NMS. Surgery

Bruce E. Jarrell, MD President University of Maryland, Baltimore Baltimore, Maryland Eric D. Strauch, MD Associate Professor of Surgery Clerkship Director, Medical Student Rotation in Surgery University of Maryland School of Medicine Baltimore, Maryland Stephen M. Kavic, MD Professor of Surgery Program Director, Residency in Surgery University of Maryland School of Medicine Baltimore, Maryland

Acquisitions Editor: Matt Hauber Senior Development Editor: Stacey Sebring Marketing Manager: Michael McMahon Production Project Manager: Barton Dudlick Design Coordinator: Stephen Druding

Editorial Coordinator: Michael Jeffrey Cohen Manufacturing Coordinator: Margie Orzech Prepress Vendor: Lumina Datamatics Seventh Edition Copyright ©2022 Wolters Kluwer Library of Congress Cataloging-in-Publication Data Names: Jarrell, Bruce E, editor. | Strauch, Eric D., editor. | Kavic, Stephen M. (Stephen Michael) editor. Title: NMS surgery / [edited by] Bruce E Jarrell, l, MD, President, University of Maryland, Baltimore, Baltimore, Maryland, Eric Strauch, M.D., Associate Professor of Surgery, Clerkship Director, Medical Student Rotation in Surgery, University of Maryland School of Medicine, Baltimore, Maryland, Stephen Kavic, MD, Professor of Surgery, Program Director, Residency in Surgery, University of Maryland School of Medicine, Baltimore, Maryland. Description: Seventh edition. | Philadelphia : Wolters Kluwer, [2021] | Series: National medical series for independent study | Includes bibliographical references and index. Identifiers: LCCN 2021027576 | ISBN 9781975112882 (hardback) | ISBN 9781975112912 (ebook) Subjects: LCSH: Surgery--Examinations, questions, etc. | Surgery--Outlines, syllabi, etc. | BISAC: MEDICAL / Education & Training Classification: LCC RD37.2 .N58 2021 | DDC 617.0076--dc23 LC record available at https://lccn.loc.gov/2021027576

I. Jarrell, Bruce E., editor. II. Strauch, Eric D., editor. III. Kavic, Stephen M. (Stephen Michael), editor. IV. Title: National medical series surgery. V. Series: National medical series for independent study. [DNLM: 1. Surgical Procedures, Operative—Examination Questions. 2. Surgical Procedures, Operative—Outlines. 3. General Surgery— methods—Examination Questions. 4. General Surgery—methods—Outlines. WO 18.2] RD37.2 617.0076—dc23 2015010501 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 on 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

We thank the many mentors who have advised us each throughout our careers. We are forever indebted to them.

I wish to thank my wife, Leslie, and my wonderful children for all of their support during my career, and for their understanding during the writing of the many editions of NMS Surgery—BEJ. I wish to thank my wife, Cecilia, my fantastic children, Jacob, Julia, Jessica, and Jenna, and my parents for all of their love and support—ES.

Dedicated to my loving wife, Jennifer, and to my lovely daughter, Emily—SMK.

Foreword

It is a tremendous honor for me to introduce the seventh edition of NMS Surgery. I accepted the Chair of Surgery at the University of Maryland School of Medicine only recently, and I have been impressed with the depth and breadth of clinical and academic work in this Department.This book, written almost entirely by the Department’s residents and faculty, continues to play an essential and unique role in educating medical students and refreshing resident knowledge of surgical disease processes. The outline format of the chapters allows for easy access to gain understanding of the basic principles of surgery. This edition has special significance to me, as it is the first time I have been asked to write a foreword. During the past year, I have been fortunate to get to know the faculty and residents who have contributed chapters to this edition. We are fortunate to have our prior Chair of Surgery, Dr. Bruce E. Jarrell, assume the role of President of the University of Maryland, Baltimore. He has continued to lend his guidance and support to the Surgery Department and to this important work. Dr. Eric D. Strauch is our Surgery Clerkship Director for the University of Maryland medical students, and he has remained a fixture here at our institution. Dr. Stephen M. Kavic, as the Program Director at the University of Maryland, continues to spearhead the writing and editing of the chapters in this educational book. As you will see, the contributors of this edition offer unique insight into surgical diseases and practice guidelines. The chapters are presented in a concise way and supplemented with pearls and key takeaways. This easy- to-read-and-understand book can fit in your lab coat pocket, making it accessible during rounding. I am very thankful for the opportunity to lead such a talented group of surgeons at the University of Maryland. I am quite proud to be a part of NMS Surgery and am sure you will find the team has done an excellent job once again with this edition. —Christine Lau, MD, MBA Dr. Robert W. Buxton Professor and Chair Department of Surgery, University of Maryland School of Medicine Surgeon-in-Chief, University of Maryland Medical Center

vi

Preface

Welcome to the seventh edition of NMS Surgery . This book is written primarily for students and residents in general surgery. It is meant to serve as an introduction to the field of surgery, rather than a comprehensive review. In this edition, we have reorganized the overall structure. First and foremost, we reduced the size to fit in a lab coat pocket, so you can carry it with you for quick reference. Accordingly, we pared down some of the text to focus on the essential information. New features to this edition include “Trusted Sources,” which are links to noncommercial websites and other sources of up-to-date details and practice guidelines on relevant topics. We have also aimed to create more alignment with the NMS Surgery Casebook . This involved changing the order of the chapters from the previous edition and adding “Cut to Casebook” cross-references to make it easier to find the appropriate cases to complement the textbook. We have also revised the outline of each chapter to open with highlights, called “Chapter Cuts.” The key points are immediately followed by “Critical Surgical Associations,” which provide triggers for medical students to remember important connections in the surgical thought process. For the tremendous work put into this edition, we thank the individual contributors. Their high-quality and frequently punctual contributions have made our jobs as editors pleasant. We are also grateful to the editorial team at Wolters Kluwer for their guidance and support throughout the process.

