local recurrence or persistent disease. Patients who undergo a complete resection have a median survival of 43 months and a 5-year survival rate of 32% to 48% compared with a median survival of 200 mEq/24 hours confirms adequate sodium loading, and urinary aldosterone < 10 µg/24 hours rules out the diagnosis of hyperaldosteronism. Confirmatory testing can also be performed via saline infusion (2 L 0.9% saline in 4 hours) followed by plasma aldosterone level (10 ng/dL makes a diagnosis of PAH highly probable). Fludrocortisone suppression testing and the captopril challenge test are alternative confirmatory tests. E Computed tomography (CT) with adrenal protocol or magnetic resonance imaging (MRI) should be performed in all patients with PA to evaluate for adrenal nodules or adrenal hyperplasia. Imaging may also help provide anatomic guidance for the interventional radiologist and surgeon.

A Although it was once thought to be relatively rare, PA may account for up to 5% to 10% of hypertensive patients, of which only a minority will present with hypokalemia. All patients with resistant hypertension (defined as a sustained blood pressure >140/90 mm Hg) who are on three or more antihypertensive agents or patients with controlled hypertension (blood pressure < 140/90 mm Hg) on four or more antihypertensive agents should be screened for PA. Patients with hypertension should also be screened for PA if they have hypokalemia, an adrenal incidentaloma, sleep apnea, cerebrovascular accident under age 40 years, a family history of early-onset hypertension, or a first-degree relative with PA.

F Adrenal venous sampling (AVS) should be performed in most patients with PA, to distinguish between bilateral and unilateral disease, because this would affect the recommendations for management. • AVS should be performed by an experienced interventional radiologist. AVS may be performed with or without cosyntropin stimulation. Adrenal vein cannulation should be confirmed by the plasma cortisol ratio of each (left and right) adrenal vein to inferior vena cava (IVC), with a ratio of ≥2.0 without cosyntropin stimulation and a ratio of ≥3.0 with cosyntropin stimulation. Once adrenal vein cannulation is confirmed, lateralization can be evaluated using the ratio of the cortisol-corrected aldosterone levels between each adrenal vein. Lateralization ratios vary by institution. A ratio of >2 : 1 may be considered as a lateralizing study without cosyntropin stimulation, whereas a ratio of >4 : 1 is considered confirmatory with cosyntropin stimulation. Patients should be off mineralocorticoid antagonists before AVS and any other medications that may elevate plasma renin levels.

B PA is caused by bilateral idiopathic adrenal hyperplasia (BIH) or a unilateral aldosterone-producing adenoma (APA). Less common causes of PA include unilateral adrenal hyperplasia, adrenal carcinoma, and familial hyperaldosteronism.

G AVS may not be necessary in patients who meet all of the following criteria: age < 35 years, with spontaneous hypokalemia, PAC > 30 ng/dL, and a solitary unilateral adrenal lesion consistent with an adenoma identified on imaging.

C The ratio of plasma aldosterone concentration (PAC) to plasma renin activity (PRA) is the most reliable screening test for PA. Samples are most sensitive in the morning when patients have been out of bed for a least 2 hours and have been seated for 5 to 15 minutes. Preferably, patients should have unrestricted salt intake and have potassium replete before testing. Mineralocorticoid receptor antagonists should be stopped for 4 weeks before testing. Other antihypertensive medications may affect the test, but this is usually limited, and the cessation of all antihypertensive medications is not usually necessary. When performed, a PAC-to-PRA ratio of >20 to 40 is considered elevated and should prompt confirmatory testing (see D). This range in the PAC:PRA ratio is based on institutional variability in diagnostic protocols and assay methods and should be interpreted based on known institutional data. Confirmatory testing may be deferred in patients with a PAC > 20 ng/dL, undetectable plasma renin level, and spontaneous hypokalemia.

H Medical management of BIH consists of mineralocorticoid receptor antagonists, such as spironolactone or eplerenone, in combination with other antihypertensive agents.

D Confirmatory testing may be performed with oral sodium loading (6 g/day of sodium for 3 days) followed by a 24-hour

I

For patients with APA, adrenalectomy is recommended, and minimally invasive approaches (transabdominal or posterior retroperitoneal) are appropriate. Preoperatively, hypertension and hypokalemia should be well controlled. Postoperatively, patients should have intravenous (IV) fluids without potassium, potassium supplements should be discontinued, and patients should be monitored for hyperkalemia because the resolution of preexisting hypokalemia can occur within the immediate postoperative period. Antihypertensive medications, including mineralocorticoid antagonists, should be titrated as tolerated; improvements in hypertension, as demonstrated by a reduction in the number and/or dosage of medications, are typically seen within the first 12 months of surgery. A serum aldosterone and renin level should be obtained in the postoperative period; this should typically be performed within the first 3 to 4 weeks postoperatively.

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Chapter 119  ◆  Primary Aldos­teronism  362.e1

Abstract

Keywords

Although it was once thought to be relatively rare, primary aldosteronism (PA) may account for up to 5% to 10% of hypertensive patients, of which only a minority will present with hypokalemia. PA is caused by bilateral idiopathic adrenal hyperplasia (BIH) or a unilateral aldosterone-producing adenoma (APA). Computed tomography (CT) with adrenal protocol or magnetic resonance imaging (MRI) should be performed in all patients with PA to evaluate for adrenal nodules or adrenal hyperplasia. Imaging may also help provide anatomic guidance for the interventional radiologist and surgeon. Adrenal venous sampling (AVS) should be performed in most patients with PA, to distinguish between bilateral and unilateral disease, because this would affect the recommendations for management. Medical management of BIH consists of mineralocorticoid receptor antagonists, such as spironolactone or eplerenone, in combination with other antihypertensive agents. For patients with APA, adrenalectomy is recommended, and minimally invasive approaches (transabdominal or posterior retroperitoneal) are appropriate.

primary aldosteronism hypertension hypokalemia adrenal venous sampling adrenalectomy

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Chapter 119  ◆  Primary Aldos­teronism  363

H A History and Physical Exam -age D -gender -number of antihypertensive medications Confirmatory testing -symptoms of hypokalemia (saline infusion or oral -sleep apnea salt load)) -blood pressure E Elevated CT scan (>20-40 ng/dL:ng/mL/hr)

B

C

Primary Hyperaldosteronism

Medical management Mineralocorticoid receptor antagonist Bilateral process

F Adrenal Vein Sampling (AVS) Unilateral process

G

Ratio of PA to PRA Normal

No confirmatory testing required -Spontaneous hypokalemia, undetectable renin, and PAC >20 ng/dL

No further testing or repeat PA/PRA

REFERENCES Funder JW, Carey RM, Mantero F, et al. The management of primary aldosteronism: case detection, Diagnosis, and treatment: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(5): 1889–1916. Lim V, Guo Q, Grant CS, et al. Accuracy of adrenal imaging and adrenal venous sampling in predicting surgical cure of primary aldosteronism. J Clin Endocrinol Metab. 2014;99(8):2712–2719.

AVS not necessary Age 30 ng/dL

I

Minimally invasive Adrenalectomy (transabdominal or posterior retroperitoneal)

Mulatero P, Monticone S, Bertello C, et al. Confirmatory tests in the diagnosis of primary aldosteronism. Horm Metab Res. 2010;42(6): 406–410. Rossi GP, Auchus RJ, Brown M, et al. An expert consensus statement on use of adrenal vein sampling for the subtyping of primary aldosteronism. Hypertension. 2014;63(1):151–160. Young WF, Stanson AW, Thompson GB, et al. Role for adrenal venous sampling in primary aldosteronism. Surgery. 2004;136(6):1227–1235.

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Chapter

120 

INITIAL EVALUATION AND RESUSCITATION Joshua J. Sumislawski, MD, and Mitchell J. Cohen, MD

A

 

PRIMARY SURVEY

Initial assessment and management of the injured patient are guided by prioritized steps defined by the Advanced Trauma Life Support (ATLS) program. Although described sequentially, these steps must be accomplished rapidly and often simultaneously. The first series of steps, the primary survey, is intended to identify and treat immediately life-threatening conditions and follows the acronym ABCDE: • Airway: Ensure patency. • Breathing: Rule out pneumo- and hemothoraces. • Circulation: Assess vital signs and peripheral pulses. Obtain intravenous (IV) access. • Disability: Perform brief neurologic examination. • Exposure: Remove patient’s clothing. Cover with warm blankets to prevent hypothermia. If the patient needs to be intubated, a brief neurologic examination should be performed before administering sedative or paralytic medications. If the patient arrives in extremis or with life-threatening external hemorrhage, circulation should precede the airway. B

 

ADJUNCTS

Although the primary and secondary surveys focus on physical examination, adjuncts may be used to assist with identifying injuries and guiding resuscitation. These adjuncts include plain radiographs (especially chest and pelvic x-rays), focused assessment with sonography in trauma (FAST), and gastric and urinary catheters. C

 

ASSESS NEED FOR RESUSCITATION

The need for resuscitation is determined during the circulation component of the primary survey based on initial vital signs and injury characteristics. New understandings of physiologic, coagulation, and inflammatory perturbations after injury have resulted in the development of multiple rules, scoring systems, and physiologic tests to assist with this determination. Hemodynamic instability in the field or upon arrival [systolic blood pressure (SBP) 100 bpm], penetrating torso injury, major pelvic fracture, or positive FAST indicate that the patient will likely require resuscitation. In these circumstances, transfusion should be initiated with a balanced ratio of red blood cells (RBCs) and fresh frozen plasma (FFP), often via a pre-established massive transfusion protocol that ensures rapid delivery of blood products from the blood bank. As soon as IV access has been obtained, laboratory tests should be sent including a type and screen, complete blood count (CBC), thromboelastography (TEG), arterial

blood gas (ABG), and lactate. Base excess < –6 and/or lactic acidosis >4 suggest severe metabolic derangements, and repeat measurements can be used to guide the effectiveness of ongoing resuscitation. D   SECONDARY SURVEY

After immediately life-threatening conditions have been addressed, the secondary survey is performed to identify all other injuries. This step consists of a complete history and physical examination and may utilize appropriate adjuncts. Moving forward, this chapter focuses on physiologic and biologic resuscitation after severe injury. E

 

BEGIN RESUSCITATION

The goals of resuscitation are threefold: identifying and stopping hemorrhage, correcting coagulopathy, and reversing metabolic derangements. It cannot be overemphasized that these steps must occur simultaneously and that the interventions described often address two or more of these goals. F

 

CONTROL HEMORRHAGE

Life-threatening hemorrhage should be approached anatomically by considering the five potential sources from which it can occur: chest, abdomen, pelvis, long-bone fractures, and external bleeding. A myriad of surgical algorithms exist to identify and address hemorrhage from these sources and are beyond the scope of this chapter. G

 

RESTORE BLOOD OXYGEN-CARRYING CAPACITY AND CORRECT COAGULOPATHY

Upon recognition of the need for resuscitation, empiric transfusion should begin with an RBC:FFP ratio > 1 : 2 while awaiting initial laboratory results. H   SERIAL COMPLETE BLOOD COUNTS

While the target hemoglobin is debated, we recommend maintaining hemoglobin > 10 mg/dL in the acute postinjury setting. I

 

SERIAL THROMBOELASTOGRAMS

TEG-guided resuscitation has been shown to be superior to resuscitation using conventional coagulation tests like international normalized ratio and partial thromboplastin time. In the bleeding patient, the following TEG parameters are used to direct correction of coagulopathy and restoration of intravascular volume: • Activated clotting time (ACT) > 128 s: Transfuse 2 units of FFP. • Alpha angle (α) < 65°: Transfuse 10 units of cryoprecipitate. • Maximum amplitude (MA) < 55 mm: Transfuse 1 unit of platelets. • Percent lysis at 30 min (LY30) > 5%: Administer 1 g of tranexamic acid (TXA). J

 

CORRECT METABOLIC DERANGEMENTS

The final consideration in postinjury resuscitation is the correction of metabolic derangements. Emerging literature suggests that endothelial, inflammatory, and immune perturbations lead to poor outcomes after trauma as a direct consequence of hyporesuscitation even when coagulation has been normalized and bleeding has stopped. The time when hemostasis is achieved and coagulation is corrected often occurs before resuscitation

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Chapter 120  ◆  Initial Evaluation and Resuscitation  366.e1

Abstract

Keywords

The initial evaluation of trauma patients follows two series of prioritized steps defined by the Advanced Trauma Life Support program, the primary and secondary surveys, which are intended to identify all injuries and treat immediately life-threatening conditions. Once the need for resuscitation has been recognized, often during the primary survey, efforts are directed toward achieving three objectives: controlling hemorrhage, restoring blood oxygen-carrying capacity and correcting coagulopathy, and reversing metabolic derangements.

advanced trauma life support hemorrhage trauma-induced coagulopathy thromboelastography targeted resuscitation

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Chapter 120  ◆  Initial Evaluation and Resuscitation  367

F Control hemorrhage

A Primary survey • Airway • Breathing • Circulation • Disability • Exposure

• Chest • Abdomen • Pelvis • Long-bone fractures • External bleeding

C Assess need for resuscitation • SBP 100 • Penetrating torso trauma • Positive FAST • Major pelvic fracture • Base excess 4

H Serial CBCs • Goal Hgb >10

I E

Initial evaluation and resuscitation

G

Begin resuscitation • Notify blood bank

D

Serial TEGs • ACT >128: 2 u FFP • α 99% of trauma team activation (TTA) patients meet one or more of the risk factors for injury. B CT is the gold standard for diagnosing cervical spine fractures when compared with clinical examination with/without supplemental plain radiography. Furthermore, when the CT scan is negative for cervical spine injury, the incidence of significant ligament injury making the cervical spine unstable is nil regardless of examination or mental status. Therefore collars should be removed as soon as possible in all patients with a CT that is negative for acute injury based on the interpretation of a boardcertified radiologist. C Isolated transverse process (TP)/spinous process (SP) fractures with no CT evidence of ligament injury are considered clinically insignificant and do not require any specialist intervention. Among these patients, however, there remains a small (2.46%) incidence of ligament injury. There are three findings that, taken together, can identify this small subset of patients: (1) neurologic symptoms, (2) midline tenderness, and (3) Glasgow Coma Scale (GCS) score < 15. D In patients with a fracture pattern that is not “isolated TP/ SP,” there is an 11% incidence of ligament injury, and the spine may be made unstable by this type of fracture. Hence, all

such patients should undergo magnetic resonance imaging (MRI) and promptly be referred for specialist consultation. Any patient demonstrating CT evidence of ligament injury should undergo an MRI examination and be referred for specialist consultation because the risk of ligament injury is higher as well. E In patients with GCS score = 15, the patient should be asked about neurologic symptoms and evaluated for midline tenderness. In the absence of these, the incidence of significant ligament injury is nil, and the collar should be removed. F Patients with isolated TP/SP fracture with GCS score < 15 persisting beyond 72 hours should undergo an MRI. This time frame allows an opportunity for the patient’s sensorium to clear and follow the GCS score = 15 algorithm with possible avoidance of an MRI. It also minimizes a false-positive MRI that may occur when the MRI is done more acutely. G Patients with clinical findings of paresthesias or focal neurologic deficits and a GCS score of 15 should undergo an MRI to rule out an unstable ligament injury. If it is negative, remove the collar. If it is positive, refer to a spine specialist. H In the large majority of patients demonstrating midline tenderness with isolated TP/SP fractures, with no attendant neurologic symptoms and GCS score = 15, the collar should be maintained for 2 weeks and the patient reexamined. This approach allows time for the tenderness associated with fracture healing to improve, allowing differentiation with ongoing pain from ligament instability. If tenderness persists, an MRI should be obtained. If the MRI is negative for an unstable ligament injury, the collar should be removed. If the MRI is positive for an unstable ligament injury, the collar should be maintained and the patient referred to a spine specialist for further evaluation. REFERENCES Chew BG, Swartz C, Quigley MR, et al. Cervical spine clearance in the traumatically injured patient: is multidetector CT scanning sufficient alone? Clinical article. J Neurosurg Spine. 2013;19:576–581. Duane TM, Mayglothling J, Wilson SP, et al. National Emergency X-Radiography Utilization Study criteria is inadequate to rule out fracture after significant blunt trauma compared with computed tomography. J Trauma. 2011;70:829–831. Duane TM, Wilson SP, Mayglothling J, et al. Canadian cervical spine rule compared with computed tomography: a prospective analysis. J Trauma. 2011;71:352–355, discussion 5–7. Duane TM, Young AJ, Vanguri P, et al. Defining the cervical spine clearance algorithm: a single institution prospective study of over 9000 patients. J Trauma Acute Care Surg. 2016;81(3):541–547. Kanji HD, Neitzel A, Sekhon M, McCallum J, Griesdale DE. Sixty-four-slice computed tomographic scanner to clear traumatic cervical spine injury: systematic review of the literature. J Crit Care. 2014;29(314): e9–e13. Raza M, Elkhodair S, Zaheer A, Yousaf S. Safe cervical spine clearance in adult obtunded blunt trauma patients on the basis of a normal multidetector CT scan–a meta-analysis and cohort study. Injury. 2013;44:1589–1595. Vanguri P, Young AJ, Weber WF, et al. Computed tomographic scan: it’s not just about the fracture. J Trauma Acute Care Surg. 2014;77:604–607.

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Chapter 122  ◆  Cervical Spine Injury  370.e1

Abstract

Keywords

Cervical spine injury evaluation is an integral part of what trauma surgeons do on a regular basis. Trauma surgeons have produced the vast majority of the evidence on the topic because we have the most extensive experience. Therefore the responsibility is ours to identify who has an injury and who does not so that collars may be removed in a timely fashion and further investigations may occur in a selective manner, reserving consultation for those patients who actually need subspecialty care. When followed, this algorithm accomplishes these goals, allowing for better outcomes with more cost-effective patient care.

cervical spine blunt trauma clearance fracture ligament injury

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Chapter 122  ◆  Cervical Spine Injury  371

B

Negative for cervical spine injury

E A Trauma patient meeting CDC TTA criteria

GCS=15

1. Isolated TP/SP fracture AND 2. CT negative for ligament injury

Noncontrast cervical spine CT

Remove collar

1. No midline tenderness 2. No paresthesia/focal deficit

No midline tenderness

1. Midline tenderness 2. No paresthesia/focal deficit

Collar X 2 weeks

Paresthesia/focal deficit

H Midline tenderness

G

C Positive for cervical spine injury

GCS persistently 70 mm Hg. EDT has the highest survival rate after isolated cardiac injury, with 20% of patients salvaged despite presenting without vital signs. For patients with penetrating torso injuries, 14% of hypotensive patients and 8% of patients without vital signs but with signs of life are salvaged. For patients sustaining blunt trauma, historically only 1% to 3% of patients survive EDT, regardless of their presenting clinical indices.

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Chapter 124  ◆  Emergency Department Thoracotomy  374.e1

Abstract

Keywords

Patients with impending cardiac arrest or those undergoing cardiopulmonary resuscitation may be salvaged with immediate thoracotomy in the emergency department. Understanding the defined indications and the key components of the associated resuscitative efforts is crucial for the appropriate use of this procedure.

emergency department thoracotomy resuscitative thoracotomy thoracic trauma cardiac arrest

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Chapter 124  ◆  Emergency Department Thoracotomy  375

A

C Patient Undergoing CPR with No Signs of Life

Blunt Trauma CPR < 10 min ---------Penetrating Torso Trauma CPR < 15 min ---------Penetrating Non-Torso Trauma CPR < 5 min

No

Dead

F

Yes

D

Tamponade? Resuscitative Thoracotomy

B Profound Refractory Shock

Cardiac Activity?

No

No

Yes

Yes Cardiac injury – repair heart

G Thoracic hemorrhage – control

Air embolism – hilar cross-clamp

E

I REBOA

H

SBP < 70, Apply Aortic Cross-Clamp

Assess Viability

OR

REFERENCES Burlew CC, Moore EE. Emergency department thoracotomy. In: Moore EE, Feliciano DV, Mattox KL, eds. Trauma. 8th ed. New York, NY: McGraw-Hill; 2017. Burlew CC, Moore EE, Moore FA, et al. Western trauma association critical decisions in trauma: resuscitative thoracotomy. J Trauma Acute Care Surg. 2012;73(6):1359–1363. Keller D, Kulp H, Maher Z, et al. Life after near death: long-term outcomes of emergency department thoracotomy survivors. J Trauma Acute Care Surg. 2013;74(5):1315–1320. Moore EE, Knudson MM, Burlew CC, et al. Defining the limits of resuscitative emergency department thoracotomy: a contemporary western trauma association perspective. J Trauma. 2011;70(2):334–339.

Moore HB, Moore EE, Bensard DD. Pediatric emergency department thoracotomy: a 40-year review. J Pediatr Surg. 2016;51(2):315–318. Moore HB, Moore EE, Burlew CC, et al. Establishing benchmarks for resuscitation of traumatic circulatory arrest: success-to-rescue and survival among 1,708 patients. J Am Coll Surg. 2016;223(1):42–50. Passos EM, Engels PT, Doyle JD, et al. Societal costs of inappropriate emergency department thoracotomy. J Am Coll Surg. 2012;214(1):18–25. Seamon MJ, Haut ER, Van Arendonk K, et al. An evidence-based approach to patient selection for emergency department thoracotomy: a practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2015;79(1):159–173.

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Chapter

125 

PENETRATING NECK TRAUMA L. D. Britt, MD, MPH, DSc (Hon), FACS, FCCM

A There are few regions of the body that are more anatomically dense and organ-system diverse as the neck. As a result, penetrating wounds of the neck have the potential for devastating and life-threatening injuries. Some notable structures in the “anatomic” regions of the neck (zones I, II, and III) include the following: • Pharynx, larynx, trachea • Carotid artery (plus internal and external branches) • Jugular vein • Esophagus • Vertebral arteries • Spinal cord • Cranial nerves IX, X, XI, and XII • Thoracic duct • Sympathetic chain Although the specific management of penetrating neck trauma (with violation of the platysma) has evolved over the past several decades, the overarching principles of initial assessment—as outlined in the Advanced Trauma Life Support (ATLS) course—are unchanged. Optimal management of major cervical penetrating injuries still dictates an ATLS-directed initial assessment or primary survey, with an unwavering and prioritizing emphasis on the ABCs (airway, breathing, circulation, and disability, exposure/environmental control). In addition, the ATLS guidelines/algorithms underscore necessary precautions when there is a possibility of associated cervical spine trauma based on the mechanism of injury and the trajectory of the missile or other piercing weapon/projectile. Resuscitation efforts are also expeditiously initiated during this time-sensitive period. After successfully completing the initial assessment (with a resulting hemodynamically stable patient), a secondary evaluation is performed—a detailed, head-to-toe (back and front) examination. It remains customary to divide the cervical region (neck) into “anatomic” zones (zones I, II, and III). The neck is also divided into an anterior triangle (bordered anteriorly by the midline, posteriorly by the sternocleidomastoid muscle, and superiorly by the lower edge of the mandible, with inferior borders being the clavicle and sternum). The posterior triangle is the area between the sternocleidomastoid (anteriorly) and the trapezius muscle (posteriorly). With the exception of the spinal cord, most vital structures are located in the anterior triangle. Based on the history, physical examination findings, and mechanism of injury, optimal management can span the full spectrum of treatment paradigms, from nonoperative management to mandatory exploration, to selective exploration (determined by significant injuries found by adjunctive invasive or noninvasive studies). A more operative approach is recommended when there is a “hard sign” of aerodigestive and/or vascular injury (e.g., stridor/ respiratory distress, subcutaneous emphysema, air bubbling at the

wound, pulsatile or expanding hematoma). All viable patients who are hemodynamically unstable should be definitively managed in the operating room. B Although there is no role for local wound exploration or probing of the neck in the trauma bay or emergency department, advanced imaging plays a pivotal role in the diagnostic evaluation of penetrating neck injuries. Multidetection computed tomography with angiography (MDCTA) has, essentially, supplanted plain radiography and arteriography in the diagnostic evaluation of the penetrating neck injury. Determination of major vascular and/or tracheal/esophageal injuries is significantly enhanced by the liberal utilization of MDCTA. The extent of the MDCTA evaluation is dependent on the zone(s) of penetration. In addition to being able to document a specific vascular injury, MDCTA also has a high sensitivity for detecting aerodigestive tract injuries. C Zone I, specifically defined as that cervical area between the clavicles/sternum (inferiorly) and the cricoid cartilage (superiorly), is the base of the neck, including the thoracic inlet. Because zone I wounds can involve mediastinal vascular injuries, operative interventions can necessitate performing a median sternotomy to achieve optimal exposure and adequate vascular control. If a patient presents in refractory shock with a zone I injury, he or she should undergo such expeditious operative intervention. Depending on institutional expertise and resources, endovascular techniques (e.g., embolization, stent placement) can be a management option. Patients who have a zone I injury and do not have an indication for surgery should undergo selective management with MDCTA. Aortic arch/great vessel aortography, tracheobronchoscopy, and esophagoscopy/esophagography are possible adjunct diagnostic modalities that could possibly be used if there are equivocal MDCTA findings. The zone II “anatomic” area is between the cricoid cartilage (inferiorly) and the angle of the mandible (superiorly). D Patients who present with a penetrating zone II injury and a “hard sign” of a vascular or aerodigestive tract injury should undergo surgical exploration. Such an exploration can be performed through an incision along the anterior border of sternocleidomastoid muscle or a transverse cervical incision. If the patient is hemodynamically stable and presents with no ominous signs/symptoms, the management can be expectant. Such an approach would require hospital observation, along with serial examinations. Those patients who present with “soft signs” or suspicion for an injury of a major structure should undergo evaluation with MDCTA. If the computed tomographic study demonstrates evidence of an injury, surgical intervention often is required. An open approach remains the standard of care. Although endovascular stenting has been entertained by more proponents, there are no long-term outcome data to support its superiority. Similar to zone I injuries and zone III injuries, aortic arch/great vessel aortography, tracheobronchoscopy, and esophagoscopy/esophagography can be incorporated in the diagnostic evaluation for equivocal MDCTA findings. E The most cephalad area of the neck is zone III, which lies between the angle of the mandible and the base of the skull. As with the other two zones, operative intervention is required in those patients who present in refractory shock. As with zone I wounds, selective management is mandatory for all zone III

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Chapter 125  ◆  Penetrating Neck Trauma  376.e1

Abstract

Keywords

In patients who sustain penetrating neck (or cervical) injuries, the two paramount variables that influence therapeutic management is the following:

penetrating anterior neck trauma management

a) The patients hemodynamic status b) The “anatomic” zones of the neck A patient with a penetrating neck injury, who is in refractory shock, requires emergency exploration. With the intense kinetics (missile speed: greater than 2,500 ft/sec) any patient who survives a high – velocity injury (HVI) will also require operative intervention, due to extensive tissue destruction. At a minimum, surgical debridement would be needed. It is customary and remains practical to divide the neck (cervical region) into “anatomic” zones (zones I, II, and III). Unless, the patient presents in extremis, penetrating injuries to zone I or III dictate selective management, with utilization of imaging studies (multidetection computed tomography with angiography; aortic arch/great vessel aortography; and esophagography) and panendoscopy (tracheobronchoscopy and esophagoscopy). A patient with a zone II injury and a “hard sign” of vascular or aerodigestive tract injury should undergo surgical exploration. Those patients who present with “soft signs” or suspicion for any injury of a major structure should undergo evaluation, with multidetection computed tomography/angiography (MDCTA).

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Chapter 125  ◆  Penetrating Neck Trauma  377

F

Refractory shock

Exploration*

A Presentation

C

Stridor (or respiratory distress) Shock Subcutaneous emphysema Air bubbling at the wound site Hemoptysis External hemorrhage Pulsatile hematoma Expanding hematoma Bruit/thrill Global neurologic deficit Impaled object

MDCTA

Zone I

Observation

Other possible diagnostic adjuncts Stable ± signs/symptoms

Aortic arch/great vessel aortography Tracheobronchoscopy Esophagram/esophagoscopy

SW signs/symptoms GSW -transcervical Refractory shock

Exploration

D Penetrating neck injury

Zone II

SW or GSW signs/symptoms

*Expectant management (observation only) MDCTA Other possible diagnostic adjuncts

B Imaging

E

Stable ± signs/symptoms

SW signs/symptoms GSW -transcervical

Zone III

Multidetector computed tomography with angiography (MDCTA)

injuries. MDCTA remains the pivotal diagnostic modality. Documentation of an injury, particularly arterial, could necessitate additional imaging studies. Such an intervention can be therapeutic, as in the case of an inaccessible arterial injury definitively being treated by angiography/embolization. F A patient with a penetrating neck injury who is in refractory shock requires emergency exploration. Also, any patient who survives a high-velocity injury (HVI) will require surgical exploration; with the high kinetics of HVI (missile speed > 2500 ft/sec), the tissue destruction is extensive, and at a minimum, surgical debridement would be required.

Aortic arch/great vessel aortography Laryngoscopy/tracheoscopy Esophagram/esophagoscopy

signs/symptoms

Refractory shock

Exploration*

REFERENCES Alterman DM. Penetrating neck trauma, MedScape. 2015. Britt L, Peyser M. Penetrating and blunt neck trauma. Trauma. 2000;20:437–449. Cozzi S, Gemma M, DeVitis A, et al. Difficult diagnosis of laryngeal blunt trauma. J Trauma. 1996;40:845–846. Demetriades D, Theodorou D, Cornwell E, et al. Evaluation of penetrating injuries of the neck: prospective study of 233 patients. World J Surg. 1997;21:41–47. Newton K. Penetrating Neck Injuries: Initial Evaluation and Management. Wolters Kluwer; 2016. Sperry JL, Moore EE, Coimbra R, et al. Pittsburgh, PA: Western Trauma Association critical decisions in trauma: penetrating neck trauma. J Trauma Acute Care Surgery. 2013;75(6).

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Chapter

126 

BLUNT CEREBROVASCULAR INJURY Walter L. Biffl, MD

A A patient with signs or symptoms of blunt cerebrovascular injury (BCVI) has an arterial injury until proven otherwise. Rapid diagnosis and treatment may improve neurologic outcome. B Screening of asymptomatic patients has become common in trauma centers, with the goal of diagnosing BCVI and providing prophylactic antithrombotic or other therapy to prevent stroke. Although associations with certain injury mechanisms or patterns have been reported, few studies have examined the true positive predictive value of various risk factors. Many large studies have found that 20% of BCVIs are found in the absence of the accepted “high-risk” factors. To never miss an injury, nearly 100% of patients would have to undergo diagnostic testing. Screening protocols should be based on institutional experience and resources. C Four-vessel biplanar cerebral arteriography (ART) has been considered the gold standard for diagnosis of BCVI. Unfortunately, it is invasive and resource-intensive. Many trauma centers have adopted multidetector-row computed tomography (CT) arteriography for screening because it is relatively easy to obtain, and at-risk trauma patients are generally undergoing CT scanning for other reasons. Its accuracy has been debated, but most studies find that clinically significant injuries are reliably diagnosed if the technical quality is good and the interpreting radiologist is experienced. D Given the potential for false-negative computed tomography arteriography (CTA), ART may be warranted in the setting of high clinical suspicion but a normal CTA, to definitively exclude an injury. Alternatively, the CTA may be repeated at an interval, with an attempt made to optimize the technique. E The Denver grading scale has been found to correlate with stroke rates and should be used to facilitate clear communication and standardize therapy.

F Grade II to Grade V injuries may be approached surgically if they are accessible. A common pitfall is that there is an arterial dissection that extends to the skull base, prohibiting distal control. G Endovascular techniques may salvage patients with grade V injuries. H The primary treatment for BCVI is antithrombotic therapy, to avoid propagation of thrombus. Systemic heparin is generally safe at a low dose, targeting a prothrombin time (PTT) of 40 to 50 sec. Antiplatelet therapy appears to be effective in stroke prevention as well, but the two have not been prospectively compared. Heparin therapy may be reversed if patients are to undergo surgery. The choice and timing of antithrombotic therapy require risk–benefit assessment and multidisciplinary communication among providers treating various injuries. I

A follow-up imaging study is recommended 7 to 10 days after injury or for any change in neurologic status. The Denver group has found that therapy was changed in 65% of Grade I and 51% of Grade II injuries and helped plan therapy for Grade III injuries. J

It has been recommended that patients receive long-term antithrombotic therapy, but the optimal drug and duration have not been studied. In the absence of documented healing of the vessel, it is reasonable to provide some treatment. Currently, the preferred long-term treatment is daily acetylsalicylic acid (ASA) 325 mg. Endovascular stenting may be considered for severe luminal narrowing. REFERENCES Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma. 1999;47:845–853. Biffl WL, Ray CE, Moore EE, et al. Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg. 2002;235:699–707. Bruns BR, Tesoriero R, Kufera J, et al. Blunt cerebrovascular injury screening guidelines: what are we willing to miss? J Trauma Acute Care Surg. 2014;76:691–695. CADISS Trial Investigators, Markus HS, Hayter E, et al. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomized trial. Lancet Neurol. 2015;14:361–367. Edwards NM, Fabian TC, Claridge JA, et al. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid artery injuries: results from longterm followup. J Am Coll Surg. 2007;204: 1007–1015. Shahan CP, Magnotti LJ, Stickley SM, et al. A safe and effective management strategy for blunt cerebrovascular injury: avoiding unnecessary anticoagulation and eliminating stroke. J Trauma Acute Care Surg. 2016;80:915–922.

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Chapter 126  ◆  Blunt Cerebrovascular Injury  378.e1

Abstract

Keywords

This algorithm offers an approach to the diagnosis and treatment of blunt cerebrovascular injuries, based on the best available evidence and expert opinion.

blunt cerebrovascular injury blunt carotid injury blunt vertebral injury screening computed tomography (CT) angiography endovascular antiplatelet anticoagulation

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Chapter 126  ◆  Blunt Cerebrovascular Injury  379

Signs/Symptoms of BCVI Potential arterial hemorrhage from neck/nose/mouth Cervical bruit in pt 50% predicted) • Deep breathing/coughing • EZ-PAP positive airway pressure system • Chest physiotherapy (CPT) • Ambulation G Failure of medical therapy can include the following: • Pneumonia • Inability to wean from the ventilator • Intractable pain H There is evidence to support early video-assisted thoraco­ scopic surgery (VATS) for retained hemothoraces. VATS performed 6 ribs fractured; and (6) >3 fractures with bicortical displacement. The combination of radiographic findings, clinical judgment, and physiologic derangements should be used when determining if rib fixation is warranted. Recent studies support that fixation should be performed early, within the first 48 hours of admission.

