The Washington Manual™ of Surgery Eighth Edition PDF

THE WASHINGTON MANUAL™ OF SURGERY Eighth Edition Department of Surgery Washington University School of Medicine St. Louis, Missouri Editors Mary E. Klingensmith, MD...

THE WASHINGTON MANUAL™ OF SURGERY Eighth Edition Department of Surgery Washington University School of Medicine St. Louis, Missouri Editors Mary E. Klingensmith, MD Paul E. Wise, MD Cathleen M. Courtney, MD Kerri A. Ohman, MD Matthew R. Schill, MD Jennifer Yu, MD, MPHS Foreword by Timothy J. Eberlein, MD Bixby Professor and Chair of Surgery Director, Siteman Cancer Center Washington University School of Medicine St. Louis, Missouri Acquisitions Editor: Keith Donnellan Development Editor: Sean McGuire Editorial Coordinator: Tim Rinehart Marketing Manager: Julie Sikora Production Project Manager: Bridgett Dougherty Design Coordinator: Stephen Druding Manufacturing Coordinator: Beth Welsh Prepress Vendor: Aptara, Inc. 8th edition Copyright © 2020 Department of Surgery, Washington University School of Medicine. Copyright © 2016 Department of Surgery, Washington University School of Medicine. Copyright © 2012 Lippincott Williams & Wilkins, a Wolters Kluwer business. Copyright © 2008 by Washington University, on Behalf of Washington University School of Medicine, Department of Surgery. Copyright © 2005, 2002, 1999 by Lippincott Williams & Wilkins. Copyright © 1996 by Lippincott- Raven Publishers. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above- mentioned copyright. To request permission, please contact Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at [email protected], or via our website at shop.lww.com (products and services). 987654321 Printed in China 978-1-9751-2006-1 Library of Congress Cataloging-in-Publication Data available upon request Library of Congress Control Number: 2019910696 This work is provided “as is,” and the publisher disclaims any and all warranties, express or implied, including any warranties as to accuracy, comprehensiveness, or currency of the content of this work. This work is no substitute for individual patient assessment based upon healthcare professionals’ examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data and other factors unique to the patient. The publisher does not provide medical advice or guidance and this work is merely a reference tool. Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources. When prescribing medication, healthcare professionals are advised to consult the product information sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things, conditions of use, warnings and side effects and identify any changes in dosage schedule or contraindications, particularly if the medication to be administered is new, infrequently used or has a narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property, as a matter of products liability, negligence law or otherwise, or from any reference to or use by any person of this work. shop.lww.com Contributors Bola Aladegbami, MD, MBA Resident in Surgery Washington University School of Medicine St. Louis, Missouri Erin G. Andrade, MD, MPH Resident in Surgery Washington University School of Medicine St. Louis, Missouri Michael M. Awad, MD, PhD, FACS Director, Washington University Institute for Surgical Education (WISE) Director, WISE Simulation Fellowship Director, Integrated Surgical Disciplines Clerkship Washington University School of Medicine St. Louis, Missouri Lauren M. Barron, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Jeffrey A. Blatnik, MD Assistant Professor of Surgery Washington University School of Medicine in St. Louis St. Louis, Missouri Grant V. Bochicchio, MD, MPH, FAS Harry Edison Professor of Surgery Department of Surgery Washington University in St. Louis St. Louis, Missouri David G. Brauer, MD, MPHS Resident in Surgery Washington University School of Medicine St. Louis, Missouri L. Michael Brunt, MD Professor of Surgery and Section Chief of Minimally Invasive Surgery Department of Surgery Washington University School of Medicine St. Louis, Missouri Sara A. Buckman, MD, PharmD Assistant Professor of Surgery Washington University School of Medicine St. Louis, Missouri Katharine Caldwell, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri William C. Chapman, MD Professor and Chief, Section of Transplant Surgery Department of Surgery Washington University Medical Center St. Louis, Missouri William C. Chapman, Jr, MD, MPHS Resident in Surgery Washington University School of Medicine St. Louis, Missouri Ina Chen, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Graham A. Colditz, MD, DrPH Professor and Chief, Division of Public Health Sciences Department of Surgery Washington University School of Medicine St. Louis, Missouri Jason R. Cook, MD, PhD Resident in Vascular Surgery Washington University School of Medicine St. Louis, Missouri Cathleen M. Courtney, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Darren R. Cullinan, MD, MSCI Resident in Surgery Washington University School of Medicine St. Louis, Missouri Jesse T. Davidson IV, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Alana C. Desai, MD Assistant Professor of Urologic Surgery Division of Urology, Department of Surgery Washington University in St. Louis St. Louis, Missouri Gayan S. De Silva, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Thomas J. Desmarais, MD Resident in Vascular Surgery Washington University School of Medicine St. Louis, Missouri Brandon D. Downing, MD, PhD Resident in Vascular Surgery Washington University School of Medicine St. Louis, Missouri M. Majella Doyle, MD, MBA, FACS Professor of Surgery Section of Abdominal Transplant Washington University School of Medicine St. Louis, Missouri J. Christopher Eagon, MD Associate Professor of Surgery Washington University School of Medicine St. Louis, Missouri Leisha C. Elmore, MD, MPHS Resident in Surgery Washington University School of Medicine St. Louis, Missouri Ryan C. Fields, MD, FACS Chief, Section of Surgical Oncology Professor of Surgery Associate Program Director, General Surgery Residency Program Director, Resident Research Department of Surgery Barnes-Jewish Hospital/Washington University School of Medicine St. Louis, Missouri Kathryn J. Fowler Assistant Professor of Radiolgy Washington University School of Medicine St Louis, Missouri Bradley D. Freeman, MD Professor of Surgery Department of Acute and Critical Care Surgery Washington University in St. Louis St. Louis, Missouri Joseph C. Fusco, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Jason M. Gauthier, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Patrick J. Geraghty, MD Professor of Surgery and Radiology Department of Surgery, Vascular Surgery Section Barnes-Jewish Hospital/Washington University School of Medicine St. Louis, Missouri William E. Gillanders, MD Mary Culver Distinguished Professor of Surgery and Vice Chair for Research Department of Surgery Washington University School of Medicine St. Louis, Missouri Sean C. Glasgow, MD Associate Professor of Surgery Washington University School of Medicine St. Louis, Missouri Trina Ghosh, MD Resident in Plastic Surgery Washington University School of Medicine St. Louis, Missouri Matthew T. Grant, MD, MPhil Resident in Surgery Washington University School of Medicine St. Louis, Missouri Julie G. Grossman, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Andrea R. Hagemann, MD, MSCI Associate Professor of Obstetrics and Gynecology Division of Gynecologic Oncology Washington University School of Medicine St. Louis, Missouri Bruce L. Hall, MD, PhD, MBA, FACS Professor of Surgery, Professor of Healthcare Administration, Vice President and Chief Quality Officer Department of Surgery Washington University and BJC HealthCare St. Louis, Missouri Rahul R. Handa, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri William G. Hawkins, MD, FACS Chief, Section of Hepatobiliary, Pancreatic, and Gastrointestinal Surgery Neidorff Family and Robert C. Packman Professor of Surgery Washington University School of Medicine, Department of Surgery St. Louis, Missouri Elspeth J.R. Hill, MB, ChB, MRes, PhD Resident in Plastic Surgery Washington University School of Medicine St. Louis, Missouri Jessica L. Hudson, MD, MPHS Resident in Surgery Washington University School of Medicine St. Louis, Missouri Steven R. Hunt, MD Associate Professor of Surgery Washington University in St. Louis St. Louis, Missouri Obeid N. Ilahi, MD Associate Professor of Surgery Section of Acute and Critical Care Surgery Washington University School of Medicine St. Louis, Missouri Omer Ismail Instructor in Surgery Washington University School of Medicine St Louis, Missouri C. Alston James, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Jared McAllister Resident in Surgery Washington University School of Medicine Saint Louis, Missouri Jeffrey Jim, MD, MPHS, FACS Associate Professor of Surgery Program Director, Vascular Surgery Training Programs Washington University in St. Louis School of Medicine St. Louis, Missouri Megan O. Kelly, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Adeel S. Khan, MD, MPH Assistant Professor of Surgery Division of Abdominal Transplant, Department of Surgery Washington University in St. Louis St. Louis, Missouri Ali J. Khiabani, MD, MHA Resident in Surgery Washington University School of Medicine St. Louis, Missouri John P. Kirby, MD, MS, FCCWS, FACS Associate Professor of Surgery, Director of Wound Healing Programs Section of Acute and Critical Care Surgery Department of Surgery Barnes-Jewish Hospital/Washington University School of Medicine in St. Louis St. Louis, Missouri Coen L. Klos, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Mary E. Klingensmith, MD Mary Culver Distinguished Professor of Surgery Department of Surgery Washington University in St. Louis School of Medicine St. Louis, Missouri Kelly Koch, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Bradley A. Krasnick, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Kelli Kreher, MD Resident in Obstetrics and Gynecology Washington University School of Medicine St. Louis, Missouri Timothy S. Lancaster, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Heidi E. L’Esperance, MD Resident in Otolaryngology Washington University School of Medicine St. Louis, Missouri Jessica Lindemann, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Robert M. MacGregor, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Julie A. Margenthaler, MD, FACS Professor of Surgery Department of Surgery Washington University School of Medicine St. Louis, Missouri Christopher M. McAndrew, MD, MSc Associate Professor Department of Orthopaedic Surgery Washington University School of Medicine St. Louis, Missouri Spencer J. Melby, MD Associate Professor of Surgery Division of Cardiothoracic Surgery