—Bruce E. Jarrell, MD —Eric D. Strauch, MD —Stephen M. Kavic, MD

vii

Contributors

Cherif Boutros, MB, ChB Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Jonathan Bromberg, MD, PhD Professor of Surgery University of Maryland School of Medicine Baltimore, MD Brandon Bruns, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Laura S. Buchanan, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Whitney Burrows, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Clint D. Cappiello, MD Assistant Professor of Surgery Johns Hopkins University School of Medicine Baltimore, Maryland

Hossam Abdou, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Brittany Aicher, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland H. Richard Alexander, MD Chief Surgical Officer Robert Wood Johnson Medical School Rutgers University New Brunswick, New Jersey Andrea Bafford, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland

Emily Bellavance, MD Surgical Oncologist Virginia Cancer Institute Richmond, Virginia

Megan Birkhold, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland

Hugo Bonatti, MD Surgeon Meritus Surgical Specialists Hagerstown, Maryland

viii

ix

Contributors

Meagan Dunne, MD Resident in Urology University of Maryland Medical Center Baltimore, Maryland

Ilaria Caturegli, MD Resident in Surgery Brigham and Women’s Hospital Boston, Massachusetts

Steven Feigenberg, MD Professor of Radiation Oncology University of Pennsylvania Philadelphia, Pennsylvania

Ifeanyi Chinedozi, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Amanda M. Chipman, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Arielle Cimeno, MD Chief Resident in Surgery University of Maryland Medical Center Baltimore, Maryland R. Gregory Conway, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Kenneth M. Crandall, MD Clinical Assistant Professor of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland Helena Crowley, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Peter Darwin, MD Professor of Medicine University of Maryland School of Medicine Baltimore, Maryland Jose J. Diaz, MD Chief, Division of Acute Care Surgery University of Maryland School of Medicine Baltimore, Maryland Laura DiChiacchio, MD, PhD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland

Jessica Felton, MD, MS Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Alison O. Flentje, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland James S. Gammie, MD Chief, Division of Cardiac Surgery University of Maryland School of Medicine Baltimore, Maryland Bryce Haac, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland R. Frank Henn III, MD Program Director, Residency in Orthopaedics University of Maryland School of Medicine Baltimore, Maryland Ajay Jain, MD Chief, Division of Surgical Oncology Oklahoma University College of Medicine Oklahoma City, Oklahoma Stephen M. Kavic, MD Program Director, Residency in Surgery Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Alexander J. Kish, MD Resident in Orthopaedic Surgery University of Maryland Medical Center Baltimore, Maryland

x

Contributors

Olivia A. Martin, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Marco Dal Molin, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Khanjan H. Nagarsheth, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Ledibabari M. Ngaage, MB, BCh Postdoctoral Fellow in Plastic Surgery University of Maryland School of Medicine Baltimore, Maryland Silke V. Niederhaus, MD Clinical Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Suliat Nurudeen, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland John A. Olson, Jr., MD, PhD Chief, Division of General and Oncologic Surgery University of Maryland School of Medicine Baltimore, Maryland Natalie A. O’Neill, MD Chief Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Christina Paluskievicz, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Jonathan P. Pearl, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland

Mark D. Kligman, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland

Andrew Kramer, MD, MBA Urologist

Chesapeake Urology Baltimore, Maryland

Natalia S. Kubicki, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Chris T. Laird, MD Chief Resident in Surgery University of Maryland Medical Center Baltimore, Maryland John C. LaMattina, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Shannon M. Larabee, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Megan Lerner, MD Resident in Urology Tulane University School of Medicine New Orleans, Louisiana Matthew Lissauer, MD Associate Professor of Surgery Robert Wood Johnson Medical School Rutgers University New Brunswick, New Jersey Kerri Lopez, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Kimberly Lumpkins, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland

xi

Contributors

Eric D. Strauch, MD Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Tara Talaie, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland

Yvonne M. Rasko, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Ace St. John, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Charles A. Sansur, MD Assistant Professor of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland Rajabrata Sarkar, MD, PhD Chief, Division of Vascular Surgery University of Maryland School of Medicine Baltimore, Maryland Joseph R. Scalea, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland

Julia Terhune, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Douglas Turner, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland

A. Claire Watkins, MD Clinical Assistant Professor, Cardiothoracic Surgery Stanford University School of Medicine Stanford, California Richelle Williams, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Jeffrey S. Wolf, MD Professor of Otolaryngology—Head and Neck Surgery University of Maryland School of Medicine Baltimore, Maryland

Thomas Scalea, MD Physician-in-Chief

R. Adams Cowley Shock Trauma Center University of Maryland School of Medicine Baltimore, Maryland

Christine Schad, MD Fellow in Colorectal Surgery Washington University in St. Louis St. Louis, Missouri

Max Seaton, MD Fellow in Surgical Oncology University of Miami Miami, Florida

Nicole Shockcor, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland

Contents

Foreword vi Preface vii Contributors viii

Part I: Foundations

1 Principles of Surgical Physiology. . . . . . . . . . . . 1 Ace St. John, Matthew Lissauer and Helena Crowley Fluid and Electrolytes 2 Acid–Base Disturbances 11 Coagulation 13 Packed Red Blood Cell Transfusion Therapy 16 Nutrition and the Surgical Patient 18 The Intensive Care Unit 24 Shock 30 2 Preoperative Considerations. . . . . . . . . . . . . 34 Silke V. Niederhaus General Principles for Evaluation and Management of the Surgical Patient 35

Prevention of Cardiac Complications 38 Prevention of Perioperative Infection 41 Prevention of Bleeding Complications 43 Prevention of Thromboembolic Disease 44 Prevention of Pulmonary Complications 45 Prevention of Renal Complications 47 Prevention of Hepatic Complications 50

xiii

xiv

Contents 3 Postoperative Considerations. . . . . . . . . . . . 53 Kerri Lopez and Kimberly Lumpkins Drains and Tubes 54

Postoperative Complications 56 Review Questions for Part I 60 Answers and Explanations 67