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Chapter 127  ◆  Rib Fractures  380.e1

Abstract

Keywords

The management of rib fractures has broadened to include various modalities, including anesthesia, nursing/respiratory care, and operative management. Pain management of rib fractures has evolved into multimodal therapies, with a focus on locoregional anesthesia. Pulmonary hygiene is still an essential component of rib fracture management. Recent studies have focused on early operative fixation of rib fractures (using both clinical and radiographic markers) to identify patients who would benefit from this intervention.

rib fractures rib fixation hemothorax pneumothorax pain control

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Chapter 127  ◆  Rib Fractures  381

A ATLS protocol Primary and secondary survey

C Retained hemothorax Persistent air leak

Pleural space evaluation

H Early VATS

D Flail chest > 3 rib fractures with bi-cortical displacement

E Rib fractures

Pain management

G Refractory to therapy

B CXR Chest CT scan

I Rib fixation

F Pulmonary care

Adequate response Stable exam, good pulmonary effort

REFERENCES Brasel K, Moore EE, Albrecht RA, et al. Western trauma association critical decisions in trauma: management of rib fractures. J Trauma Acute Care Surg. 2017;82:200–203. Bulger EM, Arneson MA, Mock CN, Jurkovich GJ. Rib fractures in the elderly. J Trauma. 2000;48(6):1040–1046.

Continue regimen No additional treatment needed

Pieracci FM, Rodil M, Stovall RT, et al. Jurcovich GJ. Surgical stabilization of severe rib fractures. J Trauma Acute Care Surg. 2015;78:883–887. Smith JW, Franklin GA, Harbrecht BG, Richardson JD. Early VATS for blunt chest trauma: a management technique underutilized by acute care surgeons. J Trauma. 2011;71:102–105.

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Chapter

128 

HEMOPNEUMOTHORAX Hunter Burroughs Moore, MD, and Ernest E. Moore, MD A Chest injury is the most common cause of hemothorax (HTX) and pneumothorax (PTX). Blood and air filling the thoracic space can pose a direct threat to life. A tension pneumothorax requires an immediate intervention because compression of the venous return of the heart will result in shock that, left untreated, will progress to cardiac arrest. In patients with a high clinical suspicion of a tension pneumothorax, immediate finger thoracostomy should be performed empirically to ventilate the chest and immediately improve breathing and circulation. B In hemodynamically stable patients without overt breathing compromise, imaging of the thoracic space is warranted to guide treatment. A PTX can be rapidly identified using the extended focused assessment with sonography for trauma (e-FAST) examination, which involves placing a probe in the intercostal space on the anterior chest and looking for pleural sliding. A lack of pleural sliding is suggestive of a PTX. The sensitivity of this study is variable, depending on the examiner, and is qualitative only. The decision to place a chest tube with a positive examination is based on the clinical scenario. In patients with respiratory distress, subcutaneous emphysema, hypoxia, or decreasing blood pressure, early tube thoracostomy without additional imaging may be warranted. However, PTXs detected by e-FAST do not always mandate chest tube placement. C The standard of care to detect HTX or PTX in a trauma patient is a supine plain x-ray film of the chest (CXR). In nontrauma patients or trauma patients without concern for spine injury, an upright film can improve the sensitivity for detecting a PTX, and a lateral decubitus film can also be used to improve the sensitivity for identifying an HTX. A plain film can rapidly identify PTX and HTX that require intervention before sending the patient to the computed tomography (CT) scanner or operating room. D CT scanning is the most sensitive imaging modality to identify a PTX. An occult PTX, one that is visible only on CT scan, is relatively common, with an incidence of roughly 15%. Treatment of occult PTX is debated, particularly in the setting of positive-pressure ventilation. E HTX/PTX greater than 20% of the pleural cavity warrants a tube thoracostomy. Although supine plain films can underestimate the size of a PTX, lung markings that have retracted within the second intercostal space indicate a 20% PTX. F An isolated PTX with 200/hr for 2 sequential hours

Primary survey Concern for tension PTX

2nd tube thoracostomy + CXR

History and physical exam

H HTX+PTX > 20%

E Hemo- or pneumothorax

B E-FAST Chest X ray CT scan

D

C

G

Positive pressure ventilation No

J

HTX < 20% Observation with repeat CXR

M In chest tubes that have a persistent air leak, the CXR should be evaluated to ensure the sentinel eye is in the chest, followed by an assessment for any potential leaks in the system. This occasionally requires replacement of the pleurovac. Air leaks can resolve on their own over several days if the visceral pleura of the lung is in contact with the chest wall. Persistent posttraumatic PTXs beyond 3 days are uncommon and should be considered for video-assisted thoracoscopic surgery (VATS) to close the lung laceration or mechanical pleurodesis if no source is identified. VATS reduces hospital length of stay and chest tube duration. Persistent PTXs in the nontrauma setting are less likely to improve with surgical intervention and should be treated conservatively for a longer duration. In patients with high-volume leaks, early bronchoscopy should be performed to rule out a proximal bronchus injury. N Timing of chest tube removal is based on re-expansion of the lung, the amount of fluid visualized in the pleural space on CXR, and the 24-hour output. The chest tube should be placed to water seal and evaluated over time to ensure no reaccumulation of a PTX. In a healthy individual, the pleural space can clear up to 500 cc of fluid a day. The cutoff for removal of a chest tube is clinician dependent. Less than 50 cc a day of drainage is a conservative volume to consider chest tube removal, but based on the clinical setting, less than 150 cc or more may be warranted to consider removing the tube. O If two chest tubes have been placed without resolution of the HTX, the patient has a caked HTX. These patients are

O

Persistent HTX/PTX

Persistent HTX/PTX

K

Yes

F PTX < 20%

Tube thoracostomy + CXR

Expansion

A

OR thoracotomy

Foley catheter +

Concern for intercostal injury

L Resolution F/u CXR Q AM

M

VATS

Persistent air leak

N CT output 10 mm, Grade III—pseudoaneurysm, and Grade IV—rupture (Fig. 129.1). Type IV injuries are seen very infrequently because these patients rarely make it to a hospital alive.

D

 

MEDICAL MANAGEMENT OF GRADE I INJURIES

Grade I injuries (small intimal flap) are increasingly being diagnosed as the resolution of CTA has increased and have become the subject of much debate over the past decade. Recent data have demonstrated that only 5% of these injuries, also called minimal aortic injuries (MAIs), will progress on follow-up imaging to require repair. They should be treated initially with medical management, with the goal of keeping the heart rate less than 100 bpm and the systolic blood pressure below 100 mm Hg. The first-line therapy should be short-acting IV beta blockers such as esmolol or labetalol. Vasodilators, such as nitroprusside, nitroglycerin, and nicardipine, should be reserved for patients whose blood pressure cannot be adequately controlled with beta blockers because of their propensity to cause reflux tachycardia, which increases aortic shear stress. If not contraindicated, patients should also receive low-dose aspirin (81 mg) to aid recovery of the intimal injury and prevent thrombus formation. Routine follow-up CTA of the chest should be performed between 3 and 7 days after the injury to assess for injury progression. Occasionally, blood pressure control is not possible or is contraindicated, for example, in patients with TBI and elevated intracranial pressure requiring elevated blood pressure. In these patients, semi-elective thoracic endovascular aortic repair (TEVAR) may be performed selectively in a manner similar to those with Grade II or III injuries. E

 

SEMI-ELECTIVE TEVAR FOR GRADE II OR III INJURIES

Patients with BTAI frequently present with more urgently lifethreatening injuries that should be dealt with first. The AAST2 study demonstrated in a retrospective analysis that delaying repair (>24 hours) to address other life-threatening injuries was associated with improved results. There is now good evidence that TEVAR is effective and has fewer short-term and midterm complications (e.g., paralysis) than open repair. Data are lacking on long-term (>15 years) outcomes; however, the modern endografts in use today have been developed to be more conformable to the aortic arch, are lower profile, and come in sizes more suitable for young trauma patients. Furthermore, most long-term complications from TEVAR can be managed electively. There is a consensus that patients with Grade II or III injuries should undergo TEVAR within 48 hours if possible or at least before discharge. Systemic heparinization is the standard practice for TEVAR; however, because the procedure can be performed rapidly, heparin can be given at a lower dose or used selectively if contraindicated (e.g., for worsening intracranial bleeding). F

 

EMERGENCY TEVAR FOR GRADE IV INJURIES

Patients with a Grade IV injury found on CTA represent the smallest subset and require immediate repair because they have a free aortic rupture with ongoing hemorrhage. Emergency TEVAR is the treatment of choice with the least morbidity. If TEVAR is not readily available, open surgical repair via a left posterolateral thoracotomy can be attempted with clamping of the aorta just proximal to the left subclavian artery; however, this is associated with much higher morbidity and mortality.

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Chapter 129  ◆  Blunt Thoracic Aortic Injury  384.e1

Abstract

Keyword

Blunt thoracic aortic injuries (BTAIs) are found in only 0.5% of trauma patients who present to the hospital alive; however, the true incidence is much higher because only 20% of patients with a BTAI survive the scene of the accident. Of all deaths at the scene of traffic accidents, 33% are because of BTAI. It is estimated that 14,000 people die annually from BTAI in the United States, making it the second most common cause of death after traumatic brain injury (TBI).

blunt thoracic aortic injury

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Chapter 129  ◆  Blunt Thoracic Aortic Injury  385

Fig. 129.1  Azizzadeh A1, Keyhani K, Miller CC 3rd, Coogan SM, Safi HJ, Estrera AL. SVS grading system for BTAI—Blunt traumatic aortic injury: initial experience with endovascular repair. Vasc Surg. 2009 Jun;49(6):14038. doi: 10.1016/j.jvs.2009.02.234.

A High risk mechanism of injury

D Blood pressure control

Follow up CTA chest in 3–7 days

C Grade I injury small intimal flap Blunt thoracic aortic injury

Grade II injury intramural hematoma Grade III injury pseudoaneurysm

Semi-elective TEVAR

Grade IV injury rupture

F B CTA chest

H

E G

Follow up CTA; 1–4 weeks and annually for 3 years

Selective revascularization for coverage of left subclavian artery

Emergency TEVAR

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386  Part VIII  ◆ Trauma G

 

COVERAGE OF LEFT SUBCLAVIAN ARTERY MANAGEMENT

The location of BTAIs is frequently just distal to the left subclavian artery, and to get at least 2 cm of proximal coverage of the injury, the left subclavian artery often must be covered by the endograft. Coverage of the left subclavian artery rarely causes any morbidity, and therefore revascularization can be safely performed selectively based on symptoms or unique anatomic considerations. The left subclavian will receive sufficient blood flow via retrograde flow in the intact left vertebral artery in the majority of patients, but in patients who have a left vertebral artery that is dominant, occluded, injured, or originates directly off the aortic arch, revascularization is more likely to be required. For patients with a left internal mammary to coronary artery bypass graft, left subclavian artery revascularization is mandatory prior to coverage of the left subclavian artery with an endograft. These considerations and data from numerous studies provide the basis for the Society of Vascular Surgery’s published guidelines that recommend selective revascularization for left subclavian coverage by TEVAR. H   FOLLOW-UP IMAGING

Routine follow-up CTA of the chest is not required before discharge but should be obtained 1 to 4 weeks postoperatively and annually thereafter for at least 3 years to evaluate for appropriate coverage of the injury with the endograft, endoleak around

the endograft, and any anatomic considerations that would warrant more frequent follow-up. REFERENCES Demetriades D, Velmahos GC, Scalea TM, et al. Diagnosis and treatment of blunt thoracic aortic injuries: changing perspectives. J Trauma. 2008a;64(6):1415–1418, discussion 1418–1419. Demetriades D, Velmahos GC, Scalea TM, et al. Operative repair or endovascular stent graft in blunt traumatic thoracic aortic injuries: results of an American association for the surgery of trauma multicenter study. J Trauma. 2008b;64(3):561–570, discussion 570–571. Demetriades D, Velmahos GC, Scalea TM, et al. Blunt traumatic thoracic aortic injuries: early or delayed repair–results of an American association for the surgery of trauma prospective study. J Trauma. 2009;66(4): 967–973. Fabian TC, Davis KA, Gavant ML, et al. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg. 1998;227(5):666–676, discussion 676–677. Lee WA, Matsumura JS, Mitchell RS, et al. Endovascular repair of traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery. J Vasc Surg. 2011;53(1):187–192. Matsumura JS, Lee WA, Mitchell RS, et al. The Society for Vascular Surgery practice guidelines: management of the left subclavian artery with thoracic endovascular aortic repair. J Vasc Surg. 2009;50(5):1155–1158. Osgood MJ, Heck JM, Rellinger EJ, et al. Natural history of grade I-II blunt traumatic aortic injury. J Vasc Surg. 2014;59(2):334–341. Starnes BW, Lundgren RS, Gunn M, et al. A new classification scheme for treating blunt aortic injury. J Vasc Surg. 2012;55(1):47–54. Tang GL, Tehrani HY, Usman A, et al. Reduced mortality, paraplegia, and stroke with stent graft repair of blunt aortic transections: a modern meta-analysis. J Vasc Surg. 2008;47(3):671–675.

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Chapter

130 

BLUNT CARDIAC INJURY Ashley K. McCusker, MD, MSc, and Bellal A. Joseph, MD, FACS

A Blunt cardiac injury (BCI) is a diagnostic quandary because it can manifest immediately, leading to the death of the patient, or in a delayed presentation. BCI can be divided into two categories: structural cardiac injuries and electrical and conduction disturbances. In investigations of fatal cardiac injuries, autopsy studies have shown that the most common structural injuries were transmural rupture of a cardiac chamber, tears at the venous-atrial confluence, or blunt coronary artery dissection or tear. The phenomenon of commotio cordis is a conduction abnormality leading to sudden death from cardiac arrest after a blunt blow to the chest in a patient with a normal heart. This is presumed to be from an impact transmitted to the myocardium during electrical repolarization. Most of these patients tend to be refractory to cardiopulmonary resuscitation (CPR) and defibrillation even within 3 minutes of the arrest. For patients with BCI who arrive alive at the hospital, their injuries tend to be less severe. However, in combination with other injuries, the signs and symptoms of BCI can be missed or masked because the most common arrhythmia associated with BCI is sinus tachycardia. Patients should be screened for BCI based on the mechanism of injury and presenting symptoms. The force of injury in BCI may be from direct, indirect, crush injury, compressive, deceleration, blast, concussive, or combined forces. All patients with blunt chest trauma should be suspected of BCI. Almost half of BCIs occur in motor vehicle crashes, with BCI also seen in pedestrians struck by vehicles, motorcycle crashes, and falls from significant height. Associated injuries are rib, thoracic spine, and sternal fractures; pulmonary contusions; pneumothorax; hemothorax; and injuries to the great vessels. However, sternal fracture alone with a normal electrocardiogram (ECG) and troponin I does not correlate with BCI. The most commonly injured area of the heart is the right ventricle because of its anterior location, followed by the right atrium and left ventricle, but more than half of patients with BCI have injury to multiple chambers. Friction rubs, new murmurs, or distant muffled heart sounds are more specific for BCI but, again, may be difficult to appreciate during a trauma evaluation. Any patient

with dyspnea, chest wall crepitus, chest wall ecchymosis, or seat-belt sign should also be suspected of having BCI. B Screening begins with a 12-lead ECG and biochemical marker testing, with troponin I being the most specific for cardiac injury. A chest x-ray should have been performed in the trauma work-up. C Studies have shown that the combination of a normal ECG and normal troponin I (less than 0.4 ng/mL) rules out a clinically significant BCI, with negative predictive values ranging from 98% to 100%. Patients may be discharged after normal ECG and troponin at time of trauma evaluation and 8 hours later. D All patients with elevated troponin I > 0.4 ng/mL or any abnormality on the 12-lead ECG should be admitted for continuous telemetry for at least 24 hours. The admission may be extended to 48 hours because most ECG abnormalities will manifest within that time frame. A repeat EKG should be done at 24 hours. E Intensive care unit (ICU) admission is warranted if the patient has signs of hemodynamic instability, a persistent arrhythmia, or a high-degree heart block, especially when associated with electrolyte disturbance or acidemia. An echocardiogram should be obtained in those instances. However, an echocardiogram is not a useful screening examination and should not routinely be performed for all suspected BCI patients. A transthoracic echocardiogram is a less invasive procedure but may be limited by body habitus, pain, chest tubes, crepitus, or other chest wall trauma. A transesophageal echocardiogram is necessary when the transthoracic echocardiogram does not show optimal images of the heart and thoracic aorta. Cardiology consult and possibly cardiothoracic surgery consult should be obtained if structural abnormalities are revealed on echocardiogram or if an arrhythmia persists. If acute heart failure occurs, consideration for pulmonary artery catheter insertion should be given. REFERENCES Clancy K, Velopulos C, Bilaniuk JW, et al. Screening for blunt cardiac injury: EAST practice management guideline. J Trauma Acute Care Surg. 2012;73:S301–S306. El-Menyar A, Al Thani H, Zarour A, Latifi R. Understanding traumatic blunt cardiac injury. Ann Cardiac Anaesth Vol. 2012;15:287–295. Marcolini EG, Keegan J. Blunt cardiac injury. Emerg Med Clin N Am. 2015;33:519–527. Peitzman AB, Schwab CW, Yealy DM, Rhodes M, Fabian TC. The Trauma Manual: Trauma and Acute Care Surgery. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013. Yousef R, Carr JA. Blunt cardiac trauma: a review of the current knowledge and management. Ann Thorac Surg. 2014;98:1134–1140.

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Chapter 130  ◆  Blunt Cardiac Injury  388.e1

Abstract

Keywords

Blunt cardiac injury (BCI) is a clinical entity that presents the physician with a diagnostic quandary because it can manifest immediately, leading to the death of the patient, or in a delayed presentation. BCI can be divided into two categories: structural cardiac injuries and electrical and conduction disturbances. Screening begins with a 12-lead electrocardiogram (ECG) and biochemical marker testing, with troponin I being the most specific for cardiac injury. A chest x-ray should have been performed in the trauma work-up. All patients with elevated troponin I > 0.4 ng/mL or any abnormality on the 12-lead ECG should be admitted for continuous telemetry for at least 24 hours. Intensive care unit (ICU) admission is warranted if the patient has signs of hemodynamic instability, a persistent arrhythmia, or a high degree heart block, especially when associated with electrolyte disturbance or acidemia. An echocardiogram should be obtained in those instances.

ECG troponin echocardiogram telemetry monitoring

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Chapter 130  ◆  Blunt Cardiac Injury  389

D

Age >50 yo Previous cardiac history steering wheel deformity, dyspnea, JVD, murmur, chest wall ecchymosis/es at belt sign, crepitus, flail chest

Arrhythmia, ST changes, ischemia, heart block

Admit for telemetry 24–48 hr, repeat EKG

Hemodynamic instability OR New persistent arrhythmia

E ICU admit, ECHO + cards consult

B EKG

A Suspected blunt cardiac injury

BLUNT CHEST INJURY: sternal fracture, rib fractures, pulmonary contustion, pneumothorax, hemothorax, great vessel injury

+

C Normal EKG normal troponin I (presentation and 8 hr later)

Clinically significant BCI ruled out

B Troponin I Elevated >0.4 ng/mL

D Admit for telemetry 24–48 hr

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Chapter

131 

ANNOTATIONS TO THORACOABDOMINAL TRAUMA Mary Condron, MD, and Karen J. Brasel, MD, MPH A The early evaluation of a patient in whom you suspect a penetrating thoracoabdominal injury must include (1) assessment of hemodynamics; (2) primary and secondary survey based on advanced trauma life support (ATLS), including a rapid but comprehensive physical examination; and in most cases (3) bedside imaging. B An upright chest x-ray should be obtained in the vast majority of patients with evidence of penetrating thoracoabdominal injury. A thoracostomy tube should be placed if there is evidence of hemo- or pneumothorax. Bedside imaging should include the extended focused assessment with sonography for trauma (eFAST) examination when there is a concern for free fluid but the patient is not appropriate for the computed tomography (CT) scanner. It should also be obtained in any patient in whom there is concern for a cardiac injury (CT scan is poor at detecting cardiac injury). C Chest tube output should lead directly to thoracotomy when there is an initial output of >1500 mL or subsequent output is >200 mL/hour for 2 to 4 consecutive hours (sources vary about duration of observation; use of clinical judgment is necessary). Two important caveats to this approach are that (1) blood in the chest may represent intraabdominal bleeding entering the chest via a diaphragm injury, and (2) the ongoing presence of an acute hemothorax despite successful placement of a thoracostomy tube likely represents ongoing, uncontrolled hemorrhage rather than a retained clot. D The decision to initially enter the abdomen versus the chest can be difficult, with the wrong cavity being entered in >20% of cases, even with the use of eFAST. The chest should be opened first to perform a resuscitative thoracotomy or in cases where there is a strong index of suspicion for cardiac tamponade. The abdominal examination can provide some guidance for your exploration but may be falsely negative in a patient in extremis or falsely positive in a patient with a thoracic injury. The eFAST examination and peritoneal lavage can provide guidance, but they are both subject to error (such as when a diaphragmatic defect leads to contamination of both cavities from one injury). E CT scanning can be very helpful in the assessment and diagnosis of patients with penetrating thoracoabdominal trauma but is only appropriate in hemodynamically stable patients without peritonitis. Care should be taken to avoid deeming patients with elevated blood pressure and narrow pulse pressure “stable” because this may reflect transient compensation for

exsanguinating injury via increased sympathetic tone. Care should also be taken to avoid deeming patients with negative CT scan “uninjured” because CT scanning frequently does not detect isolated diaphragmatic injury, particularly with right-sided injuries. Diagnostic laparoscopy and thoracoscopy have been used successfully by several groups to detect clinically occult diaphragm injuries in hemodynamically stable patients with penetrating thoracoabdominal wounds. F If thoracotomy was initially performed but there is evidence of ongoing transdiaphragmatic bleeding or ongoing shock not explained by the intrathoracic findings, the abdomen should be explored. In large studies, the rate of initially entering the “wrong” cavity is routinely more than 20%, with reported ranges above 40%. We are not aware of any studies specifically designed to look at the effect of eFAST on the problem of “double jeopardy”; however, reported rates have not changed significantly with the routine use of the eFAST examination. Initially entering the wrong cavity is associated with a dramatic increase in mortality. G In patients with a left-sided mechanism, negative examination, and negative imaging but suspicion for diaphragmatic injury based on mechanism, a nonemergent laparoscopic or thoracoscopic exploration should be performed during the next 24 hours. H The development of peritonitis, unexplained fever, or hemodynamic instability during serial examinations mandates laparotomy. Serial examination should continue for at least 36 hours post injury. I

Free air and free fluid are strong indicators for laparotomy, particularly when there is no solid organ injury to justify the free fluid. Laparotomy should additionally be considered in cases where stranding or mesenteric inflammation are suggestive of a bowel injury. J

Intraoperative evidence of ongoing thoracic bleeding, including persistent oozing through a diaphragmatic laceration or a bulging intact hemidiaphragm, should prompt thoracotomy or thoracoscopy. Elevated peak inspiratory pressures, persistent or recurrent hypotension, elevated central venous pressure, and unexplained respiratory deterioration should be repeatedly checked for (primarily via discussion with the anesthesia provider) and should prompt serious consideration of thoracotomy with or without first performing a pericardial window. K Therapeutic embolization, where promptly available, can be an excellent management strategy for isolated solid organ injuries. Injuries at grade III and above, particularly ones in which a “blush” is appreciated, may be a good fit for this management strategy. For a more detailed discussion of the decision making around pursuing therapeutic embolization, please see the Journal of Trauma practice management guidelines. L Many low-grade solid organ injuries are appropriate for initial nonoperative management, particularly in the absence of a “blush.” The majority of these patients will be appropriate for discharge after a period of close observation if they have a reliable abdominal examination.

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Chapter 131  ◆  Annotations to Thoracoabdominal Trauma  390.e1

Abstract

Keywords

Penetrating thoracoabdominal trauma is challenging because of the need to consider the variety of organs that may be injured while simultaneously evaluating the hemodynamic status of the patient. For those in shock, balanced resuscitation should be initiated coincident with physical examination, ultrasound, and chest radiograph. Intervention is dictated by both the response to resuscitation and the results of these investigations. For those patients who are hemodynamically normal, a computed tomography (CT) scan provides more information. However, even a negative CT does not exclude diaphragm injury, and consideration should be given to thoracoscopy or laparoscopy particularly when the injury is on the left.

diaphragm laparoscopy thoracoscopy extended focused assessment with sonography for trauma (eFAST)

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Chapter 131  ◆  Annotations to Thoracoabdominal Trauma  391

F

History and Physical Examination

C

Primary Survey

Prehospital details A.T.L.S. A.M.P.L.E. medical history Secondary Survey

A

Immediate Return of >1,500cc of Blood or >200cc/hr for 2-4hrs Tube

D

Thoracostomy

Hemodynamically Unstable Penetrating Thoracoabdominal Injury

B

Thoracotomy

Evidence of Tamponade or FAST Suggestive of Thoracic Source; Need for Resuscitative Thoracotomy Peritonitis, Free Intraabdominal Air, Abdominal Contents in Chest on CXR, FAST Suggestive of Abdominal Source

Laparotomy

J

Tense Pericardium or Ongoing Unexplained Shock Laparotomy

Observation and Serial Exams X24-48hrs No Injury Identified

Asymptomatic

Negative

H

Peritonitis

E CT Scan

Positive

Injury Identified

No Injury Identified

Solid Organ Injury Appropriate for NonOperative Management

Left-Sided Injury

Anderson JE, Salcedo ES, Rounds KM, Galante JM. Getting a better look: outcomes of laparoscopic versus transdiaphragmatic pericardial window for penetrating thoracoabdominal trauma at a level I trauma center. J Trauma Acute Care Surg. 2016;81:1035–1038. Asensio JA, Arroyo H Jr, Veloz W, et al. Penetrating thoracoabdominal injuries: ongoing dilemma which cavity and when? World J Surg. 2002;26:539–543. Berg RJ, Karamanos E, Inaba K, et al. The persistent diagnostic challenge of thoracoabdominal stab wounds. J Trauma Acute Care Surg. 2014;76: 418–423. Clarke DL, Gall TM, Thomson SR. Double jeopardy revisited: clinical decision making in unstable patients with thoraco-abdominal stab wounds and potential injuries in multiple body cavities. Injury. 2011;42:478–481. Como JJ, Bokhari F, Chiu WC, et al. Practice management guidelines for selective nonoperative management of penetrating abdominal trauma. J Trauma. 2010;68(3):721–733.

I

Free Air, Free Fluid without Solid Organ Injury, Evidence of Hollow Viscous Injury Liver or Spleen “Blush”

Right-Sided Injury

REFERENCES

Thoracotomy

Thoracoscopy vs Pericardial Window

Hemodynamically Stable

Trauma Bay Interventions IVF/Blood/Antibiotics NGT Foley Upright CXR eFAST Labs including T&C

Bleeding per Diaphragm Injury or Ongoing Unexplained Shock

G

Non-Emergent Laparoscopy and/or Thoracoscopy to Evaluate Diaphragm

Discharge

Laparotomy

K Therapeutic Embolization Observation and Serial Exams X24-48hrs

L

Demetriades D, Hadjizacharia P, Constantinou C, et al. Selective nonoperative management of penetrating abdominal solid organ injuries. Ann Surg. 2006;244(4):620–628. Hirshberg A, Wall MJ Jr, Allen MK, Mattox KL. Double jeopardy: thoracoabdominal injuries requiring surgical intervention in both chest and abdomen. J Trauma. 1995;39(2):225–231. Parreira JG, Rasslan S, Utiyama E. Controversies in the management of asymptomatic patients sustaining penetrating thoracoabdominal wounds. Clinics (Sao Paulo). 2008;63(5):695–700. Quinn AC, Sinert R. What is the utility of the focused assessment with sonography in trauma (FAST) exam in penetrating torso trauma? Injury. 2011;42:482–487. Ties JS, Peschman JR, Moreno A, et al. Evolution in the management of traumatic diaphragmatic injuries: a multicenter review. J Trauma Acute Care Surg. 2014;76(4):1024–1028.

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Chapter

132 

BLUNT ABDOMINAL TRAUMA Frank Z. Zhao, MD, and Walter L. Biffl, MD A The primary survey is the first key step and consists of sequential evaluation of the patient’s airway, breathing, circulation, and disability. The patient should be exposed during this time to adequately identify immediate life-threatening injuries. B Laboratory studies such as complete blood count and basic metabolic panel should be obtained as part of most trauma evaluations. Blood typing and coagulation studies should be obtained for all patients who are at risk for bleeding or require transfusions. Urinalysis and toxicology studies should also be obtained. In many hospitals, point-of-care testing now allows results to be obtained in the emergency department (ED) within the first 10 minutes of arrival. C Blunt abdominal trauma is a source of significant morbidity and preventable mortality. An expeditious and regimented evaluation algorithm can quickly identify life-threatening problems without missing other important injuries. We set forth an evidence-based algorithm to guide providers through fast and effective triage of this subset of patients. D The identification of hemodynamic instability is the first priority. The most frequent cause of instability in blunt trauma is cavitary hemorrhage. Thus for unstable patients, it is crucial to simultaneously begin resuscitation and determine the location of the hemorrhage. E If the traumatically injured patient is initially hemodynamically normal, then the evaluation can proceed to the secondary survey and adjunctive history, labs, and x-ray studies. The secondary survey includes a thorough head-to-toe physical examination. Signs of major thoracic and/or pelvic trauma should raise suspicion for intraabdominal injury. The finding of abdominal bruising such as a seat-belt sign is also associated with increased rates of intraabdominal injury. AMPLE history should be obtained for the allergies, medications, past medical history, last meal, and events surrounding the injury. Routine chest and pelvic x-rays, although not mandatory, are recommended for all patients with the potential for multisystem trauma. They can be performed and interpreted at the bedside and can identify life-threatening injuries early in the evaluation. F Focused assessment with sonography for trauma (FAST) is typically the most readily available examination modality in the ED setting. It can be reliably performed by trained surgeons, ED physicians, and advanced practice clinicians. Performance of the examination evaluates for free fluid in the right upper quadrant (Morison’s pouch), left upper quadrant (perisplenic space), pelvis (pouch of Douglas), and pericardium. Multiple

prior studies report a sensitivity of 69% to 98% and specificity from 95% to 100% for hemoperitoneum. In the setting of hemodynamic instability and thus the inability to evaluate using computed tomography (CT), the FAST examination is the optimal tool to identify the abdomen as a source of significant hemorrhage. G Peritonitis identified on secondary survey is a clear indication to proceed to laparotomy for operative exploration. H In contrast to blunt trauma patients with hemodynamic instability, there has been much debate in recent years regarding the role of FAST examination for the hemodynamically stable patient. In this population, false-negative rates as high as 29% have been reported, indicating a significant portion of missed intraabdominal injuries as compared with CT scan. Whereas stable patients with a positive FAST examination necessitate further evaluation with CT, a negative FAST examination relies on the provider’s examination and clinical suspicion regarding the next step of the evaluation. Often these patients will require further imaging with CT. Some have previously suggested the removal of FAST examinations from stable trauma patient evaluation algorithms. However, the opinion of the current authors is that the FAST examination should continue to be a part of every blunt trauma evaluation. Although a negative FAST examination does not exclude intraabdominal injury, a positive examination is an important finding, especially should the patient become unstable during the subsequent evaluation period. Routine performance of the FAST examination adds little time or cost; in addition, it can provide necessary training and experience to providers, decreasing interobserver variability and improving the reliability of the test. I

If the FAST examination is negative or equivocal, diagnostic peritoneal aspiration/lavage (DPA/DPL) may be used to exclude significant hemoperitoneum as the source of hemodynamic instability. This can be done via an open or closed technique. A catheter is inserted into the abdomen under local anesthesia. If initial aspiration returns at least 10 mL of blood, the test is considered positive. If aspiration does not reveal frank blood, then 1 L of saline is infused into the peritoneal cavity and subsequently drained and sent for laboratory analysis. A positive test is defined as fluid returning more than 100,000 red blood cells (RBCs)/mL of fluid. Bilious fluid or intestinal contents in the fluid also mandate surgical intervention. Other concerning fluid laboratory values include white blood cell (WBC) count > 500/mL, bilirubin > 0.3 mg/dL, amylase > 20 IU/L, and alkaline phosphatase > 3 IU/L. Although these latter values may not mandate laparotomy, it should be strongly considered. The reported false-negative DPL rate is 2%. Retroperitoneum hemorrhage is poorly evaluated by this technique. If DPL is not performed, a repeat FAST examination can be considered either by the same or different provider. Serial FAST examinations have been shown to improve overall sensitivity for hemoperitoneum compared with a single examination. J

Hemodynamically stable patients with negative FAST examination should undergo further imaging with CT scan as follows: (1) Patients with a Glasgow Coma Scale (GCS) score of less than 11 would be considered to have an unreliable examination for observation. (2) Abdominal pain and signs of abdominal trauma warrant further evaluation with CT. (3)

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Chapter 132  ◆  Blunt Abdominal Trauma  392.e1

Abstract

Keywords

Blunt abdominal trauma should be approached in a systematic manner to ensure prompt attention to life-threatening problems and avoid missed injuries. This algorithm offers a safe, evidencebased approach.

trauma abdomen ultrasound CT scan laparotomy

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Chapter 132  ◆  Blunt Abdominal Trauma  393 Hematuria indicates genital-urinary system injury, often from bladder rupture or renal laceration. These would be better characterized by CT with delayed phase contrast imaging and cystography. (4) Major thoracic and pelvic trauma is associated with concurrent intraabdominal injury. (5) Finally, patients with severe distracting injuries maybe unreliable for abdominal examination. If the mechanism suggests abdominal injury is possible, CT evaluation should be obtained. K CT evaluation with intravenous (IV) contrast of the abdomen and pelvis is warranted for patients who are hemodynamically stable and have either clinical indicators of possible intraabdominal injury or unreliable abdominal examination. Solid organ injury and hemoperitoneum and retroperitoneal hematomas have been detected with reported sensitivities greater than 95%. Less sensitive are evaluations of bowel, pancreas, and mesenteric injury, whose reported sensitivity falls to 70%. Specialized protocols such as delayed phase imaging and cystography should be added when clinical concern is present. L Female patients of reproductive age frequently have small amounts of physiologic fluid in the pelvis. A similar finding of isolated fluid can be seen in 3% to 5% of males. However, larger volumes of intraperitoneal fluid without solid organ injury is concerning for hollow viscous injury. Alert patients can undergo observation and serial examinations; signs of worsening pain or peritonitis should prompt laparotomy. Comatose and/or sedated patients should undergo either DPL or diagnostic laparoscopy for further evaluation. Laparotomy should be performed if there are concerning findings.