Barnes-Jewish Hospital/Washington University in St. Louis Chief of Cardiac Surgery John Cochran VA Medical Center St. Louis, Missouri Vincent Mellnick, MD Associate Professor of Radiology Mallinckrodt Institute of Radiology Washington University School of Medicine St. Louis, Missouri Bryan F. Meyers, MD, MPH Professor of Surgery Division of Cardiothoracic Surgery Washington University School of Medicine St. Louis, Missouri Matthew G. Mutch, MD Professor and Chief Section of Colon Rectal Surgery Department of Surgery Washington University School of Medicine St. Louis, Missouri Timothy M. Nywening, MD, MS, MPHS Resident in Surgery Washington University School of Medicine St. Louis, Missouri J. Westley Ohman, MD Assistant Professor of Surgery Department of Surgery, Section of Vascular Surgery Washington University School of Medicine St. Louis, Missouri Emily J. Onufer, MD, MPH Resident in Surgery Washington University School of Medicine St. Louis, Missouri Michael T. Onwugbufor, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Tiffany M. Osborn, MD, MPH, FACEP, FCCM Professor of Surgery and Emergency Medicine Barnes-Jewish Hospital/Washington University St. Louis, Missouri Roheena Z. Panni, MD, MPHS Resident in Surgery Washington University School of Medicine St. Louis, Missouri Kamlesh B. Patel, MD, MSc Associate Professor of Surgery Associate Program Director, Plastic Surgery Residency Director of Craniofacial Surgery St. Louis Children’s Hospital Washington University School of Medicine Division of Plastic and Reconstructive Surgery St. Louis Children’s Hospital St. Louis, Missouri Laurie J. Punch, MD Associate Professor of Surgery Barnes-Jewish Hospital/Washington University in St. Louis School of Medicine St. Louis, Missouri Varun Puri, MD, MSCI Associate Professor of Surgery Department of Surgery Washington University School of Medicine St. Louis, Missouri Nanette R. Reed, MD Assistant Professor Vascular and Endovascular Surgery Barnes-Jewish Hospital/Washington University in St. Louis St. Louis, Missouri Clare H. Ridley, MD Assistant Professor of Anesthesiology and Surgery Cardiothoracic Anesthesiology/Critical Care Barnes-Jewish Hospital/Washington University in St. Louis St. Louis, Missouri Jacqueline M. Saito, MD, MSCI Associate Professor of Surgery Division of Pediatric Surgery Washington University School of Medicine St. Louis, Missouri Luis A. Sanchez, MD, FACS Chief, Section of Vascular Surgery Gregorio A. Sicard Distinguished Professor of Surgery and Radiology Washington University in St. Louis – Department of Surgery St. Louis, Missouri Matthew R. Schill, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri John S. Schneider, MD, MA, FACS Assistant Professor Rhinology and Anterior Skull Base Surgery Department of Otolaryngology Washington University School of Medicine St. Louis, Missouri Douglas J. Schuerer, MD, FACS, FCCM Professor of Surgery, Trauma Medical Director Department of Surgery Washington University in St. Louis St. Louis, Missouri Kristen M. Seiler, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Surendra Shenoy, MD, PhD Professor of Surgery General Surgery Barnes-Jewish Hospital/Washington University School of Medicine St. Louis, Missouri Jason A. Snyder, MD, FACS Assistant Professor of Surgery Section of Acute and Critical Care Surgery Department of Surgery Washington University in St. Louis School of Medicine St. Louis, Missouri Tracey W. Stevens, MD Assistant Professor Department of Anesthesiology Washington University School of Medicine St. Louis, Missouri Melissa K. Stewart, MD Instructor of Surgery Acute and Critical Care Surgery, General Surgery Barnes-Jewish Hospital/Washington University in St. Louis St. Louis, Missouri Matthew S. Strand, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Melanie P. Subramanian Resident in Surgery Washington University School of Medicine Saint Louis, Missouri Steven M. Strasberg, MD, FACS, FRCS(C), FRCS(Ed) Pruett Professor of Surgery, Carl Moyer Teaching Coordinator Section of HPB Surgery, Department of Surgery Barnes-Jewish Hospital/Washington University in St. Louis St. Louis, Missouri Wen Hui Tan, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Richard Tsai, MD Instructor of Radiology Abdominal Imaging, Diagnostic Radiology Mallinckrodt Institute of Radiology/Washington University in St. Louis School of Medicine St. Louis, Missouri Isaiah R. Turnbull, MD, PhD Assistant Professor of Surgery Washington University in St. Louis School of Medicine St. Louis, Missouri Brad W. Warner, MD The Jessie L. Ternberg, MD, PhD Distinguished Professor of Pediatric Surgery Washington University School of Medicine Surgeon-in-Chief St. Louis Children’s Hospital St. Louis, Missouri Jonathan R. Weese, MD Resident in Urologic Surgery Washington University School of Medicine St. Louis, Missouri Jason R. Wellen, MD, MBA Associate Professor Director of Kidney and Pancreas Transplantation Department of Surgery, Section of Abdominal Transplant Surgery Washington University School of Medicine St. Louis, Missouri Paul E. Wise, MD Professor of Surgery and General Surgery Residency Program Director Department of Surgery Barnes-Jewish Hospital/Washington University in St. Louis St. Louis, Missouri Elisabeth K. Wynne, MD Resident in Surgery Washington University School of Medicine St. Louis, Missouri Foreword Welcome to the eighth edition of The Washington Manual™ of Surgery. Over the past 100 years, the most important focus of our Department of Surgery has been medical education of students, residents, fellows, and practicing surgeons. This commitment is clearly evident in the current edition of The Washington Manual™ of Surgery. The educational focus of our Department of Surgery has a rich tradition. The first full-time head of the Department of Surgery at Washington University was Dr. Evarts A. Graham (1919–1951). Dr. Graham was a superb educator. Not only was he an outstanding technical surgeon, but his insightful comments at conferences and ward rounds were well known and appreciated by a generation of surgeons who learned at his elbow. Dr. Graham was a founding member of the American Board of Surgery and made many seminal contributions to the management of surgical patients. His work in the development of oral cholecystography actually helped establish the Mallinckrodt Institute of Radiology at Washington University. Dr. Graham was among the first to identify the epidemiologic link of cigarette smoking to lung cancer and was instrumental in raising public health consciousness about the deleterious effect on health from cigarette smoke. Dr. Carl Moyer (1951–1965) succeeded Dr. Graham. Dr. Moyer is still regarded as a legendary educator at Washington University. He was particularly known for his bedside teaching techniques, as well as for linking pathophysiology to patient care outcomes. Dr. Walter Ballinger (1967–1978) came from the Johns Hopkins University and incorporated the Halsted tradition of resident education. Dr. Ballinger introduced the importance of laboratory investigation and began to foster development of the surgeon/scientist in our department. Dr. Samuel A. Wells (1978–1997) is credited with establishing one of the most accomplished academic departments of surgery in the United States. Not only did he recruit world-class faculty, but he increased the focus on research and patient care. Dr. Wells also placed great emphasis on educating the future academic leaders of surgery. As in previous editions, this eighth edition of The Washington Manual™ of Surgery combines authorship of residents, ably assisted by faculty coauthors and our senior editor, Dr. Mary Klingensmith, who is vice-chair for education in our department. Dr. Klingensmith is joined in this edition by a new senior editor, Dr. Paul Wise. This combination of resident and faculty participation has helped to focus the chapters on issues that will be particularly helpful to the trainee in surgery. This new edition of the manual provides a complete list of updated references that will serve medical students, residents, and practicing surgeons who wish to delve more deeply into a particular topic. This manual does not attempt to extensively cover pathophysiology or history, but it presents brief and logical approaches to the management of patients with comprehensive surgical problems. In each of the chapters, the authors have attempted to provide the most up-to-date and important diagnostic and management information for a given topic, as well as algorithms for quick reference. We have attempted to standardize each of the chapters so that the reader will be able to most easily obtain information regardless of subject matter. The eighth edition has undergone a reorganization of chapters with an emphasis on clarity and consistency. As with the past edition, evidence-based medicine has been incorporated into each of the chapters, with updated information and references to reflect current knowledge and practice. All of the sections have been updated and rewritten to reflect the most current standards of practice for each topic. These updates have been carefully edited and integrated so that the volume of pages remains approximately the same. Our goal is to keep this volume concise, portable, and user-friendly. I am truly indebted to Drs. Klingensmith and Wise for their passion for education and devotion to this project. Additionally, I am proud of the residents in our Department of Surgery at Washington University who have done such an outstanding job with their faculty coauthors in this eighth edition. I hope that you will find The Washington Manual™ of Surgery a reference you commonly utilize in the care of your patient with surgical disease. Timothy J. Eberlein, MD St. Louis, Missouri Preface As with the previous editions, this eighth edition of The Washington Manual™ of Surgery is designed to complement The Washington Manual of Medical Therapeutics. Written by resident and faculty members of the Department of Surgery at Washington University in St. Louis, we present a brief, rational approach to the management of surgical conditions and topics relevant to surgeons. The text is directed to the reader at the second- or third-year surgical resident level, although all residents, surgical and nonsurgical attendings, medical students, physician assistants, nurse practitioners, and others who provide care for patients with surgical conditions will find this Manual of interest and assistance. The book provides a succinct discussion of surgical diseases, with algorithms for addressing problems based on the opinions of the authors. Although multiple approaches may be reasonable for some clinical situations, this Manual attempts to present a single, effective approach for each. We have limited extensive details on diagnosis and therapy