Part II: Thoracic Disorders

4 Principles of Thoracic Surgery. . . . . . . . . . . . 73 Tara Talaie, Laura DiChiacchio and Whitney Burrows General Principles of Thoracic Surgery 74 Chest Wall Disorders 80 Pleural and Pleural Space Disorders 81 Pulmonary Infections 82 Solitary Pulmonary Nodules (Coin Lesions) 83 Bronchogenic Carcinoma 83 Bronchial Adenomas 87

Metastatic Tumor 88 Tracheal Disorders 88 Mediastinal Lesions 89

5 Cardiac Disorders. . . . . . . . . . . . . . . . . 91 Laura DiChiacchio, A. Claire Watkins and James S. Gammie Anatomy and General Principles 92

Aortic Valve Stenosis 95 Aortic Insufficiency 96 Mitral Stenosis 97 Mitral Insufficiency 98 Tricuspid Stenosis and Insufficiency 100 Pulmonic Valve Disease 101 Coronary Artery Disease 102 Cardiac Tumors 104 Pericardial Disorders 105 Patent Ductus Arteriosus 106 Atrial Septal Defects 106 Ventricular Septal Defects 108 Tetralogy of Fallot 109 Transposition of the Great Arteries 111

xv

Contents

Review Questions for Part II 112 Answers and Explanations 118

Part III: Vascular Disorders

6 Arterial Disease. . . . . . . . . . . . . . . . . . 123 Alison O. Flentje and Khanjan H. Nagarsheth Limb Ischemia 124 Extracranial Cerebrovascular Disease 129 Aortic Dissection 130 Aneurysms 132

Mesenteric Ischemia 136 Renal Artery Stenosis 138

7 Venous and Lymphatic Disease. . . . . . . . . . . 140 Brittany Aicher, R. Gregory Conway and Rajabrata Sarkar

Anatomy and General Principles 140 Acute Deep Venous Thrombosis 141 Pulmonary Embolism 145 Chronic Venous Disorders: Varicose Veins and Chronic Venous Insufficiency 148 Superficial Venous Thrombophlebitis 150 Lymphedema 151

Review Questions for Part III 153 Answers and Explanations 158

Part IV: Gastrointestinal Disorders

8 Esophageal Disorders. . . . . . . . . . . . . . . 163 Jonathan P. Pearl Anatomy and Physiology 164 Esophageal Motility Disorders 166

Esophageal Strictures 170 Esophageal Tumors 171 Esophageal Perforation 173 Mallory–Weiss Syndrome 174

xvi

Contents 9 Stomach and Duodenal Disorders. . . . . . . . . . 175 Natalie A. O’Neill and Cherif Boutros Stomach 176 Benign Stomach Disease 180 Gastric Cancer 186 Postgastrectomy Syndromes 191 10 Liver, Gallbladder, and Biliary Tree Disorders. . . . . . 193 Arielle Cimeno and John C. LaMattina General Principles 194 Hemangioma 197 Hepatic Adenoma 198

Focal Nodular Hyperplasia 198 Hepatocellular Carcinoma 198 Cholangiocarcinoma 199 Metastatic Malignant Tumors 200 Pyogenic Liver Abscess 200 Amebic Liver Abscess 201 Hydatid Cysts 201 Portal Hypertension 202 Cholelithiasis (Gallstones) 204 Gallbladder Carcinoma 205 Choledocholithiasis 205 Cholangitis 206 Biliary Dyskinesia 206 Primary Sclerosing Cholangitis 207 Primary Biliary Cholangitis 207 Choledochal Cysts 207

11 Pancreatic Disease. . . . . . . . . . . . . . . . 209 Richelle Williams, Peter Darwin and H. Richard Alexander Anatomy and Physiology 210 Acute Pancreatitis 212

Relapsing Pancreatitis 216 Chronic Pancreatitis 217 Pseudocyst 218 Pancreatic Malignancies 220

xvii

Contents

12 Spleen Disorders. . . . . . . . . . . . . . . . . 225 Shannon M. Larabee, Ajay Jain and Stephen M. Kavic General Principles 225 Pathology 228 Splenectomy 232

13 Small Intestine Disorders. . . . . . . . . . . . . . 234 Olivia A. Martin and Douglas Turner

Anatomy and Physiology 235 Small Bowel Obstruction 238 Tumors 240 Crohn Disease 242 Diverticular Disease 243 Short Gut Syndrome 244

14 Colon, Rectal, and Anal Disorders. . . . . . . . . . 245 Jessica Felton, Ilaria Caturegli, Bryce Haac, Christine Schad and Andrea Bafford Anatomy and Physiology 246

Patient Evaluation 250 Bowel Preparation 252 Benign and Malignant Colorectal Tumors 252 Diverticular Disease 259 Angiodysplasia 262 Inflammatory Bowel Disease 263 Anorectal Dysfunction 271 Obstructed Defecation (Pelvic Floor–Outlet Obstruction) 272 Benign Anorectal Disease 273 Perianal and Anal Canal Neoplasms 278

15 Hernia Disorders. . . . . . . . . . . . . . . . . 281 Hossam Abdou, Ifeanyi Chinedozi and Stephen M. Kavic General Principles 282

Inguinal Hernia 283 Ventral Hernia 286 Femoral Hernia 287 Obturator Hernia 287 Lumbar Hernia 288 Parastomal Hernia 288 Spigelian Hernia 289

xviii Contents

Review Questions for Part IV 291 Answers and Explanations 308

Part V: Breast and Endocrine Disorders

16 Breast Disorders. . . . . . . . . . . . . . . . . 319 Christina Paluskievicz, Steven Feigenberg and Emily Bellavance

General Principles 320 Breast Evaluation 320 Benign Breast Disease 324 Malignant Diseases 327

17 Thyroid, Parathyroid, and Adrenal Gland Disorders. . . 335 Shannon M. Larabee and John A. Olson, Jr Thyroid Gland 336 Thyroid Dysfunction Requiring Surgery 341 Parathyroid Glands 352 Adrenal Gland 358 Tumors of the Endocrine Pancreas 367