Other signs of bowel injury include focal bowel wall thickening, extraluminal air, pneumatosis, abnormal bowel wall enhancement, and mesenteric injuries. The presence of these findings should prompt operative exploration with laparotomy. Diagnostic laparoscopy may be considered if the provider is facile with the technique; however, this is not considered the current standard of care, and various studies have previously suggested a higher rate of missed intraabdominal injuries. Patients with CT-identified solid organ injuries can often become hemodynamically unstable during or after their initial evaluation. Higher grade injuries are more likely to follow this course. Laparotomy will provide the most expeditious route of hemorrhage control. Alternatively, in medical centers with interventional radiologists immediately available, angiography with embolization may also provide hemorrhage control. However, the authors caution that this decision should not delay hemorrhage control. If laparotomy can be performed more quickly, it should be the procedure of choice. Specific organ injuries and their management are covered elsewhere in this text. M If serial FAST examination or DPL results are negative for intraperitoneal hemorrhage, alternate sources of shock (e.g., hemorrhage in chest, pelvis, or extremities; neurogenic or cardiogenic shock) need to be evaluated. N Laparotomy is the definitive diagnosis and therapeutic modality for both hemorrhage control and repair of hollow visceral injuries. A midline incision provides rapid access and can be extended for additional exposure. Priorities are to first identify and control hemorrhage, followed by identification and

M

I

A F

Primary Survey ATLS

Search for alternate source of HD instability

DPL or Repeat FAST

FAST Exam

D

N

Hemodynamically unstable

G

C Blunt Abdominal Trauma

B CBC INR ABG Lactate Type & Cross UA Toxicology CXR Pelvis Xray

Laparotomy

L

Peritonitis

E Hemodynamically stable 1. Secondary Survey 2. AMPLE History 3. X-rays 4. Adjunct labs

K H FAST Exam*

CT scan of Abdomen and Pelvis

• Free fluid without solid organ injury? • Other findings of hollow viscous injury? • Solid organ injury with hemodynamic instability?

O

J • GCS < 11? • Signs of abdominal trauma? • Abdominal pain? • Distracting injury? • Major Chest or Pelvic trauma?

Observe

Discharge

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394  Part VIII  ◆ Trauma control of contamination. Once the abdominal cavity is thoroughly evaluated and all injuries identified, definitive care can be performed if the patient’s physiology allows. Management of specific injuries is outside the scope of this chapter and can be found elsewhere in this text. O Patients admitted for observation should undergo serial abdominal examinations, monitoring of vital signs, and repeated laboratory testing. Changes in patient status warrant prompt reevaluation and possible surgical intervention. Patients with no identified injuries or concerns can be discharged with counseling regarding warning signs for return to the hospital. REFERENCES American College of Surgeons Committee on Trauma. Advanced Trauma Life Support. 9th ed. Chicago, IL: 2012. Branney SW, Moore EE, Cantrill SV, et al. Ultrasound based key clinical pathway reduces the use of hospital resources for the evaluation of blunt abdominal trauma. J Trauma. 1997;42:1086–1090.

Cha JY, Kashuk JL, Moore EE, et al. Diagnostic peritoneal lavage remains a valuable adjunct to modern imaging techniques. J Trauma. 2009;67: 330–336. Henneman PL, Marx JA, Moore EE, et al. Diagnostic peritoneal lavage: accuracy in predicting necessary laparotomy following blunt and penetrating trauma. J Trauma. 1990;30:1345–1355. Miller MT, Pasquale MD, Cox J, et al. Not so FAST. J Trauma. 2003;54: 52–60. Natarajan B, Gupta PK, Forse RA, et al. FAST scan: is it worth doing in hemodynamically stable blunt trauma patients? Surgery. 2010;148: 695–701. Richards JR, McGahan JP. Focused assessment with sonography in trauma (FAST) in 2017: what radiologists can learn. Radiology. 2017;283: 30–48. Rodriguez C, Barone JE, Miller K, et al. Isolated free fluid on computed tomographic scan in blunt abdominal trauma: a systematic review of incidence and management. J Trauma. 2002;53:79–85. Rozycki RA, Ballard RB, Feliciano DV, et al. Surgeon-performed ultrasound for the assessment of truncal injuries: lessons learned from 1540 patients. Ann Surg. 1998;228:557–567. Soto JA, Anderson SW. Multidetector CT of blunt abdominal trauma. Radiology. 2012;265:678–693.

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Chapter

133 

PENETRATING ABDOMINAL INJURY Catherine Velopulos, MD, MHS

A Management of penetrating trauma to the abdomen or thoracoabdominal area is dictated by hemodynamics, physical examination, and adjunct studies. Patients with penetrating injury have a high likelihood of proceeding to operative management (60% to 70% of stab wounds and 70% to 95% of gunshot wounds), although a significant number can undergo selective nonoperative management. While undergoing the primary survey, patients should be initially resuscitated with 2 L crystalloid. If ongoing resuscitation is needed, the massive transfusion protocol should be initiated. B Patients who are normotensive but present with frank peritonitis or evisceration should proceed to the operating room (OR) for laparotomy. In some cases, a computed tomography (CT) may be obtained to evaluate the retroperitoneum and trajectory, but this should not delay proceeding to the OR. C Patients who are hypotensive and nonresponders or transient responders only should proceed to the OR expeditiously once intravenous access is obtained. If the patient is in extremis and unable to make it to the OR, resuscitative thoracotomy or resuscitative endovascular balloon occlusion of the aorta (REBOA) may be necessary. D In a normotensive patient who is fluid responsive and who does not have peritonitis, consideration is made as to the type of injury when considering nonoperative management. E Stab wounds should be evaluated by location in regard to the potential involvement of both the chest and abdomen and whether or not repair of the diaphragm would be indicated. F Gunshot wounds should be evaluated as to location and possible trajectory, which is more problematic than in stab wounds. G A stab wound to the anterior abdomen should undergo local wound exploration, with ultrasound (US) being a possible adjunct. Of note, a positive FAST may be clinically useful; however, a negative FAST does not rule out intraabdominal injury.

on the level, right-sided injuries have the potential for diaphragmatic, liver, kidney, or colonic injuries. Right-sided injuries are less likely to proceed to operative intervention, particularly because the liver protects against herniation with diaphragmatic injury. I

Left-sided injuries are more prone to diaphragmatic injuries requiring repair, and this should be ruled out.

J

Gunshot wounds are more unpredictable and should be assessed for trajectory into the thoracoabdominal region, tangential path across the anterior abdomen, or anterior-to-flank trajectory and vice versa. In a stable patient, a CT scan should be obtained to assess injury pattern. If there is concern for possible colonic injury, rectal contrast should be added to intravenous (IV) contrast when possible. Interventional radiology should be consulted for solid organ injury with blush or extravasation of blood or urine. Patients with operative findings such as free air or extravasation of enteral contrast should proceed to laparotomy. Those with no identifiable operative injuries should be evaluated with serial examinations. K Anterior stab wound with positive local wound exploration (LWE), equivocal LWE, or positive US can undergo laparoscopy or serial examinations. Patients who become symptomatic or have concerning findings on laparoscopy should proceed to laparotomy. Patients with negative LWE and negative US can have wound closure and discharge. L Patients with a flank or thoracoabdominal stab wound can undergo serial examinations with a negative US or proceed to CT in some cases. Patients with positive US or hematuria should undergo CT with double or triple contrast, followed by serial examinations. Interventional radiology should be consulted for solid organ injury with blush or extravasation of blood or urine. Patients with operative findings should proceed to laparotomy. M Patients with left-sided flank or thoracoabdominal stab wounds should be evaluated carefully for diaphragm injury. In lesions within the region of excursion of the diaphragm, laparoscopy should be used to rule out diaphragmatic injury. CT with double or triple contrast is useful here to identify associated injuries, as well as in lower stab wounds. REFERENCES Feliciano DV. Penetrating abdominal trauma. In: McIntyre R, Stiegmann G, et al, eds. Surgical Decision Making. 5th ed. Philadelphia: Elsevier; 2004. Jacobs LM, Gross R, Luk S, eds. Advanced Trauma Operative Management. Woodbury: Cine-Med; 2004. Pieracci FM, Jurkovich GJ. Penetrating abdominal trauma. In: Cameron JL, Cameron AM, eds. Current Surgical Therapy. 11th ed. Philadelphia: Elsevier; 2013.

H Management of stab wounds to the flanks or thoracoabdominal areas differs based on the site of injury. Depending

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Chapter 133  ◆  Penetrating Abdominal Injury  396.e1

Abstract

Keywords

Management of penetrating trauma to the abdomen or thoracoabdominal area is dictated by hemodynamics, physical examination, and adjunct studies. Patients with penetrating injury have a high likelihood of proceeding to operative management (60% to 70% of stab wounds and 70% to 95% of gunshot wounds), although a significant number can undergo selective nonoperative management.

penetrating trauma abdominal trauma thoracoabdominal trauma nonoperative management

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Chapter 133  ◆  Penetrating Abdominal Injury  397

A Primary survey FAST (trauma US), CXR, IV access, fluids, antibiotics, NGT, Foley Resuscitation: After 2 L crystalloid, begin Massive Transfusion Protocol

B Normotensive, Peritonitis or Evisceration

Laparotomy

C Hypotensive, is rem non-responder In ext or transient responder

Resuscitative thoracotomy or REBOA

Laparotomy

Laparotomy

G

Penetrating abdominal trauma

Anterior Abdomen

K

Positive LWE Equivocal LWE or +US Negative LWE & −US

E Stab wound CBC D INR/PTT ABG Normotensive, Lactate or responder, no TEG peritonitis Type and Cross

H

L

Right Flank/Thoracoabdominal

I

M

Left Flank/Thoracoabdominal

F Gunshot wound

Laparoscopy, or serial exams x24H + Laparoscopy, or serial exams x24H

Laparotomy

Wound closure and discharge

Negative US

Serial exams x24H +/−CXR

Positive US or hematuria

CT w/ double or triple contrast, Serial exams x24H +/−CXR

Laparotomy, or

+ High

Laparoscopy, +/− CT w/ double or triple contrast

Low

CT w/ double or triple contrast

Interventional radiology if solid organ injury with blush or extravasation of blood or urine

+

J Thoracoabdominal

CT with IV contrast

Anterior to anterior

CT with IV contrast

Anterior to flank

CT with double/triple contrast

+ -

Free air

Laparotomy

No blush or concern for bowel injury, serial exams x24H

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Chapter

134 

BLUNT SPLENIC INJURY Chasen A. Croft, MD, FACS, and Frederick A. Moore, MD, FACS, MCCM

A The initial assessment of a patient with blunt abdominal trauma and suspected splenic injury should follow the basic principles as outlined by Advanced Trauma Life Support (ATLS). B In patients with evidence of hemorrhagic shock, blood should be drawn for laboratory testing, including complete blood count, electrolytes, markers of metabolic stress (base deficit or lactate), coagulation profile, and blood typing. Adequate intravenous (IV) access should be obtained for resuscitation. After a primary survey and abdominal examination has been completed, a focused assessment with sonography for trauma (FAST) exam should be performed. In capable hands, the FAST exam has been proven to detect a minimum of 200 mL of fluid. However, FAST cannot be used to reliably grade solid-organ injuries. Therefore, in the hemodynamically stable patient, a follow-up computed tomography (CT) scan should be obtained. C There is considerable variability in the definitions of hemodynamic instability reported in the literature, but none to date has been conclusively validated. However, significant hypotension (systolic blood pressure [SBP] < 90 mm Hg) or serious tachycardia (heart rate [HR] > 130 bpm) are generally accepted parameters of hemodynamic instability. In addition to hemodynamic evaluation, response to resuscitation (i.e., crystalloid fluid resuscitation or packed red blood cell [PRBC] transfusion) should be monitored. Patients with hypotension unresponsive or transiently responsive to fluid and PRBC transfusion are also considered hemodynamically unstable. D An abdominal IV contrast-enhanced CT scan is the current gold-standard diagnostic test in diagnosing a splenic injury in the hemodynamically stable patient. Multi-slice CT scanning in both arterial and venous phases has improved the sensitivity for detecting splenic vascular injuries and contrast extravasation or “blush.” E In the hemodynamically unstable patient with a negative initial FAST exam, a repeat FAST exam should be performed as part of the secondary survey to reevaluate intraperitoneal sources of hemorrhage. F Overall, the FAST exam has a sensitivity between 73% and 88%, has a specificity between 98% and 100%, and is 96% to 98% accurate, independent of the practitioner performing

the procedure. However, a negative FAST exam does not reliably exclude intraperitoneal hemorrhage. It is not prudent to triage the hemodynamically unstable patient with a negative repeat FAST exam to the CT scanner. The patient should remain in the resuscitation bay, and a differential diagnosis of refractory shock should be pursued. In this setting, a diagnostic peritoneal aspirate (DPA) should be considered. The accuracy of DPA has been reported at between 92% and 98%. A DPA is considered positive if ≥ 10 mL of gross blood is aspirated. To avoid sampling preperitoneal hematoma because of pelvic fractures, a supra-umbilical approach has been recommended. G Therapeutic splenic angioembolization (SAE) is done if an aneurysm, arteriovenous fistula, or extravasation of contrast is found on the screening angiogram. There is some controversy over the optimal method of SAE (i.e., main splenic artery embolization vs. distal selective artery embolization vs. combination) and what material should be used to embolize the spleen. Main or proximal splenic artery embolization reduces bleeding by reducing perfusion pressure to the splenic parenchyma without causing overt infarction, but this may not prevent late pseudo­ aneurysm rupture and will likely not treat an arteriovenous fistula. On the other hand, distal selective embolization can effectively stop blood flow in polar arteries but can result in tissue infarction with local abscess formation. The decision to perform proximal or distal SAE should be based on discussion with the treating interventional radiologist and local, expert consensus. A second CT scan should be considered on all patients, regardless of embolization, to rule out persistent or new pseudoaneurysm development. H Among patients with an identified splenic injury on CT scan without evidence of splenic vascular injury or active bleeding, nonoperative management should be undertaken. This should only be considered for patients who are hemodynamically stable and have an absence of peritoneal signs and in an environment capable of hemodynamic monitoring, serial clinical evaluations, and operating room availability for urgent laparotomy should nonoperative management fail. I

The decision of whether to perform a splenectomy is dependent on the patient’s condition and associated injuries. Unfortunately, most patients undergo urgent laparotomy because of hemodynamic instability, and therefore splenectomy is the most prudent option. Splenic salvage should be pursued in the hemodynamically stable patient, although this is feasible in < 10% of patients. Techniques include topical hemostatic agents, argon-beam coagulation, direct suture repair, partial resection, wrapping the spleen with absorbable mesh, and splenic reimplantation. Pledgets are generally used when suturing splenic lacerations and margins of segmental resections. It is important to confirm hemostasis before closure of the midline fascia. Packing of the spleen in damage-control surgery should be discouraged because splenectomy is fairly simple and definitive. Splenic reimplantation in a patient without significant bacterial contamination is a safe but unproven method of preserving splenic function to protect against overwhelming postsplenectomy sepsis.

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Chapter 134  ◆  Blunt Splenic Injury  398.e1

Abstract

Keywords

The management of blunt splenic injury has evolved significantly over the past century. The treatment paradigm has shifted from operative management of all splenic injuries to the current practice of selective operative and nonoperative management. Much of the recent interest in nonoperative management in adults was stimulated by the success of nonoperative management of blunt solid-organ injuries in the pediatric population. Advances in noninvasive diagnostic imaging and therapeutic endovascular interventions have led to continued improvement of nonoperative management success rates; with documented rates greater than 90% in high-volume centers. The initial assessment of the patient with suspected blunt splenic injury follows the basic principles as outlined by Advanced Trauma Life Support (ATLS). Any patient with hemodynamic instability with evidence of intraperitoneal hemorrhage or peritonitis should undergo immediate operative exploration. Although splenic salvage may be considered in selective patients, splenectomy is most prudent in this setting. In the absence of these findings, a thorough physical and radiographic examination should be performed to diagnose the presence of a blunt splenic injury and to identify high-risk features of both early and delayed hemorrhage. Splenic angioembolization should be considered in patients with signs of active contrast extravasation, splenic vascular injuries, and clinical evidence of ongoing bleeding. Failure to successfully control hemorrhage after initial splenic angioembolization may require urgent laparotomy and splenectomy. Therefore nonoperative management should only be performed at centers capable of providing continuous hemodynamic monitoring, serial examinations, and rapidly available operative capabilities should urgent laparotomy be required.

blunt splenic injury splenic angiography splenic angioembolization nonoperative management splenectomy splenic salvage

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Chapter 134  ◆  Blunt Splenic Injury  399 No contrast extravasation or splenic vascular injury

A Initial assessment ATLS Abdominal exam

Observation

H Successful

Splenic injury identified

D Stable

Contrast extravasation Pseudoaneurysm Ongoing bleeding

Intravenous contrastenhanced CT scan

No splenic injury identified

G Angioembolization (A/E)

Other injuries requiring laparotomy

Unsuccessful or rebleeding Consider repeat A/E

Spleen injury

C Unstable

FAST exam CBC B ABG Lactate Coagulation profile Type and cross

Positive

Laparotomy

Unstable

Splenectomy

E

I

Repeat FAST exam

Stable Negative

Splenic salvage or splenectomy

Positive

F Diagnostic peritoneal aspiration Negative

REFERENCES Olthof DC, van der Vlies CH, Joosse P, et al. Consensus strategies for the nonoperative management of patients with blunt splenic injury: a delphi study. J Trauma Acute Care Surg. 2013;74(6):1567–1574. Rowell SE, Biffl WL, Brasel K, et al. Western Trauma Association Critical Decisions in Trauma: management of adult blunt splenic trauma-2016 updates. J Trauma Acute Care Surg. 2017;82(4):787–793. Skattum J, Naess PA, Eken T, Gaarder C. Refining the role of splenic angiographic embolization in high-grade splenic injuries. J Trauma Acute Care Surg. 2013;74(1):100–103, discussion 103–104.

Evaluate for other causes of instability

Stassen NA, Bhullar I, Cheng JD, et al. Selective nonoperative management of blunt splenic injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 suppl 4):S294–S300. Zarzaur BL, Kozar R, Myers JG, et al. The splenic injury outcomes trial: an American Association for the Surgery of Trauma multi-institutional study. J Trauma Acute Care Surg. 2015;79(3):335–342.

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Chapter

135 

LIVER INJURY Nicholas H. George, BS, and Rosemary A. Kozar, MD, PhD

A The initial evaluation in the setting of suspected hepatic trauma should include an abdominal examination and assessment of the patient’s vital signs and response to resuscitation. A hemodynamically unstable patient with suspected hepatic injury and a positive focused assessment with sonography for trauma (FAST) examination should be considered for immediate operative intervention. A hemodynamically stable patient may be triaged to the computed tomography (CT) scanner for a more thorough evaluation of the liver injury. If at any time the patient becomes hemodynamically unstable, operative intervention should be urgently considered. B The initial step in controlling liver bleeding is manual compression, during which time rapid assessment of the peritoneal cavity is carried out to confirm the liver as the major source of hemorrhage. Warming and resuscitative maneuvers should be instituted simultaneously. The liver should be mobilized and packs placed to adequately compress the site(s) of bleeding. C A hemodynamically stable patient with suspected liver injury should undergo a CT scan with intravenous (IV) contrast to evaluate the extent and grade of the liver injury. Liver injuries can be managed nonoperatively regardless of liver grade in hemodynamically stable patients. Because liver bleeding can sometimes be worsened by operative manipulation, it is generally considered acceptable to transfuse patients with known liver injuries if hemodynamic status permits. Transfusion requirements in the first 24 hours of observation have been shown to predict future complications. D If the CT scan reveals a vascular lesion, defined as either a pseudoaneurysm or contrast blush, angiography should be considered. Although hepatic angioembolization after high-grade liver injuries is associated with decreased mortality, there are no large prospective studies that characterize indications, outcomes, and complications of hepatic angioembolization after high-grade liver trauma. Additionally, the use of more advanced imaging such as CT scanning may lead to more selective use of angiography. Postoperative angioembolization has been associated with hepatic necrosis, particularly in patients who required perihepatic packing and damage control.

E Bleeding not controlled by packs suggests a complex hepatic injury. The next step is to perform a Pringle maneuver with the placement of a vascular clamp on the porta hepatis to control portal vein and hepatic artery bleeding. F If jaundice, abdominal pain, or signs of systemic inflammation, such as tachycardia, tachypnea, or leukocytosis, develop during the observation period, a follow-up CT scan should be obtained. G Once the decision has been made to carry out damagecontrol surgery, liver packs should remain in place, and a rapid exploration of the abdomen should be performed, with the goal being control of hemorrhage and intestinal contamination. H Other than bleeding, which usually develops early after injury, common complications of liver injury include biliary or infection-related complications, such as biloma or bile ascites, liver abscess, or infected hepatic necrosis. Most complications can be successfully managed with percutaneous drainage, although operative drainage is occasionally warranted. High-output biliary drainage may require subsequent endoscopic retrograde cholangio-pancreatography (ERCP) and stenting. I

With arterial inflow controlled, actively bleeding vessels should be directly suture ligated. Occasionally, finger fracture or extension of the laceration is needed to aid in control of vessels and injured bile ducts. Blind liver sutures can be placed, but this may lead to hepatic necrosis and is recommended only for more superficial lacerations. Hepatic artery ligation is rarely indicated with advances in interventional techniques. Omental packing once bleeding is controlled both fills in the dead space and can aid in hemostasis. J

Bleeding not controlled by a Pringle maneuver indicates a juxtahepatic injury. Manual compression of the liver should be reinstituted. If not already done, the massive transfusion protocol should be activated. Resuscitation with blood components approximating a 1:1:1 ratio of packed red cells:plasma: platelets should be employed. The patient should be actively warmed, and additional assistance in the operating room should be sought. K If not already completed, wide exposure should be obtained. Venous repair may require lobar or nonanatomic resection for visualization. Repair can be direct or done after total vascular isolation, which entails clamping of the suprahepatic vena cava, the infrahepatic vena cava, and the porta hepatis. This is not well tolerated in the hypovolemic patient and may require venoveno bypass if available. Various shunting techniques have been described, but all are associated with high mortality. Endoluminal stent grafts are likely to play a role in the future as technology advances.

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Chapter 135  ◆  Liver Injury  400.e1

Abstract

Keywords

Liver injuries are one of the most common intraabdominal injuries. Most liver injuries can be managed nonoperatively, with operative intervention reserved for patients with hemodynamic instability or the rare complication of nonoperative management. Operative technique is important and focuses on a stepwise approach to hemorrhage control.

blunt hepatic injury hepatic angioembolization juxtahepatic venous injury nonoperative management

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Chapter 135  ◆  Liver Injury  401

History and exam ATLS Diagnosed on CT

Hemodynamically stable Hemodynamically unstable

Observation

Liver injury with vascular lesion

Consider angiography

B

A

C

Liver injury with no vascular lesion

F

D

Hemodynamically unstable Diagnosed at laparotomy

Bleeding uncontrolled

CBC PT/INR PTT FAST

Follow-up CT scan

G

Damage control laparotomy Consider post-op CT or angiography

Bleeding controlled

Pack and resuscitate

Liver Injury

H

SIRS Jaundice Abdominal pain

E

Bleeding controlled

Pringle maneuver

I Control intrahepatic bleeding

J Bleeding uncontrolled

Pack and resuscitate Activate MTP Call for help

K Wide exposure Repair juxta-hepatic venous injury

REFERENCES Buckman RF, Miraliakbari R, Badellino MM. Juxtahepatic venous injuries: a critical review of reported management strategies. J Trauma. 2000;48:978. Hommes M, Nicol AJ, Navsaira PH, et al. Management of biliary complications in 412 patients with liver injuries. J Trauma Acute Care Surg. 2014;77(3):448. Kozar RA, Feliciano DV, Moore EE, et al. Western trauma association/critical decisions in trauma: operative management of adult blunt hepatic trauma. J Trauma. 2011;71(1):1–5. Kutcher ME, Weis JJ, Siada SS, et al. The role of computed tomographic scan in ongoing triage of operative hepatic trauma: a western trauma association multicenter retrospective study. J Trauma Acute Care Surg. 2015;76(9):951–956.

Ordoñez CA, Parra MW, Salamea JC, et al. A comprehensive five-step surgical management approach to penetrating liver injuries that require complex repair. J Trauma Acute Care Surg. 2013;75(2):207. Polanco PM, Brown JB, Puyana JC, et al. The swinging pendulum: a national perspective of nonoperative management in severe blunt liver injury. J Trauma Acute Care Surg. 2013;75(4):590. Sivrikoz E, Teixeira PG, Resnick S, et al. Angiointervention: an independent predictor of survival in high-grade blunt liver injuries. Am J Surg. 2015;209(4):742. Stassen NA, Bhullar I, Cheng JD, et al. Eastern association for the surgery of trauma. Selective nonoperative management of blunt hepatic injury: an eastern association for the surgery of trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 suppl 4):S288–S293.

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Chapter

136 

ABDOMINAL VASCULAR INJURIES Juan A. Asensio, MD, FACS, FCCM, FRCS, Carlos A. Fernandez, MD, FACS, Michel Wagner, MD, FACS, and Eduardo Smith Singares, MD, FACS

A More than 95% of all injuries to named abdominal vessels are caused by penetrating trauma, mostly gunshot wounds, stab wounds, and less commonly shotgun wounds. For patients sustaining gunshot wounds of the abdomen, it is estimated that approximately 20% to 25% will incur an abdominal vascular injury requiring repair and/or ligation of the injured vessel. All patients are evaluated and resuscitated per advanced trauma life support (ATLS) protocols. It is important, if possible, to define sites of entrance and exit for gunshot wounds and to determine if the missile trajectory crossed the midline. It is also important to note the presence of abdominal distention. The triad of profound shock, abdominal distention, and a gunshot wound of the abdomen is usually evidence of an abdominal vascular injury. B Routine laboratory studies are usually obtained for all trauma patients with suspected abdominal vascular injuries. Im­­ portant laboratory studies include arterial blood gases (ABGs), lactic acid, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen levels, and blood work for thromboelastography (TEG). C Patients sustaining transabdominal or transpelvic gunshot wounds presenting with overt signs of intraabdominal injury (hypotension and/or peritoneal signs) will most likely need to be intubated. Insertion of a thoracostomy tube in the trauma center is indicated if they also present with thoraco-abdominal gunshot wounds. Patients with multisystem blunt trauma or stable patients with truncal penetrating wounds that may be extracavitary may benefit from chest and abdominopelvic x-rays, surgeon-performed ultrasound of the pericardium and dependent peritoneal areas (Focused Assessment with Sonography of the Trauma Patient [FAST]), and computed tomography (CT) scan of the abdomen and pelvis. D Approximately 65% of patients sustaining abdominal vascular injuries present to trauma centers hypotensive (systolic blood pressure < 100 mm Hg). For patients presenting with multisystem blunt trauma where injuries to other body areas might be responsible for hypotension, a surgeon-performed positive abdominal ultrasound (FAST) or the presence of peritoneal signs on physical examination in the hypotensive patient confirms the abdominal cavity as the source of hemorrhage.

E Gross hematuria may be transient or totally absent with renovascular injuries; however, microscopic hematuria is generally always present. Further work-up is appropriate in all patients with this finding after blunt trauma and in a highly selected group of patients presenting with penetrating wounds to the flank or back, with no hypotension or peritonitis. F Although CTA has become the study of choice to image both the thoracic and abdominal aorta, occasionally thoracic aortograms are performed during thoracic endovascular aorta repairs (TEVARs). After a thoracic aortogram, it is worthwhile to have the angiographer perform a study of the abdominal aorta along with its visceral and terminal branches before removal of the transfemoral artery catheter. Unsuspected intimal injuries and even occlusions of the proximal renal or superior mesenteric artery have been detected with this additional study. G Patients presenting with blunt pelvic fractures, hypotension, and a continuing need for transfusion (4 to 6 units in the first 2 hours after admission) in the absence of other obvious sites of hemorrhage (negative FAST ultrasound or negative diagnostic peritoneal lavage [DPL]) will require placement of a pelvic binder if presenting with an “open book” pelvic fracture, urgent pelvic angiography with possible therapeutic embolization of bleeding sites, and consultation with an orthopedic surgeon. Consider resuscitative endovascular balloon occlusion of the aorta (REBOA). H Active hemorrhage from one or more abdominal vessels is usually found at laparotomy in patients who present hypotensive to the trauma center. I

Stable or expanding midline, perirenal, pelvic, portal, or retrohepatic hematomas (zone I supra- and inframesocolic, right or left zone III or zone III retroperitoneal hematomas) are usually found at laparotomy in patients hemodynamically stable on admission to the trauma center (systolic blood pressure ≥ 100 mm Hg) or who had rapid (but often transient) reversal of modest or moderate hypotension with the infusion of 2 L of crystalloids. J

Renovascular lesions that may be noted on CTA or selective renal arteriography if CT findings are unclear include intimal flaps with intact distal flow or occlusion 2 to 3 cm from the take-off of the abdominal aorta. K Midline supramesocolic, midline inframesocolic, portal, perirenal, and pelvic hematomas (zone I supra- and inframesocolic, right or left zone III or zone III retroperitoneal hematomas) are explored in patients sustaining penetrating wounds because large named vessels may have injuries contained by these hematomas. Perirenal and pelvic hematomas are not explored in patients sustaining blunt trauma unless they are ruptured, pulsatile, or rapidly expanding. Retrohepatic hematomas should not be explored after blunt or penetrating trauma unless, once again, they are pulsatile, ruptured, or rapidly expanding. Exploring these hematomas frequently results in torrential bleeding or exsanguination. L Intimal flaps present in renal arteries with intact distal flow diagnosed on CTA or on selective renal arteriograms may be observed with the administration of intravenous heparin in

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Chapter 136  ◆  Abdominal Vascular Injuries  402.e1

Abstract

Keywords

Most injuries to abdominal vessels are due to penetrating trauma. The majority of patients will present in shock. Initial evaluation and resuscitation is as usual for all trauma patients. When a patient is stable, CTA may be obtained to define injury. Management depends on the stability of the patient, the mechanism of injury, the location of bleeding or hematoma, and whether the injury is arterial or venous.

hematoma vascular control intimal flap extravasation stent revascularization interposition graft embolization ligation repair

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A

C

FAST X-rays (chest, abdomen) contrast-enhanced CT

Primary survey

Lab CBC Chemistries/blood alcohol Urinalysis with drug screen Type and cross-match ABG’s Lactic acid PT, PTT, fibrinogen TEG

B

BLUNT OR PENETRATING ABDOMINAL INJURY

Intubate IV fluids/blood/antibiotics Nasogastric tube Foley catheter Activate MTP

History and physical examination Prehospital information Site of injury ATLS shock category Abdominal signs

G

CTA of aorta or thoracic aortogram with abdominal aortic study

F

penetrating

blunt

Pelvic fracture with hypotension (FAST negative or diagnostic peritoneal lavage negative) Consider REBOA

blunt

blunt

Hematuria without peritonitis

E

Hypotension (if blunt, +FAST and/or peritonitis) Consider REBOA

D

Pelvic binder Pelvic angiogram Orthopedic consult

Occlusion or extravasation from superior mesenteric artery (SMA)

CT with IV and oral contrast; renal arteriogram if CT unclear

J

Hematoma at laparotomy

I

Bleeding at laparotomy

H K

L

blunt

Occlusion common or external iliac artery

N

Extravasation

Laparotomy

M

Occlusion of renal artery

blunt

all

penetrating

Intimal flap in renal artery

Retrohepatic

Perirenal Pelvic

Midline supramesocolic Midline inframesocolic penetrating Portal

If damage, control, ipsilateral below knee 4-compartment fasciotomies Consider 3 compartment fasciotomy

If stable, ipsilateral iliofemoral or contralateral-toipsilateral femorofemoral interpostion graft

Therapeutic embolization

Interposition graft from infrarenal aorta to SMA

Arteriography vs. end-toend anastomosis

If early laparotomy for other reasons, consider revascularization

Revascularize vs. heparin if absent or small contralateral kidney

Retrohepatic vena cava

SMV

Portal vein

Internal iliac vein

Common, external iliac veins

Renal vein

Superior mesenteric vein (SMV)

Infrarenal inferior vena cava (IVC)

Suprarenal inferior vena cava (IVC)

Q

Internal iliac artery

Endovascular stent, heparin Observe if contralateral kidney intact

Common, external iliac artery

Renal artery

Superior mesenteric artery (SMA)

Celiac axis

Suprarenal aorta Infrarenal aorta

P

Heparin, serial CTA’s or arteriograms

Observe

Observe

Vascular control, then GI source control

O

Vascular control, then GI source control

Repair

Ligate if damage control

Repair

Ligate

Repair

Ligate if damage control

Ligate if damage control

Repair- 1˚ venography

If ligate right, do nephrectomy

Repair

Ligate if damage control

Repair

Ligate if damage control

Repair

Repair

Ligate

Shunt if damage control

Repair if stable

Nephrectomy

Repair if solitary kidney

Shunt if damage control

Repair if stable

Ligate vs. 1˚ Repair

Repair vs. Graft

Chapter 136  ◆  Abdominal Vascular Injuries  403

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404  Part VIII  ◆ Trauma patients without other significant injuries. A follow-up CTA, renal arteriogram, or isotope renogram is appropriate before discharge to document continuing flow to the kidney through the injured artery. In some trauma centers with local expertise, an endovascular stent may be inserted with post-procedure heparinization. However, many of these patients do not require them, and short- or long-term results are not known. With blunt occlusion of the renal artery, the very low yield of reestablishment of flow after revascularization has prompted observation only if the contralateral kidney is intact on CT and the diagnosis has been made 6 hours after injury. If the contralateral kidney is absent or small, surgical revascularization is appropriate if the diagnosis has been made within 6 hours of injury. However, some trauma centers select heparinization only in the hope that recanalization will occur. If the diagnosis is known and an early laparotomy for other injuries is performed, renal revascularization should be considered if only other minor injuries are present. Outcomes, however, are not given. M Exposure for proximal control of the injured superior mesenteric artery (SMA) is obtained by a left medial visceral rotation maneuver involving the left colon, spleen, tail of the pancreas, and fundus of the stomach. A variation of this maneuver entails mobilizing the left kidney medially off the renal fossa. However, this variation should rarely be employed. On rare occasions, the pancreas may need to be transected by either a transverse anastomosis (TA) or gastrointestinal anastomosis (GIA) stapler or between Glassman clamps at the level of the neck to obtain exposure of the artery (Fullen zone I). Many injuries occur beyond the pancreas at the base of the transverse mesocolon (Fullen zone II), and exposure is obtained by elevating the transverse colon anteriorly and opening the peritoneum at the base of the mesocolon in the midline. Lacerations primarily are repaired in a transverse fashion or with resection and endto-end anastomosis with 5-0 or 6-0 polypropylene sutures. Because of the risk for a postoperative pancreatic leak from injury to the adjacent pancreas, extensive proximal injuries are ligated, and an autogenous reversed saphenous vein graft is inserted from the infrarenal abdominal aorta (end-to-side) to the distal SMA (end-to-end). Both anastomoses should be completely covered with a mobilized flap of viable omentum or with mesenteric tissues. N Extravasation from branches of the internal iliac artery, usually the superior gluteal or obturator branches and less commonly the pudendal artery, are treated by selective angiography and angioembolization. The very rare occlusion of the common or external iliac artery is addressed preferably with an ipsilateral iliofemoral or less frequently with a contralateral-toipsilateral femorofemoral bypass graft using an 8-mm externally supported polytetrafluoroethylene graft (ringed graft). In situations where “damage control” is required, an ipsilateral belowknee four-compartment fasciotomy will preserve the shank vessel and foot circulation for approximately 6 hours if a normal hemodynamic state is maintained. At this point, a graft will have to be inserted. The possibility of a thigh three-compartment fasciotomy must also be considered. O Control of active arterial bleeding is obtained by digital compression or laparotomy pad, digitally securing or “grabbing” the injured (iliac) artery with a hand, formal proximal

and distal control, or possible insertion of a Fogarty or Foley balloon catheter into the defect. In addition to the techniques listed, venous bleeding can be controlled by meticulous coadaptations of the lacerated edges with a series of Judd–Allis clamps or by proximal and distal compression with spongesticks. After active hemorrhage has been controlled and before the arterial repair is started, extensive perforations in the gastrointestinal tract are closed with Babcock, Allis, Dennis, or Glassman clamps; a rapid continuous repair with polypropylene suture; or rapid GIA stapler resection. Before exploring any hematoma, complete gastrointestinal source control is obtained using clamps or sutures as previously described. P Exposures and control of arteries are as follows: • Suprarenal aorta/celiac axis (tripod of Haller)/SMA: Bleeding → cross-clamp aorta at diaphragm. Hematoma → left-sided medial visceral rotation. • Infrarenal aorta: Hemorrhage or hematoma → base of mesocolon. • Renal artery: Bleeding → direct or medial mobilization. Hematoma → central control below left renal vein. • Iliac artery: Bleeding → eviscerate midgut, digitally control the artery. Hematoma → eviscerate midgut, proximal control at aortic bifurcation, distal control above inguinal ligament. Q Exposures and control of veins are as follows: • Suprarenal inferior vena cava (IVC): Hemorrhage or hematoma → retract liver cephalad; right medial visceral rotation and Kocher maneuver; cross-clamp infrarenal IVC; loop or cross-clamp renal veins; apply Judd–Allis, Satinsky, Cooley, or Derra versus aortic-type cross-clamp like a Crafoord–DeBakey on the IVC at edge of liver. Will need to cross-clamp the infrarenal aorta with a Crafoord–DeBakey clamp to preserve blood pressure if IVC completely clamped. • Infrarenal IVC: Hemorrhage or hematoma → right medial visceral rotation and Kocher maneuver; apply Judd–Allis, Satinsky, Cooley, or Derra clamps versus aortic-type cross-clamps like a Crafoord–DeBakey to occlude the injury to the IVC. Cross-clamp aorta as previously described. • SMV: Hemorrhage or hematoma → transect neck of pancreas if needed; otherwise incise retroperitoneum at base of mesocolon. • Renal vein: Left → base of mesocolon; right → right medial visceral rotation and Kocher maneuver. • Iliac vein: Injury to proximal right common iliac vein → retract artery with Cushing vein retractors. Very rarely requires temporary division of the overlying right common iliac artery for exposure. • Portal vein: Proximal Pringle maneuver, distal control with forceps, identify common and hepatic bile ducts before repair. • Retrohepatic vena cava: Direct lateral or transhepatic approach by transecting hepatic parenchyma, through the parenchymal laceration, or by transection through Cantlie’s line. Rarely a Schrock atriocaval shunt consisting of 36 Fr thoracostomy tube or #8 straightened endotracheal tube may need to be inserted, after median sternotomy.