as this is not meant to be an exhaustive, detailed surgical reference. Coverage of pathophysiology, the history of surgery, and extensive reference lists have been excluded from most areas. The first edition of this Manual was published in 1997, followed by editions in 1999, 2002, 2005, 2007, 2012, and 2016. As with editions in the past, we have attempted to focus on relevant and timely topics. This eighth edition continues to provide multiple choice review questions at the end of each chapter so that readers can self-assess their knowledge and practice for in-training or other examinations. We have added chapters on “Radiology,” “Trauma Resuscitation and Adjuncts,” and “Intraoperative Considerations” to complement the other chapters in this edition. A separate chapter on appendiceal diseases has been added, and many chapters have been consolidated and reorganized to best reflect the nature of today’s surgical practice. For example, we are including more information on HIPEC as well as operating on the pregnant patient in this edition. In addition, chapters have again been updated with evidence-based medicine, with the latest information and treatment algorithms in each section. As with previous editions, the eighth edition includes updates on each topic as well as new material and citations. This is a resident-prepared Manual, and each chapter was updated and revised (or authored) by a resident with assistance from faculty coauthors. Editorial oversight for the Manual was shared by four senior resident coeditors (Cathleen Courtney, MD, Chapters 10, 13, 15–20, 43, 45, and 47–48; Kerri Ohman, MD, Chapters 21, 27–31, 38–42, and 46; Matthew Schill, MD, Chapters 1–8, 11–12, 14, and 36–37; and Jennifer Yu, MD, MPHS, Chapters 9, 22–26, 32–35, 44, and 49–50). The tremendous effort of all involved—resident and faculty authors, and particularly the above-noted senior resident coeditors—is reflected in the quality and consistency of the chapters. We are indebted to the former senior editor of this work, Gerard M. Doherty, MD, who developed and oversaw the first three editions of this Manual, then handed over the role to M.E.K. as an exceptionally well-organized project. M.E.K. was proud to continue the effort through the next four editions with P.E.W. now joining as Co-Editor. We are grateful for the continued tremendous support from Wolters Kluwer Health, who have been supportive of the effort and have supplied dedicated assistance. Keith Donnellan has been a tremendously helpful Acquisitions Editor, with Sean McGuire as Development Editor and Tim Rinehart as Editorial Coordinator, keeping us on point and on schedule. Finally, we are grateful to have the fantastic mentorship and leadership of Timothy J. Eberlein, MD, our Department Chair of over 20 years. His continued support and dedication has been tremendous, and his leadership of the Department of Surgery at Washington University in St. Louis has been nothing short of inspiring. Finally, to our families, we deeply thank you for your love, support, and encouragement; we wouldn’t be who we are without you! We hope you enjoy the latest edition of The Washington Manual™ of Surgery! M.E.K. and P.E.W. Contents Contributors Foreword Preface 1 Preoperative Evaluation and Care C. Alston James and Mary E. Klingensmith 2 Intraoperative Considerations Matthew R. Schill and Michael M. Awad 3 Common Postoperative Problems Jessica L. Hudson, Melissa K. Stewart, and Isaiah R. Turnbull 4 Nutrition Kristen M. Seiler and Sara A. Buckman 5 Fluid, Electrolytes, and Acid—Base Disorders Base Matthew T. Grant and Tiffany M. Osborn 6 Hemostasis, Anticoagulation, and Transfusions Rahul R. Handa, Isaiah R. Turnbull, and Omer Ismail 7 Anesthesia Megan O. Kelly and Tracey W. Stevens 8 Critical Care Robert M. MacGregor and Clare H. Ridley 9 Trauma Resuscitation and Adjuncts Emily J. Onufer and Jason A. Snyder 10 Head, Neck, and Spinal Trauma Erin G. Andrade and Bradley D. Freeman 11 Chest Trauma Jason M. Gauthier and Grant V. Bochicchio 12 Abdominal Trauma Joseph C. Fusco and Douglas J. Schuerer 13 Extremity Trauma Trina Ghosh and Christopher M. McAndrew 14 Burns Kelly Koch and John P. Kirby 15 Wound Care Erin G. Andrade and Laurie J. Punch 16 Acute Abdomen Ali J. Khiabani and Obeid N. Ilahi 17 Esophagus Lauren M. Barron and Bryan F. Meyers 18 Stomach Bradley A. Krasnick and William G. Hawkins 19 The Surgical Management of Obesity Katharine Caldwell and J. Christopher Eagon 20 Small Intestine Darren R. Cullinan and Paul E. Wise 21 Surgical Diseases of the Liver David G. Brauer, Kathryn J. Fowler, and William C. Chapman 22 Surgical Diseases of the Biliary Tree Matthew S. Strand and Adeel S. Khan 23 Pancreas Timothy M. Nywening and Steven M. Strasberg 24 Spleen Roheena Z. Panni and M. Majella Doyle 25 Abdominal Transplantation Jessica Lindemann and Jason R. Wellen 26 Appendix Ina Chen and Sean C. Glasgow 27 Colon and Rectum Coen L. Klos, Richard Tsai, and Steven R. Hunt 28 Anorectal Disease William C. Chapman, Jr and Matthew G. Mutch 29 Hernias Wen Hui Tan and Jeffrey A. Blatnik 30 Endoscopic, Laparoscopic, and Robotic Surgery Bola Aladegbami and Michael M. Awad 31 Breast Leisha C. Elmore and Julie A. Margenthaler 32 Skin and Soft Tissue Tumors Julie G. Grossman and Ryan C. Fields 33 Diseases of the Adrenal, Pituitary, and Hereditary Endocrine Syndromes Jared McAllister and L. Michael Brunt 34 Thyroid and Parathyroid Glands Jesse T. Davidson IV and William E. Gillanders 35 Lung and Mediastinal Diseases Michael T. Onwugbufor and Varun Puri 36 Cardiac Surgery Timothy S. Lancaster and Spencer J. Melby 37 Cerebrovascular Disease Thomas J. Desmarais and Jeffrey Jim 38 Thoracoabdominal Vascular Disease Jason R. Cook, J. Westley Ohman, and Luis A. Sanchez 39 Peripheral Arterial Disease Gayan S. De Silva and Patrick J. Geraghty 40 Venous and Lymphatic Disease Brandon D. Downing and Nanette R. Reed 41 Vascular Access Ali J. Khiabani and Surendra Shenoy 42 Pediatric Surgery Elisabeth K. Wynne and Brad W. Warner 43 Otolaryngology for the General Surgeon Heidi E. L’Esperance and John S. Schneider 44 Plastic, Reconstructive, and Hand Surgery Elspeth J.R. Hill and Kamlesh B. Patel 45 Urology Jonathan R. Weese and Alana C. Desai 46 Obstetrics and Gynecology for the General Surgeon Kelli Kreher and Andrea R. Hagemann 47 Radiology Cathleen M. Courtney and Vincent Mellnick 48 Biostatistics for the General Surgeon Melanie P. Subramanian and Graham A. Colditz 49 Patient Safety and Quality Improvement David G. Brauer, Bruce L. Hall, and Jacqueline M. Saito Answer Key Index  Preoperative Evaluation and Care 1 C. Alston James and Mary E. Klingensmith I. PREOPERATIVE EVALUATION AND CARE A. General Evaluation of the Surgical Patient. The goals of preoperative evaluation are to (1) identify the patient’s medical problems and functional status; (2) determine if further information is needed to characterize the patient’s medical status; (3) estimate the patient’s level of risk for the planned procedure; and (4) establish if the patient’s condition is medically optimized. Much of this can be accomplished with a thorough history and physical examination. For minor surgical procedures and procedures on young, healthy patients, routine diagnostic testing is often unnecessary. For patients with existing comorbidities, or in patients undergoing certain complex procedures, preoperative laboratory studies and imaging should be decided on an individual basis. B. Specific Considerations in Preoperative Management 1. Cardiovascular disease is one of the leading causes of death after noncardiac surgery. In a cohort study looking at the 8,351 patients who were included in the PeriOperative ISchemic Evaluation (POISE) trial (noncardiac surgery), 5% of patients suffered a perioperative MI. Most of these MIs occurred within 48 hours of surgery (74%) and the majority did not experience ischemic symptoms (65%). The 30-day mortality rate was 11.6% among patients who had a perioperative MI, compared with 2.2% among those who did not (Ann Intern Med. 2011;154(8):523–528). Risk stratification for major adverse cardiac events (MACE, defined as death, Q-wave MI, and need for revascularization) by the operating  surgeon, anesthesiologist, and consulting internist is important. a. Risk factors. A number of patient factors have been identified and are associated with perioperative cardiac morbidity and mortality. These include age above 70 years, unstable angina, recent (prior 6 months) MI, untreated CHF, diabetes mellitus, valvular heart disease, cardiac arrhythmias, peripheral vascular disease, and functional impairment. Factors related to the surgical procedure under consideration also convey risk. In their most recent guidelines published in 2014, the American Heart Association has condensed procedures into two risk levels: low risk (MACE risk 1%). The category of intermediate risk is no longer used, as the management of patients undergoing these and elevated risk procedures is similar. TABLE 1-1 Revised Cardiac Risk Indexa Risk Factor Comment High-risk surgery Intrathoracic, intraperitoneal, major vascular Ischemic heart History of myocardial infarction, positive exercise disease stress test, angina, nitrate therapy, electrocardiogram with abnormal Q waves History of CHF History of CHF, pulmonary edema, or paroxysmal nocturnal dyspnea, bilateral rales, S3 gallop, chest x-ray showing pulmonary vascular redistribution History of History of transient ischemic attack or stroke cerebrovascular disease Preoperative insulin therapy for diabetes Preoperative serum  creatinine >2 mg/dL aRates of major cardiac complication with 0, 1, 2, or 3 of these factors were 0.4%, 0.9%, 7.0%, and 11.0%, respectively. Adapted from Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043–1049. b. Cardiac risk indices/calculators. Several tools have been created to aid in predicting preoperative risk of a MACE. The Revised Cardiac Risk Index is one such tool, and its criteria are shown in Table 1-1. The American College of Surgeons NSQIP Surgical Risk Calculator combines cardiac and noncardiac factors to calculate the risk of overall postoperative complications and can be found at riskcalculator.facs.org. c. Functional status. Patients with poor functional status are at significantly elevated risk of perioperative cardiac events. This can usually be assessed from a patient’s activities of daily living (ADLs) and is often expressed in metabolic equivalents (METs), with 1 MET equaling the resting oxygen consumption of an average 40-year-old male (Table 1-2). Functional capacity can be classified as excellent (>10 METs), good (7 to 10 METs), moderate (4 to 6 METs), or poor (65 years old) undergoing intermediate- or high-risk surgical procedures (i.e., those with a cardiac risk higher than 1%). (b) Multiple screening tools exist (frailty index, FRAIL scale, etc.); however, none have been shown as superior. b. Application. Once made, a diagnosis of frailty can then impact several phases of patient care (J Clin Anesth. 