Multiple Endocrine Neoplasia 370 Review Questions for Part V 373 Answers and Explanations 377

Part VI: Special Subjects

18 Acute Abdominal Surgical Emergencies. . . . . . . . 381 Megan Birkhold, Laura S. Buchanan and Jose J. Diaz Acute Abdomen 382

Obstruction 389 Hemorrhage 392

19 Trauma and Burns. . . . . . . . . . . . . . . . . 395 Amanda M. Chipman, Brandon Bruns and Thomas Scalea Trauma 396 Specific Injuries 402 Burn Injury 408

xix

Contents

20 Pediatric Surgery. . . . . . . . . . . . . . . . . 411 Chris T. Laird, Clint D. Cappiello and Eric D. Strauch General Principles 412 Congenital Pulmonary Malformations (CPAM) 412 Esophageal Atresia (EA) and Tracheoesophageal Fistula (TEF) 413 Congenital Diaphragmatic Hernia (CDH) 415

Congenital Abdominal Wall Defects 416 Infantile Hypertrophic Pyloric Stenosis 419 Biliary Atresia 419 Necrotizing Enterocolitis (NEC) 420 Intestinal Malrotation With or Without Midgut Volvulus 423 Intestinal Atresia 425

Hirschsprung Disease 426 Anorectal Malformation 428 Solid Tumors 429

21 Surgical Oncology. . . . . . . . . . . . . . . . . 430 Marco Dal Molin, Julia Terhune and Suliat Nurudeen Cancer 431 Cancer Etiology and Epidemiology 431

Screening and Diagnosis 434 Diagnostic Procedures 436 Staging 437 Surgical Treatment 437 Multidisciplinary Treatment 440 Research and Training 442

22 Organ Transplantation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444 Tara Talaie, Joseph R. Scalea, Max Seaton, Silke Niederhaus

and Jonathan Bromberg General Principles 445 Heart Transplantation 453 Pulmonary Transplantation 454

Hepatic Transplantation 455 Kidney Transplantation 458 Pancreatic Transplantation 461 Small Bowel and Multivisceral Transplantation 463 Composite Tissue Allograft and Vascularized Composite Allograft Transplants 464

xx

Contents 23 Minimally Invasive Surgery and Robotics. . . . . . . 466 Hossam Abdou, Natalia S. Kubicki, Hugo Bonatti and Stephen M. Kavic General Principles 466 Selected Laparoscopic Procedures 470 Robotic Technology 476 24 Bariatric Surgery. . . . . . . . . . . . . . . . . 479 Nicole Shockcor and Mark D. Kligman General Principles 480 Surgical Treatment of Obesity 481 25 Head and Neck Surgery . . . . . . . . . . . . . . 488 Jeffrey S. Wolf Anatomy 488 Disease Processes 491 Head and Neck Cancer 501

Benign Parotid Neoplasms 513 Review Questions for Part VI 515 Answers and Explanations 527

Part VII: Surgical Subspecialties

26 Neurosurgery. . . . . . . . . . . . . . . . . . . 535 Kenneth M. Crandall and Charles A. Sansur General Principles 536 Evaluating the Neurosurgical Patient 540 Head Injury 541 Spinal Cord Injury 545 Neurovascular Disease 547 Central Nervous System Tumors 549

Functional Neurosurgery 555 Degenerative Spine Disease 556 Tumors of the Spine 559

Spinal Deformity 561 Peripheral Nerves 561

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Contents

27 Plastic and Reconstructive Surgery . . . . . . . . . 564 Ledibabari M. Ngaage and Yvonne M. Rasko General Principles 565 Reconstructive Plastic Surgery 565 Skin and Soft Tissue Reconstruction 570 Craniofacial Surgery 582 Hand Surgery 584 Aesthetic Plastic Surgery 587 Innovation in Plastic Surgery 590

28 Urologic Surgery. . . . . . . . . . . . . . . . . 591 Megan Lerner, Meagan Dunne, Jessica Felton and Andrew Kramer

Urologic Emergencies 592 Urinary Tract Stones 594 Benign Prostatic Disorders 596 Genitourinary Malignancies 600 Erectile Dysfunction 608 Voiding Dysfunction 609

29 Orthopedic Surgery. . . . . . . . . . . . . . . . 613 Alexander J. Kish and R. Frank Henn III Orthopedic General Principles 614

Orthopedic Emergencies 615 Orthopedic Urgencies 618 Arthritis 630 Infections 631 Tumors 633 Adult Orthopedics 636 Review Questions for Part VII 641 Answers and Explanations 649

Index 655

Chapter 1

Part I: Foundations

Principles of Surgical Physiology Ace St. John • Matthew Lissauer • Helena Crowley

Chapter Cuts ◆◆ No one formula best determines fluid and electrolyte management. ◆◆ High insensible losses occur during and after surgical procedures. ◆◆ Hyperkalemia is a common, life-threatening electrolyte disorder that leads to cardiac dysrhythmia. It is treated by shifting potassium into cells (insulin/ glucose), stabilizing cardiac cells (calcium), and increasing potassium excretion (potassium binders). ◆◆ New anemia in a surgical patient is surgical bleeding until proven otherwise. ◆◆ Enteral nutrition is preferred for most patients. ◆◆ Adequate oxygenation is reflected in blood pressure, pulse, urine output (end- organ function), pH, and overall appearance. ◆◆ Patients with inadequate oxygenation or increased work of breathing should be intubated for mechanical ventilation. ◆◆ Shock is the state of physiologic decompensation resulting in oxygen demand outstripping oxygen supply, and inadequate tissue perfusion. Critical Surgical Associations