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Chapter 136  ◆  Abdominal Vascular Injuries  405 REFERENCES Asensio JA, Berne JD, Chahwan S, et al. Traumatic injury to the superior mesenteric artery. Am J Surg. 1999;178:235–239. Asensio JA, Britt LD, Borzotta A, et al. Multi-institutional experience with the management of superior mesenteric artery injuries. J Am Coll Surg. 2001;193:354–366. Asensio JA, Chahwan S, Hanpeter D, et al. Operative management and outcome of 302 abdominal vascular injuries. Am J Surg. 2000;180: 528–534. Asensio JA, Forno W, Roldan G, et al. Abdominal vascular injuries: injuries to the aorta. Surg Clin North Am. 2001;81:1395–1416. Asensio JA, Forno W, Roldan G, et al. Visceral vascular injuries. Surg Clin North Am. 2002;82:1–20, xix. Asensio JA, Kuncir E, Garcia-Nuñez LM, et al. 298 femoral vessel injuries: analysis of factors predicting outcome. J Am Coll Surg. 2006;203: 512–520. Asensio JA, McDuffie L, Petrone P, et al. Reliable variables in the exsanguinated patient which indicate damage control and predict outcome. Am J Surg. 2001;182:743–751.

Asensio JA, Petrone P, Garcia-Nuñez LM, et al. Superior mesenteric venous injuries. To ligate or repair remains the question. J Trauma. 2007;62: 668–675. Asensio JA, Petrone P, Kimbrell B, et al. Lessons learned in the management of thirteen celiac axis injuries [review]. South Med J. 2005;98:462–466. Asensio JA, Petrone P, Roldan G, et al. Analysis of 185 iliac vessel injuries. Risk factors and predictors of outcome. Arch Surg. 2003;138:1187–1193, discussion 1193–1194. Davis TP, Feliciano DV, Rozycki GS, et al. Results with abdominal vascular trauma in the modern era. Am Surg. 2001;67:565–571. Haas CA, Dinchman KH, Nasrallah PF, et al. Traumatic renal artery occlusion: a 15-year review. J Trauma. 1998;45:557–561. Kumar SR, Rowe VL, Petrone P, et al. The vasculopathic patient: uncommon surgical emergencies [review]. Emerg Med Clin North Am. 2003;21: 803–815. Tillou A, Romero J, Asensio JA, et al. Renal vascular injuries. Surg Clin North Am. 2001;81:1417–1430, xx. Tyburski JG, Wilson RF, Dente C, et al. Factors affecting mortality rates in patients with abdominal vascular injuries. J Trauma. 2001;50:1020–1026.

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Chapter

137 

PANCREATIC INJURY Lung W. Lau, MD, and Vanessa P. Ho, MD, MPH

A Pancreatic injury severity is determined by location and degree of parenchymal and ductal involvement (Table 137.1). Ductal injury is the strongest prognostic factor for patient outcome. Complications include pancreatitis, abscesses, fistulas, pancreatic pseudocysts, sepsis, and death. Given the low incidence of pancreatic injuries, management recommendations are extrapolated from retrospective case series and meta-analysis. B Unstable patients or patients with obvious indications for laparotomy (such as evisceration or peritonitis) should be taken immediately for an operation. Wide exposure of the pancreas should be performed when there is suspicion of retroperitoneal injury. Careful inspection of the injured tissues is required to determine whether the pancreatic duct is involved. Approach the body and tail via the lesser sac, and Kocherize the duodenum to fully visualize the anterior and posterior pancreatic head. Unroof and examine all contusions. C Stable patients without an indication for immediate surgery should be evaluated by computed tomography (CT) scan. The sensitivity of CT for the detection of any pancreatic injury ranges from 47% to 91%. A CT finding of a ductal injury is an indication for an operation, as described previously.

TABLE 137.1  Pancreatic Organ Injury Severity

(American Association for the Surgery of Trauma [AAST] Organ Injury Scaling Committee) Grade

Injury

Description

I

Hematoma Laceration Hematoma

Minor contusion without duct injury Superficial laceration without duct injury Major contusion without duct injury or tissue loss Major laceration without duct injury or tissue loss Distal transection or parenchymal injury with duct injury Proximal (to the right of the superior mesenteric vein) transection or parenchymal injury with duct injury Massive disruption of pancreaticoduodenal complex or devascularization of pancreas

II

Laceration III

Laceration

IV

Laceration

V

Laceration

D If a CT scan does not clearly rule out the involvement of the pancreatic duct, further imaging is warranted. Endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) is the next best choice to evaluate the duct. Patients without ductal injury may be observed. Ductal injury warrants an operative treatment, as described previously. ERCP treatment of ductal injuries has been described, but outcomes are not well studied. Stable patients with duct injuries managed by ERCP should be observed for complications such as a leak or intraabdominal abscess. E If no ductal injury is identified intraoperatively, expectant management is preferred. Devitalized tissue should be debrided and drained. A surgical drain should be placed for grade I and II injuries. F High-grade pancreatic injuries are best managed with pancreatic resection, dictated by duct injury location. Resection is associated with lower mortality and postoperative fistulae than management without resection. G Grade I and II injuries identified by CT scan are best managed nonoperatively. Complication rates are low, and rare late complications of fistula or pseudocyst can be managed with percutaneous drain placement with interventional radiology. H For transections of body and/or tail or parenchymal injuries that include the pancreatic duct (grade III), the recommended procedure is a distal pancreatectomy. Splenic preservation has not shown to affect short-term outcomes. Intraoperative stability and surgeon experience with the procedure should guide the decision for splenic preservation. I

For pancreatic injuries that involve the head, with ampullary ductal injury (grade IV) or complete destruction of the pancreatic head (grade V), resection with reconstruction is preferred. Current literature does not indicate a preferred reconstruction, although Roux-en-Y with pancreaticojejunostomy and pancreaticoduodenectomy have been described. Immediate reconstruction for stable patients should be individualized to a patient’s injury pattern. Grade V injuries are rare but are associated with high mortality. Damage-control surgery with drainage of the pancreas may be the best immediate intervention if there are other life-threatening injuries causing intraoperative instability. For these complex patients, a planned, staged reconstruction should occur after the patient is stabilized. Surgeons should use the opportunity of delayed reconstruction to plan a multidisciplinary approach, use expert consultation when available and appropriate. Post-treatment complications can usually be treated with nonoperative intervention. Interventional radiology consultation should be made for intraabdominal abscesses and peripancreatic fluid collections. Fistulae are usually self-limiting but may require a period of bowel rest and parenteral nutrition to reduce pancreatic stimulation and secretions. Octreotide has not been proven to improve outcomes after pancreatic injuries. Pseudocysts are managed similarly to those that develop in the nontraumatic setting. Infected cysts or cysts involving the duct may require stenting or cyst enterostomy.

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Chapter 137  ◆  Pancreatic Injury  406.e1

Abstract

Keywords

Pancreatic injury management is largely dictated by the presence of ductal injury, which is the strongest prognostic factor for patient outcome. Complications include pancreatitis, abscesses, fistulas, pancreatic pseudocysts, sepsis, and death.

pancreas pancreatic injury

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Chapter 137  ◆  Pancreatic Injury  407

E Grade I/II: Drain

H Laparotomy Ductal injury?

F

Body/tail

Duct injury location?

B Immediate laparotomy

I Head

A Pancreatic injury?

C CT Scan Ductal injury?

O.R. Yes

Unclear

No

Grade III: Distal pancreatectomy

Grade IV/V: Resect and reconstruct

D ERCP/MRCP Duct injury?

G Grade I/II: Observe

REFERENCES Biffl W, Moore E, Croce M, et al. Western Trauma Association critical decisions in trauma: management of pancreatic injuries. J Trauma Acute Care Surg. 2013;75:941–946. Hamidian J, D’Agostino H, Zibari G, et al. Surgical versus nonsurgical management of traumatic major pancreatic duct transection: institutional experience and review of the literature. Pancreas. 2013;42:76–87. Ho V, Nimitt P, Bokhari F, et al. Management of adult pancreatic injuries: a practice management guideline from Eastern Association for the Surgery of Trauma. J Trauma. 2017;82:185–199.

Lee KJ, Kwon J, Kim J, et al. Management of blunt pancreatic injury by applying the principles of damage control surgery: experience at a single institution. Hepatogastroenterology. 2012;59:1970–1975. Moore E, Cogbill T, Malangoni M, et al. Organ injury scaling, II: pancreas, duodenum, small bowel, colon, and rectum. J Trauma. 1990;30: 1427–1429.

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Chapter

138 

DUODENAL INJURY Abid D. Khan, MD, and Thomas J. Schroeppel, MD, MS

A Duodenal injury occurs with penetrating trauma to the abdomen or with blunt-force trauma to the epigastrium (e.g., handlebar or kick injuries). They are present in 1% to 2% of blunt abdominal trauma and 5% to 7% of penetrating abdominal trauma. B Laboratory studies include a complete blood count (CBC) and lactate. An abdominal computed tomography (CT) scan with intravenous (IV) and (if possible) oral (PO) contrast is obtained in a stable patient. Visible intramural hematoma, intramural edema, or focal duodenal wall thickening suggest the presence of a duodenal hematoma. Findings indicative of a duodenal laceration include extraluminal air, extraluminal fluid, or PO contrast extravasation, any of which can be contained in the retroperitoneum or free in the peritoneal cavity. Focused assessment with sonography in trauma (FAST) and diagnostic peritoneal lavage (DPL) are unreliable in the diagnosis of duodenal injury and have an unacceptable rate of missed injury. C The presence of peritonitis or hemodynamic instability is an indication to forgo imaging studies and to proceed directly to laparotomy. Findings on CT scan indicative of duodenal laceration should likewise prompt operative exploration. Hemodynamic instability, worsening acidosis, hypothermia, and/or coagulopathy should lead to consideration of damage-control laparotomy. D Duodenal hematomas discovered on imaging can usually be managed nonoperatively. If the hematoma causes gastric outlet obstruction, the patient is made nil per os (NPO) and started on total parenteral nutrition, and a nasogastric (NG) tube is placed. Most obstructions will resolve in 2 weeks. An upper gastrointestinal (GI) contrast study can be obtained to ensure the obstruction has resolved. Hematomas that fail to resolve in 2 weeks should undergo operative drainage. E The key to the intraoperative evaluation of the duodenum is exposure. Aside from the first portion, the duodenum is a retroperitoneal structure that must be exposed to be properly examined for injury. A wide Kocher maneuver is performed to expose the second and third portions of the duodenum. The fourth portion can be exposed by right medial visceral rotation or by dividing the ligament of Treitz. F A duodenal hematoma discovered at laparotomy is evaluated for expansion and for degree of luminal obstruction. Those that are not expanding and cause less than 50% luminal obstruction are left in place. Those that are actively expanding or create a greater than 50% luminal obstruction are opened, with care taken not to violate the mucosa. Hemostasis is important to prevent recurrence. The defect is closed primarily.

G Anatomy and physiology specific to the duodenum make lacerations especially difficult to manage. The duodenum has a high rate of suture/staple line leak and is the conduit for 6 L of gastric, biliary, and pancreatic secretions each day. Leaks can have a devastating physiologic effect. The proximity to multiple large vascular structures, the common bile duct (CBD), and the pancreas means that duodenal lacerations are often accompanied by major hemorrhage or concomitant biliary or pancreatic injuries. Extraluminal drains are unnecessary with isolated duodenal injuries but are placed if a biliary or pancreatic injury is also present. The location and grade of the duodenal lacerations dictate operative management. More than 80% of duodenal injuries are amenable to simple primary repair where the defect is debrided to healthy tissue and is closed transversely in one or two layers. Omental or jejunal serosal patches are reserved for repairs with an increased risk for leak because of a comorbid condition, such as chronic steroid use. See Table 138.1 for the American Association for the Surgery of Trauma (AAST) grading scale for duodenal injuries. H Injuries to the second portion of the duodenum require an assessment of the proximity of the injury to the ampulla and evaluation for concomitant pancreatic or biliary injuries. The location within the second portion is an important consideration in the management of these injuries. I

Grade I or II injuries to the first part of the duodenum undergo a simple primary repair. Grade III injuries require an antrectomy with Billroth 1, Billroth 2, or Roux-en-Y gastrojejunostomy reconstruction if not amenable to primary repair. J

Lacerations to the lateral wall of the second part of the duodenum are less likely to involve the ampulla and are treated with primary repair. Pyloric exclusion can be considered for these injuries but should be reserved for grade IV injuries, those that present >24 hours after injury, or otherwise tenuous repairs. K Lacerations to the medial wall or near the ampulla require assessment of the CBD with an intraoperative cholangiogram. If the cholangiogram is negative, a primary repair of the

TABLE 138.1  Duodenal Injury Severity (AAST

Organ Injury Scaling Committee) Grade

Injury

Description

I

III

Hematoma Laceration Hematoma Laceration Laceration

IV

Laceration

V

Laceration

Involving single portion of duodenum Partial thickness, no perforation Involving more than one portion Disruption 75% of circumference of D2 Involving ampulla or distal common duct Massive disruption of duodenopancreatic complex, devascularization of duodenum

II

Advance one grade for multiple injuries up to grade III. D1, first portion of duodenum; D2, second portion of duodenum; D3, third portion of duodenum; D4, fourth portion of duodenum

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Chapter 138  ◆  Duodenal Injury  408.e1

Abstract

Keywords

Duodenal injury is relatively rare. This chapter outlines an algorithm for the repair and management of these injuries. Greater than 80% of injuries can be simply managed with primary repair. Complicated repairs or adjuvant procedures are reserved for the most tenuous of repairs.

duodenal injury Abdominal trauma pyloric exclusion triple-tube therapy duodenum

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Chapter 138  ◆  Duodenal Injury  409 Grade I or II

A History and physical exam Abdominal trauma

DUODENAL INJURY

Peritonitis, hemodynamic instability, evidence of duodenal laceration on imaging

Lateral wall

E H

C Duodenal hematoma at laparotomy

Duodenal laceration

2nd part of duodenum

Medial wall or near ampulla

G

B

Disruption of duodenopancreatic complex

D Duodenal hematoma on imaging

Grade III

Primary repair or antrectomy with gastrojejunostomy

Grade I-III

Primary repair

J Grade IV

Primary repair +/− pyloric exclusion

Grade I-IV with − cholangiogram

Primary repair with triple-tube therapy

Laparotomy

F Diagnostic workup CT with IV contrast Labs-WBC, lactate

Primary repair

I

1st part of duodenum

Greater than 50% luminal obstruction

Grade V

L Grade I or II

3rd or 4th part of duodenum Observation NPO NG tube suction TPN

K Grade IV with + cholangiogram

M Grade III

Hematoma evacuation

defect is indicated, and the patient should also undergo “tripletube therapy.” A nasogastric tube, an afferent jejunostomy tube, and a distal feeding jejunostomy tube are placed. The afferent jejunostomy tube is passed retrograde to the site of injury to provide internal drainage. A positive cholangiogram without complete disruption of the duodenopancreatic complex requires a biliary reconstruction in addition to a duodenal repair. CBD injuries with less than 50% circumferential involvement can be primarily repaired over a T tube. Larger defects are prone to stricture with repair and require hepaticojejunostomy. If possible, pancreaticoduodenectomy should be avoided. L Complete disruption of the duodenopancreatic complex or devascularization of the duodenum will require pancreaticoduodenectomy. Invariably, these patients have profound physiologic derangements. Resection can be performed at the index operation, but reconstruction is reserved for a later date, after resuscitation in the intensive care unit (ICU). M Injuries to the third and fourth portions of the duodenum are managed similarly to injuries to the rest of the small intestine. Grade I or II injuries are primarily repaired, whereas

Damage control laparotomy

Primary duodenal repair with biliary repair or reconstruction

Pancreaticoduodenectomy

Primary repair Primary repair or resection with primary duodenoduodenostomy or duodenojejunostomy

grade III injuries are primarily repaired or are resected with primary duodenoduodenostomy reconstruction. If the injury is directly behind the superior mesenteric artery, a duodenojejunostomy allows for a technically easier anastomosis because of improved exposure. REFERENCES Biffl WL. Duodenum and pancreas. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 7th ed. New York: McGraw-Hill; 2013:603–619. Dubose JJ, Inaba K, Teixeira PG, et al. Pyloric exclusion in the treatment of severe duodenal injuries: results from the National Trauma Data Bank. Am Surg. 2008;74:925–929. Malhotra A, Biffl WL, Moore EE, et al. Western Trauma Association critical decisions in trauma: diagnosis and management of duodenal injuries. J Trauma Acute Care Surg. 2015;79(6):1096–1101. Mayberry J, Fabricant L, Anton A, et al. Management of full-thickness duodenal laceration in the damage control era: evolution to primary repair without diversion or decompression. Am Surg. 2011;77:681–685. Moore EE, Cogbill TH, Malangoni MA, et al. Organ injury scaling. II: pancreas, duodenum, small bowel, colon, and rectum. J Trauma. 1990;30:1427–1429. Schroeppel TJ, Saleem K, Sharpe JP, et al. Penetrating duodenal trauma: a 19-year experience. J Trauma Acute Care Surg. 2016;80(3):461–465. Stone HH, Fabian TC. Management of duodenal wounds. J Trauma. 1979;19:334–339.

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Chapter

139 

PENETRATING INJURY OF THE COLON David J. Ciesla

A The circumstances of the injury are ascertained from first responders and/or the patient on arrival, including prehospital vital signs, time and mechanism of injury, and medical/ surgical history. B The majority of colon injuries occur secondary to penetrating abdominal trauma, and the colon is the second most commonly injured organ, following the small intestine. Firearms account for 75% to 90% of these injuries, and most are diagnosed on operative exploration, some by endoscopy and some by imaging. C Baseline hematology laboratory studies are obtained. Resuscitation with blood products should be guided by coagulation studies. The authors use thromboelastography and guidance from collateral history when available. D Gunshot wound to the abdomen mandates laparotomy if the bullet violates the peritoneal cavity because visceral injury occurs in greater than 80% of patients. Plain abdominal and thoracic x-rays are obtained to assess for bullet location and/or penetration of the diaphragm. Triple-contrast computed tomography (CT) scanning can be useful in evaluating for evidence of visceral injury in the stable patient with a flank wound. Wounds near the retroperitoneal colon or rectum warrant laparotomy or diagnostic laparoscopy, even in the absence of abdominal signs, unless diagnostic findings are unequivocally normal. E At laparotomy, hemorrhage and contamination control are the first priority, followed by full exploration to evaluate for concomitant injury. Fecal contamination is controlled by stapling and resecting the area of injury with a gastrointestinal anastomosis (GIA) stapler. Intraoperative resuscitation with the goal of normalizing the metabolic derangements is guided by measurements of arterial pH, temperature, and coagulation laboratory studies. F If resuscitation successfully normalizes the patient’s metabolic parameters, the surgeon can proceed to definitive management of the colon injury. G Intraoperative indications for a damage-control procedure are hypothermia (initial temperature < 35 °C [95 °F], acid–base status (pH < 7.2, base deficit < –15 mmol/L in pt < age 55, < –6 mmol/L in > age 55, lactate > 5 mmol/L) and coagulopathy (prothrombin time [PT] and/or partial thromboplastin time [PTT] > 50% of normal).

After hemorrhage and contamination control, if the patient remains unstable and/or metabolic derangements are not successfully corrected, a temporary abdominal closure is performed, and the patient is transferred to the intensive care unit (ICU) for continued aggressive resuscitation. Intraabdominal packing may be required if the patient is coagulopathic. H The goal is to restore normal metabolic parameters, with a return to the operating room (OR) within 24 hours for definitive management of all injuries. Continuity of the previously stapled colon segments is restored with delayed primary anastomosis if closure can be achieved during the second laparotomy; otherwise, an ostomy is fashioned. The complication rate of delayed primary anastomosis does not appear to be higher than that for anastomosis performed during the initial operation. However, the anastomotic complication rate does increase substantially if delayed primary anastomosis is performed without closure of the abdomen on the first re-exploration. I

Colon injury is graded according to the American Association for the Surgery of Trauma (AAST), as follows: Grade I: Contusion or hematoma without devascularization or laceration—partial thickness, no perforation Grade II: Laceration < 50% of circumference Grade III: Laceration > 50% of circumference Grade IV: Transection of the colon Grade V: Transection with segmental tissue loss

J

Rectal injury is graded similarly to colon injury and is scored according to the grading scale published by the AAST, as follows: Grade I: Contusion or hematoma without devascularization or laceration—partial thickness, no perforation Grade II: Laceration < 50% of circumference Grade III: Laceration > 50% of circumference Grade IV: Full-thickness laceration with extension into the peritoneum Grade V: Devascularized segment Before laparotomy and while the patient is under anesthesia, rigid or flexible proctosigmoidoscopy should be performed in all patients with a suspected rectal injury. Transanal palpation or visualization of a perforation is diagnostic. Occasionally, intraluminal blood or submucosal hematoma is the only evidence of rectal injury, which is associated with colon or rectal injury in approximately 90% of cases. K Nondestructive (American Association for the Surgery of Trauma Organ Injury Scale [AAST-OIS] grades I to III) injuries not requiring segmental resection are treated with debridement of only contaminated or ischemic tissue with primary suture repair. We close transversely using a single layer of absorbable monofilament suture. L Destructive injuries (AAST-OIS grades IV to V) proximal to the middle colic vessels are resected, and a primary ileocolostomy is created. Injuries distal to the middle colic vessels treated with primary anastomosis have as good as or better results than routine colostomy when considering postoperative complications of a leak, an abscess, or abdominal sepsis. Colostomy is considered in the setting of significant bowel wall edema secondary to large-volume resuscitation, continued shock, multiple injuries, spillage, or poor tissue condition.

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Chapter 139  ◆  Penetrating Injury of the Colon  410.e1

Abstract

Keywords

Penetrating colon injuries present a difficult diagnostic and therapeutic challenge. Diagnosis is often made at the time of operative exploration but can be made preoperatively as in the case of iatrogenic colonoscopy injuries. Treatment is determined by the location of the injury, the amount of surrounding tissue destruction, and the physiologic status of the patient.

penetrating abdominal injury rectum colon colostomy diversion presacral drainage

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Chapter 139  ◆  Penetrating Injury of the Colon  411

G A History and physical examination

B PENETRATING INJURY OF THE COLON

C Labs

Resuscitation

Primary anastomosis

Return to OR In 24 hours Unable to close

Colostomy

K

E Laparotomy 1. Hemorrhage control 2. Contamination control 3. Restore perfusion 4. Restore physiology 5. Restore function

Able to close

H

Damage control procedures Temporary abdominal closure

Non-destructive Improved physiology

F

Yes

Destructive

Consider laparoscopy

No

Resection, primary anastomosis or ostomy

Proximal to middle colic vessels

Non-destructive

D

Proximal No

Resection, primary anastomosis

M

Injury above peritoneal reflection

Imaging

Yes

L

I

Definitive reconstruction

Debridement, primary repair

N Destructive

J

Non-destructive Distal

O

Destructive

P

Debridement, primary repair

Resection with reconstruction or ostomy Exclude intraperitoneal injury, proximal diversion, consider nonoperative management

Loop colostomy, consider presacral drainage

M Nondestructive injuries to the proximal intraperitoneal and extraperitoneal rectum that do not require resection based on the intraoperative evaluation (American Association for the Surgery of Trauma Rectal Injury Scale [AAST-RIS] grades I to III) are repaired primarily. These injuries are generally lacerations, and with mobilization, they are easily repaired with a single layer of absorbable monofilament suture. Injuries with surrounding tissue destruction, as with gunshot wounds, require debridement to healthy tissue before primary suture repair. Routine placement of pelvic drains after primary repair of proximal rectal injuries should be avoided. Drains do not reduce the complication rate and may increase the risk for fistula.

the ostomy should be matured immediately. Nonoperative management has been achieved in select patients. Intraperitoneal rectal injury and bladder injury must be excluded when considering treatment without proximal diversion.

N Proximal rectal injuries with extensive loss of the rectal wall or devascularization (AAST-RIS grades IV to V) are more safely managed by resection and proximal diversion than by primary repair. The rectum is resected distal to the injury with construction of a proximal end colostomy, followed by delayed reconstruction. Patients with minimal comorbid injuries, minimal contamination, and normal physiology can be considered for resection and immediate primary colorectal anastomosis, with or without protective proximal loop ostomy. Patients with extensive abdominal injuries, significant contamination, or persistent shock should undergo resection and proximal diversion.

REFERENCES

O Nondestructive wounds to the distal extraperitoneal rectum are treated with a proximal diverting colostomy. Extensive dissection to visualize the injury should be avoided because of the potential for vascular, urologic, neurologic, or iatrogenic rectal injury. The fecal stream must be completely diverted, and

P Distal destructive extraperitoneal rectal injuries require a proximal diverting colostomy; consider presacral drainage. Reconstruction occurs at a future operation. Concomitant genitourinary injuries should be repaired and separated with an omental pedicle flap. Extensive anorectal injuries may require abdominoperineal resection (APR).

Demetriades D, Murray JA, Chan L, et al. Penetrating colon injuries requiring resection: diversion or primary anastomosis? An AAST prospective multicenter study. J Trauma. 2001;50(5):765–775. Navsaria P, Edu S, Nicol AJ. Civilian extraperitoneal rectal gunshot wounds: surgical management made simpler. World J Surg. 2007;31:1345–1351. Ordoñez CA, Pino LF, Badiel M, et al. Safety of performing a delayed anastomosis during damage control laparotomy in patients with destructive colon injuries. J Trauma. 2011;71(6):1512–1517, discussion 1517–1518. Rombeau JL, Wilk PJ, Turnbull RB Jr, et al. Total fecal diversion by the temporary skin-level loop transverse colostomy. Dis Colon Rectum. 1978;21(4):223–226. Sharpe JP, Magnotti LJ, Weinberg JA, et al. Impact of location on outcome after penetrating colon injuries. J Trauma Acute Care Surg. 2012;73(6): 1428–1432, discussion 1433. Weinberg JA, Fabian TC, Magnotti LJ, et al. Penetrating rectal trauma management by anatomic distinction improves outcome. J Trauma. 2006;60:508–513, discussion 513–514. Wyrzykowski AD, Feliciano DV. Chapter 38. Trauma damage control. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 7th ed. New York, NY: McGraw-Hill; 2013.

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Chapter

140 

PENETRATING RECTAL INJURY Morgan Schellenberg, MD, MPH, and Kenji Inaba, MD, FACS, FRCSC

A As with any trauma patient, management starts with the primary survey and attention to airway, breathing, and circulation. The initial history and physical examination, including vital signs, are of paramount importance. The vast majority of rectal injuries occur after penetrating mechanisms, in particular, gunshot wounds, and a rapid evaluation of the front, back, and perineum should be conducted. Abdominal examination should follow. Because of the high incidence of associated genitourinary tract injuries, a Foley catheter should be placed to allow inspection of the urine for gross hematuria to screen for a bladder injury. B The necessary investigations hinge on the clinical stability of the patient. Even an unstable patient should have plain x-rays taken quickly in the trauma bay whenever possible to provide information about the bullet trajectory and presence of any fragments that may injure the operator. A focused assessment with sonography for trauma (FAST) examination demonstrating free intraabdominal fluid signals blood until proven otherwise. C Hemodynamic instability, peritonitis, evisceration, or an unevaluable abdomen should trigger immediate laparotomy. Because of the proximity of the major abdominal vasculature, pulse discrepancy, a hard sign of vascular injury, also mandates operation. The rectum can be evaluated directly at laparotomy. D Patients with suspected penetrating rectal injury and hemodynamic instability, peritonitis, evisceration, or an unevaluable abdomen proceed to the operating room. If they are hemodynamically normal, they should be positioned in lithotomy to allow for a rigid proctosigmoidoscopy before operative intervention. Rigid proctosigmoidoscopy plays a number of important roles. First, in a patient with a computed tomography (CT) scan that is suggestive but not conclusive for rectal injury, a rigid proctosigmoidoscopy that is negative for blood or a defect rules out rectal injury with a negative predictive value of 100%. Second, in the setting of a rectal injury, it allows for the determination of the distance of that injury from the anal verge and its circumferential extent and location. This classifies rectal injuries into intra- or extraperitoneal, which is critical in the surgical decision making that ensues. E Patients who are hemodynamically normal, evaluable without peritonitis, and do not have evisceration should undergo

CT scan with intravenous (IV) contrast, which will detect pelvic injury after gunshot wounds with a sensitivity of 100% and specificity of 98%. If gross hematuria is found, a CT cystogram should also be performed. If the CT scan is positive or equivocal for rectal injury, the patient should proceed to the operating room for rigid sigmoidoscopy as described previously. F Intraperitoneal rectal injuries occur in the proximal rectum—more specifically, the upper two-thirds of the rectum anteriorly and the upper third laterally. Injury to the intraperitoneal rectum will typically manifest clinically with peritonitis. G Extraperitoneal rectal injuries should be considered separately from colonic injuries. Because they are outside of the peritoneal cavity, exposure of and surgical access to these injuries can be challenging. Additionally, an intact peritoneal reflection provides a barrier between the injury and the peritoneal cavity, an anatomic distinction that effectively prevents the development of intraabdominal sepsis after penetrating injury to the extraperitoneal rectum. This further distinguishes these injuries from colonic injuries, and therefore their management is different. H If the location of the rectal injury is uncertain, diagnostic laparoscopy may be used to confirm an intraperitoneal component. I

Because the intraperitoneal rectum is anatomically analogous to the sigmoid colon, injuries to the intraperitoneal rectum should be treated as colonic injuries. J

Penetrating rectal injuries that can be accessed transanally and are not destructive can be treated with simple primary repair. Although fecal diversion, presacral drainage, and distal rectal washout make up the traditional management of extraperitoneal rectal injuries, recent studies have called the necessity of these interventions into question. Contemporary management of simple extraperitoneal rectal injuries should consist of primary repair alone without proximal diversion. K Penetrating injuries to the extraperitoneal rectum that cannot be accessed transanally or that are too extensive for primary repair should be managed with proximal diversion in the form of a loop colostomy. The absolute necessity of diversion for a simple high rectal injury is unknown. A well-constructed sigmoid loop colostomy can allow for complete fecal diversion, and small leaks will seal without further intervention. Destructive injuries to the distal rectum or anus can be managed with proximal diversion in the form of a loop sigmoid colostomy followed by reconstruction, which can be delayed to optimize patient physiology and operating conditions. The ideal timing of colostomy closure is controversial. There is evidence supporting reversal of loop colostomy from anywhere between the index hospitalization to at least 3 months after ostomy creation. In practice, colostomy closure should be individualized and occur after all other critical injuries have been fully addressed and the patient’s physiologic and nutritional status have been normalized.