2018;47:33–42). (1) Shared decision making (a) Surgery is higher risk in the frail population; therefore, a frailty diagnosis makes it essential to establish upfront goals of care and confirm that these are in keeping with anticipated surgical outcomes. (2) Prehabilitation (a) Although no established, standardized preoperative exercise  therapy regimen currently exists, there is a growing body of evidence to suggest that in select patient populations preoperative interventions can improve patients’ perioperative morbidity and mortality. (3) Interdisciplinary geriatric comanagement (a) Similarly, inpatient geriatric comanagement programs are an increasingly popular strategy that have been shown to improve perioperative morbidity and mortality. Although the majority of this data is in orthopedic fracture surgery, there is promising initial data from its application in other surgical fields. CHAPTER 1: PREOPERATIVE EVALUATION AND CARE Multiple Choice Questions 1. Which of the following factors is associated with the highest elevated cardiac risk? a. Diabetes controlled with metformin and glyburide b. Mild renal impairment with a preoperative creatinine level of 1.7 mg/dL c. History of a transient ischemic attack 9 months ago d. History of hypertension controlled with three medications 2. Classify the functional status of a patient who is able to golf with a cart and climb two flights of steps but unable to jog or do push-ups: a. Poor b. Moderate c. Good d. Excellent 3. Which of the following is a recommendation endorsed by the Centers for Disease Control and Prevention to reduce the risk of surgical site infection? a. Hair removal from surgical site by shaving b. Tight glucose control perioperatively with goal of 90%. Morphine may be administered to manage the pain and to decrease the sympathetic drive (1 to 4 mg IV every hour), and nonenteric coated aspirin administration can be lifesaving (325 mg). In the absence of hypotension, initial management for cardiac chest pain includes sublingual nitroglycerin (0.4 mg) every 5 minutes until the pain resolves. Hemodynamically stable patients without CHF, significant bradycardia, and/or heart block should also receive beta-blockade, usually metoprolol 15 mg IV in 5-mg doses every 5 minutes, as this has been shown to improve patient outcomes (Am J Cardiology. 1999; 84:76). Patients with any sign of hemodynamic changes should be urgently transferred to an ICU pending expert consultation. D. Congestive Heart Failure (CHF) 1. Presentation. CHF exacerbations typically present with shortness of breath or hypoxia. Physical examination often reveals signs of fluid overload. CHF can occur in the immediate postoperative period as a result of excessive intraoperative administration of fluids or 24 to 48 hours postoperatively related to mobilization of fluids that are sequestered in the extracellular space. Patients frequently have a history of asymptomatic heart failure. 2. Evaluation. Bedside evaluation includes pulse oximetry and assessment of net fluid balance and weight for the preceding days. Laboratory studies include troponin I, B-type natriuretic peptide (BNP), ABG, CBC, electrolytes, and renal function tests. CXR and ECG are frequently indicated. 3. Differential diagnosis: pneumonia, atelectasis, PE, reactive airway disease (asthma, COPD exacerbation), and pneumothorax. 4. Treatment is aimed at maximizing cardiac perfusion and efficiency. a. Supplemental oxygen should be administered. Mechanical ventilation is indicated in patients with refractory hypoxemia. b. Diuresis should be initiated with furosemide (20 to 40 mg IV push), with doses up to 200 mg every 6 hours as necessary. Furosemide drips can be effective in promoting adequate diuresis. Fluid intake should be limited, and serum potassium should be monitored closely. If contraction alkalosis occurs, acetazolamide may be substituted for furosemide.  c. Arterial vasodilators. To reduce afterload and help the failing heart in the acute setting, ACE inhibitors can be used to lower the systolic BP to 90 to 100 mm Hg. Negative inotropes such as calcium channel blockers and beta-blockade should be avoided. d. Inotropic agents. Digoxin increases myocardial contractility and can be used to treat patients with mild failure. Patients with florid failure may need invasive monitoring and continuous inotrope infusion. III. PULMONARY COMPLICATIONS A. Dyspnea 1. Diagnostic considerations: Shortness of breath is often thought of as being a primary respiratory problem, but it can be a symptom of systemic illness such as CHF and PE. Differential diagnoses include atelectasis, lobar collapse, pneumonia, CHF, COPD, asthma exacerbation, pneumothorax, PE, and aspiration. Shortness of breath can also be a result of MI, intra-abdominal complications, systemic sepsis, and fever. Additional factors that help to differentiate disease entities include smoking history, fever, chest pain, and the time since surgery. 2. Examination may reveal jugular venous distention, abnormal breath sounds (wheezing, crackles), asymmetry, and increased respiratory effort. 3. Evaluation. CBC, pulse oximetry, ABG, and CXR are mandatory for all persistently dyspneic patients. ECG should be obtained for any patient older than 30 years with significant dyspnea or tachypnea to exclude myocardial ischemia and in any patient who is dyspneic in the setting of tachycardia. 4. Treatment: a. Atelectasis commonly occurs in the first 36 hours after operation and typically presents with dyspnea and hypoxia. Therapy is aimed at reexpanding the collapsed alveoli. For most patients, deep breathing, coughing, and incentive spirometry are adequate. Postoperative pain should be controlled so that pulmonary mechanics are not impaired. In patients with atelectasis or lobar collapse, chest physical therapy and nasotracheal suctioning might  be required. In rare cases, bronchoscopy can aid in clearing mucus plugs that cannot be cleared using less invasive measures. b. Gastric aspiration usually presents with acute dyspnea and fever. CXR might be normal initially but subsequently demonstrates a pattern of diffuse interstitial infiltrates. Therapy is supportive, and antibiotics are typically not given empirically. c. Pneumothorax is treated with tube thoracostomy. If tension pneumothorax is suspected, immediate needle decompression should precede controlled placement of a thoracostomy tube. d. Volume overload, pneumonia, and PE are discussed elsewhere in this chapter. B. COPD and Asthma Exacerbations 1. Reactive airways are common in postoperative smokers and asthmatic patients. The local trauma of an endotracheal tube can induce bronchospasm. 2. Presentation may include wheezing, dyspnea, tachypnea, hypoxemia, and possibly hypercapnia. 3. Treatment: a. Acute therapy includes administration of supplemental oxygen and inhaled beta-adrenergic agonists (albuterol, 3.0 mL [2.5 mg] in 2-mL normal saline every 4 to 6 hours via nebulization). Beta- adrenergic agonists are indicated primarily for acute exacerbations rather than for long-term use. b. Anticholinergics such as ipratropium bromide (Atrovent, two puffs every 4 to 6 hours) can also be used in the perioperative period, especially if the patient has significant pulmonary secretions. c. Patients with severe asthma or COPD may benefit from parenteral steroid therapy (methylprednisolone, 50 to 250 mg IV every 4 to 6 hours) as well as inhaled steroids (beclomethasone metered- dose inhaler, two puffs four times a day), but steroids require 6 to 12 hours to take effect. IV. RENAL COMPLICATIONS A. Oliguria is defined as urine output of less than 0.5 mL/kg/hr. The most common early perioperative cause of oliguria is hypovolemia from underresuscitation or bleeding. Other important considerations include  preoperative renal dysfunction, home diuretic use, and perioperative urinary retention due to general anesthesia. Initial evaluation should include serum electrolytes, hematocrit/hemoglobin level, and a bladder ultrasound to assess for urinary retention. Persistent oliguria necessitates Foley catheter placement. For patients with normal cardiac and renal function, a fluid challenge with 0.5 to 1 L of crystalloid IV can be diagnostic and therapeutic for hypovolemia. B. Urinary Retention. Perioperative patients are at risk for acute urinary retention. Urinary retention can present as failure to void or with acute pain due to an overdistended bladder. In the perioperative patient, failure to void within 6 hours should prompt a workup for oliguria as described above, including a bladder ultrasound. Patients with subjective symptoms of bladder distension or patients with greater than 500 mL of urine on bladder ultrasound should undergo catheterization. An initial trial of bladder decompression with immediate removal of the catheter (“straight cath”) is reasonable, although others advocate for a short duration (24 hours) of bladder decompression with an indwelling Foley catheter. Treatment with alpha-blockade (tamsulosin 0.4 mg daily) may decrease the probability of a second episode of urinary retention (Rev Urol. 2005;7 Suppl 8:S26–S33). C. Acute Kidney Injury (AKI) 1. Presentation: AKI is defined by an increase in serum creatine level by 0.3 mg/dL or 1.5-fold above baseline in the setting of oliguria. The etiologies of AKI can be classified as prerenal, intrinsic renal, and postrenal (Table 3-1). a. Prerenal azotemia results from decreased renal perfusion that might be secondary to hypotension, intravascular volume contraction, or decreased effective renal perfusion. b. Intrinsic renal causes include drug-induced acute tubular necrosis, pigment-induced renal injury, radiocontrast dye administration, acute interstitial nephritis, rhabdomyolysis, and prolonged ischemia from suprarenal aortic cross-clamping. TABLE 3-1 Laboratory Evaluation of Oliguria and Acute Renal Failure  c. Postrenal causes can result from obstruction of the ureters or bladder. Operations that involve dissection near the ureters, such as colectomy, colostomy closure, or total abdominal hysterectomy, have a higher incidence of ureteral injuries. In addition to ureteral injuries or obstruction, obstruction of the bladder from mechanical (enlarged prostate, obstructed urinary catheter) or functional (narcotics, anticholinergics) means can contribute to postrenal AKI. 2. Evaluation. Urinalysis with microscopy and culture (as indicated) can help in differentiating between etiologies of AKI. Additionally, urinary indices including fractional excretion of sodium (FENa), renal failure index, and fractional extraction of urea (FEUr) help to classify AKI into the above listed categories. In the setting of diuretic administration, FEUr is favored over FENa. Renal ultrasonography can be used to exclude obstructive uropathy, assess the chronicity of renal disease, and evaluate the renal vasculature with Doppler ultrasonography. Radiologic studies using IV contrast are contraindicated in patients with suspected AKI due to potential exacerbation of renal injury. 