If You Hear/See

Think

Adequate urine output

½ mL/kg/hr, or 250 mL per 8 hr

Maintenance fluid

½ Normal saline + 20 mEq KCl

Maintenance rate

60 mL/hr + 1 mL/hr per kg over 20 kg

Potassium replacement

10 mEq of IV KCL raises serum concentration by 0.1 mEq/L

Prothrombin time

Reflects extrinsic pathway

(continued) 1

2

Part I ♦ Foundations

If You Hear/See

Think

Partial thromboplastin time Reflects intrinsic pathway Spontaneous bleeding

Platelet dysfunction or thrombocytopenia

Nutritional supplements Use the gut first Increased work of breathing Intubate early Shock

Inadequate oxygen delivery relative to demand

Septic shock

Norepinephrine

Nitroprusside

Cyanide toxicity

FLUID AND ELECTROLYTES Normal Body Composition I. Body water: Water accounts for 50%–70% of total body weight (Fig. 1-1) and is higher in young people, thin people, and men. A. Two-thirds rule: Total body water comprises about two thirds of body weight. B. Plasma volume: ~5% of body weight is plasma volume (e.g., 3.5 L of plasma for a 70 kg male). Plasma is ~60% of the blood volume if the hematocrit is 40% (e.g., 5.8 L of blood for a 70 kg male). II. Electrolyte composition: Electrolyte concentrations differ between intracellular and extracellular compartments due to ion pumps, principally Na + /K + ATPase (Table 1-1). Osmotic pressure changes between compartments causes water to redistribute. A. Intracellular compartment: The principle osmotic cation is potassium. The concentration of osmotic and oncotic (protein) particles is higher than the extracellular compartment, thus allowing water to flow into the cell creating turgidity. B. Extracellular compartment: The principle osmotic cation is sodium. Interstitial and plasma composition is nearly equal. Water and Electrolyte Maintenance I. Water: Required amount depends on the person’s weight, age, gender, and health. A. Water calculation methods 1. Amount of body water excreted a. Most water lost from the body is through urine production. Generally, 0.5 mL/kg/hr is the minimum needed to excrete the daily solute load. b. The next highest daily water loss is from insensible losses (i.e., sweat, respiration, stool). This is estimated at 600–900 mL/24 hr.

3

Chapter 1 ♦ Principles of Surgical Physiology

Total body water: 60% of total body weight

Intracellular: 40% of total body weight (2/3 of the total body water)

Extracellular: 20% of total body weight (1/3 of the total body water)

Interstitial: 15% total body weight (3/4 of the extracellular fluid)

Plasma: 5% total body weight (1/4 of the extracellular fluid)

Figure 1-1: Water compartments.

Table 1-1: Electrolyte Composition by Water Compartment

Intracellular Compartment

Extracellular Compartment

Electrolytes

Anions/Cations Sodium (Na + )

10 mEq/L

142 mEq/L

Potassium (K + )

140 mEq/L

4 mEq/L

Chloride (Cl − )

4 mEq/L

103 mEq/L

Bicarbonate (HCO 3 − )

10 mEq/L

28 mEq/L

3− )

Phosphate (PO 4

75 mEq/L

4 mEq/L

2− )

Sulfate (SO 4

2 mEq/L

1 mEq/L

Calcium (Ca ++ )

<1 mEq/L

5 mEq/L

Magnesium (Mg ++ )

18 mEq/L

2 mEq/L

Organic acids

—

5 mEq/L

Various proteins

40 mEq/L

1 mEq/L

4

Part I ♦ Foundations 2. Water maintenance a. Adult patients: (70 kg × 0.5 mL/kg/hr × 24 hr) + (750 mL/24 hr) = 1,590 mL/24 hr. b. Pediatric patients: 4 mL/kg/hr for the first 10 kg of body weight, 2 mL/kg/hr for the second 10 kg of body weight, and 1 mL/kg/hr for each additional kilogram of body weight. B. Evaluating maintenance rates: 1. Monitor urine output: If urine output is low (i.e., <0.5 mL/kg/hr), then more water may be required. 2. Monitor heart rate: Tachycardia can be a sign of low intravascular volume. C. Adjusting fluid rates and types for individual patients: First, calculate the patient’s maintenance rate, and then adjust the amount up or down based on the need for resuscitation and the replacement of gastrointestinal (GI) losses. Adjust the type of fluid based on the type of losses (Table 1-2). 1. Injury, illness, and surgery: These may result in fluid losses due to blood loss, third spacing, insensible losses from diarrhea, fever, etc. It may be necessary to provide more than calculated maintenance fluid to replace losses. 2. Hypervolemia and diuresis: Patients who require diuresis are often overloaded with fluid. In these instances, intravenous (IV) fluids should be limited. II. Sodium: 150–200 mEq/day of sodium is typically consumed; most is excreted in the urine. A. If the body needs to conserve sodium, then it can reduce renal excretion to less than 1 mEq/day. B. Daily homeostasis is easily maintained with 1–2 mEq/kg/day. III. Potassium: The normal daily intake of potassium is ~40–120 mEq/day. 10%–15% is excreted in the urine, and 0.5–1 mEq/kg/day is appropriate to maintain homeostasis.

Table 1-2: Electrolyte Composition of Gastrointestinal Secretions

HCO 3 − (mEq/L)

Volume/ day Na + (mEq/L) K + (mEq/L) Cl − (mEq/L)

Organ

Stomach 1–5 L

20–150

10–20 10–20

120–140

Nil

Duodenum 0.1–2 L 100–120

110

10–20 30–50 30–50

Ileum 1–3 L

80–140

5–10

60–90

Colon

0.1–2 L 100–120

10–30

90

Gallbladder 0.5–1 L 140 Pancreas 0.5–1 L 140

5 5

100

25

30 (higher when not stimulated)

115 (lower when not stimulated)