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Chapter 140  ◆  Penetrating Rectal Injury  412.e1

Abstract

Keywords

The management of penetrating rectal injuries has evolved over time. Patients who sustain a pelvic gunshot wound or stab wound may have an injury to the rectum. Patients who are hemodynamically stable without peritonitis or evisceration and who are evaluable should undergo computed tomography (CT) scanning. All others should be brought for immediate laparotomy. The contemporary management of rectal injuries begins with a rigid sigmoidoscopy to identify the location of the rectal injury relative to the peritoneal reflection. Intraperitoneal rectal injuries are managed as colon injuries, and extraperitoneal rectal injuries are managed with either transanal repair or proximal diversion, depending on the location and extent of injury. If the location of the injury is unclear, a diagnostic laparoscopy can be performed to exclude an intraperitoneal component.

rectal trauma penetrating rectal injury gunshot wounds to the rectum

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Chapter 140  ◆  Penetrating Rectal Injury  413

D

Hemodynamic instability, peritonitis, evisceration, or unevaluable No

B

E

Equivocal

Yes

H

Operating Room + Rigid Proctosigmoidoscopy Positive or

C

Manage as colon injury

Intraperitoneal Rectal Injury

Transpelvic/Lower Abdominal Trajectory • Vital Signs • Abdominal Exam • Lower Extremity Pulse Exam

Potential Penetrating Rectal Injury

I

F

A

CT Scan +/− Cystogram

Investigations • Plain X-rays • FAST • Blood Work

REFERENCES Bosarge PL, Como JJ, Fox N, et al. Management of penetrating extraperitoneal rectal injuries: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma. 2016;80:546–551. Demetriades D, Inaba K. Colon and rectal trauma. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 7th ed. New York: The McGraw Hill Companies; 2013:620–631. Navsaria PH, Edu S, Nicol AJ. Civilian extraperitoneal rectal gunshot wounds: surgical management made simpler. World J Surg. 2007;31(6):1345–1351.

Location Unclear

Diagnostic Laparoscopy

J G Extraperitoneal Rectal Injury

Transanal primary repair

K Proximal diversion

Schellenberg M, Inaba K, Priestley EM, et al. The diagnostic yield of commonly used investigations in pelvic gunshot wounds. J Trauma. 2016;81(4):692–698. Velmahos GC, Degiannis E, Wells M, et al. Early closure of colostomies in trauma patients - a prospective randomized trial. Surgery. 1995;118(5): 815–820.

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Chapter

141 

DAMAGE-CONTROL LAPAROTOMY Erik Peltz, DO, FACS, and Franklin L. Wright, MD

A A key update from prior versions of this algorithm involves the recognition that deranged pathophysiology from trauma and hemorrhagic shock, leading to physiologic decompensation, begins at the time of injury, and acute therapy may limit the number of damage-control interventions done. Identification of patients at risk for hemorrhagic shock and need for massive transfusion (MT) allows for goal-directed resuscitation to attenuate the “bloody vicious cycle” and may allow more patients to undergo definitive laparotomy in the acute setting. • Prediction of the need for MT: Patients may be identified in the pre-hospital setting using validated scoring systems (i.e., Assessment of Blood Consumption scoring tool, Resuscitation Outcomes Consortium) that predict the need for MT. • Physiologic indications: Critically injured patients who develop metabolic failure are at imminent risk for death and should undergo “damage control” or “abbreviated laparotomy.” The “bloody vicious triad” is characterized by the following: 1. Hypothermia (body temperature [BT] < 35 °C), 2. Acidosis (pH < 7.2, lactate > 5 mmol/L, base deficit < 15 mmol/L in patient < 55 years or < 6 mmol/L in patient > 55 years of age), and 3. Coagulopathy prothrombin time/international normalized ratio (PT/INR), partial thromboplastin time (PTT) > 50% above normal • Therapies initiated during pre-hospital and emergency department (ED) resuscitation may limit the need for damage-control surgery and should be incorporated within the trauma system. • Therapeutic hypotension with support of systolic blood pressure (SBP) to 90 mm Hg • Limited crystalloid resuscitation and early administration of blood products, including fresh frozen plasma (FFP), for patients in shock after trauma • Active rewarming (heated trauma bay, warm air convection heating, warm blankets, active warming systems for infusion of intravenous fluid [IVF] and blood products) B Damage-control surgery is an abbreviated surgical approach performed on injured patients with profound shock and metabolic failure. Tenets of this approach are as follows 1. Control hemorrhage. 2. Control contamination. 3. Focus on resuscitative efforts and rewarming to normalize metabolic derangements. Restoration of physiologic equipoise is paramount before return to the operating room (OR) for definitive surgical

reconstruction. Surgeons use damage-control principles when dealing with cervical, thoracic, abdominal, vascular, orthopedic, and neurosurgical injuries. Damage-control principles are also applicable during acute care surgery and elective surgical procedures with similar, profound metabolic derangement. • Physiologic indications: hypothermia, acidosis, or coagulopathy, as noted previously. The OR should be actively warmed, and warm air convection devices should be placed on the patient as operative exposure will allow. Irrigation fluids must be warm, and all fluids and blood products to be infused intravenously should be actively warmed. • Other surgical indications are as follows: • Trauma patients requiring intraabdominal packing for hemorrhage control (liver packing, pre-peritoneal pelvic packing, retroperitoneal hemorrhage) • Gastrointestinal injury requiring time-consuming or complex reconstruction (e.g., trauma Whipple) • Mesenteric vascular injury/ischemia requiring a second-look operation for intestinal viability • Need for separate endovascular interventions (e.g., angioembolization of pelvis fracture) • Need to proceed to surgical procedures for other life-threatening injuries (e.g., ruptured descending thoracic aorta) • Inability to perform definitive closure of abdomen because of bowel edema • Impending abdominal compartment syndrome (ACS) C Hemorrhage control is rapidly achieved using nonanatomic resection, laparotomy sponge packing, suture control and ligation of vessels, retained vascular clamps, or temporary vascular shunt placement for destructive injuries. If shunt application is possible, this may allow critical perfusion during further resuscitation (e.g., transected iliac or extremity arteries). Intestinal injuries are stapled, ligated with umbilical tape, or whip-stitched and left in discontinuity. Definitive repair/reconstruction is planned after resuscitation to normal physiologic parameters. D The abdomen is temporarily closed by placing a series of penetrating towel clamps on the skin edges to prevent further heat and fluid loss. Intraoperative resuscitation continues with blood product transfusion, attempting 1 : 1 : 1 (packed red blood cells:fresh frozen plasma:platelet [PRBC:FFP:PLT]) ratio, or component transfusion is guided by whole-blood clotting assay (thromboelastograph [TEG]/rotational thromboelastometry [ROTEM]) directed at restoring perfusion, correcting acidosis, and normalizing coagulopathy. All infusion fluids are warmed. Operating room temperature is maximized. Warm air convection heating devices are used as operative exposure will allow. Wet drapes and blankets are replaced. All exposed body surfaces are covered. After 30 to 45 minutes, the towel clips are removed and the abdomen is re-explored while the patient’s physiologic status is reassessed (vital signs, temperature, pH, lactate, base deficit, PT, and PTT). E Restored physiology allows for definitive operation and fascial closure. F The abdomen is briefly re-explored for additional sources of surgically controllable hemorrhage, and the patient’s physiology is reassessed (coagulopathy, hypothermia, acidosis).

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Chapter 141  ◆  Damage-Control Laparotomy  414.e1

Abstract

Keywords

Damage-control surgery is an abbreviated surgical approach performed on injured patients with profound shock and metabolic failure. Tenets of this approach are to (1) control hemorrhage, (2) control contamination, and (3) focus on resuscitative efforts and rewarming to normalize metabolic derangements. Restoration of physiologic equipoise is paramount before return to the operating room (OR) for definitive surgical reconstruction. Surgeons use damage-control principles when dealing with cervical, thoracic, abdominal, vascular, orthopedic, and neurosurgical injuries. Damage-control principles are also applicable during acute care surgery and elective surgical procedures with similar, profound metabolic derangement.

damage control trauma abdominal compartment syndrome

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Chapter 141  ◆  Damage-Control Laparotomy  415 G With persistent damage-control criteria, several techniques are available for temporary abdominal closure. Two easily performed methods include towel clip or segmental suture of the skin only. These techniques, however, create a rigid closure and may contribute to the development of ACS with ongoing resuscitation. The towel clips may also interfere with visualization if the patient is to undergo angiography. A variety of improvised and commercial vacuum devices use towels or perforated plastic sheets placed over the bowel and under the fascial edges. An impervious, adhesive material (e.g., Ioban sheet) is placed over the abdomen, and suction is applied between the layers to remove pooling fluids and decrease visceral edema. Techniques may be combined and individualized to the operative need (e.g., upper laparotomy penetrating towel clamps to provide tamponade over liver packing and an open abdomen wound vacuum for control of the lower abdomen). H Active rewarming and continued balanced resuscitation with blood products and judicious crystalloids is continued in the intensive care unit (ICU). The ICU is notified before patient transfer to allow continued rewarming on patient arrival. Resuscitation efforts are focused on normalization of physiologic and metabolic derangements to allow the patient to return to the OR for reassessment and potential definitive repair of all injuries within 24 to 48 hours. I

ACS is a potentially lethal complication of massive resuscitation. Swelling and edema associated with the injury, coagulopathy, and resuscitation cause an increased volume of the intraabdominal organs and tissues beyond the constraints of

the semirigid abdominal cavity. Physiologic indicators of the ACS include elevated intraabdominal pressure (IAP), hypotension, tachycardia, hypoxemia, hypercarbia, high peak airway pressures, oliguria, and new or worsening organ failure. J

A graded, sequential escalation of therapeutic approaches is taken to limit intraabdominal hypertension and the progression to ACS. Therapies directed at optimizing abdominal wall compliance (neuromuscular blockade), avoiding Trendelenburg or prone position, decompressing intra-luminal volume (nasogastric tube), draining/decompressing extra-luminal intraabdominal volume (percutaneous drains), judicious fluid man­­ agement, and goal-directed/balanced resuscitation are employed. Continued serial abdominal pressures are assessed. ACS can occur and is described in patients with open abdominal management (e.g., towel clamp or suture skin closure, restrictive adhesive dressings for wound vacuum, occluded wound vacuum sponge or towel with clotted blood). In patients with an open abdomen closure technique and ACS, the closure device should be removed in the ICU, after prep and drape, and transitioned to a more accommodating closure technique (e.g., clamps and sutures removed; wound vacuum applied) or a more loosely applied wound vacuum, with new sponge or towel, is replaced. See the ACS algorithm for additional management details. K Ideally the patient is completely resuscitated before return to the OR and undergoes a successful definitive operation within 24 to 48 hours. Packing is removed for assessment of ongoing bleeding. Definitive organ resection may be performed (e.g., destructive liver lacerations with nonviable parenchyma).

A Abdominal Trauma Pre-hospital, ED, pre-operative strategies - Limit crystalloid - Therapeutic hypotension - Early blood product support - Active rewarming

B DamageControl Laparotomy

C Control hemorrhage Minimize contamination Resuscitate Rewarm

CBC PT/INR, PTT Whole blood clotting assay (TEG / ROTEM) ABG Lactate

E Definitive operation with fascial closure

D Packing/towel clip closure Intraoperative resuscitation and active warming

Rapid G re-exploration Temporary Closure Damage Control Criteria Reassessment

F

Definitive operation with fascial closure

H ICU Resuscitation Monitor for ACS

I ACS

Definitive operation with fascial closure

J Graded therapeutic Approach

K Partial closure Coverage of exposed viscera

L Delayed Abdominal Wall Reconstruction

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416  Part VIII  ◆ Trauma Omental pedicle flaps may be used to buttress areas of injury (liver laceration, bowel/vascular anastomosis). Non-viable bowel is resected, and bowel continuity is restored with anastomosis (proximal small bowel or colon), or ostomies are created as necessary (end colostomy, proximal diverting loop ileostomy). Enteral access for nutrition is obtained to optimize ongoing alimentation for critical care support. • Several techniques have been described for sequential closure of the open abdomen. A common feature of these techniques is sequential re-intervention, every 24 to 48 hours, with progressive closure of the upper and lower ends of the laparotomy and application of moderate tension to the midportion of the open laparotomy fascia with sutures (sequential abdominal closure) or traction dressing (e.g., Wittman patch) to prevent loss of domain and bring fascial edges to approximate in the midline. These techniques are often combined with re-application of woundvacuum devices to facilitate removal of edema and peritoneal fluids. It is critical that these sequential interventions be performed every 24 to 48 hours, with evidence suggesting that delays >48 hours are associated with failure to ultimately achieve fascial closure. L Patients with an open abdomen for more than 7 to 10 days often cannot undergo fascial closure secondary to abdominal wall retraction. This small subset of patients will have skin-only closure, which may be combined with the placement of a biologic mesh underlay or the placement of an absorbable bridging mesh (e.g., Vicryl) to the fascial edges. Complex abdominal reconstruction with flaps or extensive myofascial release is avoided during the acute/subacute operative phase. These may be necessary for

a later, definitive abdominal wall reconstruction. In the extreme case, skin grafting is done on the omentum or bowel once it has a bed of granulation tissue. These patients undergo complex flap or myofascial release with repair of the large ventral hernia in a delayed (6 to 12 months) fashion. REFERENCES Burch JM, Ortiz VB, Richardson RJ, et al. Abbreviated laparotomy and planned reoperation for critically injured patients. Ann Surg. 1992; 215(5):476–483, discussion 483–4. Burlew CC, Moore EE, Biffl WL, et al. One hundred percent fascial approximation can be achieved in the postinjury open abdomen with a sequential closure protocol. J Trauma Acute Care Surg. 2012;72(1): 235–241. Cotton BA, Reddy N, Hatch QM, et al. Damage control resuscitation is associated with a reduction in resuscitation volumes and improvement in survival in 390 damage control laparotomy patients. Ann Surg. 2011; 254(4):598–605. De Waele JJ, Leppaniemi AK. Temporary abdominal closure techniques. Am Surg. 2011;77(suppl 1):S46–S50. Feliciano DV, Moore EE, Mattox KL. Trauma damage control. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 7th ed. New York: McGraw-Hill; 2013. Higa G, Friese R, O’Keeffe T, et al. Damage control laparotomy: a vital tool once overused. J Trauma. 2010;69(1):53–59. Johnson JW, Gracias VH, Schwab CW, et al. Evolution in damage control for exsanguinating penetrating abdominal injury. J Trauma. 2001;51(2): 261–269, discussion 269–271. Kashuk JL, Moore EE, Millikan JS, et al. Major abdominal vascular trauma–a unified approach. J Trauma. 1982;22(8):672–679. Raeburn CD, Moore EE, Biffl WL, et al. The abdominal compartment syndrome is a morbid complication of postinjury damage control surgery. Am J Surg. 2001;182(6):542–546. Rotondo MF, Schwab CW, McGonigal MD, et al. Damage control: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35(3):375–382, discussion 382–383.

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Chapter

142 

ABDOMINAL COMPARTMENT SYNDROME Erik Peltz, DO, FACS, and Franklin L. Wright, MD A Intraabdominal hypertension (IAH) and the progression to abdominal compartment syndrome (ACS) is a potentially lethal complication of massive resuscitation. Swelling and edema associated with the injury, coagulopathy, and resuscitation cause an increased volume of the abdominal organs and tissues beyond the constraints of the semirigid abdominal cavity. Abdominal sepsis, retroperitoneal edema associated with resuscitation from necrotizing pancreatitis, bowel distention with associated adynamic ileus, Ogilvie’s syndrome, and gastric distention all contribute to increased intra-luminal volume and pressure. Conditions that limit abdominal wall compliance, such as burns, further limit the tolerance of the abdominal cavity to increased volume, resulting in increased pressure. Risk factors include the following: Diminished abdominal wall compliance: • Respiratory failure/pulmonary pathology with high intrathoracic pressure, abdominal surgery—tight fascial closure, restrictive open abdominal dressing, major trauma/torso burns, prone positioning, head of bed (HOB) > 30 degrees Increased intraabdominal volume: • Severe pancreatitis; hemoperitoneum/intra-peritoneal fluid collections, including cirrhosis with uncontrolled ascites; intraabdominal abscess/infection; intraabdominal and retroperitoneal tumors Resuscitation/tissue edema/capillary leak: • Acidosis (pH < 7.2), hypotension, hypothermia, coagulopathy • Transfusion (>6 units in 6 hours, >10 units/24 hours) • Crystalloid resuscitation (>500 mL/h for 4 hours, > 5 L/24 hours) • Pancreatitis, sepsis, major trauma/burns Patients with two or more risk factors or with risk factors associated with new or worsening organ dysfunction should have intraabdominal pressure assessed at the time of intensive care unit (ICU) admission. For patients found to have IAH (see later discussion), serial assessment should continue every 4 to 6 hours. B Polycompartment syndrome: Increased intraabdominal pressure (IAP) impairs perfusion within the abdomen and translates pressure to the systemic arteries (increased afterload); to the systemic veins, leading to impaired venous return to the heart (decreased preload); and across the diaphragm, which increases intra-thoracic pressure (increased right ventricular [RV] afterload). These changes result in decreased mean arterial pressure (MAP), decreased cardiac output, prolonged acidosis, and further impairment of systemic perfusion and organ function. Polycompartment syndrome has adverse effects on systemic perfusion and abdominal organ function (i.e., liver, kidneys,

bowel). Intra-thoracic pressure and impaired cardiopulmonary function can contribute to impaired cerebral venous drainage and elevated intracranial pressures. • Physiologic indicators of ACS include elevated IAP, hypotension, tachycardia, hypoxemia, hypercarbia, high peak airway pressures, oliguria, and cardiac index < 3.0 despite apparent adequate central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). However, increased intraabdominal pressure can falsely elevate CVP and PCWP. C Screening: Patients with two or more risk factors (as outlined previously) or risk factors with new or worsening organ dysfunction should have IAP assessed at the time of ICU admission. For patients found to have IAH (see later discussion), serial assessment should continue every 4 to 6 hours. • Assessment of IAP: A Foley catheter is attached to a manometer or to the bedside hemodynamic monitoring system. The bladder is partially distended with instillation of 25 cc of room-temperature saline, the transducer is zeroed at the mid-axillary line, and pressure is assessed at end expiration, in a supine position, with adequate analgesia and sedation, or with paralytics to eliminate muscular contraction. IAP is expressed in mm Hg. The technique of assessment must be consistent to provide reliable serial measurements to guide therapy. • ACS is at the end of a continuum of pathologic IAH: Normal intraabdominal pressure = 5 to 7 mm Hg in adults IAH grade I IAH grade II IAH grade III IAH grade IV

= IAP = IAP = IAP = IAP

12 to 15 mm Hg 16 to 20 mm Hg 21 to 25 mm Hg > 25 mm Hg

*ACS is IAP > 20 with new/worsening organ dysfunction. D A graded, sequential, escalation of therapeutic approaches is applied to attenuate IAH and limit the progression to ACS: • Step 1: Optimize sedation and analgesia. Remove/loosen and re-apply open abdomen closure devices; avoid Trendelenburg position. Decompress intraabdominal contents and volume. Evacuate hollow viscous air and fluid with a nasogastric tube (NGT) and enemas. Assess for drainable peritoneal fluid. Avoid excessive fluid administration, follow goal-directed therapy, and provide balanced resuscitation with blood component therapy. • Step 2: Consider rectal tube for colon distention refractory to enemas and percutaneous drainage of peritoneal fluid collections. Consider limiting enteral nutrition and hypotonic and crystalloid fluid administration, and consider reverse Trendelenburg position. If physiologic endpoints (pH, coagulopathy, hypothermia, and adequate oxygen perfusion) are met, then consider active diuresis for volume removal. • Step 3: Consider colonoscopic decompression if significant colon dilation persists, consider continuous neuromuscular blockade for refractory IAH and hemodialysis, or consider hemofiltration if diuresis ineffective and resuscitation goals are met. ACS can occur and is described in patients with open abdominal management (i.e., towel clamp or suture closure of the skin, tight adhesive dressings for wound vacuum, occluded

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Chapter 142  ◆  Abdominal Compartment Syndrome  418.e1

Abstract

Keywords

Intraabdominal hypertension (IAH) and the progression to abdominal compartment syndrome (ACS) is a potentially lethal complication of massive resuscitation. Swelling and edema associated with the injury, coagulopathy, and resuscitation cause an increased volume of the abdominal organs and tissues beyond the constraints of the semirigid abdominal cavity. Abdominal sepsis, retroperitoneal edema associated with resuscitation from necrotizing pancreatitis, bowel distention with associated adynamic ileus, Ogilvie’s syndrome, and gastric distention all contribute to increased intra-luminal volume and pressure. Conditions that limit abdominal wall compliance, such as burns, further limit the tolerance of the abdominal cavity to increased volume, resulting in increased pressure.

intraabdominal hypertension

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Chapter 142  ◆  Abdominal Compartment Syndrome  419 wound vacuum sponge, or towel with clotted blood). In patients with an open abdomen closure technique and ACS, the closure device should be removed in the ICU, after prep and drape, and transitioned to a more accommodating closure technique (clamps/sutures removed; apply negative pressure vacuum closure device), or a more loosely applied wound vacuum, with new sponge or towel, is replaced.

• Several techniques have been described for sequential closure of the open abdomen. Common features of these techniques are sequential re-operation or bedside procedure every 24 to 48 hours, progressive closure of the upper and lower ends of the laparotomy, and application of moderate tension to the mid-portion of the open laparotomy fascia with sutures (sequential abdominal closure) or traction dressing (i.e., Wittman patch) to prevent loss of domain and bring fascial edges toward the midline. These techniques are often combined with the application of wound-vacuum devices to facilitate removal of edema and peritoneal fluids. • It is critical that sequential interventions are performed every 24 to 48 hours, with evidence suggesting that delays > 48 hours are associated with failure to ultimately achieve fascial closure.

E Step 4: If new/progressive organ dysfunction occurs and IAP is > 25, consider decompressive laparotomy. F If successful at relieving ACS, goal-directed resuscitation continues in the ICU with serial assessment of intraabdominal pressures (every 4 to 6 hours) and with continued therapy to limit progression. Continue treatment for the primary disease process (i.e., sepsis, trauma/burn resuscitation) and support of multiple-organ dysfunction.

H Patients with an open abdomen for more than 7 to 10 days often cannot undergo fascial closure secondary to abdominal wall retraction. This small subset of patients will have skin-only closure, which may be combined with the placement of a biologic mesh underlay or the placement of an absorbable bridging mesh (i.e., Vicryl) to the fascial edges. Complex abdominal reconstruction with flaps or extensive myofascial release is avoided during the acute/subacute operative phase. These may be necessary for a later definitive abdominal wall reconstruction. In the extreme case, skin grafting is done on the omentum or bowel once it has a bed of granulation tissue. These patients undergo complex

G Ideally the patient is resuscitated before return to the operating room (OR) and undergoes a successful definitive operation with abdominal fascial closure. Often this cannot be achieved in a single intervention, and the patient must undergo continued ICU support with cycles of resuscitation and operative intervention for sequential closure. At each operation an assessment is made if it is possible to close the abdomen. The abdomen often cannot be fully closed until the visceral edema resolves, which may take several days.

A Risk factor Decreased abdominal wall compliance Increased intraabdominal volume Resuscitation/Edema Favorable response

Intraabdominal Hypertension/ Abdominal Compartment Syndrome

C Intra-abdominal Pressure

B Clinical Signs “Poly-compartment Syndrome” Decreased BP Increased HR Decreased PaO2 Increased PaCO2 Increased peak airway pressure Decreased urine output

D Graded Management • Optimize abdominal wall compliance • Remove and replace abdomen closure (i.e., wound vacuum, sutures) • Supine or reverse Trendelenburg position • Decompress intra-luminal volume • Decompress extra-luminal volume and drain ascites/ peritoneal fluid • Judicious fluid management/ balanced resuscitation, diuresis, HD, or hemofiltration

Successful sequential fascial closure

Continue management

E • IAP > 25 with new/ worsening organ dysfunction, refractory to graded therapeutics • Decompressive laparotomy

F • Continued resuscitation • Treat primary pathology

G Return to OR 24–48 hours

H Partial closure Coverage of exposed visceral

Delayed hernia repair/ abdominal wall reconstruction

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420  Part VIII  ◆ Trauma flap or myofascial release with repair of the large ventral hernia in a delayed (6 to 12 months) fashion. REFERENCES Balogh ZJ, Leppaniemi A. Patient populations at risk for intra-abdominal hypertension and abdominal compartment syndrome. Am Surg. 2011;77(suppl 1):S12–S16. Burlew CC, Moore EE, Biffl WL, et al. One hundred percent fascial approximation can be achieved in the postinjury open abdomen with a sequential closure protocol. J Trauma Acute Care Surg. 2012;72(1): 235–241. Burlew CC. The open abdomen: practical implications for the practicing surgeon. Am J Surg. 2012;204(6):826–835. De Waele JJ, Leppaniemi AK. Temporary abdominal closure techniques. Am Surg. 2011;77(suppl 1):S46–S50.

Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013;39(7): 1190–1206. Malbrain ML, Cheatham ML. Definitions and pathophysiological implications of intra-abdominal hypertension and abdominal compartment syndrome. Am Surg. 2011;77(suppl 1):S6–S11. Malbrain ML, De Laet IE, De Waele JJ, et al. Intra-abdominal hypertension: definitions, monitoring, interpretation and management. Best Pract Res Clin Anaesthesiol. 2013;27(2):249–270. Raeburn CD, Moore EE, Biffl WL, et al. The abdominal compartment syndrome is a morbid complication of postinjury damage control surgery. Am J Surg. 2001;182(6):542–546.

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Chapter

143 

TRAUMATIC HEMATURIA Rodrigo Donalisio de Silva, MD, and Fernando J. Kim, MD, MBA, FACS A Gross hematuria or microscopic hematuria with a systolic pressure < 90 mm Hg warrants investigation and can result from blunt, penetrating, or even iatrogenic injuries. Following general guidelines, surgical decision making should focus on signs of clinical stability, grade of injury, and presence of associated injuries. B In patients with suspected bladder and/or urethral injury, refer to Bladder and Urethral Trauma (Chapter 145). Patients with gross hematuria and stable vital signs can be evaluated with computed tomography (CT) scanning of the abdomen and pelvis with intravenous (IV) contrast. CT scanning can precisely identify and classify renal and ureteral injuries. Patients with microscopic hematuria and systolic blood pressure < 90 mm Hg, if responsive to initial resuscitation, will proceed with CT of the abdomen and pelvis with IV contrast and delayed images. It is mandatory to get delayed images (10 minutes) after contrast injection to rule out urine extravasation and ureteral injuries. If no urethral injury is suspected, a Foley catheter can be placed to monitor urinary output. If not responsive to initial resuscitation, the patient is referred to step C. Patients with persistent microscopic hematuria but stable vital signs and stable hemoglobin (Hb) and hematocrit (Ht) can be safely managed conservatively. C Patients who are unstable and have multisystem trauma, a major mechanism of injury (e.g., deceleration injuries), or penetrating injuries may require urgent laparotomy. If the patient becomes stable after initial resuscitation, imaging should be performed. D Patients with isolated high-grade renal injuries that responded at first to resuscitation can be candidates for conservative management. If a transient response occurs after initial resuscitation and isolated renal injury, interventional radiology (IR) embolization may be an option to control bleeding. E Patients with low-grade renal injuries (American Association for the Surgery of Trauma [AAST] grades I to III) who are hemodynamically stable can be safely managed conservatively by monitoring serial Hb and Ht, basic metabolic panel (BMP), and bedrest. If patients become unstable during their observation period, the patient needs to be reevaluated (refer to step C).

F High-grade renal injuries (AAST grades IV and V) can also be managed conservatively if hemodynamically stable. Contrast extravasation in CT-scan delayed phases can initially be managed conservatively with a Foley catheter (decompress upper urinary tract), bedrest, and serial BMP and Ht/Hb. Repeat CT scan with delayed images after 48 to 72 hours to compare with initial image. It is important to monitor for signs of infection (fever, chills, worsening of pain). G Exploratory laparotomy should be performed if multisystem or penetrating injuries occur or there is an indication for laparotomy because of other associated injuries. During exploratory laparotomy, all associated injuries should be addressed and controlled. A nonexpanding retroperitoneal hematoma can be observed. If the retroperitoneal hematoma is expanding, exploration is required. Surgeons must inspect the ureters during exploratory laparotomy if they suspect ureteral injury. A single-shot intravenous pyelogram (IVP) cannot reliably exclude ureteral injury. Intravenous (IV) or intraureteral injectable dyes such as methylene blue or indigo carmine can be used. A retrograde pyelogram is an option to identify ureteral injuries and possible treatment (stent placement); however, that may be time-consuming and require a radio-translucent bed and fluoroscopy. H Patients with urine extravasation in the initial CT/IVP and elected for conservative management should have the CT scan repeated in 48 to 72 hours. If the urinoma increases in size and/or signs of infection are present, consider ureteral stent placement and/or IR drainage. I

Grade IV and grade V renal injuries that show a continuous decrease in Hb/Ht and/or multiple transfusions can be managed with IR selective embolization. REFERENCES Iverson AJ, Morey AF. Radiographic evaluation of suspected bladder rupture following blunt trauma: critical review. World J Surg. 2001;25: 1588–1591. Kim FJ. Urologic trauma. In: Moore EE, Feliciano DV, Mattox KL, eds. Trauma Companion Handbook. 4th ed. New York: McGraw-Hill; 2002. Lumen N, Kuehhas FE, Djakovic N, et al. Review of the current management of lower urinary tract injuries by the EAU trauma guidelines panel. Eur Urol. 2015;67(5):925–929. [Epub 2015 Jan 6]. McAninch JW. Traumatic and Reconstructive Urology. Philadelphia: WB Saunders; 1996. Moore EE, Cogvill TH, Jurkovich GJ, et al. Organ injury scaling, III: chest wall, abdominal vascular, ureter, bladder, and urethra. J Trauma. 1992;33:337–339. Moore EE, Feliciano DV, Mattox KL. Trauma. New York: McGraw-Hill Education; 2016. Morey AF, Brandes S, Dugi DD, et al. Urotrauma: AUA Guideline. Accessible at: https://www.auanet.org/education/guidelines/urotrauma.cfm. Accessed February 16, 2017. Serafetinides E, Kitrey ND, Djakovic N, et al. Review of the current management of upper urinary tract injuries by the EAU trauma guidelines panel. Eur Urol. 2015;67(5):930–936. [Epub 2015 Jan 8].

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Chapter 143  ◆  Traumatic Hematuria  422.e1

Abstract

Keywords

Genitourinary injury occurs in 2% to 5% of all trauma patients and in at least 10% of patients with abdominal trauma, emphasizing the need for close collaboration between the general and urologic trauma surgeon. This unique relationship that the urologist and general trauma surgeon share in the management of urologic injuries requires common philosophies of management to be applied. Gross hematuria is one of the most common signs of trauma to the urinary tract. Hematuria is commonly seen in renal, bladder, and urethral injuries. Surgeons must identify patients with suspected urologic injuries and proceed with the appropriate work-up to identify and treat these patients.

hematuria renal injury renal trauma bladder trauma bladder injury urethral trauma urethral injury pelvic fracture

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Chapter 143  ◆  Traumatic Hematuria  423 Lower urinary tract trauma (refer to chapter 145)

Stable Serial Hb/Ht, BMP checks, bed rest

E

Unstable - Refer to UNSTABLE

Grade I-III

History and physical exam Gross Hematuria

Stable

B

CT Scan abdomen & pelvis w/IV contrast & Microscopic Hematuria + delayed images Systolic Pressure (CT-IVP) 3 red blood cells per high-power field [RBC/HPF]) following blunt abdominal trauma because it will guide subsequent management. Similar assessment criteria may be applied to pediatric patients, except for SBP. Pediatrics patients have a high reserve and do not develop hypotension in the same manner as adults. B Stable patients should undergo computed tomography (CT) imaging with early corticomedullary phase (corresponds to portal venous phase used to evaluate liver/spleen injuries) and 10-minute delayed intravenous contrast phases. The early corticomedullary phase evaluates for a renal parenchymal injury, and the delayed phase evaluates for collecting-system injuries and urine extravasation. C Unstable patients or patients with nonrenal findings (e.g., positive focused assessment with sonography in trauma examination [FAST]) necessitating abdominal exploration should forego CT imaging and proceed directly to the operating room for abdominal exploration. D Patients with uncomplicated American Association for the Surgery of Trauma (AAST) grade I, II, or III renal injuries should initially undergo nonoperative management that may include intensive care unit (ICU) admission, hemodynamic monitoring, serial hematocrit evaluation, and bedrest. Routine follow-up CT imaging (after 48 hours) should not be performed in patients with uncomplicated injuries and a stable clinical picture. E Patients with AAST grade IV, grade V, and complicated grade III (e.g., multiple grade III injuries or penetrating injury) renal injuries may undergo operative or nonoperative (expectant) management depending on the clinical scenario. Nonoperative management may include ICU admission, hemodynamic monitoring, serial hematocrit evaluation, and bedrest.