3. Treatment: a. Prerenal. In most surgical patients, oliguria is caused by hypovolemia. Initial management includes a fluid challenge (i.e., a normal saline bolus of 500 mL). Patients felt to be adequately resuscitated and/or patients with underlying CHF may benefit from invasive monitoring and optimization of cardiac function.  b. Intrinsic renal. Treat the underlying cause, if possible, manage volume status, and avoid nephrotoxic agents. c. Postrenal. Ureteral injuries or obstruction can be treated with percutaneous nephrostomy tubes and generally are managed in consultation with a urologist. Urinary retention and urethral obstruction can be managed with a Foley catheter or, if necessary, a suprapubic catheter. d. In all cases, careful attention to intravascular volume is paramount. Patients should be weighed daily and have carefully recorded intakes and outputs. Hyperkalemia, metabolic acidosis, and hyperphosphatemia are common problems in patients with AKI and should be managed as discussed in Chapter 4. Medication doses should be adjusted appropriately and potassium removed from maintenance IV fluids. e. Dialysis. Indications for dialysis include intravascular volume overload, electrolyte abnormalities (especially hyperkalemia), metabolic acidosis, and complications of uremia (encephalopathy, pericarditis). V. GASTROINTESTINAL COMPLICATIONS A. Postoperative Nausea and Vomiting 1. Presentation. On postoperative days 0 to 1, postanesthesia nausea can affect up to 30% of patients (Anesthesiology. 1992;77:162). Other common causes of nausea in the early perioperative period include medication side effects (especially from opiate analgesics), perioperative gastroparesis, and paralytic ileus. Patients who have undergone extensive intra-abdominal procedures and are more than 24 hours out from anesthesia should be evaluated for the underlying causes of nausea before administration of antiemetics. Up to 20% of these patients will suffer an ileus requiring nasogastric decompression (Dis Colon Rectum. 2000;43:61). 2. Treatment. Aggressive management with antiemetics can be employed. Multimodal therapy with ondansetron, promethazine, prochlorperazine, scopolamine, and dexamethasone can be required. B. Postoperative Paralytic Ileus 1. Presentation. Paralytic ileus typically presents with obstipation,  persistent nausea despite antiemetic use, intolerance of oral diet, belching, and abdominal distension/discomfort. 2. Differential diagnosis: bowel obstruction, constipation, Ogilvie syndrome, intra-abdominal infection, and retroperitoneal bleeding. 3. Evaluation. Upright and lateral decubitus radiographs of the abdomen should be obtained to evaluate for dilated stomach and loops of bowel. Air should be seen in the colon, thus helping to differentiate from bowel obstruction. When this imaging is insufficient to rule out obstruction, abdominal CT with oral contrast is both sensitive and specific (90% to 100%), though is less reliable for partial versus complete small bowel obstructions. If the diagnosis remains uncertain, an upper gastrointestinal study with water-soluble contrast material may be necessary. 4. Treatment. Patients with an ileus should be made NPO and started on IVF. Strong consideration should be made for placing a decompressive nasogastric tube, even in the absence of emesis or gastric distension on plain film. A patient with an NG tube in place who complains of nausea should have the NG tube manipulated until functioning properly. This may even require replacement with a larger-bore NG tube. Deficiencies of potassium and magnesium as well as excess opioids can prolong ileus. Since the etiology is nonmechanical, patience must then be employed as one awaits return of bowel function. Should the ileus persist beyond 7 days, a TPN consultation should be placed. VI. INFECTIOUS COMPLICATIONS A. Diagnostic Considerations. Infection can manifest with obvious signs such as erythema, induration, drainage, necrosis, or tenderness on examination. Infection can also manifest with more subtle symptoms such as chills, malaise, hypothermia, and/or unexplained leukocytosis. While due attention to the multitude of peri- and postoperative infections complications is paramount, it is beyond the scope of this chapter. The discussion below is designed to serve as an initial starting point and will touch briefly on management of specific infectious pathologies. B. Generalized Fever 1. Presentation. In the immunocompetent adult, fever is defined as a  body temperature greater than 38.5°C. Evaluation of fever should take into account the amount of time that has passed since the patient’s most recent operation. a. Intraoperative fever may be secondary to malignant hyperthermia, a transfusion reaction, or a pre-existing infection. b. Fever in the first 24 hours usually occurs as a result of atelectasis. A high fever (>39°C) is commonly the result of a streptococcal or clostridial wound infection, aspiration pneumonitis, or a pre- existing infection. However, fever in this time period can also be seen in trauma or burn patients as a part of an expected inflammatory response. c. Fever that occurs more than 72 hours after surgery has a broad differential diagnosis, including but not limited to the following: wound infection (including fascial or muscle), pneumonia, gastroenteritis, infection colitis (including Clostridium difficile), abscess, peritonitis, UTI, infected prosthetic materials or catheters, deep venous thrombosis (DVT), thrombophlebitis, drug allergy, or devastating neurologic injury. In immunocompromised hosts, viral and fungal infections should also be considered. Transfusion reactions can also be confused for infection due to the presence of fever, though the treatment is vastly different and will not be discussed here. 2. Evaluation. The new onset of fever or leukocytosis without an obvious source of infection requires a thorough history and physical examination, including inspection of all wounds, tubes, and catheter sites, and obtainment of CBC, urinalysis, and CXR. Gram stain/cultures of the blood, sputum, urine, and/or wound should be dictated by the clinical situation. Imaging such as an ultrasound or CT should be chosen based on clinical context, usually to evaluate for a deep space infection in the cavity where surgery was performed. 3. Treatment. Empiric antibiotics may be initiated after collection of cultures, with therapy directed by clinical suspicion, but are not always warranted. Therapy usually begins with broad-spectrum IV antibiotics and narrows as more information is known about the infectious pathogen. C. Surgical Site Infections (SSI) are the second leading cause of nosocomial infections, leading to significant patient care costs, longer  length of hospital stays, and increased rates of readmission. They typically present with erythema, pain, induration, and/or drainage. Fever and leukocytosis may be present. 1. Prevention of SSI begins with appropriate selection of prophylactic antibiotics (Table 3-2). Consideration should be given to the classification of the preoperative field, which places a patient at increased risk for SSI despite antibiotic therapy (Table 3-3). Finally, the Surgical Care Improvement Project (SCIP) is a quality improvement partnership aimed at reducing significant surgical complications and improving surgical outcomes nationally. Of the 2018 SCIP core measurement, 6 of the 11 indicators relate to infection prevention. 2. Treatment is to open the wound to allow drainage, with culture if possible. Parenteral antibiotics are used only if extensive erythema or a deeper infection is present and are not required for superficial infections. Wound infections in the perineum or after bowel surgery are more likely to be caused by enteric pathogens and anaerobes. More aggressive infections involving underlying fascia require operative débridement and broad-spectrum IV antibiotics. Streptococcal wound infections present with severe local erythema and incisional pain. Penicillin G or ampicillin is effective adjuvant treatment. Patients with a severe necrotizing clostridial infection present with tachycardia and signs of systemic illness, pain, and crepitus near the incision. Treatment includes emergent operative débridement and metronidazole (500 mg IV every 6 hours) and clindamycin (600 to 900 mg IV every 8 hours). TABLE 3-2 Recommendations for Antibiotic Prophylaxis Nature of Operation Likely Recommended Adult Pathogens Antibiotics Dose Before Surgerya Cardiac: prosthetic Staphylococci, Vancomycin and 1–1.5 g IV valve and other corynebacteria, Cefazolin 1–3 g IV procedures enteric gram- Vancomycin and 1–1.5 g IV Device insertion negative bacilli Aztreonama 1–2 g IV Cefazolin or 1–3 g IV Vancomycin 1–1.5 g IV Thoracic Staphylococci Cefazolin 1–3 g IV Vancomycina 1–1.5 g IV Vascular: peripheral Staphylococci, Cefazolin 1–3 g IV bypass or aortic streptococci, Vancomycin and 1–1.5 g IV surgery with enteric gram- Aztreonama 1–2 g IV prosthetic graft negative bacilli, clostridia Abdominal wall hernia Staphylococci Cefazolin 1–3 g IV Clindamycina 900 mg IV Orthopedic: total joint Staphylococci Cefazolin +/− 1–3 g IV replacement or Vancomycin 1–1.5 g IV internal fixation of Vancomycin and 1–1.5 g IV fractures Aztreonama 1–2 g IV Gastrointestinal Upper GI and Enteric gram- Cefotetan 1–2 g IV hepatobiliary negative bacilli, Cefoxitin 1–2 g IV enterococci, Clindamycin and 900 mg IV clostridia Gentamicina 5 mg/kg Ciprofloxacin IV and 400 mg IV Metronidazolea 500 mg IV Colorectal Enteric gram- Cefoxitin 1–2 g IV negative bacilli, Cefotetan 1–2 g IV anaerobes, Ertapenem 1 g IV enterococci Cefazolin and 1–3 g IV Metronidazolea 500 mg IV Appendectomy (no Enteric gram- Cefoxitin 1–2 g IV perforation) negative bacilli, Cefotetan 1–2 g IV  anaerobes, Ciprofloxacin 400 mg IV enterococci and 500 mg IV Metronidazolea Obstetrics/gynecology Enteric gram- Cefotetan 1–2 g IV negative bacilli, Cefoxitin 1–2 g IV anaerobes, Cefazolin 1–3 g IV group B Clindamycin and 900 mg IV streptococci, Gentamicina 1.5–5 enterococci mg/kg IV aIndicated for patients with penicillin/cephalosporin allergy. For vancomycin, dose of 1 g is recommended for patients 250 IU/L aminotransferase Initial 48 hr Hematocrit >10% decrease Blood urea nitrogen >5 mg/dL elevation Serum calcium 6 L sequestration Mortality Number of Ranson Approximate Mortality (%) Signs 0–2 0 3–4 15 5–6 50 >6 70–90 TABLE 23-2 CT Severity Grading Index (CTSI) Scoring Based on Imaging Characteristics Scoring for pancreatic necrosis 0 Points No pancreatic necrosis 2 Points ≤30% pancreatic necrosis 4 Points >30% necrosis Evaluation of pancreatic morphology, not including necrosis 0 Points (grade A) Normal pancreas 2 Points (grade B/C) Focal or diffuse enlargement of the gland, including contour irregularities and inhomogeneous attenuation with or without peripancreatic inflammation 4 Points (grade D/E) Pancreatic or peripancreatic fluid collection or peripancreatic fat necrosis Additional 2 points Extra pancreatic complications including one or more of the following: pleural effusion, ascites, vascular complications, parenchymal complications, or gastrointestinal tract involvement 3. The Acute Physiology and Chronic Health Evaluation (APACHE) II, using a total of 14 variables, can be calculated at admission and updated daily to allow continual reassessment. More recently, the APACHE IV score, using 52 variables, has also been validated in acute pancreatitis with a score >44 predicting mortality in 100% of cases (Pancreas. 