5

Chapter 1 ♦ Principles of Surgical Physiology

IV. Maintenance IV: Table 1-3 gives electrolyte concentrations of several IV fluids. A. Minimal sodium maintenance would require 70–140 mEq/day. B. Minimal potassium requirements would be 35–70 mEq/day. Water and Electrolyte Deficits and Excesses I. Water A. Hypovolemia 2. Signs and symptoms of gradual volume loss: Loss of skin turgor, thirst, alterations in body temperature, and changes in mental status. 3. Treatment: Acute deficits should be replaced rapidly, whereas chronic deficits should be replaced slowly, with half of the deficit replaced over the first 8 hours and the rest in 24–48 hours. B. Hypervolemia: Well tolerated in healthy patients. 1. Signs and symptoms of acute hypervolemia: Acute shortness of breath, tachycardia. 2. Signs and symptoms of chronic hypervolemia: Peripheral edema, pulmonary edema. 3. Treatment: With normal kidneys, volume restriction and/or diuretics. For nonfunctioning kidneys, renal replacement therapy (hemodialysis). 1. Signs and symptoms of acute volume loss: Tachycardia, hypotension, and decreased urine output. a. Hyperosmolar: Hyperglycemia, mannitol infusion, or presence of other osmotically active particles that draw in water. b. Normo-osmolar (pseudohyponatremia): Hypertriglyceridemia, hyperlipidemia, and hyperproteinemia; large, minimally osmotic molecules displace water and interfere with the lab measurement. c. Hypo-osmolar (1) Hypovolemic: Renal losses, renal tubular acidosis, cerebral salt wasting, GI losses, “tea and toast syndrome”, transcutaneous losses (burns, trauma). (2) Hypervolemic: Related to low cardiac output (the kidneys have less blood flow, and free water is conserved) or hypoalbuminemia (e.g., cirrhosis) or other edematous states wherein salt and free water cannot be excreted by the kidneys (e.g., renal failure). (3) Euvolemic: Syndrome of inappropriate antidiuretic hormone (SIADH) secretion or other disorders (e.g., glucocorticoid deficiency, hypothyroidism, water intoxication from psychogenic polydipsia). II. Sodium: Close relationship to volume status. A. Hyponatremia (Na + <130 mEq/L): (Fig. 1-2) 1. Causes

6

Part I ♦ Foundations

Table 1-3: Electrolyte Concentration in Various Intravenous Fluids Fluid Na + (mEq/L) K + (mEq/L) Mg ++ (mEq/L) Ca ++ (mEq/L) Cl − (mEq/L) Normal saline (0.9% NaCl) 154 0 0 0 154 0 308 1/2 normal saline (0.5% NaCl) 77 0 0 0 77 0 154 Hypertonic saline (3% saline) 513 0 0 0 513 0 1027 Lactated Ringer’s 130 4 0 2.7 98 28 525 Plasmalyte* 140 5 3 0 98 0 294 Lactate (mEq/L) Osmolarity (mOsm/L)

*Plasmalyte also contains 27 mEq/L acetate and 23 mEq/L gluconate.

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Chapter 1 ♦ Principles of Surgical Physiology

Hyponatremia

Hypo-osmotic

Normo-osmotic

Hyperosmotic

Hypovolemic

Euvolemic

Hypervolemic

Figure 1-2: Hyponatremia.

2. Signs and Symptoms a. Acute hyponatremia: Acute cerebral edema, seizures, and coma. b. Chronic hyponatremia: Tolerated to Na + concentrations of 110 mEq/L; signs and symptoms include confusion, irritability, and decreased deep tendon reflexes. 3. Diagnosis and categorization: Clinical exam and lab determination of osmolar state are often enough for diagnosis; when in doubt, check urine osmolarity and sodium. a. Hypovolemic, hypo-osmolar hyponatremia: Urine Na + greater than 20 mEq/L = renal losses; urine Na + less than 10 mEq/L = extrarenal losses. b. Hypervolemic, hypo-osmolar hyponatremia: Urine Na + greater than 20 mEq/L = renal failure; Na + less than 10 mEq/L = cirrhosis, heart failure. c. Euvolemic, hypo-osmolar hyponatremia: Urine osmolarity usually high; urine Na + usually greater than 20 mEq/L except in water intoxication. 4. Treatment (if minimally symptomatic) a. Hyperosmolar: Correct hyperglycemia or other active osmotic particles. b. Normo-osmolar: Treat the underlying disease process. c. Hypo-osmolar (1) Hypovolemic: Treat with isotonic fluid infusion to restore deficits. (2) Hypervolemic: Treat underlying medical cause first, and then initiate salt and free water restrictions. (3) Euvolemic: If SIADH, free water restriction usually is sufficient.

8

Part I ♦ Foundations B. Hypernatremia (Na + > 150 mEq/L) 1. Categories a. Hypovolemia: Hypernatremia represents a free water deficit; total body sodium may be low. b. Hypervolemia: Iatrogenic infusion of too much sodium can lead to hypervolemic hypernatremia, but this is rare. 2. Signs and symptoms: Similar to volume depletion (e.g., tachycardia, hypotension, dry mucous membranes, decreased skin turgor); water shifts from the intracellular compartment can produce neurological signs and symptoms (lethargy, confusion, and coma). 3. Diagnosis/etiology (usually simple): High serum sodium with obvious free water losses. a. Extrarenal losses: Insensible losses due to fever, mechanical ventilation, burns, diarrhea, or measured losses from the GI tract. b. Renal losses: Excessive free water excretion. (1) Osmotic diuresis from hyperglycemia or mannitol administration. (2) High-output dilute urine from acute tubular necrosis (ATN). 4. Treatment a. Hypovolemia: Need to replace volume; calculate free water deficit first: (1) Water deficit = 0.6 × body weight (kg) × (serum Na+/140−1). (2) Replace half the deficit in the first 8 hours; the rest in the next 16 hours. (3) If the hypovolemic state is severe (i.e., shock), then initial resuscitation can be isotonic fluids. If the deficit is less severe, use dextrose 5% in water (D5W) to complete the free water replacement. b. Hypervolemia (1) If total body water is increased, then decrease the amount of sodium administered. (2) If sodium intake (e.g., antibiotics, total parenteral nutrition [TPN]) cannot be decreased, free water can be infused to lower the serum sodium level. (3) Diuretics can be used, but sodium can rise. (4) Consider natriuresis. III. Potassium A. Hypokalemia (K + <3.5 mEq/L): Severe hypokalemia is a serum potassium level of 3.0 mEq/L or less; in some patients (e.g., cardiac), a K + higher than 4.0 is desirable. 1. Signs and symptoms: Ileus, weakness, and cardiac dysrhythmias.