Nonoperative management for select penetrating renal trauma has gained support over the past few decades, more commonly following stab wounds (no blast effect) than GSWs. The ability to perform nonoperative management for penetrating injuries is often limited by the high rate of multiple-organ injury. F Patients identified with a pulsatile or expanding retroperitoneal hematoma during abdominal exploration should undergo renal exploration. Manual palpation should be performed to evaluate for the presence and pulse of a contralateral kidney. Intraoperative one-shot intravenous pyelogram (IVP) is an alternative method to evaluate for a contralateral kidney and ipsilateral collecting-system injury; however, obtaining an IVP may be logistically challenging and not practical unless it is seamlessly built into the trauma operating room protocol. Identifying the presence of a functioning contralateral kidney is important before attempted reconstruction if a nephrectomy is required. G Patients identified with a stable retroperitoneal hematoma may undergo evaluation by manual palpation of the contralateral kidney or one-shot IVP before proceeding with renal exploration. Alternatively, the stable retroperitoneal hematoma may be managed nonoperatively by obtaining CT imaging once stable. The latter is a suitable option for patients who are unable to undergo renal exploration because of clinical instability or who will undergo delayed abdominal closure at a later time. H Patients without a retroperitoneal hematoma and without penetrating renal trauma do not require renal exploration and should undergo CT imaging once stable if renal injury is still suspected. I

Indications for open or endoscopic evaluation include a shattered kidney, suspected renal pedicle avulsion, and ureteropelvic junction (UPJ) disruption. UPJ disruption was not included in the original AAST Organ Injury Scale from 1989 but was introduced as a proposed revision in 2011. Traditional teaching suggests that vascular control of the renal pedicle should be obtained before exploring the retroperitoneum and opening Gerota’s fascia; however, the benefit of this maneuver is debatable. When devitalized renal tissue is debrided during renorrhaphy, surgeons should be careful not to excise the renal capsule because it will provide strength for the sutures placed during renorrhaphy. If sufficient capsule is not present, polyglactin mesh or an omental pedicle flap may be used to facilitate closure. J

Renal exploration should be considered if a patient is to undergo abdominal exploration for other, nonrenal causes. Patients may benefit from primary repair of renal injuries because devitalized renal parenchyma and hematoma are a risk for developing an infected urinoma or perinephric abscess, which can further complicate coexisting intraperitoneal injuries. Husmann et al. (1993) identified that patients who underwent operative versus nonoperative management of devitalized renal parenchyma developed lower rates of urological morbidity (23% vs. 85%). Therefore some surgeons recommend surgical intervention for grade IV renal injuries with >25% devascularized parenchyma. K Patients with grade IV or V injuries who become hemodynamically unstable or experience down-trending hematocrits

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Chapter 144  ◆  Renal Injury  424.e1

Abstract

Keywords

Renal trauma management has evolved to primarily non-operative or minimally invasive management in an effort to preserve the injured kidney. Following initial evaluation, patients should be stratified to stable or unstable, as it will determine if radiologic staging can be performed before a possible intervention. When able, CT imaging with immediate and 10 minute delayed contrast phases is crucial to accurately determine renal injury grading. Select AAST grade 3-5 blunt renal injuries may require acute intervention. Utilization of repeat CT imaging in 48 hours should be considered to evaluate for injury progression when nonoperative strategies are employed. Minimally invasive techniques should be used, when necessary, to encourage renal healing.

renal injury management

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Chapter 144  ◆  Renal Injury  425

D History and Physical Mechanism of injury Vital signs Flank ecchymosis Rib fractures Wound entry and exit sites Gross hematuria

B

A

Operative management Stable patient should undergo CT imaging with immediate and delayed contrast phases

Suspicion for Renal Injury -Blunt abdominal trauma and gross hematuria -Blunt abdominal trauma, microscopic hematuria, and shock (SBP2 units of RBC transfusions or have intravascular contrast extravasation or perirenal hematoma >25 mm on imaging are at risk for requiring angioembolization. Patients with a history of renal trauma may develop pseudo­ aneurysms or arteriovenous malformations, which typically present as flank pain or gross hematuria 7 to 14 days after injury. Typical CT imaging to assess trauma does not include an arterial phase; therefore these patients should undergo an arterial-phase CT scan and may require selective angioembolization. L Patients with main or segmental renal vessel thrombosis are managed conservatively, especially in the setting of a normal contralateral kidney. Patients with such vascular injuries are often unable to receive thrombolytics because they are diagnosed outside of the therapeutic window or have concomitant injuries susceptible to bleeding. Similarly, patients also infrequently undergo open vascular repair because of the morbidity of the surgery and the inability to receive anticoagulation afterward as a result of concomitant injuries. M Patients with deep renal injuries (grade IV or V), complicated grade III injuries (e.g., multiple grade III injuries or penetrating injury), or worsening clinical picture (e.g., fever, worsening flank pain, ongoing blood loss, abdominal distention) should undergo repeat imaging (48 hours) to evaluate for previously unidentified or worsening collecting-system injuries. Patients with segmental renal vascular injuries without perinephric hematomas do not require repeat imaging because of the low risk for requiring subsequent intervention. N No specific management recommendations exist as to whether collecting-system injuries should be managed proactively before possible clinical symptoms develop from a

Renal exploration

urinoma or reactively when clinical symptoms develop (e.g., fever, leukocytosis, pain, nausea) because they may heal without intervention. Patients with complex urinomas at presentation or enlarging urinomas on repeat imaging may undergo ureteral stent and catheter placement. Patients who develop an infected urinoma or perinephric abscess may require perinephric drain placement. REFERENCES Bjurlin MA, Jeng EI, Goble SM, et al. Comparison of nonoperative management with renorrhaphy and nephrectomy in penetrating renal injuries. J Trauma. 2011;71:554. Buckley JC, McAninch JW. Revision of current American Association for the Surgery of Trauma renal injury grading system. J Trauma. 2011;70:35. Carroll PR, McAninch JW, Wong A, et al. Outcome after temporary vascular occlusion for the management of renal trauma. J Urol. 1994;151:1171. Charbit J, Manzanera J, Millet I, et al. What are the specific computed tomography scan criteria that can predict or exclude the need for renal angioembolization after high-grade renal trauma in a conservative management strategy? J Trauma. 2011;70:1219. Gonzalez RP, Falimirski M, Holevar MR, et al. Surgical management of renal trauma: is vascular control necessary? J Trauma. 1999;47:1039. Husmann DA, Gilling PJ, Perry MO, et al. Major renal lacerations with a devitalized fragment following blunt abdominal trauma: a comparison between nonoperative (expectant) versus surgical management. J Urol. 1993;150:1774. Lin WC, Lin CH, Chen JH, et al. Computed tomographic imaging in determining the need of embolization for high-grade blunt renal injury. J Trauma Acute Care Surg. 2013;74:230. Long JA, Fiard G, Descotes JL, et al. High-grade renal injury: non-operative management of urinary extravasation and prediction of long-term outcomes. BJU Int. 2013;111:E249. Malaeb B, Figler B, Wessells H, et al. Should blunt segmental vascular renal injuries be considered an American Association for the Surgery of Trauma grade 4 renal injury? J Trauma Acute Care Surg. 2014;76:484. Morey AF, Brandes S, Dugi DD 3rd, et al. Urotrauma: AUA guideline. J Urol. 2014;192:327. van der Wilden GM, Velmahos GC, Joseph DK, et al. Successful nonoperative management of the most severe blunt renal injuries: a multicenter study of the research consortium of New England centers for trauma. JAMA Surg. 2013;148:924.

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Chapter

145 

URETERAL INJURIES Maxx Gallegos and Richard A. Santucci

A Ureteral trauma is rare, accounting for 1% of all genitourinary injuries. The ureter is flexible and well protected by its position in the retroperitoneum. The dorsal musculature, spinal vertebral column, and abdominal contents provide protection. Approximately 80% of ureteral injuries result from iatrogenic causes. The remaining 20% of ureteral injuries are caused by blunt and penetrating extremal trauma. Ureteral injury occurs in 1% of blunt traumatic events and in 4% of penetrating events. Penetrating ureteral trauma is highly correlated with injury to other organ systems (98%). Blunt trauma is more likely to cause ureteral injury in children. This is because of hyperextension of the vertebral column causing disruption of the ureteral pelvic junction (UPJ). Gunshot wounds account for 55% of all penetrating ureteral injuries. The distribution of injury to the ureter is 26% proximal, 37% mid, and 37% distal. Bullets injure the ureter in two distinct ways. One is by direct destruction or transection and the other is by disruption of the blood supply, leading to necrosis. B The American Association for the Surgery of Trauma (AAST) grades ureteral injuries by the severity of the injury: Grade I: Contusion or hematoma without devascularization Grade II: Laceration with less than 50% transection Grade III: Laceration with more than 50% transection Grade IV: Laceration with complete transection and less than 2-cm devascularization Grade V: Laceration with avulsion and more than 2-cm devascularization C Iatrogenic ureteral injury can occur in the setting of open, laparoscopic, and even endoscopic surgery. Mechanisms of injury include resection of the ureter, ischemia caused by tissue stripping or cautery, transection, ligation, crush injury caused by clamping, and angulation leading to obstruction. Iatrogenic ureteral injury remains most common in gynecologic surgery. The incidence of injury ranges from 0.05% to 2.3% in this setting. Other surgical settings of ureteral injury include colorectal, vascular, and urologic surgery. Predisposing factors for injury during gynecologic surgery include the size of the uterus, large ovarian cysts, history of radiation therapy, and urinary tract anomalies. The ureter is most often injured during hysterectomy because the ureter runs inferior to the uterine artery. The risk for ureteral injury during laparoscopic gynecologic operations is equal to that of open operations. Ureteral injuries are less likely to be recognized at the time of laparoscopy than in open gynecologic surgery. In the setting of colorectal surgery, inflammation and malignancy are correlated with increased risk for injury. In vascular surgery, ureteral injuries are more likely during procedures involving large pelvic vascular aneurysms. Ureteroscopy is the most common urologic setting of injury. The rates of injury resulting from ureteroscopy are declining as

technology and technique improve. Oftentimes, ureteral injury at the time of ureteroscopy can be managed with ureteral stenting alone. D Prompt diagnosis is key in limiting morbidity and mortality. Maintaining a high index of suspicion is key in early detection. Despite this, 66% of all ureteral injuries are diagnosed in a delayed fashion. The sequelae of delayed ureteral injury include abdominal pain, flank pain, fevers, leukocytosis, elevated creatinine, prolonged ileus, fistula formation, and sepsis. Ureteral trauma must be considered in all instances of penetrating trauma, especially in the setting of gunshot wounds. Hematuria, although common in most genitourinary (GU) injuries, doesn’t reliably indicate ureteral injury. The absence of hematuria doesn’t rule out ureteral injury. E Computed tomography (CT) scanning with delayed excretory imaging is the mainstay in the detection of ureteral injury. CT scanning will often detail the presence and degree of renal and ureteral injury. In the setting of ureteral injury, this examination shows extravasation of contrast or the absence of contrast filling the distal ureter. If these exist, it should prompt further evaluation or surgical repair. Especially when the injury is detected in a delayed fashion, CT scanning can also demonstrate hydronephrosis, urinoma, or abscess formation. F If further evaluation is called for, cystoscopy with retrograde pyelography is the study of choice because of its high sensitivity. It is performed under anesthesia and provides the chance for diagnosis and treatment. G Early detection of ureteral injury after trauma typically occurs at the time of trauma laparotomy, although the detection rate is variable at 39% to 92%. Direct visualization is the most reliable method for evaluating the viability of the ureter. Signs such as contusion, discoloration, or lack of or decreased peristalsis can indicate ureteral injury. In the setting of trauma, the patient’s stability should lead the decision to repair or temporize. H Intraureteral or intravenous instillation of indigo/carmine or methylene blue can be helpful in identifying the injury. When injury is identified at the time of surgery, intraureteral and intravenous dye instillation can also be used to localize the injury. I

The majority of iatrogenic ureteral injuries are discovered postoperatively. If a diagnosis is made within 7 to 10 days, repair should be attempted then. If the injury is discovered after this, ureteral repair is less likely to be successful as a result of inflammation. A nephrostomy tube should then be placed, followed by repair 3 months later. J

In stable patients, primary repair provides durable long-term patency. Ureteral repair must include careful debridement/ mobilization of the ureter. It should also include a spatulated, tension-free, and watertight anastomosis. It is also wise to leave a means for retroperitoneal drainage and a temporary stent. The method of repair is often dictated by the location and length of the ureteral injury. The ureter is divided into three sections: upper, middle, and lower. The upper segment extends from the UPJ to the sacrum. The middle ureter runs along the sacrum.

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Chapter 145  ◆  Ureteral Injuries  426.e1

Abstract

Keywords

Ureteral trauma is rare, accounting for 1% of all genitourinary injuries. Most injuries result from iatrogenic causes, although some result from external trauma. The majority of ureteral injuries are discovered in a delayed manner. This delay in diagnosis often leads to considerable morbidity, including fevers/sepsis, abdominal pain, hematuria, elevated creatinine, and loss of renal function. Gynecologic surgery is the most common setting for ureteral injury, although other common settings include colorectal surgery, vascular surgery, and even urologic surgery. Prompt recognition of injury and treatment can mitigate morbidity. Computed tomography (CT) urography is the best imaging study for the diagnosis of a suspected ureteral injury. When patients are unstable, ureteral injuries should be temporized with nephrostomy tubes. Ureteral repair can be done after the patient is more clinically stable. When patients are stable, repair of the ureteral injury can be performed. The type of repair largely depends on the location, length, and nature of the injury. Tenets of ureteral repair include careful mobilization and debridement of the ureter, spatulation, and tension-free anastomosis. Repair methods range from primary repair to pyeloplasty in the upper ureter and ureteroneocystostomy with or without psoas hitch and Boari flap maneuvers in the distal ureter. If ureteral continuity is suspected on imaging, cystoscopy and ureteral stenting should be attempted. This step is often the definitive treatment for ureteral injuries. Nephron preservation should be a urologist’s primary goal. Early recognition and prompt treatment of ureteral injury are paramount in achieving this objective.

ureter trauma iatrogenic injury delayed diagnosis computed tomography (CT) urogram anastomosis

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Imaging - CT scan E - Retrograde pyelogram

Ureteral Injury

F

History and Physical Exam Trauma A B Iatrogenic injury C Keys in evaluation D - Abdominal pain - Hematuria - Fevers/sepsis

K

L

Ureteral continuity

Delayed diagnosis

I

O

Mid ureteral injury

N

No ureteral continuity

P Unsuccessful

Successful

O

Discontinue stent

Nephrectomy vs long-term nephrostomy tube

Ileal ureter vs autotransplant

Boari flap with ureteroneocystostomy

Psoas hitch with ureteroneocystostomy

Normal healing Placement of nephrostomy tube and delayed repair

Retrograde pyelogram

T

Ureteroneocystostomy

Pyeloplasty or ureterocalycostomy

Replace stent or repair

S

R

Q

Q

Ureteroureterostomy

Primary closure

Persistent leakage

Bad reconstructive candidate

Good reconstructive candidate

Lowest 1/6 ureter Lowest 1/3 ureter Lowest 2/3 ureter

Transureteroureterostomy

N

Primary closure/ureteroureterostomy

Partial transection Complete transection UPJ or severe pelvis injury

Placement of nephrostomy tube and delayed repair

Distal ureteral injury Complete ureteral destruction Placement of nephrostomy tube and delayed repair

Primary repair

Attempt Double J stent

Unstable patient

Early diagnosis

G H

Stable patient

J

M Proximal ureteral injury

V

U

Chapter 145  ◆  Ureteral Injuries  427

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428  Part VIII  ◆ Trauma The lower ureteral segment extends from the lower border of the sacrum to the bladder. K In an unstable patient, when other organ systems are injured, temporizing the patient’s urinary status with a percutaneous nephrostomy tube is prudent. Ureteral repair should never preclude treatment of other vital organs or blood vessels. Another option is to ligate the ureter with clips or suture and then place a nephrostomy tube. Finally, a transected ureter can be exteriorized to the skin through the abdominal wall. Once the patient is stable, reconstruction can be attempted. L If ureteral continuity exists, ureteral stenting should be attempted. If successful, the stent should be maintained for 6 weeks. This will promote healing and occasionally definitively treat the injury. A retrograde pyelogram must be done to ensure resolution of the ureteral injury at the time of stent removal. M Upper ureteral injury often is treated by performing primary repair, ureteroureterostomy, pyeloplasty, and less commonly ureterocalicostomy. N Injuries in the mid-ureter can be repaired by primary closure and ureteroureterostomy as described previously. For long injuries of the distal half of the ureter or when bladder capacity is insufficient, transureteroureterostomy can be performed. This technique involves mobilization and debridement of the injured ureter. It is then transposed and anastomosed to the contralateral ureter via a 1.5-cm ureterotomy in an end-to-side fashion. Note: This procedure is contraindicated in patients with a history of transitional cell carcinoma or urolithiasis. It is also important to note that this technique should be performed only as a last option. Operating on both ureters inherently puts both renal units at risk for obstruction, need for future operation, and even renal failure. O Injuries involving the lower ureter are best treated with ureteroneocystostomy with or without the use of either psoas hitch or Boari flap techniques. If ureteroneocystostomy is performed alone, a tension-free anastomosis of the ureter to the bladder is critical. This method is only feasible when the injury is very distal or for short defects. P If retrograde stent placement is not successful, a nephrostomy tube should be placed, with a plan for delayed repair. This is typically done 3 months later. Q Both primary closure and ureteroureterostomy can be used in all three segments of the ureter. Primary closure is rarely used because it is only applicable for short stab injuries. It should never be used for gunshot injuries because of delayed tissue breakdown resulting from the blast effect. Ureterouretostomy involves mobilization and debridement of nonviable ureteral edges. A spatulated, tension-free anastomosis is then created with absorbable sutures. Internal stents should always be used and maintained for at least 6 weeks. If a tension-free repair is

not possible, several centimeters can be gained by performing nephropexy. In this step the kidney capsule is sutured to the quadratus lumborum. R If the entire ureter is injured and the patient is a good operative candidate, ileal ureter substitution and autotransplantation are options. Ileal substitution requires a creatinine level of less than 2.5. Typically, a 25-cm segment of ileum is liberated and anastomosed proximally to the renal pelvis and distally to the bladder. Complications are similar to those of an ileal conduit. Autotransplantation of the kidney to the iliac fossa is another option but requires comfort in performing venous and arterial anastomoses. The renal pelvis is anastomosed to the bladder. S Patients who are not good operative candidates can be managed with chronic nephrostomy tubes. A nephrectomy can also be performed if the contralateral kidney is normal, although preserving renal function should always be a urologist’s primary goal. T When there is considerable damage to the UPJ or the proximal ureter, pyeloplasty can be performed. When the renal pelvis is extensively damaged, ureterocalicostomy can be performed. During ureterocalicostomy, the lower pole is amputated to expose a lower pole infundibulum. An anastomosis is then formed using the healthy proximal ureter and the lower pole infundibulum. This technique has a high risk for stenosis and requires extensive dissection. As such, ureterocalicostomy should be employed only when absolutely necessary. U If the distal ureteral defect is longer or more distant from the bladder, a psoas hitch is performed. In this method, the bladder is mobilized aggressively. Ligation of the contralateral pedicle can be performed to gain additional length. These maneuvers will aid in fixing the bladder to the ipsilateral psoas tendon with longitudinally placed sutures. A ureteroneocystostomy is then performed as described previously. V For even longer distal ureteral defects, an anterior bladder flap (Boari flap) can be used to bridge gaps as long as 15 cm. This technique involves aggressive mobilization of the bladder and incising a U-shaped anterior bladder wall flap. This is tubularized, and a ureteroneocystostomy is done. REFERENCES Armenakas N. Ureteral trauma: surgical repair. Atlas Urol Clin North Am. 1998;6(2):71–84. Brandes SB, McAninich JW. Reconstructive surgery for trauma of the upper urinary tract. Urol Clin North Am. 1999;26(1):183–199. Hohenfellner N, Santucci RA. Emergencies in urology. In: Pfetzenmaier J, et al, eds. Trauma of the Ureter. Springer; 2007:233–245. Morey AF, Brandes S, et al. Urotrauma: AUA guidelines. J Urol. 2014; 192(2):327–335. Png JCD, Chapple CR. Principles of ureteric reconstruction. Curr Opin Urol. 2000;10:207–212. Wein AJ, Kavoussi LR., Campbell MF., Walsh PC. Campbell-Walsh urology. In: Santucci RA, Doumanian LR, eds. Upper Urinary Tract Trauma. Elsevier Saunders; 2012:1178–1189.

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Chapter

146 

BLADDER AND URETHRAL TRAUMA Rodrigo Donalisio de Silva, MD, and Fernando J. Kim, MD, MBA, FACS

A The presence of hematuria or blood in the urethral meatus in patients with suspected genitourinary trauma warrants investigation. Penetrating trauma to the pelvis, perineum, and abdomen can involve the lower urinary tract. Identification of entrance and exit wounds can give the surgeon an idea of possible organs affected in that region. Blunt trauma can cause injury to the lower urinary tract and is usually associated with pelvic fracture, saddle injury, or direct trauma to the pelvis and genitals. B Patients with pelvic fracture and hematuria are assumed to have injuries to the lower urinary tract until proven otherwise. Urinary retention can also be a sign of injury to the lower urinary tract. The initial investigation of these patients when hemodynamically stable should start with hematuria work-up including a retrograde urethrogram. C Patients with penetrating injuries to the lower urinary tract should have imaging studies of the lower urinary tract if they are hemodynamically stable. A computed tomography (CT) cystogram should be performed in patients with suspected bladder injuries, and retrograde urethrography (RUG) should be performed in patients with suspected urethral injuries. For unstable patients who need emergent laparotomy, bladder exploration should be performed to identify and treat bladder injuries. During the exploration, if a bladder lesion is found, surgeons must carefully inspect the bladder for foreign bodies and exit wounds, sometimes extending the cystotomy. If no obvious bladder lesion is found, surgeons can fill the bladder with fluids and inspect for extravasation. If a bladder injury is found, it should be repaired with absorbable sutures. D Pelvic fracture urethral injuries (PFUIs) should trigger prompt urological evaluation. The urologist can sometimes attempt a Foley catheter placement. When able to place the Foley catheter, it should remain in the urethra for at least 7 days, and pericatheter RUG should be performed before Foley removal. In patients with failed Foley catheter placement, cystoscopy at the bedside can be performed in an attempt to find the urethral lumen, and a guidewire can be placed into the bladder, guiding the passage of a Council-tip urethral catheter. If the urethral lumen cannot be found during bedside cystoscopy, the placement of a suprapubic catheter (SPT) is recommended. Primary urethral realignment can be attempted 7 to 10 days after the initial urethral injury using cystoscopic guidance and flexible scopes through the suprapubic (anterograde) tract. Primary urethral realignment can be as effective as primary treatment for posterior urethral

disruption. Some patients will develop a urethral stricture after primary realignment, but stricture length tends to be smaller, facilitating future reconstruction. E In patients with pelvic fracture and no hematuria who will require Foley catheter placement (surgery, urinary output, intensive care unit [ICU], and others), one attempt of Foley placement can be performed. If unable to place a catheter, RUG should be performed. F When bladder injury is suspected in patients with a pelvic fracture, RUG should be performed to rule out urethral injury. If no contrast extravasation is in the urethra, a catheter can be placed to facilitate contrast injection (around 150 to 200 mL) into the bladder to proceed with the CT cystogram. If CT scanning is not available, a traditional cystogram including post-void films can be performed; however, 45-degree images should also be obtained. G Patients with bladder injury should have a urologic consultation when the diagnosis is made. An intraperitoneal bladder injury identified at laparotomy for associated injuries is repaired once critical injuries are addressed. In stable patients who do not need exploratory laparotomy with intraperitoneal bladder rupture, the CT cystogram will show contrast inside the peritoneal cavity. Exploration of intraperitoneal bladder rupture is the treatment of choice and can be performed with laparoscopy or open, performing bladder repair with absorbable sutures and bladder drainage with a Foley catheter for 7 to 10 days. Extraperitoneal bladder rupture can be managed with bladder drainage from Foley catheter and repeated image studies in 7 to 10 days. If it is a complicated extraperitoneal bladder rupture or the patient is going for surgery for pelvic fracture, bladder repair can be performed. H In unstable patients who underwent exploratory laparotomy in which a bladder injury was found, there is suspicion for ureteral injury. Cystoscopy and RUG can be performed to identify associated ureteral injuries. If found, endoscopic treatment with placement of ureteral stents should be attempted. In complete ureteral transection, ureteral repair should be performed, and the surgical decision will be based on the location and length of the injury (ureteral reimplant, psoas hitch, ureteroureteral anastomosis, Boari flap, ileoureter, and other techniques). REFERENCES Groen J, Pannek J, Castro Diaz D, et al. Summary of European Association of Urology (EAU) guidelines on neuro-urology. Eur Urol. 2016;69(2): 324–333. Kim FJ, Chammas MF Jr, Gewehr EV, Campagna A, Moore EE. Laparoscopic management of intraperitoneal bladder rupture secondary to blunt abdominal trauma using intracorporeal single layer suturing technique. J Trauma. 2008;65(1):234–236. Kim FJ, Pompeo A, Sehrt D, et al. Early effectiveness of endoscopic posterior urethra primary alignment. J Trauma Acute Care Surg. 2013;75(2): 189–194. Moore EE, Cogvill TH, Jurkovich GJ, et al. Organ injury scaling, III: chest wall, abdominal vascular, ureter, bladder, and urethra. J Trauma. 1992;33:337–339. Moore EE, Feliciano DV, Mattox KL. Trauma. New York: McGraw-Hill Education; 2016. Morey AF, Brandes S, Dugi DD, et al. Urotrauma: AUA Guideline. Accessible at: https://www.auanet.org/education/guidelines/urotrauma.cfm. Accessed February 16, 2017.

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Chapter 146  ◆  Bladder and Urethral Trauma  430.e1

Abstract

Keywords

Lower urinary tract trauma is more frequent in patients with pelvic fracture. The presence of blood in the urethral meatus, hematuria, and/or urinary retention are signs that should raise suspicion for lower urinary tract injuries. Radiologic evaluation is recommended in stable patients before any manipulation of the urinary tract; however, unstable patients may require surgery to treat other associated injuries, and intraoperative evaluation and treatment of the lower urinary tract injuries can be performed during the same procedure. It is important that surgeons recognize patients at risk for lower urinary tract lesions to proceed with the work-up and management of these lesions because a delay in diagnosis can affect patient outcomes.

hematuria renal injury renal trauma bladder trauma bladder injury urethral trauma urethral injury pelvic fracture

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Chapter 146  ◆  Bladder and Urethral Trauma  431

F Hematuria &/or urinary retention History and physical exam

G

RUG ± CTCystogram

Urology Consult

Extraperitoneal bladder rupture

Bladder Injury

No Hematuria

Pelvic Fracture

If urinary drainage needed

1 attempt Foley placement

D Urethral Injury

Urology Consult

Bladder/ Urethral Trauma

Stable

Fail

Catheter & repeat imaging at 7 days

RUG

Observe ± RUG before cath. pull

Fail

Attempt retrograde cystoscopic cath.

Attempt retrograde cath. placement 1x

Repair and urethral drainage

Complicated &/or open surgery for pelvic fracture

Pass

Primary realignment

Pass Fail

SPT Placement Urethroplasty ~3 months

CT-Cystogram & CT-IVP

C Penetrating Injury w/ suspected bladder &/or ureteral injury

Exploration

Uncomplicated

E

B

A

Intraperitoneal bladder rupture

H Unstable

Intraoperative exploration of bladder & repair

Possible ureteral injury

Retrograde pyelogram

Labs UA/BMP/Hb/Ht

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Chapter

147 

PELVIC FRACTURES Jason W. Stoneback, MD, and Melissa A. Gorman, MD

A Traumatic pelvic fractures are typically the result of highenergy mechanisms and come with significant risk for concomitant injuries, many of which can be life-threatening. The high mortality rate of these fractures may be a result of multiple factors, including intra-pelvic hemorrhage (either venous or arterial), injury to vital organs in the thoracic and abdominal cavities, and significant traumatic brain injuries. A multidisciplinary approach, including the use of a pelvic fracture protocol, can aid in reducing morbidity and mortality in this patient population. Numerous institution-specific pelvic fracture protocols exist and have been shown to improve outcomes by identifying injuries and prioritizing the management of these injuries in a logical and efficient manner. By following a protocol in a systematic fashion, significant and potentially life-threatening injuries can be identified and treated quickly by allowing the treatment team to focus on key organ systems and injuries. In some institutions, the implementation of a multidisciplinary pelvic fracture protocol has been shown to decrease the mortality rate in unstable pelvic fracture patients, bringing it down to a rate similar to that of stable pelvic fracture patterns. B Determining hemodynamic stability is the first key component in the treatment of a patient with a suspected pelvic fracture. Hemodynamic stability is determined by a systolic blood pressure > 90 mm Hg and no blood products required to maintain stable vital signs. If the patient is hemodynamically stable, appropriate pelvic radiographs and a computed tomography (CT) scan of the abdomen and pelvis with intravenous contrast can be obtained at that time. Any other trauma work-up required at that time can also be performed as long as the patient remains hemodynamically stable. C If the patient is deemed hemodynamically unstable by the previously outlined criteria, trauma activation should be immediately initiated. The massive transfusion protocol should be started. This protocol is important to avoid the coagulopathy that can occur with transfusion of packed red cells alone. A pelvic binder should be placed and orthopedics consulted to assist in the management of any unstable patient. If a pelvic binder is not available, a sheet may be used in order not to delay further care and resuscitation of the patient. This early mechanical stability should help control any venous or bony bleeding from an unstable pelvic fracture and assist in hemostasis. D A focused abdominal sonography for trauma (FAST) examination should be performed in all unstable pelvic fracture patients. It is essential to determine if bleeding is coming

from a source other than the pelvis because intraabdominal injuries are very common in unstable pelvic fracture patterns. A positive FAST examination with hemodynamic instability necessitates an urgent/emergent laparotomy. Laparotomy should not be delayed to obtain specialized pelvic radiographs. Orthopedics should be available at that time to place a pelvic external fixator if necessary. The external fixator should be positioned to allow access for the laparotomy and pelvic packing. All potential sources of bleeding should be addressed at the time of laparotomy, and if the retroperitoneum is entered, pelvic packing should be considered. E If the FAST scan is negative, the next step in care can involve two different interventions. If the patient remains hemodynamically unstable despite adequate resuscitation and mechanical compression with a pelvic binder, the involvement of interventional radiology for angiography and possible embolization should be considered, especially if a pelvic blush is seen on CT scan. Only 10% to 15% of pelvic fractures, however, have significant arterial bleeding, with the majority of pelvic bleeding coming from a venous source or from cancellous bony surfaces. Mechanical compression will typically be effective in these cases, and embolization is not indicated. In the case of arterial injury, however, angiographic embolization has been found to be very effective. Embolization has been shown to cause a significant decrease in mortality and a significant reduction in blood transfusions, particularly in anterior-posterior compression (APC) fracture patterns. If angiography/interventional radiology is not immediately available, the patient who remains hemodynamically unstable should be taken to the operating room for external fixator placement and consideration of pelvic packing. Pelvic packing is effective to control venous bleeding and may help stabilize the patient while awaiting the arrival of an interventional radiologist. The patient can then be taken for subsequent angiography and embolization if arterial hemorrhage is also suspected. F On the other side of most protocols is a patient with a pelvic fracture who remains hemodynamically stable. If a pelvic blush is seen on CT scan, the patient should be taken for angiography to determine if embolization is possible to mitigate blood loss and avoid the potential complications that arise from multiple blood transfusions. This should also assist in ensuring that the stable patient does not become unstable from persistent hemorrhage. G Any patient with multisystem injury, unstable fracture patterns, hemodynamic instability, and age > 60 should be monitored closely in the trauma intensive care unit (ICU). The majority of patients who die from their injuries do so within the first few days after a trauma event, either from severe head injuries or hemorrhagic shock, and should be monitored closely. Avoiding complications such as multiple-system organ failure and sepsis is critical. Follow-up imaging of the pelvis may be necessary and can be obtained once the patient is stable enough to do so for preoperative planning for definitive stabilization of the pelvic ring injury. Young patients with isolated pelvic fractures without hemodynamic instability can oftentimes be managed by the orthopedic service with trauma consultation.

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Chapter 147  ◆  Pelvic Fractures  432.e1

Abstract

Keywords

Traumatic pelvic fractures are typically the result of high-energy mechanisms and come with significant risk for concomitant injuries, many of which can be life-threatening. The high mortality rate of these fractures may be a result of multiple factors, including intra-pelvic hemorrhage (either venous or arterial), injury to vital organs in the thoracic and abdominal cavities, and significant traumatic brain injuries. A multidisciplinary approach, including the use of a pelvic fracture protocol, can aid in reducing morbidity and mortality in this patient population.

pelvic fracture hemodynamically unstable protocol

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Chapter 147  ◆  Pelvic Fractures  433

G

F

1. AP/Inlet/outlet pelvis radiographs 2. CT pelvis with IV contrast and reconstructions 3. Other trauma work up and consultation as indicated

No

B

Yes

Admit to orthopedics Consider trauma consult

Yes

To IR for angiography vs pelvic packing No

Hemodynamically stable?

Trauma patient with suspected pelvic fracture

No

Pelvic blush? Yes

A

Does the patient have any of the following? Age ≥ 60 years Multisystem injury Unstable fracture

To OR for: Pelvic external fixation Consider pelvic packing

SBP > 90 and no blood products to maintain vitals

E

No

C Trauma activation Consult orthopedic surgery Activate massive transfusion protocol (MTP) Consult interventional radiology Place pelvic binder Trauma work up as indicated

Now Yes Admit to trauma ICU hemodynamically stable? No

Yes

Candidate for external fixation? Negative

D

E-FAST or DPA/DPL exam

Positive To OR for laparotomy

REFERENCES Black SR, Sathy AK, Jo C, et al. Improved survival after pelvic fracture: 13-year experience at a single trauma center using a multidisciplinary institutional protocol. J Orthop Trauma. 2016;30(1):22–28. Burlew CC, Moore EE, Stahel PF, et al. Preperitoneal pelvic packing reduces mortality in patients with life-threatening hemorrhage due to unstable pelvic fractures. J Trauma Acute Care Surg. 2017;82(2):233–242. El-Haj M, Bloom A, Mosheiff R, Liebergall M, Weil YA. Outcome of angiographic embolization for unstable pelvic ring injuries: factors predicting success. Injury. 2013;44:1750–1755.

Filiberto DM, Fox AD. Preperitoneal pelvic packing: technique and outcomes. Int J Surg. 2016;33:222–224. Holstein JH, Culemann U, Pohlemann T, Working Group Mortality in Pelvic Fracture Patients. What are predictors of mortality in patients with pelvic fractures? Clin Orthop Relat Res. 2012;470:2090–2097. Ruatti S, Guillot S, Brun J, et al. Which pelvic ring fractures are potentially lethal? Injury. 2015;46:1059–1063. Tai DKC, Li W, Lee K, et al. Retroperitoneal pelvic packing in the management of hemodynamically unstable pelvic fractures: a level I trauma center experience. J Trauma. 2011;71(4):E79–E86.

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Chapter

148 

CLOSED HEAD INJURY David Mann, MD, and Robert E. Breeze, MD

A The initial trauma assessment begins with a history and physical examination. When a detailed history is unavailable, the loss of consciousness may have preceded the traumatic injury, and one should always maintain an index of suspicion for other causes of loss of consciousness (e.g., aneurysmal hemorrhage, hypoglycemia, and seizure). B Brain injury from trauma is thought to result from two separate processes. Primary brain injury occurs at the time of injury and results from mechanical forces or direct penetrating injury. This phase is irreversible. Secondary injury develops subsequent to the initial injury and results from edema, hypoxemia, ischemia related to elevated intracranial pressure or hypotension, or vasospasm. The goal of resuscitation and subsequent management is to minimize the effects of this secondary injury. C The neurologic examination is a critical part of the primary survey recommended by the American College of Surgeons advanced trauma life support (ATLS) protocols. The postresuscitation Glasgow Coma Scale (GCS) is the most widely used scale for the assessment of head trauma. There are a number of valid criticisms of the GCS; it is insensitive to localized neurologic deficits, and it is nonlinear; a decrease of several points in one category is not necessarily equal to a similar decline in another category. In general, the severity of a head injury is stratified by a GCS score of 14 to 15 = mild, a GCS score of 9 to 13 = moderate, and a GCS score of 3 to 8 = severe. D Strategies have been proposed to identify patients who require intracranial imaging. In general, patients with a severe head injury who require imaging are immediately obvious; those who appear to have only a minor head injury but have or may develop a significant intracranial injury are more difficult to identify. In general, patients can be stratified into low-, moderate-, or high-risk groups. Those who are asymptomatic or have headache and dizziness only, without a history of loss of consciousness, have a low risk for intracranial injury, and a computed tomography (CT) scan is usually not indicated; these patients can often be observed at home. For those patients with a history of change in or loss of consciousness, progressive headache, intoxication, posttraumatic seizure, inadequate history, vomiting, posttraumatic amnesia, polytrauma, signs of basilar skull fracture, significant facial injury, or subgaleal swelling, clinical grounds alone may miss intracranial injury in this group. The most frequent finding in this group is a hemorrhagic contusion, and 8% to 46% of patients with minor head injury have intracranial

findings on CT head scans. Patients with a depressed level of consciousness not attributable to intoxication or postictal state, focal neurologic findings, decreasing level of consciousness, or suspected penetrating injury or depressed skull fracture are at high risk for intracranial injury and require urgent investigation. E General measures in the trauma patient should include maintaining adequate oxygenation and systemic blood pressure. Hypotension is rarely attributable to the head injury itself, except in the terminal stages where downward herniation can lead to medullary compression and resultant cardiopulmonary collapse. Hypotension (defined as a single systolic blood pressure [SBP] < 90 mm Hg) has been shown to double mortality. The airway should be secured in patients presenting with a depressed level of consciousness who cannot protect their airway and in those who remain hypoxic despite supplemental oxygen. The combination of hypotension and hypoxia triples mortality. In general, prophylactic hyperventilation (HPV) (PaCO2 < 25 mm Hg) should be avoided during the first 24 hours after traumatic brain injury (TBI), when cerebral blood flow is often decreased, and should be reserved only as a temporizing measure if there are signs of transtentorial herniation (pupillary dilation, asymmetric light reflex, decerebrate or decorticate posturing, or progressive neurologic decline not attributable to extracranial factors). Similarly, the use of hyperosmolar therapy before intracranial pressure (ICP) monitoring is established should be reserved for patients with signs of transtentorial herniation or progressive neurologic decline who are adequately volume resuscitated. The use of steroids is not recommended; in patients with severe TBI, high-dose methylprednisolone was found to be associated with increased mortality and is contraindicated. Prophylactic antiepileptic drugs (AEDs) may be used to decrease the incidence of early posttraumatic seizures ( 40 years, unilateral or bilateral motor posturing, or SBP < 90 mm Hg.