2015;44(8):1314–1319). However, these scores are somewhat cumbersome and difficult to calculate that limits their everyday use. TABLE 23-3 Prognosis Based on CTSI Score Index Predicted Predicted Mortality (%) Morbidity (%) 0–3 8 3 4–6 35 6 7–10 92 17 4. Multiple Organ Dysfunction Score (MODS) and Sequential Organ Failure Assessment (SOFA) have been shown to be important predictors of disease severity in critically ill patients and have been extended to patients with severe acute pancreatitis and are predictive of mortality and development of complications (Br J Surg. 2009;96(2):137–150). 5. Bedside Index for Severity in Acute Pancreatitis (BISAP) is a validated 5-point scoring system assigning a point for presence of serum BUN >25 mg/dL, impaired mental status, systemic inflammatory response syndrome (SIRS), age >60 years, or presence of pleural effusion within the first 24 hours. Observed mortality was 90%) test for the diagnosis of chronic pancreatitis (Gastrointest Endosc. 2003;57:37–40). c. Pancreatic endocrine function. Fasting and 2-hour postprandial blood glucose levels or glucose tolerance tests may be abnormal in 14% to 65% of patients with early chronic pancreatitis and in up to 90% of patients when calcifications are present. Serum trypsinogen levels correlate with residual acinar cell mass and levels 50% direct-reacting bilirubin. b. Elevated alkaline phosphatase. c. Prolonged obstruction may lead to mild increase in AST and ALT. (a, b, and c are seen with biliary obstruction) d. Tumor markers. Serum CA19-9 is often elevated (>37 U/mL) in patients with pancreatic cancer but may be falsely elevated in cases of nonmalignant biliary obstruction. Approximately 15% of patients with pancreatic cancer will demonstrate normal CA19-9 levels (≤37 U/mL) and low levels (5 ng/mL) in 40% to 50% of patients with pancreas cancer. 3. Radiologic studies a. CT imaging should be a fine-cut (≤3 mm slices), “pancreatic protocol CT” including two contrast phases (arterial and venous) to allow for assessment of the relationship of the mass to vascular structures as this is crucial to determine resectability. Pancreatic cancer on CT usually appears as a hypoattenuating mass that distorts the normal architecture of the gland, often paired with findings of a dilated pancreatic and biliary ductal system (the so- called “double-duct” sign). Preoperative assessment of tumor resectability using the National Comprehensive Center Network (NCCN) guidelines classifies pancreatic adenocarcinoma into  three categories (Table 23-4): (1) Resectable. No distant metastases; no arterial tumor contact (celiac axis [CA], common hepatic artery [CHA], and SMA); no tumor contact with the SMV or portal vein (PV); ≤180- degree contact with vein contour irregularity. (2) Borderline resectable. No distant metastases; solid tumor arterial contact without extension to CA or CHA allowing for complete resection and reconstruction; tumor contact with the CA or SMA ≤180 degrees; tumor contact with the CA >180 degrees without aortic involvement and an uninvolved GDA (permitting modified Appleby procedure), tumor contact with variant arterial anatomy (as it effects surgical planning); solid tumor contact with the SMV or PV >180 degrees; contact ≤180 degrees with contour irregularity of the vein or thrombosis but amenable to complete vein resection and reconstruction; solid tumor contact with the IVC. (3) Unresectable. Distant metastases (including nonregional lymph nodes) or solid tumor contact of the CA or SMA >180 degrees; unreconstructable SMV/PV due to tumor involvement or occlusion (bland or tumor thrombus); tumor contact with the most proximal draining jejunal branch of the SMV (for head/uncinate lesions). b. EUS and ERCP, especially the former, play an important role in patients in whom a mass is not seen on CT, obtaining tissue diagnosis when necessary (e.g., to determine candidacy for neoadjuvant therapy or when the diagnosis is in doubt). In addition, ERCP can be performed for drainage of biliary obstruction. Preoperative stenting in patients suitable for surgery at the time of presentation is controversial as it has been associated with an increase in postoperative complications (NEJM. 2010;362(2):129–137). However, it is advisable in patients whose bilirubin is very high and in those whose surgery will be delayed due to neoadjuvant therapy or treatment of comorbidities. c. MRI and MRCP can provide information similar to that in conventional CT. d. Staging laparoscopy is used sparingly in cancer of the head of the  pancreas where palliative operations are useful. A high suspicion for metastatic disease would be an indication (e.g., high CA19-9). It is advisable for cancers of the distal pancreas where peritoneal metastases are common and surgical palliation is not performed. E. Treatment 1. Resection a. PD (Whipple procedure) consists of en bloc resection of the head of the pancreas, distal common bile duct, duodenum, jejunum, and gastric antrum. Pylorus-sparing PD has been advocated by some, but there are no data demonstrating improved survival or lower morbidity (Cochrane Database Syst Rev. 2011;(5):CD006053). There has been a sharp decline in morbidity and mortality in specialized centers, with a 30-day mortality of less than 3%. TABLE 23-4 NCCN 2019 Imaging Criteria for Resectability of Pancreatic Adenocarcinoma  b. Distal pancreatectomy. The procedure of choice for lesions of the body and tail of the pancreas is distal pancreatectomy. Distal pancreatectomy consists of resection of the pancreas, generally at the SMV laterally to include the spleen. We have described a technique that provides a more radical resection with improved R0 resection rates, the radical antegrade modular pancreatosplenectomy (RAMPS), when compared to traditional series, which is the procedure of choice for malignant tumors of the distal pancreas at our institution (J Hepatobiliary Pancreat Sci. 2016;23(7):432–441). c. Minimally invasive pancreatectomy is emerging as a feasible strategy for patients with overall survival, rate of R0 resection, and adjuvant therapy being similar to open procedures in a large meta-analysis (Eur J Surg Oncol. 2019;45(5):719–727). 2. Postoperative considerations. Delayed gastric emptying, pancreatic fistula, and wound infection are the three most common complications of PD. a. Delayed gastric emptying (20%) almost always subsides with conservative treatment. b. Pancreatic fistula (20%) may be reduced by meticulous attention to the blood supply of the pancreaticoenteric duct-to-mucosa anastomosis (J Am Coll Surg. 2002;194:746). Most surgeons routinely place abdominal drains, with a recent Cochrane Review citing modest-quality evidence that routine drain placement may slightly reduce 90-day mortality (Cochrane Database Syst Rev. 2018;6:CD010583). c. Surgical site infection (10% to 15%). d. Superficial incisional infection (192 ng/mL) and high amylase levels (suggestive of MPD communication) are consistent with mucinous neoplasm of the pancreas. Cytology, DNA molecular analysis (high-amplitude  KRAS mutation), and elevated CA19-9 levels in the cyst fluid may be suggestive of malignant transformation. 3. Treatment. Surgery should be strongly considered in the medically fit patient with any “high-risk stigmata,” cytology suggestive of malignancy, or symptoms related to pancreatic mass (pancreatitis, pain, obstructive jaundice). In the absence of these features, management per consensus guidelines is determined by IPMN subtype. When indicated, standard oncologic resection (PD or distal pancreatectomy) with lymph node dissection should be performed. The use of intraoperative frozen section is recommended to confirm the resection margin is free of high-grade dysplasia or invasive carcinoma, although the presence of low-grade dysplasia at the margin does not require further intervention (Surgery. 2011; 149(1):79–86). a. Main duct IPMN carries a high incidence of malignancy with >70% having high-grade dysplasia or invasive carcinoma in a large retrospective study and warrants resection in selected medically fit patients (Ann Surg. 2015;261(5):976–983). While MPD dilation >10 mm is a clear indication for pancreatectomy, surgical resection for MPD dilation of 5 to 9 mm remains controversial but should be considered in young, healthy patients with life expectancy >10 years. Surgery should remove all tumor, and intraoperative frozen section is recommended to confirm that the resection margin is free of high-grade dysplasia or invasive carcinoma, although the presence of low-grade dysplasia at the margin does not require further intervention (Surgery. 2011;149(1):79–86). b. Side branch IPMNs are less likely to evolve to invasive disease and management by current consensus guidelines indicates resection be considered for cysts >3 cm, mural nodules >5 mm, symptomatic patients, and cytology concerning for malignancy. Lesions without these findings may undergo routine surveillance imaging. c. Mixed IPMNs have similar malignant risk and surgical management as main duct IPMN. D. Mucinous Cystic Neoplasms (MCNs) 1. Epidemiology. MCNs are considered premalignant lesions that  account for approximately 25% of all resected cystic pancreatic neoplasms. They are most commonly located in the pancreatic body or tail and occur almost exclusively in middle age women. Most are asymptomatic and identified incidentally. 2. Diagnosis. MCNs are mucin-producing cystic lesions that do not communicate with the pancreatic ductal system. Histologically, they have a columnar epithelium lining with an ovarian-type stroma. Cyst fluid analysis reveals viscous fluid with an elevated CEA level (>192 IU) and low amylase levels. 