Electrocardiogram (ECG) changes may occur below a K + of 3.0 mEq/L and include, in increasing order of severity, T-wave flattening or inversion, depressed ST segments, development of U waves, prolonged QT interval, and ventricular tachycardia.

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Chapter 1 ♦ Principles of Surgical Physiology

2. Diagnosis/etiology: Rarely found in healthy humans with normal diet and kidneys. a. Renal: Diuretics, vomiting (renal excretion of K + to preserve Na + ), renal tubular acidosis. b. Extrarenal: Diarrhea, burns. c. Intracellular shift: Insulin, alkalotic state. d. Medical disease: Hyperaldosteronism, Cushing syndrome. 3. Treatment a. If symptoms are severe, then administer potassium IV centrally in a monitored setting. b. If symptoms are mild, then infuse 20 mEq/hr maximum in the unmonitored patient and 40 mEq/hr in the monitored patient. c. Administration for more chronic conditions can be via the enteral route. B. Hyperkalemia (K + ≥ 6 mEq/L) 1. Signs and symptoms: Diarrhea, cramping, nervousness, weakness, and flaccid paralysis; more often, cardiac dysrhythmias occur before other symptoms. (ECG changes include peaked T waves and widened QRS, and ventricular fibrillation.) 2. Diagnosis/etiology (numerous): Most common include the following: a. Renal failure: With inappropriate consumption and administration of K + . b. Extracellular shift: Rhabdomyolysis, massive tissue necrosis, metabolic acidosis, hyperglycemia. c. Medical disease: Addison disease, major burns, uncontrolled diabetes. 3. Treatment a. Acutely symptomatic patient (1) IV calcium stabilizes cardiac myocyte membranes and can prevent dysrhythmias. (1 g Ca++ gluconate IV is a standard dose.) (2) Glucose/insulin shifts K+ intracellularly acutely and quickly. (1 ampule of D50 with 10 units of regular insulin is often sufficient.) (3) Bicarbonate shifts K + intracellularly. b. To remove K + and lower body stores permanently: (1) Ion-exchange resin: oral or rectal: binds K+, facilitating excretion. (2) Furosemide: Only use if kidneys are functional; monitor electrolytes and fluid balance. (3) Dialysis. IV. Chloride A. Hypochloremia (Cl − < 90 mEq/L) 1. Signs and symptoms: Associated with dehydration or hypokalemia due to GI losses. 2. Diagnosis/etiology a. Gastric hydrochloric acid (HCl) is lost from vomiting, leading to low chloride and a buildup of bicarbonate, causing a metabolic alkalosis . b. Hypochloremia is often associated with paradoxical aciduria . As the dehydration worsens, the kidneys’ drive to retain sodium predominates, and the kidneys excrete both K + and H + to conserve sodium.

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Part I ♦ Foundations 3. Treatment: Replace the chloride and volume deficit with sodium chloride solutions and replace K + as needed. B. Hyperchloremia (Cl − > 110 mEq/L) 1. Signs and symptoms: Muscle weakness, fatigue, thirst, hypertension. 2. Cause: Iatrogenic chloride in IV solutions. (The chloride content in normal saline [154 mEq/L] is significantly higher than that in plasma [90–110 mEq/L].) 3. Diagnosis/etiology: Excess chloride causes more water to dissociate and more H + ions to be present, leading to metabolic acidosis. 4. Treatment: Decrease the amount of chloride being infused.

V. Calcium A. Hypocalcemia (Ca ++ < 8 mg/dL)

1. Signs and symptoms: Neuromuscular irritability with perioral and extremity numbness that may progress to carpopedal spasm and tetany;

premature ventricular contractions. 2. Diagnosis/etiology (numerous)

a. Surgical patients: Removal of adenomatous or hyperplastic parathyroid glands and parathyroid injury during thyroid surgery. b. Critically ill patients: Lactate, citrate from blood transfusions, and medicines. c. Other: Vitamin D deficiency, chronic renal failure, intestinal malabsorption, excess dietary or therapeutic (laxative) magnesium, mercury exposure, chelation therapy. 3. Treatment a. Asymptomatic outpatients: Provide oral supplement. b. Symptomatic patients: Monitor and treat. (1) If symptoms are mild, then oral calcium is often sufficient. (2) Severely symptomatic patients should be repleted with IV calcium until symptoms resolve and an appropriate oral regimen is tolerated. B. Hypercalcemia (Ca ++ ≥ 10.5 mg/dL) 1. Signs and symptoms: Fatigue, confusion, nausea, vomiting, diarrhea, dehydration, and anorexia are common; when secondary to hyperparathyroidism, renal calculi and ulcer disease are more common. 2. Diagnosis/etiology (numerous) a. Endocrine: Primary hyperparathyroidism (most common), thyrotoxicosis. b. Malignancy: Most common (up to 20%–30% of cancer patients), often from osteolytic or parathyroid hormone-related protein (PTHrP) secreting lesions. c. Granulomatous disease: Sarcoidosis, tuberculosis. d. Medications: Excess calcium ingestion, vitamin D toxicity, thiazide diuretics. e. Other: Renal disease, milk alkali syndrome, familial hypocalciuric hypocalcemia.

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Chapter 1 ♦ Principles of Surgical Physiology

3. Treatment a. First-line therapy: Aggressive isotonic resuscitation, leading to diuresis and calcium excretion; if unsuccessful, then add furosemide. b. Medical therapy: Medications to stop osteoclastic activity are the mainstay of therapy (i.e., bisphosphonates, calcitonin, and steroids).

Quick Cuts • Two-thirds rule: Total body water = 2/3 total body weight. • Adequate urine output is ½ mL/kg/hr or 250 mL per 8 hour shift.

• Maintenance fluid estimate: 60 mL/hr + 1 mL/kg/hr for each kg above 20 kg. • Hyperkalemia is life threatening: Treat aggressively to shift K intracellularly, and then work on potassium excretion. • Severe, symptomatic hypocalcemia is life threatening and should be treated with calcium supplementation.

ACID–BASE DISTURBANCES Regulatory Systems

I. Carbon dioxide: CO 2 production can exceed 15,000 mmol/day from metabolic processes (e.g., lung excretion). If Pco 2 increases, then water dissociates into HCO 3 − and H + based on the Henderson–Hasselbalch equation , thus decreasing pH. Either a loss of bicarbonate or a gain in protons can cause acidosis. II. Strong ions: Ions that completely dissociate in water (e.g., Na + , Cl − , Ca ++ , Mg ++ , K + ). In a pure salt solution, ion concentrations are equal, and pH is neutral. In plasma, cations outnumber anions. To maintain electrical neutrality, water dissociates, H + is excreted, and HCO 3 − concentration increases, creating a pH of 7.4, not 7.0. III. Weak acids: Weak acids can exist as negatively charged molecules or accept H + and exist uncharged. These buffering systems include proteins and phosphates. Acidosis The body’s pH decreases when the Pco 2 increases, the concentration of HCO 3 − decreases, the concentration of strong anions increases, or the concentration of weak acids increases. A pH less than 7.35 is considered pathologic. I. Respiratory acidosis A. Causes 1. Decreased ventilation: Leads to increased CO 2 concentration. 2. Increased CO 2 production: Excess enteral or parenteral carbohydrate administration increases the respiratory quotient and production of CO 2 . B. Treatment: Increase alveolar ventilation. Most alveolar hypoventilation requires intubation with mechanical ventilation.

12

Part I ♦ Foundations II. Metabolic acidosis: Results either from HCO 3

− loss or accumulation of

strong anions (measured or non-measured) or weak acids. A. Causes 1. Weak acid accumulation (anion gap): Loss of HCO 3 − . a. Acid accumulation can occur because of renal failure and the inability to clear acid by-products of metabolism. b. Lactic acidosis: Inadequate tissue perfusion and anaerobic metabolism. c. Diabetic ketoacidosis: Acetoacetate and beta-hydroxybutyrate are weak acids. d. Toxins (polyethylene glycol, methanol): Methanol is metabolized to formaldehyde and then formic acid. 2. Strong anion accumulation: Normal anion gap; in hyperchloremic acidosis, excess chloride induces water to dissociate and pH to drop. B. Treatment: Correct the underlying metabolic disorder. Bicarbonate administration should rarely be used unless pH is dangerously low (<7.2). Alkalosis I. Respiratory alkalosis A. Causes 1. Spontaneously breathing patient: Caused by alveolar ventilation increase and subsequent reduction in CO 2 levels (anxiety, pain, shock, sepsis, toxic substances [salicylate poisoning], or central nervous system dysfunction). 2. Mechanically ventilated patient: Iatrogenic overventilation is common. B. Treatment: Decrease minute ventilation. Most cases are self-limited. II. Metabolic alkalosis: pH increases to >7.45, and HCO 3 − is >26 mEq/L. A. Causes 1. Most common non-iatrogenic cause is loss of gastric contents (HCl and large volumes of water are lost). 2. Drugs that limit renal excretion of HCO 3 − (e.g., steroids and diuretics). 3. Over-administration of alkali (e.g., in ulcer therapy), acetate in TPN that is used to replace other anions, and citrate in transfused blood that is converted to CO 2 and water and then to HCO 3 − by the kidneys. B. Treatment: Stop the loss of chloride and replace the water and chloride with isotonic sodium chloride and potassium supplementation. For other causes, stopping the offending agent is usually sufficient. Diagnosing Acid–Base Disorders (Table 1-4) Quick Cuts • Acidosis is a pH-lowering process; acidemia is a low blood pH. • Paradoxical aciduria: The kidney exchanges H for Na, so the urine may be acidotic when the patient is alkalotic. 3. Loss of bicarbonate: Normal anion gap. a. Excess renal excretion of bicarbonate. b. Diarrhea.

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Chapter 1 ♦ Principles of Surgical Physiology

Table 1-4: Acid–Base Disorders

Expected Compensation 1–4 mEq/L HCO 3 − for each 10 mm Hg Pco 2 rise

−

Disorder

Phase

Pco 2

HCO 3

pH

↑

Respiratory acidosis

Acute

Normal

<7.35

↑

↑

Compensated

7.35–7.40

↓

Respiratory alkalosis

Acute

Normal

>7.45

2–5 mEq/L HCO 3 − for each 10 mm Hg Pco 2 drop

↓

↓

Compensated

7.40–7.45

↓

Metabolic acidosis

Acute

Normal

<7.35

Expected Pco 2 = 1.5(HCO 3

− ) + 8

↓

↓

Compensated

7.35–7.40

↑

Metabolic alkalosis

Acute

Normal

>7.45

Expected Pco 2 = 0.7(HCO 3

− ) + 20

↑

↑

Compensated

7.40–7.45

COAGULATION Hemostasis Mechanism Phases I. Primary Hemostasis

A. Platelet adherence: The first step in controlling hemorrhage is platelet adherence via glycoprotein (Gp) receptor Ib in conjunction with von Willebrand factor. B. Platelet activation: Activated platelets produce thromboxane A 2 and other vasoconstrictors, which reduce blood flow. Expression of Gp IIb/IIIa promotes platelet–platelet adhesion (fibrinogen required) and platelet plug formation. II. Clot formation: Tissue factor exposed due to vessel injury or in response to inflammation begins the clotting cascade (traditionally taught as having an intrinsic and extrinsic pathway; however, in vivo, both pathways act in concert). A. Extrinsic pathway: Tissue factor binds factor VII and activates it (VIIa). VIIa subsequently activates factor X. Xa then converts prothrombin to thrombin.