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Chapter 148  ◆  Closed Head Injury  434.e1

Abstract

Keywords

Closed head injury is an important cause of neurologic disability. Early recognition and management of patients who require intracranial imaging and early resuscitation aimed at minimizing the effects of secondary brain injury are crucial to reducing morbidity and mortality. This chapter provides a stepwise approach to the identification and management of closed head injury and provides guidelines for identifying patients who require neurosurgical consultation and/or operative intervention.

trauma closed head injury

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Chapter 148  ◆  Closed Head Injury  435 History and physical exam Mechanism of trauma A Level of consciousness Localizing signs Evidence of elevated ICP on exam Adequacy of ventilation Arterial blood pressure Antiplatelet/Anticoagulation

D

Fully alert Normal exam No risk criteria

Observe

Assessment of risk of intracranial injury

Abnormal

C GCS

Normal

E Unconscious

Intubate Ventilate Hyperosmolar/ Hypertonic administration

Emergency CT scan of the head

Labs Arterial blood gas O2 saturation, pulse oximeter PT/PTT, INR Thromboelastogram

G

Focal signs not explained by CT head findings

CT scan of the head

Conscious CLOSED HEAD INJURY

Observe

Normal

High/medium risk criteria

B

F

Abnormal

CTA Further imaging as warranted EEG

Interval CT of the head Neurosurgical consultation

>2 factors present H on admission: Age >40 Unilateral or bilateral posturing SBP 50 cm3, or GCS score of 6 to 8 with frontal or temporal ICH volume > 20 cm3 with midline shift ≥ 5 mm. In general, an epidural hematoma volume of >30 cm3 should be evacuated regardless of GCS score. An acute subdural hematoma with a thickness of > 10 mm or midline shift of > 5 mm should be evacuated regardless of GCS score. A subdural hematoma (SDH) < 10 mm and a midline shift < 5 mm should be evacuated if the GCS score drops by ≥2 points from admission, pupils become asymmetric, or ICP > 20 mm Hg.

herniation, or compressed basal cisterns.1 Treatment for intracranial hypertension should be initiated for ICP ≥ 20 mm Hg. Cerebral perfusion pressure (CPP) should also be supported by maintaining adequate mean arterial pressure (MAP); aggressive fluids and pressors should be avoided to maintain CPP > 70 mm Hg because of the risk for acute respiratory distress syndrome (ARDS). The optimal value for CPP has yet to be determined; however, the threshold for ischemia is in the range of CPP < 50 mm Hg, which should be avoided. General measures to lower ICP include positioning (elevate head of bed [HOB]; ensure head is midline to prevent jugular venous outflow obstruction), avoiding hypotension, normalizing intravascular volume, controlling hypertension, and preventing hyperglycemia (exacerbates cerebral edema). If intracranial hypertension persists, heavy sedation or paralysis may be necessary; however, this should be done with caution because the ability to follow the neurologic examination may be lost. Cerebrospinal fluid (CSF) diversion and administration of osmotic therapy should be pursued if sedation alone fails to lower intracranial pressures. Mannitol is generally administered as a 0.25- to 1-g/kg bolus followed by

J

1

ICP should be monitored in all salvageable patients with a post-resuscitation GCS score of 3 to 8 and an abnormal CT scan of the head, including hematomas, contusions, swelling,

Brain Trauma Foundation: Guidelines for the management of severe traumatic brain injury, ed 4, September 2016, Palo Alto, CA: Brain Trauma Foundation.

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436  Part VIII  ◆ Trauma intermittent dosing of 0.25 g/kg as necessary. If ICP remains refractory to mannitol, hypertonic saline can be considered, either as a continuous 3% saline infusion or as boluses of 23.4% saline. Second-tier therapy for persistent intracranial hypertension includes high-dose barbiturate therapy, hyperventilation, and hypothermia. K Decompressive craniectomy for refractory intracranial hypertension is controversial, and further randomized controlled trials are warranted. At the time of publication of the most recent Brain Trauma Foundation TBI guidelines, the results of the RESCUEicp trial were not yet released. The RESCUEicp trial aimed to assess the effectiveness of decompressive craniectomy offered as a last-tier treatment for refractory intracranial hypertension. The trial demonstrated that at 6 months, decompressive craniectomy resulted in mortality that was 22% lower than medical management alone; however, it was also associated

with higher rates of vegetative state and severe disability than medical management. REFERENCES Bullock MR, Chestnut RM, Ghajar J, et al. Surgical management of acute epidural hematomas. Neurosurgery. 2006;58:S7–S15. Bullock MR, Chestnut RM, Ghajar J, et al. Surgical management of acute subdural hematomas. Neurosurgery. 2006;58:S16–S24. Bullock MR, Chestnut RM, Ghajar J, et al. Surgical management of traumatic parenchymal lesions. Neurosurgery. 2006;58:S25–S46. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364:1493–1502. Greenberg MS. Handbook of neurosurgery. Acta Chir Belg. 2016;116(4):269. Guidelines for the Management of Severe Traumatic Brain Injury, 4th ed. September 2016. Mayer SA, Chong J. Critical care management of increased intracranial pressure. J Intensive Care Med. 2002;17:55–67. RESCUEicp Trial Collaborators. Trial of decompressive craniectomy for traumatic intracranial hypertension. N Engl J Med. 2016;375(12): 1119–1130.

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Chapter

149 

CERVICAL SPINE FRACTURES Daniel Craig, MD, and Robert E. Breeze, MD The purpose of this chapter is to outline a stepwise approach to C-spine fractures to aid in the safe and expedient work-up for these potentially complex injuries. The inclusion of some of the specific classifications employed by spine surgeons and the stepwise progression through localization, anatomy, neurologic status, stability, and disposition allow the reader to critically evaluate the nuances of the injury in anticipation of definitive management by a specialist or to make safe and reasonable management decisions in the absence of tertiary care resources. Unfortunately, the complexity and variety of C-spine fractures defy a straightforward algorithmic approach. However, every surgeon should feel equipped to define the injury, maintain appropriate precautions during work-up, complete appropriate initial imaging, consider factors involved in stability, and have an understanding of the most likely definitive management (e.g., surgery, immobilization, observation, etc.). This text will follow the flow of the diagram from the starting point of having already identified the presence of a fracture, presumably on either x-ray (XR) or noncontrast computed tomography (CT). Keep in mind the end goal of C-spine fracture management: to protect neurologic function and preserve alignment. The work-up is tailored to vulnerable neurologic structures and potential deformity. Specifically outside the scope of this chapter are details of cervical collar clearance, isolated subluxation/dislocation, and the management of cervical spinal cord injury. A   CERVICAL SPINE PRECAUTIONS

At the identification or suspicion of a C-spine injury, the patient should be placed in a cervical collar and maintained on bedrest until stability and the disposition plan are clarified. In the absence of concurrent thoracolumbar spine injuries, log-roll precautions are generally not necessary. Often patients arrive from the field in a one-piece, wraparound collar placed by the emergency medical services (EMS) team. Our practice is to replace this as soon as possible with a sturdier and more comfortable Aspen or Philadelphia-type collar. During the rest of the work-up, the patient should be in the collar at all times with the head supported.

Localization The cervical spine comprises several anatomically distinct sections, each with unique stability variables and common fracture morphologies, ranging from the skull base (occipital condyle) to the axial C-spine (C1 and C2) to the subaxial C-spine (C3 to C7). After employing appropriate precautions, the next step is to define the exact level of the injury. B   FRACTURE ANATOMY

After localization to a particular level or levels, it is critical to have a detailed anatomic definition of the fracture. Although plain radiography (XR) can identify many if not most fractures,

an unenhanced computed tomography (CT) scan of the C-spine is the best way to clearly identify bony anatomy. This allows segregation of fractures into their common types, which in turn dictates evaluation of stability. In an awake and intact patient with a low-velocity mechanism, relatively simple fractures such as a mild vertebral body compression fracture or an isolated spinous process fracture may not require CT evaluation. However, with any suggestion of a more complex or high-velocity mechanism of injury, and especially in obtunded, altered, and polytrauma patients, CT should be considered the standard to define any fracture. The basic classification systems commonly used for occipital, C1, C2, and C3 to C7 fractures are noted briefly in the algorithm and represent a treatment-based stratification, giving the surgeon an initial impression of the likelihood of stability and risk for neurologic injury or deformity. The details of these systems are complex. However, with the help of the radiologist, the majority of fractures can be assigned to one of the morphologic types.

Vascular Imaging At this stage one should consider the risk for injury to the vertebral artery in its course through the transverse foramina, typically from C6 to C2; its turn over the lateral mass of C1; and posternmedial-superior trajectory past the occipital condyle toward its intra-dural extension. Many C-spine fractures are accompanied by vertebral artery injury. The work-up of any fracture or subluxation approaching or directly involving its course should include computed tomography angiography (CTA) of the neck. Specifically, occipital condyle fractures, C1 fractures involving any portion other than the anterior ring, C2 fractures involving the pedicle/pars/transverse foramen, and subaxial fractures involving the transverse foramina merit CTA. Isolated odontoid, vertebral body, and spinous process/lamina fractures generally do not require CTA evaluation. Remaining fracture morphologies and multilevel injuries must be considered at the discretion of the provider, and the prudent surgeon will err on the side of obtaining vascular imaging in the absence of contraindications to contrast administration. C   NEUROLOGIC STATUS

The presence of any neurologic injury will guide the next stage of evaluation, specifically toward obtaining magnetic resonance imaging (MRI) to evaluate traumatic injury to the nerve roots and spinal cord. Only rarely will management of a fracture proceed without MRI in the context of a new neurologic deficit, because even a simple, nondisplaced fracture may be accompanied by potentially serious disk herniation or other soft tissue pathology incompletely shown on CT scan. In cases where MRI is contraindicated, CT myelography should be considered. Evaluation of the neurologic status in C-spine patients should always include mental status, Glasgow Coma Scale (GCS) score, cranial nerves, upper and lower extremity strength in all muscle groups, sensation at least to light touch with identification of a sensory level versus a focal sensory deficit, and deep tendon reflexes, specifically with an eye toward asymmetry and hyperreflexia. In high-mechanism injuries and whenever strength or sensation is symmetrically compromised, rectal tone and the bulbocavernosus reflex should be noted. The localization of the fracture should guide the suspicion of specific neurologic injuries. Occipital condyle fractures threaten the hypoglossal nerve. Upper C-spine injuries will uncommonly present with cord or nerve root injuries except in cases of

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Chapter 149  ◆  Cervical Spine Fractures  438.e1

Abstract

Keywords

A survey of and brief guide to the evaluation, classification, and clinical management of cervical spine fractures.

cervical spine fracture spine stability alignment immobilization fracture classification vertebral artery injury

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Chapter 149  ◆  Cervical Spine Fractures  439 devastatingly severe upper cord injuries, whereas subaxial fractures commonly present with new radiculopathy, myelopathy, or central cord syndrome.

C-spine fractures even in the neurologically intact patient. This stage must include evaluation by a spine surgeon if at all possible. Many fractures, especially in the axial C-spine, are unsafe to mobilize for flexion–extension radiographs. The decision of appropriate stability-defining imaging should be at the discretion of the provider who will be ultimately responsible for the definitive management of the patient.

D   STABILITY

Perhaps the most challenging aspect of C-spine fracture evaluation is the determination of stability. Outside of the need to decompress neurologic structures, this is the most important factor guiding the need for surgery or immobilization. Few fractures are patently unstable by anatomic definition. The majority are indeterminate based on CT imaging. Each fracture location carries its specific radiographic parameters to identify gross instability/malalignment. Atlanto-occipital dislocation is commonly evaluated by the atlanto-occipital interval (normal < 1.4 mm in adults, < 2.5 mm in children) and the Powers’ ratio on sagittal CT. C1 to C2 instability can be assessed by the atlanto-dental interval (ADI; normal is up to 3 mm in adults and 4 mm in children) and the rule of Spence (combination overhang of C1 lateral mass on C2 > 7 mm) on coronal CT. These values were defined on plain radiographs, and an updated set of parameters for CT was suggested. Angulation and subluxation of C2 pars fractures dictate Levine and Francis scale classification. In the subaxial C-spine, subluxation of adjacent vertebral bodies > 3 mm or facet dislocation (perched, jumped, or locked facets) are considered unstable by definition. In the absence of a clear misalignment on CT imaging, the next set of tools to determine stability is noncontrast MRI and flexion–extension/upright radiographs to assess ligamentous integrity. In general, without abnormal alignment on CT imaging, flexion–extension radiographs can be safely obtained in more straightforward fractures such as isolated vertebral body, spinous process, nondisplaced lamina, and transverse process fractures. This is assuming a lack of neurologic deficit; otherwise, an MRI is likely already indicated. Because of the high consequence of occult instability, it is wise to default to including MRI in the work-up of axial, occipital, and complex subaxial

E   DISPOSITION

At this point, the surgeon has identified the level, location, and morphologic classification of the fracture. Vascular imaging has been completed where appropriate to identify vertebral artery injury. Neurologic evaluation and assessment of CT alignment parameters are complete, and MRI or dynamic radiography has helped determine ligamentous injury/instability (with the aid of a spine surgery consult). These factors will all culminate in a need for surgical fixation, protracted immobilization (halo or cervical collar), traction, or proceeding down the pathway of cervical collar clearance. Common classification systems evolve with new imaging modalities but remain the foundation of surgical decision making. Tools, such as the Subaxial Cervical Spine Injury Classification System (SLIC), based on fracture morphology, disco-ligamentous integrity, and neurologic injury have been widely accepted as an easy-to-use and objective method for the initial estimation of surgical versus nonsurgical intervention. Even with detailed classification systems and rigorous radiologic evaluation, decision making among spine practitioners can vary widely among similar injuries. The proceeding algorithm indicates the most likely trend of treatment from the surgical fixation of unstable and neurologically compromised patients to expectant observation in a cervical collar for intact/aligned/ simple fractures. This decision point should involve conclusive evaluation by a spine surgeon wherever possible, and C-collar precautions should continue until definitive management is decided.

B History and exam Trauma Obvious C spine injury Polytrauma High energy mechanism Altered mental status

Occipital condyle Type 1: comminuted Type 2: linear Type 3: avulsion

Clinical C-Spine Clearance Pathway Neuro Exam Radiographic Stability

Atlas – C1 Type 1: single arch Type 2: burst (Jefferson) Type 3: lateral mass

D Normal neurologic exam

Cervical Collar Clinic Follow-Up Repeat Radiography 2-6 Weeks

Stable

C C spine injury

A

Axis – C2 Odontoid Type 1, 2, 3 Pars: Hangman, Levine/Francis Grade 2 Misc: body, spine/transverse process, facet

MRI

New neurologic deficit

Imaging Non-enhanced CT C spine

Sub axial – C3-7 Body: Compression, Burst, Teardrop Avulsion, Quadrangular, Dislocation/sublux Facet/lateral mass/pedicle Fracture-linear Perched/jumped facet Subluxation Lamina/spinous process Linear Comminuted/avulsed Transverse process

E

Unstable

Rigid Immobilization Halo Traction

Surgical Fixation/Fusion Decompression of Neural Elements

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440  Part VIII  ◆ Trauma REFERENCES Al-Mahfoudh R, Beagrie C, Woolley E, et al. Management of typical and atypical hangman’s fractures. Global Spine. 2016;6(3):248–256. Anderson LD, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg. 1974;56A:1663–1674. Anderson PA, Montesano PX. Morphology and treatment of occipital condyle fractures. Spine. 1988;13(7):731–736. Hadley MN, Dickman CA, Browner CM, Sonntag VK. Acute axis fractures: a review of 229 cases. J Neurosurg. 1989;71(5):642–647. Joaquim AF, Ghizoni E, Tedeschi H, et al. Upper cervical injuries - a rational approach to guide surgical management. J Spinal Cord Med. 2014;37(2): 139–151. Levine AM, Edwards CC. The management of traumatic spondylolisthesis of the axis. J Bone Joint Surg Am. 1985;67(2):217–226. Li XF, Dai LY, Lu H, Chen XD. A systematic review of the management of hangman’s fractures. Eur Spine J. 2006;15(3):257–269.

Mead IILB, Millhouse PW, Krystal J, Vaccaro AR. C1 fractures: a review of diagnoses, management options, and outcomes. Curr Rev Musculoskelet Med. 2016;9(3):255–262. Rojas CA, Bertozzi JC, Martinez CR, Whitlow J. Reassessment of the craniocervical junction: normal values on CT. Am J Neuroradiol. 2007;28:1819–1823. Section on disorders of the spine and peripheral nerves of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. Management of vertebral artery injuries after nonpenetrating cervical trauma. Neurosurgery. 2002;50(suppl 3):s173–s178. Vaccaro AR, Hulbert J, et al. The sub-axial cervical spine injury classification system (SLIC): a novel approach to recognize the importance of morphology, neurology, and integrity of the disco-ligamentous complex. Spine. 2007;32(21):2365–2374.

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Chapter

150 

SPINAL CORD INJURY Todd F. VanderHeiden, MD, and Philip F. Stahel, MD

INTRODUCTION Spinal cord injury (SCI) is a devastating, life-altering event for patients and their families. In spite of decades of innovative research in the field, no pharmacologic “silver bullet” has been developed that can mitigate or cure the extent of neurologic impairment in SCI patients. Preservation of function by providing early stability to the injured spine followed by neurorehabilitation remains the current standard of care. Surgical decision making should hinge on evaluation and early restoration of the “Holy Trinity” of the spine (alignment, stability, and neurology) to provide the best baseline opportunity for recovery of the injured spinal cord. Compression of neural elements should be mitigated by early surgical management, and episodes of postinjury hypoxia and hypotension should be strictly avoided to prevent secondary insults to the injured spinal cord. A protocol-driven multidisciplinary approach to the management of SCI patients is imperative to reduce the risk for preventable complications and to improve long-term patient outcomes. A Assume that all trauma patients have a spinal injury until proven otherwise. Start by ensuring that the patient is adequately immobilized while maintaining strict log-roll precautions. Initially, all trauma patients should be placed in a rigid cervical immobilizer. These cervical collars (C-collars) should be kept in place until the cervical spine is “cleared.” Clearance is the process by which the treatment team confirms that a spinal injury is absent. Once this is done, the C-collar can be removed. On the contrary, if a spinal injury is identified, then a spine surgery consult should be placed to determine the proper course of treatment. Patients should be removed from the backboard as soon as possible, using a team-based log-rolling maneuver. Simultaneously, a care provider should inspect the entire spine for external trauma while also investigating for irregularities and areas of palpable step-off. A complete and thorough neurologic examination must occur. Muscle strength is assessed in all myotomes of the four extremities. The sensory examination includes the assessment of light touch, proprioception, pain, and temperature in all dermatomes. A reflex examination is performed to evaluate the upper and lower extremities while also evaluating pathologic reflexes like Hoffmann’s and clonus. A complete sphincter examination must also be performed. This includes inspection of the anus, evaluation of perianal sensation with dull and sharp probes, detection of resting rectal tone with digital insertion, evaluation of voluntary anal sphincter contraction, and determination of the presence or absence of the bulbocavernosus reflex. The examiner should also check for priapism. All examination results should be completely and thoroughly documented.

B Members of the treatment team should be aware of the mechanism of injury and the presence of distracting injuries. This knowledge can be invaluable when attempting to assess for SCI because the neurologic examination can be extremely difficult in polytrauma patients who exhibit severe injuries to multiple organ systems. Further complicating the assessment of such patients can be the presence of intoxicating substances that alter the level of consciousness and render a patient uncooperative or unresponsive. Even in severely obtunded patients with multiple concomitant injuries, however, there can be an injury pattern that suggests to the care provider a need to be extremely vigilant about the possibility of SCI. An example of such a scenario is a patient involved in a high-speed MVC who also has severe facial and cranial injuries suggesting a hyperextension mechanism to the neck. In this situation, providers need to be alerted to the likelihood of a significant cervical spine hyperextension injury that could be associated with an SCI. Close evaluation of the cervical spine with advanced imaging is mandatory in this situation. C The treatment team should adhere to an algorithmic approach to SCI when assessing a trauma patient. The first step must be to ask if a neurologic injury is present. If so, the care provider must ask if the encountered neurologic deficit is attributable to the spine. To do so, neurologic dysfunction associated with cranial or extremity injuries must be considered carefully and then confirmed as absent or occurring simultaneously with the SCI. Once the possibility of an SCI is either identified, excluded, or deemed indeterminate, then the care provider can follow each branch of the decision tree and arrive at an appropriate conclusion regarding surgical decision making. Multiply-injured patients with cranial trauma and other injuries can be very difficult to examine. In addition to significant cranial trauma that limits the neurologic evaluation, these patients are also frequently intubated, sedated, and can even be pharmaceutically paralyzed. It is important for the examiner to be aware of these confounding variables. Despite these challenges, it is still possible to obtain important information concerning the neurologic examination and spinal cord function. Flaccid motor tone and absent reflexes should raise suspicion of SCI. In contrast, these findings are extremely unusual with isolated brain injury. When patients cannot be assessed for motor and sensory function, it is important to examine reflexes and also to perform a complete and thorough sphincter examination. Spinal-cord-injured patients typically have flaccid paralysis with associated areflexia. It is important to compare the reflexes of the upper and lower extremities. The examiner should check for priapism. Priapism is common with SCI but is not caused by head injury. The examiner should also perform a thorough anorectal examination. This detailed examination can be a “window” to the spinal cord. Radiographic imaging should also be used liberally when a neurologic deficit is suspected. D There is a high incidence of noncontiguous spinal injuries when a major spinal injury is identified in a polytrauma patient. Therefore it is imperative to visualize the entire spinal column using a high-resolution computed tomography (CT) scan with reconstructed coronal and sagittal reformations when an SCI is suspected. It is not unusual for such patients to need spinal surgery in more than one spinal region. Furthermore, SCI in more than one site can lead to very complicated neurologic findings. As such, it is imperative that care providers be able to

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Chapter 150  ◆  Spinal Cord Injury  442.e1

Abstract

Keywords

Spinal cord injury (SCI) is a devastating, life-altering event for patients and their families. In spite of decades of innovative research in the field, no pharmacologic “silver bullet” has been developed that can mitigate or cure the extent of neurologic impairment in SCI patients. Preservation of function by providing early stability to the injured spine followed by neurorehabilitation remains the current standard of care. Surgical decision making should hinge on evaluation and early restoration of the “Holy Trinity” of the spine (alignment, stability, and neurology) to provide the best baseline opportunity for recovery of the injured spinal cord. Compression of neural elements should be mitigated by early surgical management, and episodes of postinjury hypoxia and hypotension should be strictly avoided to prevent secondary insults to the injured spinal cord. A protocol-driven multidisciplinary approach to the management of SCI patients is imperative to reduce the risk for preventable complications and to improve long-term patient outcomes.

spinal cord injury timing of surgery spine damage control neurorehabilitation

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Chapter 150  ◆  Spinal Cord Injury  443 discern these findings based on the various levels of involvement of the neural tissue. Instruments are available to guide the treatment team in proper neurologic assessment. The most important example of this is the American Spinal Injury Association (ASIA) impairment scale. E A magnetic resonance imaging (MRI) scan of the affected spinal region (cervical, thoracic, lumbar) is important to help clarify the neurologic deficit and is invaluable for surgical planning. This study allows visualization of the neurologic elements and characterization of the location, extent, and type of neural compression. This study is essential for preoperative surgical templating. Spinal surgeons pay close attention to the integrity of the spinal bones and the intervertebral disks and the posterior ligamentous complex (PLC). The PLC includes the ligamentum flavum, the interspinous and supraspinous ligaments, and the facet-joint capsules and the intertransverse ligaments. Injury to the PLC is a significant finding that can render the spinal column mechanically unstable. Spinal surgeons also thoroughly evaluate the morphology of the injury as evidenced by the CT and MRI images. Injury morphology is interpreted carefully to infer the injury mechanism. Once mechanism and morphology are confirmed, then the spinal surgeon couples this information with the neurologic assessment of the patient and the stability of the spinal column, paying close attention to the disco-ligamentous and bony structures. Compiling all of this information soon leads to a conclusive surgical decision-making process. F Clarifying the neurologic deficit and classifying the injury severity will significantly affect surgical timing. Incomplete SCI is a surgical spinal emergency with the goal of preserving the precious remaining function of the spinal cord. Incomplete injury to the spinal cord involves the preservation of some motor or sensory function below the damaged level. Typically, there is also variable sparing of sacral nerve-root function manifesting as some appreciation of peri-anal sensation and some existence of sphincter control. Cauda equina syndrome (CES) is a surgical urgency that requires decompression of the lumbar nerve rootlets. CES exists as a spectrum of disease ranging from subtle bowel and bladder dysfunction to full-blown flaccid lower-extremity paralysis and loss of sensation with areflexia and complete sphincter incompetence. Complete SCI is a less urgent clinical scenario given the extremely limited potential for neurologic recovery in these patients. Despite this, surgical stabilization of the spine should be strongly considered when appropriate so as to ensure early and safe mobilization of these patients. Early mobilization of critically ill patients is of paramount importance. This will allow prevention of dreaded complications associated with recumbency: pneumonia, urinary tract infections, thromboembolic events, and pressure sores are pertinent examples. Nerve root and plexus injuries are urgent elective conditions that may or may not respond to surgical intervention. Penetrating injuries to nerve roots or the brachial plexus often accompany surgical indications for exploration and repair. Compressive lesions about the nerve roots or brachial plexus (e.g., hematoma, bone or disk fragments, bullets or shrapnel) may also be surgically removed. It is mandatory to classify the injury to the spine because this can assist in guiding surgical treatment. Multiple classification systems exist. Pertinent examples include the Subaxial Cervical and Thoracolumbar Injury Classification Systems and Severity-Scores

(SLICSS and TLICSS) by the Spine Trauma Study Group and the AO/OTA Spine Injury Classification System by the Orthopaedic Trauma Association (AO/OTA). Although these classification systems can be very detailed and somewhat cumbersome, they all have certain characteristics in common. These characteristics include the analysis of the mechanism and morphology of the injury, the presence and classification of the neurologic injury, and the integrity of the intervertebral disk and posterior ligamentous complex. When considering these three important areas together, spinal surgeons can quickly make conclusions about the necessity for surgery and the desired approach and techniques. The classification of SCI relies on the full understanding of the following clinical/neurologic entities: • Tetraplegia involves an injury to the cervical spinal cord leading to impairment of function in the upper extremities, trunk, lower extremities, and pelvic organs. • Paraplegia involves an injury to the thoracic, lumbar, or thoracolumbar spinal cord leading to impairment of function in the trunk, lower extremities, and pelvic organs. Upper-extremity function is preserved. • Pentaplegia is an SCI at or above the C4 level that results in the complete loss of motor, sensory, and reflexive functions below the injured level. Importantly, this also includes paralysis of the respiratory muscles. Patients enduring this type of SCI often remain ventilator dependent. • Complete SCI may result from transection, stretch, or contusion of the spinal cord. All function—motor, sensory, and reflexive—below the level of the lesion is lost. This injury is associated with the worst prognosis. • Incomplete SCI involves some preservation of motor or sensory function below the neurologic lesion. There is often sacral sparing. • Anterior cord syndrome results from an injury of the anterior two-thirds of the spinal cord (the distribution of the anterior spinal artery), which carries motor, pain, and temperature tracts. Vibration sense and proprioception are left intact because the posterior columns are typically preserved. This injury usually stems from a vascular insult. The prognosis is poor. • Posterior cord syndrome results from an injury to the posterior one-third of the spinal cord (the distribution of the posterior spinal artery), which carries proprioceptive and sensory tracts. Motor function and interpretation of painful and temperature stimuli are preserved. This injury usually results from a vascular problem, and the prognosis is variable. However, the outlook for patients with this syndrome is much better than for those with anterior cord syndrome. • Central cord syndrome results from injury to the central area of the spinal cord. This entity is often found in patients with preexisting cervical stenosis resulting from spondylotic changes. Characteristic deficits are more severe in the upper extremities than in the lower extremities because of the axial arrangement of the neuronal tracts. Distal deficits are more profound than proximal deficits within the limbs. Injury is thought to be a result of buckling of a thickened posterior ligamentum flavum into the spinal cord with an extension moment of the neck. Histological analysis shows there is hemorrhage in the center of the spinal cord. Motor function is typically affected more than sensory function. The prognosis is variable, but there tends to be some

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444  Part VIII  ◆ Trauma clinically detectable recovery. Patients are often left with clumsiness of the hands. • Brown–Séquard syndrome is usually seen in penetrating injuries that affect one side of the spinal cord through unilateral hemisection. This entity may also be seen in blunt injury, especially with unilateral traumatically herniated disks. The syndrome results from injury to half of the spinal cord where clinical manifestations result in motor, position, and vibration deficits on the ipsilateral side of the injury, whereas the contralateral side shows deficits in pain and temperature sensation. This pattern of deficits occurs as a result of the decussation level of the neuronal tracts within the spinal cord. The prognosis is typically good. • Spinal shock is a clinical syndrome caused by trauma marked by the absence of all spinal cord function below the level of the injury. This condition results in flaccid motor paralysis, complete loss of sensation, and areflexia. As spinal shock evolves, the return of reflex activity begins to occur. This happens in phases and begins with the bulbocavernosus reflex around 48 to 72 hours. Deep tendon reflexes may take days or weeks to return. The term “shock” in spinal shock does not involve end-organ hypoperfusion. Spinal shock, however, can lead to neurogenic shock. Although both of these clinical entities should be recognized, understood, and treated, they should not be confused. • Neurogenic shock refers to diminished end-organ perfusion caused by hypotension that can result from cervical or upper-thoracic SCI. Hypotension results from a lack of sympathetic tone below the neurologic lesion. It is characterized by bradycardia from unbalanced vagal input to the heart, decreased systemic vascular resistance, and blood pooling in the extremities. Fluid resuscitation should be used judiciously, and vasopressors should be used to keep the systolic blood pressure (SBP) > 90 mm Hg. Atropine may be necessary to treat bradycardia. G A pragmatic and simplistic approach to decision making for operative versus nonoperative management in SCI relates to the concept of the “Holy Trinity” of the spine. The “Holy Trinity” of the spine is simply defined as “alignment, stability, and neurology.” Elaborating on this concept reveals that a normally functioning spinal column and its associated neurologic elements maintain anatomic alignment, preserve stability under physiological conditions, and manifest normal function of the spinal cord and the nerve roots. When assessing a patient with SCI, the care providers and treating spinal surgeon must ask themselves simple yes/no questions related to spinal alignment, stability, and neurology: □ Is the spine aligned—yes or no? □ Is the spine stable—yes or no? □ Is the spinal neurologic function normal—yes or no? If the answer to any of these questions is no, then the spinal surgeon needs to be acutely ready to perform surgery. The answers to the questions related to alignment and neurology are typically straightforward. However, the answer to the question about stability can be somewhat challenging. A working definition of spinal stability should consider that under physiological loads, the spine does not experience increasing deformity, onset of neurologic insult, or a drastic increase in the patient’s pain. If spinal stability can be confirmed without the need for surgical

intervention, then immediate mobilization of patients with or without bracing may be possible. If the spine is deemed unstable, then early surgical treatment is necessary to enable immediate mobilization. One must also consider the difference between mechanical and neurologic stability. Mechanical stability is often a binary concept—mechanical stability is either present or absent. Neurologic stability is a much more dynamic process that can include rapid improvement or decline. In cases where neurologic improvement begins to abruptly plateau, spine surgeons often consider surgical intervention even if initial closed treatment was indicated. An example of this is a patient with central-cord syndrome who shows initial improvement but then either plateaus or declines in the setting of ongoing neurologic compression. H The surgical restoration of the “Holy Trinity” of the spine consists of realigning, stabilizing, and decompressing the spine and its neurologic elements. Although spine surgical techniques are many and variable, the goals of providing and maintaining proper spinal alignment, ensuring immediate and rock-solid stabilization, and decompressing impinged neurologic structures remain constant. Spine surgeons may employ anterior approaches, posterior approaches, lateral approaches, or a combination of approaches to ensure that the principles of spinal surgery are upheld. Modern spine surgery techniques often involve the application of screws, rods, plates, and bone grafting, with the ultimate goal being bony fusion. Protection of the neurologic elements is done acutely by meticulous and thorough decompression of the spinal cord and nerve roots, whereas longer-term protection is accomplished by providing stability to the spinalcolumn around these structures. “Holy Trinity” of spinal surgery: • Provide and maintain anatomic alignment of spinal segments. • Provide immediate, rock-solid stability to the unstable spine. • Decompress neurologic structures (brainstem, spinal cord, spinal nerve rootlets, cauda equina, conus medullaris, nerve roots) if indicated and clinically relevant. Once spinal injuries are stabilized, immediate mobilization of these critically ill patients must be allowed. After surgery, patients often have ongoing “spinal precautions,” which typically involve some limitation of bending, lifting, and twisting. Even when nonoperative care of spinal injuries is initially considered, if the spinal precautions are too prohibitive to the care team to adequately rehabilitate the patient, then the spine surgeon must consider surgical fixation and stabilization. This will allow removal of activity restrictions and mobility limitations, thus facilitating the proper care by intensivists, therapists, nurses, and SCI specialists. After spinal surgery, patients should be placed on an SCI protocol. These patients have a long list of needs that are specific to SCI. All care-team members should be acutely aware of these needs, and treatment should be protocolized to ensure proper delivery of care. Modern trauma centers typically have clinical practice guidelines specifically for SCI that assist the treatment team in caring for these critically ill patients. Examples of such guidelines include the manner in which SCI patients are properly protected from blood clots, skin ulcerations, pneumonia, and gastric bleeding, to name a few common issues. Prophylaxis against these and other commonly encountered complications I

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Chapter 150  ◆  Spinal Cord Injury  445 • Continue diagnostic work-up • Evaluate for other causes of neurologic impairment

A

NO

• History & physical examination • Meticulous documentation

• Spinal origin? • Concern for SCI? • Level of injury? YES

Trauma patient with suspected spine injury: Neurologic impairment?