3. Treatment. MCNs undergo an adenoma–adenocarcinoma sequence of evolution and invasive cancer is present in 17.5% of resected MCN. Malignancy is associated with larger size (>4 cm) and advanced age (>55). Five-year survival was 100% for noninvasive MCN and 57% for patients with malignant lesions (Ann Surg. 2008;247(4):571–579). As there is a clear survival advantage for those patients who undergo resection prior to the development of invasive cancer, pancreatectomy is recommended for all patients with MCN. E. Serous Cystadenoma (SCA) 1. Epidemiology. SCAs are benign lesions that account for 16% of all resected cystic neoplasms. They are most commonly located in the pancreatic head, and the majority (75%) is diagnosed in women, usually in the fifth or sixth decade of life. Symptoms correlate with size (>4 cm); however, most lesions are asymptomatic. 2. Diagnosis. Lesions are characterized by an epithelial lining and are microcystic (“honeycomb” appearance) with a calcified central scar present in 30% of lesions on imaging studies. Cyst fluid analysis reveals nonviscous fluid with low CEA (5 years) and remains the treatment of choice in patients with platelets less the 30,000/mm3 or with a high risk of bleeding (Fig.24-2). Most patients will achieve a response to splenectomy within 10 days postoperatively (Am J Surg. 2004;187:720–723). Alternatives to splenectomy include Rituximab (anti-CD20 monoclonal antibody) and thrombopoietin receptor agonists which have shown efficacy as second-line agents (Blood. 2012;120:960–969). When the short- and long-term outcomes after laparoscopic splenectomy are assessed in patients with ITP, the conversion rate to open surgery was 5.6%, and the immediate nonresponder rate was 8.2%. However, in these patients, a clinical response was achieved in 72% of the patients on 5-year long-term follow-up (Am J Hematol. 2009;84:743–748). Urgent splenectomy, in conjunction with aggressive medical therapy, may play a role in the rare circumstance of severe, life-threatening bleeding in both children and adults with ITP. FIGURE 24-2 Simplified approach to the treatment of patients with ITP. Clinical symptoms and patients’ concerns must be taken into account, and the decision for which management modality to use first (splenectomy, rituximab, or a thrombopoietin receptor agonist) is determined by patient and physician preference. The treatment of serious bleeding also requires additional therapy including platelet transfusions. ITP, idiopathic thrombocytopenia purpura; IVIG, intravenous immune globulin; TPO, thrombopoietin receptor agonist. b. Thrombotic thrombocytopenic purpura (TTP) is a serious systemic disease resulting in the pentad of thrombocytopenia, microangiopathic hemolytic anemia, altered mental status, renal failure, and fever. It is a result of decreased ADAMT13, a protease responsible for cleaving von Willebrand factor, leading to platelet aggregation and thrombosis of the microvasculature. TTP may be distinguished from autoimmune causes of thrombocytopenia, such as Evans syndrome (ITP and autoimmune hemolytic anemia) or systemic lupus erythematosus, by a negative result on Coombs test. It is more common in adults and is usually idiopathic or drug related (e.g., cyclosporine, gemcitabine, clopidogrel, quinine). First-line TTP treatment includes plasmapheresis, which improves initial response and 6-month survival compared with plasma infusion (N Engl J Med. 1991;325:393–397). Steroid therapy in addition to plasmapheresis is used in the treatment of relapse. Second-line agents include rituximab, cyclosporine, and increased frequency of plasmapheresis. Plasma exchange consists of the daily removal of a single volume of the patient’s plasma and its replacement with fresh-frozen plasma until the thrombocytopenia, anemia, and associated symptoms are corrected. Therapy is then tapered over 1 to 2 weeks. Splenectomy plays a key role for patients who experience relapse or who require multiple plasma exchanges to control symptoms, and it is generally well tolerated without significant morbidity. Furthermore, splenectomy has only shown benefit when used in conjunction with plasmapheresis in order to achieve durable remission (Br J Haematol. 2005;130:768–776). 4. Myeloproliferative and myelodysplastic disorders a. Chronic myelogenous leukemia (CML) is a myelodysplastic disorder of the primitive pluripotent stem cells in the bone marrow that results in a significant increase in erythroid, megakaryocytic,  and pluripotent progenitors in the peripheral blood smear. Genetically it is characterized by the bcr–abl fusion oncogene, known as the Philadelphia chromosome. This oncogene results in a constitutively active tyrosine kinase, and thus first-line therapy utilizes the tyrosine kinase inhibitor (TKI) imatinib mesylate (Gleevec). Alternative TKI treatments (dasatinib and nilotinib) are used in cases of intolerance or suboptimal response. Stem cell transplantation is used for cases of treatment failure in eligible patients (Blood. 2006;108:1809–1820). In the management of CML, early splenectomy has no effect on disease progression or overall survival, however, it increased the rate of thromboembolic events and vascular accidents (Cancer. 1984;54;333–338). Splenectomy is indicated only for palliation of symptomatic splenomegaly (pain control, early satiety, etc.) or hypersplenism that significantly limits therapy. b. Polycythemia vera is a clonal, chronic, progressive myeloproliferative disorder characterized by an increase in RBC mass, leukocytosis, thrombocytosis, and splenomegaly. Physical findings include ruddy cyanosis, hepatomegaly, splenomegaly, and hypertension. Treatment ranges from phlebotomy and aspirin administration to the use of chemotherapeutic agents. Splenectomy is not helpful in the early stages and is most useful with late-stage disease when patients have developed severe splenomegaly-related symptoms. Splenectomy can result in severe thrombocytosis, causing thrombosis or hemorrhage, which requires perioperative antiplatelet, anticoagulation, and myelosuppressive treatment. c. Myelofibrosis is a chronic, malignant hematologic disease associated with bone marrow fibrosis, extramedullary hematopoiesis, splenomegaly, and the presence of RBC and white blood cell (WBC) progenitors in the bloodstream. Asymptomatic patients are closely followed, whereas symptomatic patients undergo therapeutic intervention targeted to their symptoms. Allogeneic bone marrow transplantation in younger, high-risk patients is the only curative treatment. Supportive therapy for clinically symptomatic anemia includes steroids, danazol, erythropoietin, or blood transfusion (Clin Adv Hematol Oncol.  2008;6:278,281–282). Splenomegaly-related symptoms are best palliated with splenectomy, but the cytopenias frequently recur. In addition, these patients are at increased risk for postoperative hemorrhage and thrombotic complications after splenectomy. 5. Lymphoproliferative disorders a. Non-Hodgkin lymphoma (NHL) includes a wide range of disorders ranging from indolent to highly aggressive and includes a variety of clinical presentations. Splenomegaly exists in some forms. As with other malignant processes, splenectomy is indicated for palliation of hypersplenism and cytopenias or for diagnosis in patients with suspected persistent or recurrent disease after systemic therapy. Splenectomy plays an important role in the diagnosis and staging of patients with isolated splenic lymphoma. In these cases, improved survival has been shown in patients undergoing splenectomy. b. Hairy cell leukemia is an uncommon blood disorder, representing only 2% of all adult leukemias, and is characterized by splenomegaly, pancytopenia, and large numbers of abnormal lymphocytes in the bone marrow. The lymphocytes have cytoplasmic projections which can be identified on peripheral smear. Splenectomy does not correct the underlying disorder, but cell counts do return to normal with some alleviation of symptoms as well. Splenectomy was previously regarded as the primary therapy for this disease, but improvements in systemic chemotherapy (e.g., rituximab, pentostatin, cladribine) have reduced the role of splenectomy, which is reserved only for refractory disease. c. Hodgkin lymphoma historically had required splenectomy for diagnostic staging. However, due to refinements in imaging techniques and progress in the methods of treatment, splenectomy for Hodgkin lymphoma is rare. Indications for surgery are similar to those for NHL. d. Chronic lymphocytic leukemia (CLL), a B-cell leukemia, is the most common of the chronic leukemias and is characterized by the accumulation of mature but nonfunctional lymphocytes. Primary therapy is medical, with palliative splenectomy reserved for those patients with symptomatic splenomegaly to improve  cytopenias and severe hypersplenism. 6. Neutropenia a. Felty syndrome involves the triad of rheumatoid arthritis, splenomegaly, and neutropenia. It exists in approximately 3% of all patients with rheumatoid arthritis, two-thirds of whom are women. The size of the spleen varies from nonpalpable to massively enlarged. The primary treatment is corticosteroids, but refractory cases may require splenectomy to reverse the neutropenia. After splenectomy, >80% of patients show a durable increase in WBC count. Besides symptomatic neutropenia, other indications for splenectomy include transfusion-dependent anemia and profound thrombocytopenia. 7. Nonhematologic conditions a. Trauma is the most common indication for splenectomy. In the unstable trauma patient, the procedure is traditionally performed via laparotomy. With current imaging modalities, grading of splenic injuries allows for conservative management in selected patients (J Trauma. 