D

YES

• Obtain spinal MRI: • Assess for integrity of ligaments, disk, neural elements NO

NO UNCLEAR

C

UNCLEAR

• Obtain total spine CT scan: • Evidence of spinal injury, fracture, or dislocation?

NO

• Trauma mechanism? • Level of consciousness? • Distracting injuries?

E

• Continue ATLS • Resuscitation • Repeat neurologic examination and documentation

G

I

Violation of the “Holy Trinity” of the spine? * YES

YES

F B

• Consider non-operative management • Adjunctive bracing as indicated

• Continue management of associated injuries • Physical/occupational therapy • Early referral to a dedicated center for neurorehabilitation

*Holy Trinity of the spine: Classify SCI severity: • Alignment • Stability • Fracture classification? • Neurology • Complete vs incomplete SCI? • Central cord syndrome? • Cauda equina syndrome? • Nerve root injury? • Plexus injury? • Recognize and treat neurogenic shock • Understand spinal shock

in SCI patients is paramount. Furthermore, the SCI team should be involved very early in the process of care. The SCI team is typically composed of intensivists, respiratory therapists, physiatrists, and therapists of myriad types who are experienced in delivering care to patients suffering from an acute traumatic SCI. In addition, a multidisciplinary approach to critically injured patients with SCI is mandatory. Explicit communication is required between care providers to ensure all body systems are appropriately managed, with specific attention paid to the effect that serious spinal injury can have on each of these areas. It is also highly recommended to involve clinical social workers and spiritual-care specialists early in the treatment process. These ancillary providers can be extremely helpful in dealing with the psychological and emotional challenges that accompany SCI. This can not only be said of the patient but also of the involved family members. It is also frequently helpful to employ the expert services of a psychologist, psychiatrist, or other behavioral health specialist. In short, the care of SCI patients after surgery is equally or more important than a very wellexecuted surgical intervention. Patients with SCI should be mobilized by physical therapy (PT)/occupational therapy (OT) in a timely fashion to reduce preventable complications, with the goal of referral to a neurorehabilitation facility at the earliest time point, once all associated injuries have been definitely managed and patients are fully resuscitated.

SPECIAL CONSIDERATIONS Gunshot wounds (GSWs) to the spine are most frequently nonoperative entities. This can be said of most low-velocity missile injuries caused by civilian handguns. SCI from GSW is most frequently a result of the concussive injury to the neural tissue delivered by the missile. This neuropraxic-type injury does not respond to surgical decompression. In rare instances, a low-velocity GSW can destabilize the spine such that a stabilization procedure is required. High-velocity GSWs to the spine, however, may require debridement and stabilization because of the much higher-energy injury to the tissues. Shotgun blasts from close range are also typically managed with surgery. A spinal GSW that includes retained bullet or bony fragments within the spinal canal, causing ongoing neurologic compression, may require surgical removal when patients present with incomplete or

H

• Early surgical management: • Restoration of sagittal alignment, stability of spinal column, and decompression of neural elements, as indicated

changing neurologic injuries. Shrapnel within the thecal sac that leads to persistent cerebrospinal fluid leak or concern for lead poisoning can also cause the surgeon to pursue operative intervention. When missiles traverse the intestines before damaging the bony architecture of the spine, then osteomyelitis prophylaxis is indicated. Antibiotics should target intestinal flora and are typically given for 7 days. Ankylosing conditions of the spine, such as ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis (DISH), require special consideration when involved with SCI. This can also be said for spines with previous surgical fusions. Whereas the normal spine is a supple structure, these conditions render the spine extremely stiff. As such, the spine acts more like a long bone. Therefore fractures can more readily lead to instability. The spinal surgeon must be acutely aware of these conditions and have a lower threshold to provide stability to the spine in a surgical manner. Additionally, surgical techniques required for procedures in this patient population typically entail an increased number of bony fixation points to ensure proper stability. These stiffened spines can also be accompanied by fairly dramatic deformities. The spinal surgeon should work to restore the baseline alignment and not “normal” alignment. In fact, restoring normal alignment can further threaten the spinal cord. An example would be a patient with a chin-on-chest deformity in the setting of ankylosing spondylitis. A fractured neck in this setting mandates a very careful positioning effort during all phases of care to ensure that baseline deformity is maintained so as to protect the spinal cord.

CONCLUSION Surgical decision making for patients with SCI is a challenging task because of the heterogenic patient population and multiple confounding variables that affect the decision-making process. Patients with SCI can present with unclear neurologic manifestations that can puzzle the care team and examining physicians. Protocol-driven assessment and management are therefore imperative, as illustrated in the algorithm. Executing a thorough and detailed history, examination, and evaluation of the injury patterns is paramount. Once this is done, the care provider can begin to march through the steps of the algorithm, which will allow arrival at a surgical decision point. Along the way, it is

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446  Part VIII  ◆ Trauma important to clarify the neurologic deficit, classify the injury, and determine the status of the “Holy Trinity” of the spine. The spine surgeon should work swiftly to restore alignment, establish stability, and decompress threatened neurologic structures once the trauma- and critical-care teams have given the green light for surgery. After the goals of surgery are accomplished, SCI patients require a multidisciplinary approach to care by many skilled providers to enable optimal outcomes. Even when care is delivered to these critically ill patients in a highly effective manner, SCI patients often experience life-long sequelae from their injuries. REFERENCES Bellabarba C, Fisher C, Chapman JR, et al. Does early fracture fixation of thoracolumbar spine fractures decrease morbidity or mortality? Spine. 2010;35(9 suppl):S138–S145. Fehlings MG, Perrin RG. The timing of surgical intervention in the treatment of spinal cord injury: a systematic review of recent clinical evidence. Spine. 2006;31(11 suppl):S28–S35. Harris MB, Sethi RK. The initial assessment and management of the multiple-trauma patient with an associated spine injury. Spine. 2006;31(11 suppl):S9–S15. Jakoi A, Iorio J, Howell R, Zampini JM. Gunshot injuries of the spine. Spine J. 2015;15(9):2077–2085. Kossmann T, Payne B, Stahel PF, Trentz O. Traumatic paraplegia: surgical measures. Swiss Med Wkly. 2000;130:816–828. Marsh JL, Slongo TF, Agel J, et al. Fracture and dislocation classification compendium - 2007: Orthopaedic Trauma Association classification, database and outcomes committee. J Orthop Trauma. 2007;21(10 suppl):S1–S133.

Piazza M, Schuster J. Timing of surgery after spinal cord injury. Neurosurg Clin N Am. 2017;28(1):31–39. Platz A, Stahel PF, Kossmann T, Trentz O. Civilian gunshot injuries to the spine: diagnostic procedures and therapeutic concepts. Eur J Trauma. 2001;27:104–109. Schinkel C, Anastasiadis AP. The timing of spinal stabilization in polytrauma and in patients with spinal cord injury. Curr Opin Crit Care. 2008;14: 685–689. Schmidt OI, Gahr RH, Gosse A, Heyde CE. ATLS and damage control in spine trauma. World J Emerg Surg. 2009;4:9. Schuld C, Franz S, Bruggemann K, et al. EMSCI study group. International standards for neurological classification of spinal cord injury: impact of the revised worksheet on classification performance. J Spinal Cord Med. 2016;39(5):504–512. Stahel PF, Flierl MA. Targeted modulation of the neuroinflammatory response after spinal cord injury: the ongoing quest for the “holy grail. Am J Pathol. 2010;177:2685–2687. Stahel PF, Flierl MA, Moore EE, et al. Advocating “spine damage control” as a safe and effective treatment modality for unstable thoracolumbar fractures in polytrauma patients: a hypothesis. J Trauma Manag Outcomes. 2009;3:6. Stahel PF, VanderHeiden T, Finn MA. Management strategies for acute spinal cord injury: current options and future perspectives. Curr Opin Crit Care. 2012;18(6):651–660. Stillman MD, Barber J, Burns S, Williams S, Hoffman JM. Complications of spinal cord injury over the first year after discharge from inpatient rehabilitation. Arch Phys Med Rehabil. 2017;Jan 20, Epub ahead of print. Westerveld LA, Verlaan JJ, Oner FC. Spinal fractures in patients with ankylosing spinal disorders: a systematic review of the literature on treatment, neurological status and complications. Eur Spine J. 2009; 18(2):145–156.

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Chapter

151 

POPLITEAL ARTERY INJURY Caleb Mentzer, MD, Nicholas Namias, MD, MBA, FACS, FCCM, and Lori Baird, MD, MBA

A This algorithm begins with the suspicion of popliteal artery injury. It is assumed that all of the basics of the trauma work-up have been completed or are in progress and that if there is obvious exsanguinating bleeding, that hemorrhage control would be immediately obtained by direct pressure or by tourniquet. Suspicion of popliteal artery injury, other than obviously visible bleeding or hematoma, would be raised by the following: a. Perigeniculate fractures or a floating knee b. Posterior knee dislocation or ligamentous instability (The dislocated knee that has been relocated intentionally or spontaneously may have suffered an intimal injury.) c. Difference between the left and right pedal pulses, regardless of mechanism d. Penetrating injury with even a remote possibility of involving the popliteal artery B When there is exsanguinating injury, remember to consider life over limb. Tourniquets have been reintroduced into trauma practice, and it is unacceptable to have a death from extremity bleeding without a tourniquet. In the situation of exsanguination, the patient must have pressure or a tourniquet applied in the emergency department (ED) and be moved expeditiously to the operating room. If associated life-threatening injuries require imaging (e.g., brain), it is permissible to move briskly through computed tomography (CT) of the brain so that the neurosurgeon can intervene simultaneously, so long as hemorrhage is stopped. C There is no diagnostic dilemma to be solved with a pulseless extremity and a single-level injury (stab, gunshot). These patients should go directly to the operating room for exploration and revascularization, even with temporary intravascular shunts. As surgical training evolves to subspecialization, it is no dishonor to call for experienced or vascular-trained help with popliteal injuries. It is, however, better to be in the operating room, prepping, draping, exposing, and identifying the injury while waiting for help, if it is called, rather than delaying the time to reperfusion by waiting for the vascular surgeon. Multiple levels of injury do present a diagnostic dilemma because there may be multiple levels of obstructing injury. With multiple levels, it is best to have a roadmap. CT angiography, interventional radiology (IR)

suite angiography, and on-table angiogram are all acceptable based on local resources and practices. D The arterial pressure index (API) distinguishes between those injuries with a pulse that will need further work-up and those that will not. The systolic pressure in the injured extremity is divided by the systolic pressure in an uninvolved arm to yield the API. The sensitivity and specificity of an API of less than 0.90 are 95% and 97%, respectively, and the negative predictive value of an API greater than 0.90 is 99%. E A detailed discussion of the operative management of popliteal arteries is beyond the scope of this algorithm. However, some basic principles apply. At the popliteal level, the surgeon is faced with flexion at the knee and relatively small vessel size. For these reasons, the autologous greater saphenous vein is the preferred conduit. A polytetrafluoroethylene (PTFE) of the size needed to repair a popliteal artery (4 mm) is likely to suffer premature occlusion. Kinking across the knee joint will also likely lead to occlusion. If concomitant venous injury is present, there is a high risk for thrombosis if the vein is repaired. Either thrombosis or ligation can lead to a high risk for leg compartment syndrome. It is safest to perform four-compartment fasciotomies in the setting of combined arterial and venous injuries. Ensure adequate fasciotomies. Loss of a limb to compartment syndrome after doing inadequate fasciotomies is a problem. Closing overzealous fasciotomies a few days later is not. Finally, if concomitant life-threatening injuries or a mangled extremity involving soft tissue, bone, and nerve make amputation likely, primary amputation is sometimes the best option. (The factors in the decision to amputate are beyond the scope of this algorithm.) F Imaging undertaken for an API < 0.90 in the extremity that didn’t obviously need surgery because of hard signs of vascular injury is likely to reveal injuries that are amenable to a variety of modern options. The data for all of these options are poor and are evolving, with practice evolving faster than the data. Open surgery remains a safe and reliable option. Endovascular surgery is rapidly replacing open surgery. Although there are no good long-term data for stenting across popliteal artery injuries, it is being done, and depending on locale, we can expect to see this performed by vascular surgeons, interventional radiologists, and interventional cardiologists. Likewise, the role of antiplatelet and anticoagulation therapy for dissections or small intimal injuries is widely accepted but poorly defined, yet these adjuncts are often the sole treatment for small intimal injuries or pseudoaneurysms. REFERENCES Frykberg ER, et al. Popliteal vascular injuries. Surg Clin North Am. 2002;82(1):67–89. Ganapathy A, et al. Endovascular management for peripheral arterial trauma: the new norm? Injury. 2017;48(5):1025–1030. Johansen J, et al. Non invasive vascular reliably exclude occult arterial trauma in injured extremities. J Trauma. 1991;31:515. Medina O, et al. Vascular and nerve injury after knee dislocation: a systematic review. Clin Orthop Relat Res. 2014;472(9):2621–2629.

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Chapter 151  ◆  Popliteal Artery Injury  448.e1

Abstract

Keywords

An algorithm for decision making in suspected popliteal artery injury is presented. Algorithm junction points include the presence or absence of hemorrhage, pulses, and degree of diminution of pulses when pulses are present.

popliteal artery tourniquet arterial pressure index repair stent

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Chapter 151  ◆  Popliteal Artery Injury  449 Tourniquet or pressure and operating room

Yes

Operating room

Single level injury?

Yes

B

Suspect Popliteal Artery Trauma

Multiple level injury?

API < .9

Exsanguinating?

No No

Operative management

C Imaging and OR

Pulseless

A

E

D

API > .9

Imaging

Pos

Neg

Open surgery and/or Endovascular surgery and/or Interventional radiology and/or Antiplatelet and/or Anticoagulation

F Discharge

No vascular injury

Discharge

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Chapter

152 

BURNS Arek Wiktor, MD, FACS, and Anne Lambert Wagner, MD, FACS

A In the initial evaluation of a burn patient, obtaining an accurate history of the mechanism of burn injury and following Advanced Trauma Life Support (ATLS) principles are essential. A burn injury alone typically does not cause an immediate life threat unless the airway is in question. ATLS management provides an excellent framework for the comprehensive evaluation of the burn patient. Priority is given to all life-threatening injuries first, and surgical approaches should not be limited because of overlying burned skin. Additional consideration must be made for possible inhalation injury and toxic gas exposure as well. A history of exposure to smoke in an enclosed space, prolonged exposure, and a loss of consciousness are important risk factors to ascertain. Hypothermia prevention measures such as increasing the room temperature, using warm intravenous (IV fluids), and utilizing warm blankets are warranted. Chemical injuries should be treated by brushing off excess liquid or powder and then dilution of the agent with copious water irrigation. Adherent, hot materials, such as tar or melted plastics, should be cooled and removed as expediently as possible. Tar can be removed with many petroleum-based products by emulsifying it (mineral oil, mayonnaise, and vegetable shortening have been used with success). IV access should be promptly established. Peripheral IVs through nonburned skin are preferable. In patients who are severely burned and IV sites are compromised, interosseous (IO) and central lines are options; both can be placed through burned skin if need be. IO access can be established much faster than a central line. Fluid boluses should be avoided unless necessary because these may lead to overresuscitation. If burns are suspected to be > 10% of total body surface area, before formal estimation of burn size is done, fluids (lactated Ringer’s) can be started according to Advanced Burn Life Support (ABLS) prehospital criteria: 500 cc/hr for 14 years of age to adult, 250 cc/hr for children 6 to 13 years of age, 125 cc/hr for small children/infants 5 years old and younger. Dextrose-containing fluids should be given to infants < 10 kg. B Initial labs such as a basic metabolic panel, complete blood count, and coagulation studies are helpful for burns that may require inpatient admission, may require surgery, or have other medical comorbidities. Urine toxicology screening should also be routinely performed. For those patients with smoke inhalation, a carboxyhemoglobin level is warranted, along with an arterial blood gas and cyanide level if one is very suspicious of exposure. Serum lactate can be useful as an initial marker of hypoperfusion or anaerobic metabolism, such as in cyanide exposure. A chest x-ray is often normal in cases of inhalation injury and is not diagnostic. For electrical burns, specifically, high-voltage (>1000 volts) burns, a creatine kinase level and electrocardiogram (ECG) are mandatory.

C One of the most important assessments in caring for a burned patient is determining the percent total body surface area (% TBSA) burned. The % TBSA burned can be estimated using the rule of nines, the Lund and Browder diagram, or the 1% palmar rule (patient’s entire palmar surface, including digits, is roughly equivalent to 1% TBSA). The Lund and Browder diagram is more accurate and makes age-related adjustments to surface area. For instance, an infant under the age of 6 months may have up to 18% of the body surface area accounted for by the head alone. Most importantly, superficial (first-degree) burns are not counted in the % TBSA. Burns smaller than 20% TBSA are generally regarded as not requiring a formal burn fluid resuscitation. However, compensation should be made for wound losses with higher-than-normal maintenance fluid rates. These patients will require some debridement of their wounds, pain control, assessment for admission and/or operative need. D Patients with ≥ 20% TBSA burns are regarded as having a severe burn injury and require admission with formal burn resuscitation because of the profound capillary leak. In these patients, the catabolic response to severe burn injury is profound, and the basal metabolic rate can double in burns greater than 40% TBSA. Patients are typically unable to meet their caloric needs and will need enteral nutrition access via nasogastric/ Dobhoff tube. Tube feeds are started within 24 hours of injury. Adjunctive treatments to modulate the stress response, preserve lean body mass, and improve outcomes have focused on heart-rate optimization with propranolol and the oral synthetic androgen oxandrolone. These adjuncts are typically started after the burn resuscitative period and are continued throughout the hospital course. Propranolol can cause hypotension, and oxandrolone can cause an elevation in transaminases; scheduled weekly monitoring is recommended. E The diagnosis and management of smoke inhalation injury pose a unique challenge in caring for the burn patient. Patients may also be exposed to toxic gases, such as carbon monoxide, without obvious external evidence. In addition, singed nasal hairs, facial burns, carbonaceous sputum, and soot in the oropharynx do not correlate with the presence or severity of inhalation injury or upper airway compromise. Chest x-ray is usually unremarkable and non-diagnostic. These factors can complicate the assessment for definitive airway management. Extensive and deep facial burns, inability to clear secretions, respiratory distress, stridor, and retractions are clinical indicators of early intubation. Upper airway injury (above the glottis) is predominantly a heat injury and is often not apparent at presentation, but it can develop in the first 8 hours, creating an airway obstruction. If an upper airway injury is suspected, early assessment by nasal bronchoscopy can be performed. Lower airway injury (below the glottis) is predominantly a chemical injury. Inhalation injury is an independent predictor of mortality and imparts an additive inflammatory effect to the burn injury; resuscitative fluid amounts can double. Carbon monoxide (CO) poisoning is the most common toxic gas patients are exposed to during a fire. The signs and symptoms of CO poisoning can be quite nonspecific, and all patients should be placed on 100% oxygen during evaluation. Standard pulse oximetry will yield falsely high results; thus, a CO-oximeter is required to directly measure carboxyhemoglobin levels. Cyanide poisoning is uncommon but potentially fatal. Signs and symptoms mirror CO poisoning, such as altered mental status and tachypnea. Other clues

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Chapter 152  ◆ Burns  450.e1

Abstract

Keywords

The initial evaluation and treatment of a burn patient can be intimidating and complex. This algorithmic approach helps simplify the initial care and stabilization of a burn patient. Smoke inhalation, toxic gases, burn depth, and strategies for basic wound care are all discussed.

burn inhalation injury carbon monoxide poisoning cyanide toxicity burn resuscitation burn depth partial-thickness burns full-thickness burns

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Chapter 152  ◆ Burns  451 include progressive metabolic acidosis, serum lactate ≥ 10, and an elevated mixed venous oxygen saturation. F Resuscitation is usually performed with lactated Ringer’s solution to minimize the hyperchloremic metabolic acidosis seen with normal saline. Various formulas estimate expected resuscitation needs in the first 24 hours after a burn. Local practices vary, but the American Burn Association (ABA) consensus formula combines the modified Brooke and Parkland formulas to allow a range of fluid to be administered: 2 to 4 cc per kg of body weight per % TBSA burned within the first 24 hours of burn injury. The rule of 10s developed by the U.S. military is a simple and elegant way to estimate initial fluid rates: Estimate the % TBSA burned to the nearest 10, multiply that by 10, and the result is the initial starting rate of IV fluids (adjustments for patients weighing above 80 kg are also made). It is critical to remember that formulas are only starting points of resuscitation, and fluid rates are dynamically titrated in response to urine output (UOP) and markers of organ perfusion. Goal UOPs for adult and pediatric patients are 0.5 cc/kg/hr and 1 cc/kg/hr, respectively. Colloids (albumin and fresh frozen plasma [FFP]) are adjuncts to resuscitation and can be considered when UOP is not improving (despite increasing crystalloid fluid rates) and to avoid overresuscitation. Overresuscitation complications include abdominal compartment syndrome, pulmonary edema, and burn depth conversion. G Treatment of any suspected inhalation injury begins with 100% oxygen therapy. Assessment for intubation follows. If the patient is intubated, bronchoscopy can be performed to diagnose inhalation injury. Daily therapeutic bronchoscopies are also routinely performed to remove any airway debris or cast formation. Other adjuncts employed by burn units

for inhalation injury include nebulized albuterol/heparin/Nacetylcysteine/epinephrine along with specialized mechanical ventilator therapies such as intermittent positive-pressure ventilation (IPPV), high-frequency percussive ventilation (HFPV), and airway pressure-release ventilation (APRV). For CO poisoning, the standard of therapy is administration of 100% oxygen via high-flow mask. Treatment of CO poisoning with hyperbaric oxygen is controversial, and local practices vary. For cyanide poisoning, hydroxocobalamin is the mainstay of treatment, and many prehospital agencies have medical authority to administer this drug in the prehospital setting. Typical dosing of hydroxocobalamin is 70 mg/kg, and it is packaged in 5-g vials. One vial is usually enough for an average-size person, although it can be redosed as necessary. Common side effects include hypertension and chromaturia. There are mixed results in the literature on the efficacy of empiric cyanide treatment. H Admission/transfer to a burn center versus home care with clinic follow-up is an important decision point to be made when treating these patients. Factors to consider include size/ depth of burn, location of burn, degree of pain, ability to tolerate wound care on oral medications, and social factors such as resources and the capability to perform wound care independently or with assistance. Burns are characterized as superficial (first degree), partial thickness (second degree), and full thickness (third degree). Superficial burns are akin to a sunburn and are mildly painful, are pink/red, and blanch. There is no blistering or dermal damage. These will usually heal within a week with lotion, and no scarring will develop. Partial-thickness burns damage the dermis and will usually have a blister. Blisters greater than 2 cm should be debrided (removal of the loose epidermis), and the underlying dermis exposed, so that topical wound agents can be applied.

A History and PE Mechanism Trauma Concern for inhalation Toxic gas exposure

I Topical Antimicrobials

C 1-19% TBSA

H D Burn

> 20% TBSA

F

Evaluate for burn center transfer Basic burn wound care

Burn resuscitation

B Labs and initial imaging CBC Chem7 Coags CK If suspect inhalation injury: Cyanide level Carboxyhemoglobin level

Escharotomy

K

E Inhalation Injury Toxic gases: Carbon monoxide and cyanide poisoning

J

G Bronchoscopy Inhaled heparin Albuterol Mucomyst 100% oxygen Hydroxocobalamin

Wound excision and grafting

L Biological dressings

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452  Part VIII  ◆ Trauma Once the blister has been debrided, the exposed dermis is pink/red, moist, and very tender. These burns will generally heal in 7 to 21 days, primarily by reepithelization. Full-thickness burns represent the complete destruction of the dermis extending to the subcutaneous tissues. They appear waxy and leathery, with colors ranging from white, to punctate hemorrhage red to charred black. There is no blistering or blanching, and they are insensate. Without surgical intervention (excision and grafting), these may heal only by autolysis of eschar and contraction, leading to significant morbidity and mortality. The ABA has developed criteria for patients who will likely require referral/transfer to a local burn center. Patients meeting these criteria or those in question should be discussed with a local burn center to assess the appropriateness of transfer and tips for care. These include partial-thickness burns greater than 10% TBSA; burns that involve the face, hands, feet, genitalia, perineum, or major joints; full-thickness burns; electrical burns, including lightning injury; chemical burns; inhalation injury; and any patient with burns and concomitant trauma in which the burn injury poses the greatest risk for morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit. Other indications for transfer are burned children in hospitals without qualified personnel or equipment for the care of children, and burn injury in patients who will require special social, emotional, or rehabilitative intervention. Before transferring a burn patient, IV access and fluid rates should be confirmed. Patients are typically dressed in dry gauze over their burn wounds. This not only expedites transfer but also improves wound examination accuracy at the receiving burn center while preventing hypothermia. Blisters are left alone, and no debridement should be undertaken before transfer. Tetanus status needs to be checked and updated. No prophylactic systemic antibiotics should be given. Do not apply topicals because they will need to be removed for wound examination at the burn center. I

There are myriad ways to perform burn wound care. The simplest method is to apply an antibiotic ointment (e.g., bacitracin) to the burn, cover with a petroleum gauze, secure, and change daily. Formulations with silver have been a mainstay of burn wound care for decades. Silver sulfadiazine (SSD) is excellent on full-thickness burns; however, it is falling out of favor for partial-thickness burns because it has been shown to inhibit wound healing. An entire product line of silver-containing dressings has also been developed. These include both ionic and nanocrystalline silver that are incorporated into fabrics, silicone sheets, nylon sheets, gels, and alginates. All of these can be used depending on local practice and familiarity. These products typically allow for longer wear times (up to 7 days) and easier application, which may help avoid the pain and cost of daily dressing changes. Because of protein build-up, topical debriding agents can also be useful, such as medical-grade honey and enzymatic agents such as collagenase. Eschar penetration and open excised wound coverage can be accomplished with 2.5% mafenide acetate, 0.5% silver nitrate, or 0.5% acetic acid soaks. Mafenide acetate cream is used for ear and nose burns to prevent liquefactive necrosis of cartilaginous structures. J

Full-thickness circumferential burns on the extremities can act as a tourniquet during burn resuscitation (extremity

eschar syndrome, EES), whereas these burns on the torso impede chest wall compliance, alter respiratory mechanics, and lead to hypoxia and hypercapnia, as evidenced by rising airway pressures or decreasing tidal volumes. To prevent EES, judicious fluid resuscitation is warranted, and elevation of the burn extremity is mandatory. Despite these measures, escharotomies may still be necessary and are ideally performed before any signs of compartment syndrome. They can be performed at the bedside under moderate sedation with a Bovie cautery or scalpel. Incisions should only be made over full-thickness areas. Remember, these are not fasciotomies. The goal is to release the dermis only; cutting into fat only causes bleeding and scarring. Escharotomies rarely need to be performed at outside facilities before transfer to a burn center; discussions with the accepting burn center should be held before this occurs. K Full-thickness burns require excision and grafting to achieve wound closure. Early excision and grafting of the burn within the first few days of injury have been shown to decrease complications, decrease transfusion requirements, and improve outcomes. Some centers employ immediate excision with the goal of removing all full-thickness burn and covering the excised beds with autograft, allograft, or skin substitute within the first 48 hours of injury. Most centers employ an early-excision approach, with all full-thickness burn excised within the first 2 weeks of the burn. During burn excision, adjunctive measures to prevent blood loss, such as tumescence with dilute epinephrine and use of tourniquets, are warranted. Autografting can be accomplished with full-thickness and split-thickness skin grafts (STSGs). STSGs are the most commonly used because of the availability of donor sites and the ability to reharvest donor sites if needed. Autografts can also be meshed or nonmeshed (sheet grafts). Sheet grafts are preferred whenever possible, especially on the hands and face. When meshing is required, the smallest size is picked to decrease scarring and contracture. L Biologic skin substitutes and dressings have also been developed to allow for coverage of wounds and prevent infection. These include polyurethane, acrylamide, and nylon films combined with other biological materials. Porcine xenograft and human cadaver allograft are commonly used as well. Porcine xenograft can be used as a biological bandage over partialthickness burns, minimizing painful dressing changes. Large burns may not have enough native skin available for complete autograft coverage. Temporary skin substitutes, such as cryopreserved allograft, or other acellular dermal replacement products such Integra® and Primatrix® can be applied to cover the wound after burn eschar removal while donor sites are healing for reharvesting. Dehydrated human amniotic chronic membrane allografts have also gained popularity as dressings for partialthickness burns or debrided wounds. REFERENCES American Burn Association. 2016. Advanced Burn Life Support (ABLS) Provider Manual 2016 Update. Deutsch CJ, Tan A, Smailes S, Dziewulski P. The diagnosis and management of inhalation injury: an evidence based approach. Burns. 2018;44:1040–1051. Kagan RJ, Peck MD, Ahrenholz DH, et al. Surgical management of the burn wound and use of skin substitutes: an expert panel white paper. J Burn Care Res. 2013;34(2):e60–e79. Lundy JB, Chung KK, Pamplin JC, et al. Update on severe burn management for the intensivist. J Intensive Care Med. 2016;31(8):499–510.

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Chapter

153 

ACUTE FROSTBITE Anne Lambert Wagner, MD, FACS, Arek Wiktor, MD, and John Twomey, MD Skin and soft tissue are readily susceptible to injury at either end of the temperature spectrum. With exposure to cold, unprotected tissues can readily become frostbitten and/or hypothermic (aka frostnip); these are two distinct but often linked injuries. In the past, skin, limbs, and digits sustaining severe frostbite injury had predictable outcomes: sloughing or amputation. The only question was how long to wait to amputate. Essentially, no progress was made in the treatment of frostbite until the early 1990s when the development of a treatment protocol for frostbite patients was developed using thrombolytics to restore blood flow to damaged tissue. Frostbite has two separate mechanisms to the injury itself. The initial insult is the cold injury that leads to direct cellular damage from actual freezing of the tissues. Rewarming of the affected tissues leads to the second, a reperfusion injury resulting in patchy microvascular thrombosis and tissue death. A There are two classification methods used to determine the severity of frostbite. The traditional classification uses a first- through fourth-degree injury scale, similar to burn injury. Frostnip is the stage just before frostbite, which is chilling of the skin without any cellular damage. It may present with blanched, cool skin that becomes warm and reddened upon rewarming. It often presents with significant but limited discomfort and no evidence of cutaneous damage such as blistering. • First-degree frostbite: Superficial damage to the skin from tissue freezing, with redness (erythema), some edema, hypersensitivity, and stinging pain. • Second-degree frostbite: Deeper damage to skin, with a hyperemic or pale appearance, significant edema with clear or serosanguineous fluid-filled blisters, and severe pain. Frostnip and first- and second-degree frostbite will generally heal without significant tissue loss. • Third-degree frostbite: Deep damage to the skin and subcutaneous tissue. Cold, pale, and insensate without a lot of tissue edema. Shortly after rewarming, edema rapidly forms, along with the presentation of hemorrhagic blisters. Significant pain often occurs after rewarming. • Fourth-degree frostbite: All the elements of a third-degree injury with evidence of damage extending to the muscle, tendon, and bone of the affected area. Determining the extent of frostbite injury starts with a detailed history regarding how the affected area appeared on presentation. The history of a cold, white, and insensate extremity on presentation is consistent with severe frostbite injury (third- and/ or fourth-degree frostbite). A severe frostbite injury requires emergent therapy with thrombolytics unless the patient meets one of the exclusion criteria. If in question regarding the depth of the injury, a clinical examination can be supported by a vascular study as indicated. A digital Doppler examination is a simple and quick modality to further clarify the diagnosis of severe frostbite.

B

 

PREHOSPITAL OR EMERGENCY DEPARTMENT MANAGEMENT

• Correct hypothermia (warm room, remove wet clothing and jewelry, provide warmed fluids, etc.). • If there are areas of frozen tissue, do not thaw if the transport time to a referring center is within 2 hours. Rapid rewarming is associated with the best outcomes and salvage rates. However, never thaw until the risk for refreezing has been eliminated. Patients who have undergone freeze–thaw cycles do not respond to thrombolytics and are treated with standard frostbite therapy. • Protect affected areas from further trauma with padding, splinting, and immobilization while transporting. • Minimize manipulation or rubbing of the affected area. • The patient should be made completely non–weight bearing to avoid incurring additional injury to frozen tissue (ice crystals) and/or forming blisters. • Elevate the affected extremities, when able, to decrease tissue edema. • Obtain a large-bore peripheral intravenous (IV) line and start warmed fluids. Most patients will present with dehydration secondary to hypothermia and/or intoxication. • Avoid direct radiant heat to prevent iatrogenic burns to the cold tissue. • Update the patient’s tetanus status. • Complete admission labs, including: • Complete blood count (CBC) with platelets, basic metabolic panel, prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), blood alcohol, ionized calcium, magnesium, phosphorus, liver function tests, and a urine toxicology screen • Pain management should include ibuprofen (800 mg if no contraindication) to block the arachidonic cascade and narcotics as needed. C

 

RAPID EXTERNAL REWARMING

Rapid rewarming should be instigated as soon as possible after arrival in the treating facility once the risk for refreezing has been eliminated. Rewarming is a simple but often painful process. Current recommendations for treatment are submersion of the affected digits or limb(s) in 100 to 104° F (38 to 40° C) water bath. Dry heat should be avoided secondary to the risk for thermal injury. Continue to avoid unnecessary manipulation. Narcotics will frequently be required during the rewarming process, which typically takes between 30 and 40 minutes. Allow the tissues to air-dry. Rewarming will be associated with a return of sensation, movement, and possible initial flushing of the skin. The vessels in the case of severe frostbite (third or fourth degree) quickly become thrombotic (24 hours since time of rewarming Platelets < 50,000

History and PE: Male 40 years old + Alcohol Homeless No freeze-thaw cycles, hands & feet involved + Schizophrenia Thawed Extremities Presented to OSH with frozen fingers & toes, outside freezing temperatures for >24 hours

A Frostbite

CONTRAINDICATIONS TO THE THROMBOLYTIC PROTOCOL

No clinical evidence of decreased perfusion or mottled tissues