2008;207(5):646–655). b. Incidental splenectomy occurs when the spleen is iatrogenically injured during an intra-abdominal procedure. Injury may result from a retractor placed in the left upper quadrant or during mobilization of the splenic flexure. Small injuries such as capsular tears may be controlled with hemostatic agents or electrocautery, but injuries resulting in significant blood loss may require splenectomy to achieve rapid hemostasis. c. Wandering spleen is an uncommon abnormality in which the spleen floats inside the abdominal cavity due to anomaly of embryogenesis. The wandering spleen is not normally attached to adjacent viscera in the splenic fossa which may lead to splenic torsion and infarction. Splenectomy or splenopexy is indicated. d. Splenic artery aneurysm is the most common visceral artery aneurysm and is typically an incidental finding. It occurs more commonly in females and is associated with a high incidence of rupture during pregnancy with significant maternal and fetal mortality. Indications for intervention include aneurysm size ≥2 cm, females of child-bearing age who may become pregnant, and  inflammatory pseudoaneurysms. e. Primary infections of the spleen are infrequent. Parasitic infections account for more than two-thirds of splenic cysts worldwide but are rare in the United States. The majority are hydatid cysts caused by Echinococcus species. They are typically asymptomatic but may rupture or cause symptoms due to splenomegaly. The primary treatment is splenectomy, with careful attention not to spill the cyst contents. The cyst may be aspirated and injected with hypertonic saline prior to mobilization if concern about rupture exists. f. Splenic abscesses are rare, but potentially lethal if not accurately diagnosed and treated. Two-thirds arise from seeding of the spleen by a distant site, most commonly endocarditis and urinary tract infections. Abdominal CT and/or ultrasound (US) imaging are the diagnostic modalities of choice. CT images reveal a low intensity lesion that does not enhance with contrast. The most common organisms are aerobic microbes (Streptococci, Escherichia coli), but other microorganisms have also been isolated (Mycobacterium tuberculosis, Salmonella typhi). Treatment includes broad- spectrum antibiotics for 14 days. Splenectomy is the operation of choice, but percutaneous and open drainage are options for patients who cannot tolerate splenectomy. g. Cystic lesion of the spleen may be either true cysts or pseudocysts, but this differentiation is difficult to make preoperatively. True cysts (or primary cysts) have an epithelial lining and are most often congenital. Rare true cysts include epidermoid and dermoid cysts. Pseudocysts (or secondary cysts) lack an epithelial lining and make up more than two-thirds of nonparasitic cysts. They typically result from traumatic injury and will resorb. Treatment of splenic cysts depends on the size of the lesion and associated symptoms. Most are typically asymptomatic, but they may present with left upper abdominal or shoulder pain. If smaller than 5 cm, the cysts can be followed with US and often resolve spontaneously. Larger cysts risk rupture and require cyst unroofing or splenectomy. Percutaneous aspiration is associated with infection and recurrence and therefore not indicated. Laparoscopic management of splenic cysts yields shorter hospital  length of stay and fewer complications with no adverse effects (Surg Endosc. 2007;21:206–208). h. Tumors and metastasis. Sarcoma is the most common primary tumor of spleen. Most metastases to the spleen are carcinomas, commonly lung cancer. If isolated splenic metastasis is confirmed, a laparoscopic splenectomy with intact spleen retrieval should be considered. B. Preoperative Preparation for Splenectomy 1. Imaging: CT or MRI may be required in patients with concern for malignancy or clinical splenomegaly to accurately estimate splenic size and evaluate for hilar adenopathy that may complicate a laparoscopic approach. Right upper quadrant US is indicated for preoperative assessment of gallstone disease in patients with hemolytic or sickle cell anemias for planning of possible concomitant cholecystectomy. 2. Vaccination: Infection is the most common complication after splenectomy, and vaccination for encapsulated organisms is the mainstay of preventive therapy. Asplenic patients are at higher risk of infection caused by Streptococcus pneumoniae, Haemophilus influenzae type b, Neisseria meningitidis (J Clin Pathol. 2001;54(3):214–218). 3. Transfusions: Patients with hematologic disease, particularly those with autoimmune disorders, often have autoantibodies and are difficult to cross-match. Thus, blood should be typed and screened at least 24 hours prior to surgery, and patients with splenomegaly should have 2 to 4 units of packed RBCs cross-matched and available for surgery. Patients with severe thrombocytopenia (particularly those with counts 30 cm) Moderate splenomegaly (>23 cm) Portal hypertension Severe, uncorrectable cytopenia Splenic trauma (unstable patient) Splenic vein thrombosis Splenic trauma (stable patient) Bulky hilar adenopathy Morbid obesity Pregnancy Extensive previous surgeries 3. Robotic splenectomy offers a unique three-dimensional visualization. The overall outcomes of robotic approach are very similar to standard laparoscopy, although not as cost effective. 4. Partial splenectomy is indicated to minimize the risk of postsplenectomy sepsis in children, in lipid storage disorders with splenomegaly (Gaucher disease), and certain cases of blunt and penetrating splenic trauma. Both open and laparoscopic approaches have been well described. The spleen must be adequately mobilized, and the splenic hilar vessels attached to the targeted segment should be ligated and divided, with the spleen then transected along the devascularized line of demarcation. D. Splenectomy Complications 1. Intraoperative complications a. Hemorrhage is the most common intraoperative complication (open: 2% to 3%, laparoscopic: 5%) of splenectomy, which can  occur during the hilar dissection or from a capsular tear during retraction. Bleeding during laparoscopic splenectomy may necessitate conversion to a hand-assisted or open approach. Strong consideration should be given to splenorrhaphy in minor injuries. Overall, the patient’s hemodynamic condition is the primary determinant of whether splenic salvage can be attempted. b. Pancreatic injury occurs in up to 6% of splenectomies, whether open or laparoscopic. A retrospective review of one center’s experience with laparoscopic splenectomy found pancreatic injury in 16% of patients, of which half were simply isolated instances of hyperamylasemia (J Surg. 1996;172(5):596–599). If pancreatic parenchymal injury is suspected during laparoscopic splenectomy, a closed suction drain should be placed adjacent to the pancreas, and a drain amylase obtained prior to removal after the patient is eating a regular diet. c. Colonic injuries. Due to the close proximity of the splenic flexure to the lower pole of the spleen, it is possible to injure the colon during mobilization, but it is rare. Mechanical bowel preparation is not indicated preoperatively. Identification and primary repair are appropriate. d. Gastric injuries can occur by direct trauma or can result from thermal injury during division of the short gastric vessels. Use of energy devices too close to the greater curvature of the stomach can result in a delayed gastric perforation. High index of suspicion and low threshold to oversew any areas of concern is warranted. e. Diaphragmatic injury has been described during the mobilization of the superior splenic pole, especially with perisplenitis, and is of no consequence if recognized and repaired. In laparoscopic splenectomies, careful dissection of the splenophrenic ligament can minimize its occurrence. The pleural space should be evacuated under positive-pressure ventilation prior to closure to minimize the pneumothorax. 2. Early postoperative complications a. Pulmonary complications develop in nearly 10% of patients after open splenectomy, and these range from atelectasis to pneumonia and pleural effusion which are significantly less common with the laparoscopic approach (Surgery. 2003;134:647–653).  b. Subphrenic abscess occurs in 2% to 3% of patients after open splenectomy but is uncommon after laparoscopic splenectomy (0.7%). Treatment usually consists of percutaneous drainage and IV antibiotics. c. Ileus can occur after open splenectomy, but a prolonged postoperative ileus should prompt the surgeon to search for concomitant problems such as a subphrenic abscess or PVT. d. Wound problems such as hematomas, seromas, and wound infections are common after open splenectomy (4% to 5%). Splenectomy utilizing minimally invasive techniques is associated with wound complications that are usually minor and less frequent (1% to 2%). e. Thrombocytosis and thrombotic complications can occur after either open or laparoscopic splenectomy. The presumed causes of thrombosis after splenectomy may relate to the occurrence of thrombocytosis, alterations in platelet function, and a low- flow/stasis phenomenon in the ligated splenic vein. As a result, splenomegaly is a major risk factor for splenic/PVT. Symptomatic PVT occurs more commonly than expected (8% to 12.5%) and can result in extensive mesenteric thrombosis if not recognized promptly and treated expeditiously (Surg Endosc. 2004;18:1140– 1143). 3. Late postoperative complications a. Overwhelming postsplenectomy infection (OPSI) can occur at any point in an asplenic or hyposplenic patient’s lifetime. The estimated mortality with OPSI averages 0.73/1,000 patient years (Ann Intern Med. 1995;122:187–188). Patients present with nonspecific flu-like symptoms rapidly progressing to fulminant sepsis, consumptive coagulopathy, bacteremia, and ultimately death within 12 to 48 hours. Encapsulated bacteria, especially S. pneumoniae, H. influenzae type B, and N. meningitidis, are the most commonly involved organisms. Successful treatment of OPSI requires early supportive care and high-dose third- generation cephalosporins. OPSI appears to have a higher incidence in children, particularly below the age of 5. All patients who have had a splenectomy should be vaccinated and educated about the risk of OPSI (Table 24-3).  b. Splenosis is the presence of disseminated intra-abdominal splenic tissue, which usually occurs after splenic rupture. Care should be taken during splenic morcellation to avoid bag rupture and spillage of splenic tissue. TABLE 24-3 Centers for Disease Control and Prevention Vaccine Recommendations for Asplenic Patients Vaccine Recommendation Tetanus (Td/Tdap) One dose every 10 yr Human papillomavirus Three doses for women through age 26 years (0, 2, 6 months) Measles, mumps, rubella One or two doses Varicella Two doses (0, 4–8 weeks) Zoster One dose Influenza One dose annually Pneumococcal polysaccharide One or two doses Hepatitis A Two doses (0, 6–12 months or 0, 6–18 months) Hepatitis B Three doses (0, 1–2 months, 4–6 months) Meningococcal One dose E. Antibiotics and the Asplenic Patient. Early antibiotic therapy for the asplenic patient can be considered in three contexts: deliberate therapy for established or presumed infections, prophylaxis in anticipation of invasive procedures (e.g., dental procedures), and general prophylaxis. Daily prophylactic antibiotics (oral penicillin) have been recommended after operation in all children younger than 5 years and in immunocompromised patients because these patients are unlikely to produce adequate antibodies in response to pneumococcal vaccination. Some also advocate continuation of prophylactic antibiotics into at least young adulthood, though this is not as widely practiced. CHAPTER 24: