Step-Up to Surgery PDF

10164-00_FM.qxd 1/3/07 2:41 PM Page ii McFadden_FM.qxd 5/30/08 12:50 PM Page i Step-Up to Surgery McFadden_FM.qxd 5/30/08 12:50 PM Page ii McFadden_FM.qxd 5/30/08 12:50 PM Page iii...

10164-00_FM.qxd 1/3/07 2:41 PM Page ii McFadden_FM.qxd 5/30/08 12:50 PM Page i Step-Up to Surgery McFadden_FM.qxd 5/30/08 12:50 PM Page ii McFadden_FM.qxd 5/30/08 12:50 PM Page iii Step-Up to Surgery STANLEY ZASLAU, MD, MBA, FACS Urology Residency Program Director Associate Professor Division of Urology Department of Surgery West Virginia University Morgantown, West Virginia DAVID W. MCFADDEN, MD, FACS Stanley S. Fieber Professor and Chair Department of Surgery University of Vermont College of Medicine Surgical Services Leader, Surgeon-in-Chief Fletcher Allen Health Care Burlington, Vermont McFadden_FM.qxd 5/30/08 12:50 PM Page iv Acquisitions Editor: Charley Mitchell Senior Managing Editor: Stacey Sebring Marketing Manager: Jennifer Kuklinski Production Editor: Kevin Johnson Compositor: International Typesetting and Composition Printer: Data Reproductions Corp. Copyright © 2009 Lippincott Williams & Wilkins 351 West Camden Street Baltimore, MD 21201 530 Walnut Street Philadelphia, PA 19106 All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form or by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner. The publisher is not responsible (as a matter of product liability, negligence, or otherwise) for any injury resulting from any material contained herein. This publication contains information relating to general principles of medical care that should not be construed as specific instructions for individual patients. Manufacturers’ product information and package inserts should be reviewed for current information, including contraindications, dosages, and precautions. Printed in the United States of America Library of Congress Cataloging-in-Publication Data Step-up to surgery / [edited by] Stanley Zaslau, David W. McFadden. p. ; cm. —(Step up series) ISBN-13: 978-0-7817-7454-3 ISBN-10: 0-7817-7454-3 1. Surgery—Outlines, syllabi, etc. I. Zaslau, Stanley. II. McFadden, David W., MD. III. Series. [DNLM: 1. Surgical Procedures, Operative—Outlines. 2. Surgical Procedures, Operative—Problems and Exercises. WO 18.2 S827 2009] RD37.3.S738 2009 617—dc22 2008014717 The publishers have made every effort to trace the copyright holders for borrowed material. If they have inadvertently overlooked any, they will be pleased to make the necessary arrangements at the first opportunity. To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 824-7390. International customers should call (301) 714-2324. Visit Lippincott Williams & Wilkins on the Internet: http://www.LWW.com. Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6:00 pm, EST. 04 05 06 07 08 1 2 3 4 5 6 7 8 9 10 McFadden_FM.qxd 5/30/08 12:50 PM Page v Dedication To our students, whose interest in surgery fuels our energy and enthusiasm to further our own knowledge of this great specialty. McFadden_FM.qxd 5/30/08 12:50 PM Page vi McFadden_FM.qxd 5/30/08 12:50 PM Page vii Preface Step-Up to Surgery evolved from our desire to provide To this end, we have recruited the authors from our medical students with a concise, easy-to-read, up-to-date department of surgery faculty and residents. These dedi- overview of the key concepts of general surgery, applica- cated teachers are our front-line educators for our students ble to students taking the third-year clerkship rotation. and have provided didactic education to them. We wanted our book to be different from others currently Because of our location in rural West Virginia and three available in the following ways: campuses throughout the state, it is our hope that Step-Up to Surgery will allow a standardization of general surgical 1. Provide a core overview of not only general surgery clerkship education at all sites. We are hopeful that our topics, but key concepts in the surgical subspecialties readers will share the same enthusiasm for surgical educa- 2. Provide numerous “quick hits” to illustrate important tion as we do. points for licensure examinations 3. Provide authentic case-based questions to further illus- With best regards, trate concepts and allow students to apply them to typ- SZ ical patient presentations DWM 4. Provide many pictures, figures, and tables to further illustrate key concepts and allow for easy recall when students are questioned on rounds, in the operating room, and on written examinations vii McFadden_FM.qxd 5/30/08 12:50 PM Page viii McFadden_FM.qxd 5/30/08 12:50 PM Page ix Contributing Authors Laura Buchanan, MD Charles Goldman, MD Resident Associate Professor Department of Surgery Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia Riaz Cassim, MD Cynthia Graves, MD Assistant Professor General Surgery Residency Program Director Department of Surgery Assistant Professor West Virginia University Department of Surgery Morgantown, West Virginia West Virginia University Morgantown, West Virginia Adam Cassis, MD Resident Syed Hashmi, MD Department of Otolaryngology Assistant Professor West Virginia University Division of Trauma Morgantown, West Virginia Department of Surgery West Virginia University Morgantown, West Virginia Felix Cheung, MD Resident Hannah Hazard, MD Department of Orthopedic Surgery Instructor West Virginia University Division of General Surgery Morgantown, West Virginia Department of Surgery West Virginia University Alexandre D’Audiffret, MD Morgantown, West Virginia Associate Professor Division of Vascular Surgery Marissa Howard-McNatt, MD Department of Surgery Assistant Professor West Virginia University Division of General Surgery Morgantown, West Virginia Department of Surgery West Virginia University Kevin Day, MD Morgantown, West Virginia Resident Department of Surgery Antony Joseph, MD West Virginia University Resident Morgantown, West Virginia Department of Surgery West Virginia University Bruce Freeman, MD, PhD Morgantown, West Virginia Chief Division of Plastic Surgery Kamran Karimi, MD Associate Professor Resident Department of Surgery Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia ix McFadden_FM.qxd 5/30/08 12:50 PM Page x x CONTRIBUTING AUTHORS Jennifer Knight, MD Muhammad Nazim, MD Resident Resident Department of Surgery Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia Tarun Kumar, MD Matthew Oliverio, MD Instructor Resident Division of Pediatric Surgery Department of Otolaryngology Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia Jessica Partin, MD James Longhi, DO Resident Assistant Professor Department of Surgery Division of General Surgery West Virginia University Department of Surgery Morgantown, West Virginia West Virginia University Morgantown, West Virginia Kumar Pillai, MD Chief Matthew Loos, MD Division of Vascular Surgery Resident Associate Professor Department of Surgery Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia Christopher McCullough, MD Ganga Prabhakar, MD Chief Assistant Professor Division of Transplantation Services Division of Cardiovascular Surgery Professor Department of Surgery Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia Irfan Rizvi, MD David W. McFadden, MD, FACS Resident Stanley S. Fieber Professor and Chair Department of Surgery Department of Surgery West Virginia University College of Medicine Morgantown, West Virginia University of Vermont Morgantown, West Virginia Larry Roberts, MD Surgical Services Leader, Surgeon-in-Chief Associate Professor Fletcher Allen Health Care Division of Trauma Burlington, Vermont Department of Surgery West Virginia University Stephen McNatt, MD Morgantown, West Virginia Associate Professor Division of General Surgery Daniel Rossi, DO Department of Surgery Resident West Virginia University Department of Surgery Morgantown, West Virginia West Virginia University Morgantown, West Virginia Bradford Mitchell, MD Assistant Professor Walter Samora, MD Division of General Surgery Resident Department of Surgery Department of Orthopedic Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia McFadden_FM.qxd 5/30/08 12:50 PM Page xi CONTRIBUTING AUTHORS xi Susan E. Saunders, MD Giridhar Vedula, MD Resident Resident Division of Urology Department of Surgery Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia Alison Wilson, MD Farooq Shahzad, MD Director Resident Jon Michael Moore Trauma Center Department of Surgery Assistant Professor West Virginia University Department of Surgery Morgantown, West Virginia West Virginia University Morgantown, West Virginia Santosh Shenoy, MD Stanley Zaslau, MD, MBA, FACS Resident Urology Residency Program Director Department of Surgery Associate Professor West Virginia University Division of Urology Morgantown, West Virginia Department of Surgery West Virginia University Magesh Sundaram, MD Morgantown, West Virginia Chief Division of Surgical Oncology Pamela Zimmerman, MD Associate Professor Instructor Department of Surgery Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia Richard Vaughan, MD Jamshed Zuberi, MD Chairman Assistant Professor Department of Surgery Division of Trauma Professor Department of Surgery West Virginia University West Virginia University Morgantown, West Virginia Morgantown, West Virginia McFadden_FM.qxd 5/30/08 12:50 PM Page xii McFadden_FM.qxd 5/30/08 12:50 PM Page xiii Acknowledgments To Stacy Sebring and Donna Balado for their support and guidance throughout this process. To our wives and families who allowed us to spend more time on our laptops writing chapters instead of being with them. xiii McFadden_FM.qxd 5/30/08 12:50 PM Page xiv McFadden_FM.qxd 5/30/08 12:50 PM Page xv Contents COLOR PLATES after page............... 176 Chapter 10. Breast.............................. 156 Preface................................ vii Anatomy and Development.............. 156 Contributing Authors....................... ix Breast Workup........................ 157 Acknowledgments......................... xiii Breast Complaints and Disorders.......... 159 Breast Cancer......................... 162 Chapter 1. Surgical Physiology...................... 1 Special Problems...................... 169 Fluids and Electrolytes.................... 1 Hemostasis/Coagulation................... 9 Chapter 11. Skin and Soft Tissue.................. 172 Surgical Nutrition....................... 12 Anatomy............................ 172 Chapter 2. Trauma and Burns..................... 17 Wounds and Scars..................... 173 Neoplasms of the Skin.................. 178 Chapter 3. Hernias.............................. 35 Chapter 12. Vascular Surgery..................... 184 Chapter 4. Esophagus and Stomach................ 46 Aneurysmal Vascular Disease............. 184 Esophagus............................. 46 Cerebrovascular Occlusive Disease........ 189 Stomach............................... 60 Aortoiliac Occlusive Disease.............. 191 Femoropopliteal and Tibial Chapter 5. Small Bowel.......................... 66 Occlusive Disease.................... 193 Anatomy............................... 66 Upper Extremity Occlusive Disease........ 194 Physiology............................. 68 Splanchnic Occlusive Disease............. 195 Immune Function....................... 70 Venous Disease: Acute Venous Crohn Disease.......................... 70 Thromboembolic Disease.............. 196 Small Bowel Obstruction.................. 72 Postphlebitic Syndrome and Chronic Meckel Diverticulum..................... 75 Venous Insufficiency.................. 198 Benign Small Bowel Tumors............... 76 Superficial Thrombophlebitis............. 199 Small Bowel Malignancy.................. 77 Vascular Noninvasive Diagnostic Studies.... 199 Chapter 6. Colon, Rectum, and Appendix........... 80 Chapter 13. Pediatric Surgery..................... 201 Colorectal and Anal Disorders............. 80 Head and Neck........................ 201 Anorectal Disorders...................... 94 Chest................................ 204 Appendix and Appendicitis................ 98 Abdominal Wall....................... 208 Abdomen............................. 211 Chapter 7. Hepatobiliary System................. 100 Abdominal Cysts....................... 221 Hepatic System......................... 100 Oncology............................ 223 Biliary System.......................... 111 Chapter 14. Orthopedic Surgery................... 226 Chapter 8. Pancreas and Spleen.................. 117 Fractures............................. 226 Pancreas.............................. 117 Orthopedic Syndromes.................. 236 Spleen................................ 134 Orthopedic Oncology................... 237 Chapter 9. Endocrine Surgery.................... 140 Chapter 15. Neurosurgery........................ 242 Thyroid.............................. 140 Congenital Malformations and Disorders Parathyroid Glands and of Cerebrospinal Fluid Circulation....... 242 Hyperparathyroidism.................. 146 Intracranial Bleeding.................... 243 Adrenal Glands........................ 149 Diseases of the Spine: Spinal Pancreas............................. 153 Cord Injury......................... 244 Carcinoid Tumors...................... 154 Benign and Malignant CNS Tumors........ 245 xv McFadden_FM.qxd 5/30/08 12:50 PM Page xvi xvi CONTENTS Chapter 16. Urology............................ 247 Chapter 18. Cardiothoracic Surgery................ 280 Kidney.............................. 247 Diagnostic Tests....................... 280 Bladder.............................. 251 Cardiac Disease........................ 281 Prostate............................. 255 Pulmonary Disease..................... 292 Penis............................... 258 Urethra.............................. 261 Chapter 19. Transplantation...................... 297 Scrotum............................. 262 Immunobiology....................... 297 Spermatic Cord....................... 263 Organ Supply and Demand.............. 303 Testis............................... 264 Transplantation of Specific Organs......... 306 Chapter 17. Otolaryngology...................... 267 Chapter 20. Acute Abdomen..................... 312 Common Otolaryngologic Severe Abdominal Pain.................. 312 Conditions......................... 267 Acute Appendicitis..................... 319 Congenital Conditions................. 270 Abdominal Pain in Women.............. 322 Otitis............................... 271 Fractures............................ 273 Appendix A: Next Step Questions........... 325 Neoplasms........................... 275 Appendix B: Shelf Questions............... 337 Squamous Cell Answers.............................. 351 Carcinoma......................... 277 Index................................ 359 McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 1 SURGICAL PHYSIOLOGY TER CHAP 1 Surgical Physiology Larry Roberts, MD Jamshed Zuberi, MD Farooq Shahzad, MD FLUIDS AND ELECTROLYTES All surgical patients need intravenous access and most receive intravenous fluids. The gen- eral surgeon must be well versed in the kinds and quantities of fluids to be used, the dif- ferences in crystalloids, colloids, and blood products, and the electrolyte disturbances common in surgical diseases. I. Body Water and Distribution A. The human body is 45% to 60% water by weight. For a 70-kg adult, there are 31.5 to 42 liters of water throughout the body. Body mass and habitus play roles in percentage of water, as does gender (females have a slightly lower water percentage than males). B. The total body water (TBW) is distributed in the following ways: 1. Extracellular compartment (40% TBW). In a 70-kg adult, a. Intravascular/plasma space (25% extracellular water). the intravascular b. Extravascular/interstitial space (75% extracellular water). volume ⫽ 70 ⫻ 0.4 ⫻ 0.25 2. Intracellular compartment (60% TBW). ⫽ 7 liters. C. The extracellular water electrolyte composition is primarily that of sodium, chloride, and bicarbonate. The intracellular water electrolyte composition is primarily that of potassium, organic phosphate, and sulfate. D. The intravascular water also has many proteins (mostly albumin), which account for plasma colloid oncotic pressure. E. The kidneys maintain volume and composition of body fluid by two mecha- nisms: regulation of water excretion via antidiuretic hormone (ADH), and reab- sorption of sodium. 1. By regulating sodium and water metabolism, the kidneys maintain volume and body fluid composition body in a very narrow range. Urinalysis is a 2. Osmolality throughout all compartments remains similar even if the solutes valuable tool, are different. Regulation is primarily by the kidneys: if water intake because changes in the urine decreases, the kidneys can concentrate the urine to a solute concentration reflect changes in body water four times that of the plasma, thus maintaining body osmolality. composition. II. Volume Disorders A. Starling fluid flux equation 1. The movement of fluids and proteins between the intravascular and intersti- tial spaces is governed by the Starling fluid flux equation: Q ⫽ Kf (Pmv ⫺ Pt) ⫺ σ(pmv ⫺ pt) where σ is the osmotic reflection coefficient, pmv is the capillary colloid osmotic pressure, pt is the tissue interstitial colloid osmotic pressure, Kf is the filtration coefficient, Pmv is the capillary hydrostatic pressure, and Pt is the tissue interstitial hydrostatic pressure. 1 McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 2 2 STE P-U P TO S U R G E RY SURGICAL PHYSIOLOGY 2. The net fluid flux in normal patients favors movement of fluid from the intravascular to the interstitial space. 3. Example: During hemorrhage, the initial Pmv drops, favoring the influx of fluid from the interstitial to the intravascular space. In cardiac failure, Pmv increases, and fluid flux into the interstitial space can result in pulmonary edema. B. Volume overload 1. Syndrome of inappropriate antidiuretic hormone secretion (SIADH). This syndrome can occur after head injury, some cancers, and burns. The patient is hyponatremic, and hypervolemic (the extracellular fluid volume is increased). The patient also has concentrated urine and high urine sodium concentrations. Lethargy and coma can ensue. Treatment includes free-water intake restriction, replacing lost sodium with intravenous saline infusion, and a loop diuretic such as furosemide (Lasix). 2. Iatrogenic conditions. In the majority of hospitalized surgical patients, volume overload is iatrogenic (caused by management of the health care team). Attention to the volume of administered fluids is required, and can be anticipated by the increase in patient weight. C. Volume depletion 1. Diabetes insipidus (DI) occurs in head trauma patients due to damage in the hypothalamic nuclei or hypophyseal stalk. Large urine outputs that may reach 2 liters/hour are characteristic. Urine sodium is low, and the patient is hypernatremic and hyperosmolar. a. Treatment is supportive, with replacement of free water as guided by the following estimate: (Body weight) ⫻ (% water) ⫽ normal TBW (140/current serum sodium) ⫻ TBW ⫽ current body water TBW ⫺ current body water ⫽ water deficit b. Example: In a 70-kg man with a serum sodium of 156 meq/L, (70) ⫻ (0.6) ⫽ 42 L normal TBW (140/156) ⫻ (42 L) ⫽ 37.7 L current TBW 42 L ⫺ 37.7 L ⫽ 4.3 L water deficit 2. Gastrointestinal (GI) fluid losses a. Table 1-1 lists the typical electrolyte compositions and volumes of differ- ent gastrointestinal fluids. Often, this can aid in fluid and electrolyte replacement strategy. b. Example: In a patient on a proton-pump inhibitor, or H2 blocker therapy (that is, low acid stomach fluid), who has emesis, the typical replacement fluid would be 0.45% normal saline with 20 mEq KCl (Na⫹ ⫽ 72, Cl⫺ ⫽ 92, K⫹ ⫽ 20), and to maintain isotonicity, the commercially available fluid adds 5% dextrose. Therefore, D51/2 NS with 20 mEq KCl is the typi- cal crystalloid fluid replacement for protracted emesis. c. Choosing fluids and amounts. In response to a fall in blood pressure and intravascular volume, angiotensin I is released, converted to angiotensin II by angiotensin converting enzyme. This causes vasoconstriction. Angiotensin II also stimulates the release of aldosterone from the adrenal gland. Aldos- terone affects the kidney by reabsorbing more sodium and thereby “holding onto” more water. A byproduct is renal potassium wasting, or excretion of potassium in the urine. (1) In most surgical patients, a balanced isotonic salt crystalloid solution is used for intravenous fluid replacement and management. The body loses water in the urine, stool, and via insensible (evaporative) losses. Open wounds dramatically increase the latter. It is estimated that during open abdominal surgery, up to 1 L insensible losses occur per hour. McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 3 S U R G I CAL P HYS I O LO GY 3 SURGICAL PHYSIOLOGY T A B L E 1-1 Electrolyte Composition and Volumes of Gastrointestinal Fluids Volume Na⫹ (mEq/L) K⫹ (mEq/L) Clⴚ(mEq/L) HCO3ⴚ (mEq/L) (mL/24 hr) Stomach, high acid 20 10 120 0 1,000–9,000 Stomach, low acid 80 15 90 15 1,000–2,500 Pancreas 140 5 75 80 500–1,000 Bile 148 5 100 35 300–1,000 Proximal small bowel 110 5 105 30 1,000–3,000 Distal small bowel 80 8 45 30 1,000–3,000 Colon/diarrhea 120 25 90 45 500–17,000 (2) In resuscitation, blood loss volume is estimated, and three times that volume is replaced with a crystalloid. (Crystalloids readily leave the intravascular space within 20 minutes after a one-liter infusion of crystalloid, and only 200 mL remain intravascularly!) However, the clinical scenario must guide the volume of fluid resuscitation. In blunt trauma patients, the volume tends to be greater initially than that given to penetrating trauma victims. (3) In the adult, fluid maintenance requirements approximate 30 mL/kg body weight/24 hours. Maintenance fluid after resuscitation is also estimated using the 4-2-1 formula: 4 L/kg for the first 10 kg body weight. 2 mL/kg for the second 10 kg body weight. 1 mL/kg for all additional weight. (4) The postoperative, or physiologically stressed, patient is glucose intol- erant as a result of high circulating glucagon levels and relative insulin Based on an esti- resistance. Diabetics tend to be particularly hyperglycemic at these mated need of 30 mL/kg/hr, a 70-kg man requires times, and the high serum glucose can function as an osmotic agent 2,100 mL crystalloid per day to promote inappropriate diuresis. During the first 48 to 72 hours replacement and maintenance postsurgery and after trauma, it is unlikely that exogenous glucose fluid, or approximately 88 mL will provide an energy substrate. Therefore, crystalloid solutions fluid per hour. The patient’s tem- with dextrose should be avoided during this time. See the nutrition perature, degree of GI fluid losses section later in the chapter for guidance. Commonly, lactated (urine output), and overall cardio- Ringers or normal saline solutions are appropriate choices for surgi- vascular state may favor a higher cal patients until specific restrictions are necessary. replacement rate. III. Electrolyte Abnormalities A. Hypernatremia. Commonly, hypernatremia is seen in free water deficit. This condition may occur as a result of DI or a significant renal condition. Please refer to the section on volume deficit. B. Hyponatremia. This condition, which may occur as a result of isotonic fluid loss, can be seen in SIADH (discussed above), in adrenal insufficiency, or in hyperglycemia, where the osmotic effects of glucose lead to inappropriate fluid loss from the kidney. In usual circumstances, a balanced salt solution can be used to replace sodium deficits. C. Hyperkalemia 1. This serious condition mandates prompt attention. It can result from any catabolic state, such as crush injuries in trauma, burns, prolonged illness, hemolysis, renal failure, and from adrenal insufficiency (addisonian crisis). Depolarizing paralytics such as succinylcholine (commonly used McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 4 4 STE P-U P TO S U R G E RY SURGICAL PHYSIOLOGY for rapid-sequence induction anesthesia) can cause massive muscle potas- sium release and acute hyperkalemia. In acute scenarios, most clinical manifestations are absent. However, an abnormal electrocardiogram (EKG) demonstrating progressive peaked T-waves and widening of the QRS complex can ultimately lead to cardiac arrest. Hyperkalemia also occurs in acidosis (see later in the chapter). 2. Treatment is based on rapidity of rise of serum potassium and the underly- ing cause. a. Serum potassium is actively transported intracellularly with insulin. There- fore, initial treatment is administration of intravenous glucose (1 ampule of D50%) and intravenous regular insulin (20 U). b. Correcting a metabolic acidosis with sodium bicarbonate can lower serum potassium levels. c. Calcium gluconate is another option—calcium antagonizes the tissue effects of hyperkalemia and thereby minimizes cardiac effects. The infusion of calcium does not by itself lower serum potassium levels. d. If hyperkalemia is due to adrenal insufficiency, hydrocortisone can be administered. Hyperkalemia due to renal failure may require hemodialysis or peritoneal dialysis. e. A slower treatment is Kayexalate (sodium polystyrene sulfonate, a cation exchange resin), which can be given orally or by enema, and binds potas- sium in the GI tract in exchange for sodium. D. Hypokalemia 1. Obligatory potassium losses occur in both the urine (30–60 mEq/day) and stool (30–90 mEq/day). Increased potassium loss can result from emesis, diarrhea, diuretic use, DI, and metabolic alkalosis. 2. Increased urinary excretion of potassium occurs when the serum potassium level rises above 4 mEq/L. Aldosterone release is increased as a result of hyperkalemia, promoting excretion of potassium in the distal tubule of the kidney. In patients with emesis, the loss of hydrogen ion in the emesis results in potassium retention in the kidney (to maintain electrical neutrality) at the expense of hydrogen ion excretion. The emesis causes a hypochloremic, hypokalemic metabolic alkalosis, worsened paradoxically over time by the kidney, leading to a paradoxical aciduria. 3. Another cause of hypokalemia is potassium loss, primarily from the kidney. This is called renal wasting of potassium. Greater than 30 mEq/L of urinary potassium when the serum potassium is ⬍3.5 mEq/L defines renal potas- sium wasting. The three causes of renal potassium wasting are diuretic ther- apy, effects of aldosterone, or alkalosis. 4. When assessing for hypokalemia, the acid-base status of the patient must be ascertained first. If the patient is alkalemic, the hypokalemia may simply be an ion exchange issue; the more alkalemic the intravascular space is, the more hydrogen ion is shifted intravascularly and potassium shifts extravas- cularly. Figure 1-1 suggests a replacement strategy for potassium when alka- losis exists. Often correcting the underlying alkalosis resolves the hypokalemia and should be considered first. This is depicted in Table 1-2. 5. Treatment most often consists of potassium replacement once the acid–base status of the patient has been ascertained. Intravenous potassium (usually potassium chloride) generally is given at rates of 20 mEq/hour, and causes local discomfort if given peripherally. A preferable route is through a central venous line. If the patient can tolerate it, oral administration is preferred. If the cause of hypokalemia is diuretic therapy, consider alternatives to that therapy. E. Hypercalcemia. This condition occurs with hyperparathyroidism, cancer, hyperthyroidism, adrenal insufficiency, and prolonged immobilization. Serum calcium levels of 12 g/dL and greater are a medical emergency and should be managed with intravenous saline. Loop diuretics, steroids, and calcitonin are additional treatments. McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 5 S U R G I CAL P HYS I O LO GY 5 SURGICAL PHYSIOLOGY F I G U R E 1-1 Relationship of serum potassium to total body potassium stores at different blood pH levels. 7.0 8.0 pH Serum potassium concentration (meq/L) 7.1 7.0 7.2 6.0 7.3 /L 7.4 eq +] n 7.5 5.0 [H 0 7.6 10 7.7 4.0 79 63 50 3.0 40 32 25 2.0 1.5 −20 −10 0 +10 +20 Potassium depletion or excess (%) (Reprinted, with permission, from Scribner B, ed. University of Washington Teaching Syllabus for the Course on Fluid and Electrolyte Balance.) F. Hypocalcemia. This is a more common calcium abnormality in surgical patients and may result from hypoparathyroidism, pancreatitis, severe trauma and crush injuries, necrotizing fasciitis, and severe renal failure. Clinically, patients develop hyperactive deep tendon reflexes and a Chvostek sign (an abnormal reaction to stimulation of the facial nerve), abdominal cramps, and carpopedal spasm. Treatment initially involves treating a metabolic alkalosis if it exists, then replacing calcium with calcium chloride or glu- conate. G. Hypermagnesemia. Hypermagnesemia is rare in surgical patients, but can occur with renal disease. Iatrogenic hypermagnesemia can occur in these patients with excessive magnesium intake through antacid and laxative therapy. Patients with hypermagnesemia are lethargic and weak. EKG abnormalities are similar to those in hyperkalemia. Progressive hypermagnesemia result in the loss of deep tendon reflexes, somnolence, coma, and death. Treatment consists of intravenous normal saline, calcium infusions (similar to hyperkalemia, calcium antagonizes the neuromuscular effects of hypermagnesemia), and possibly dialysis if the patient has severe renal failure. T A B L E 1-2 Prediction of Serum Potassium Concentrations in Acid–Base Abnormalities Assuming No Potassium Wasting If Serum pH is: The Predicted Serum Kⴙ (mEq/L) 7.10 5.9 7.20 5.1 7.30 4.7 7.40 (normal) 4.1 7.50 3.8 7.60 3.1 7.70 2.6 McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 6 6 STE P-U P TO S U R G E RY SURGICAL PHYSIOLOGY H. Hypomagnesemia 1. This abnormality occurs as a result of poor dietary intake, malabsorption in the GI tract, excessive GI loss (for example, diarrhea), enteric fistulas, chronic alcohol use and abuse, acute pancreatitis, severe burns, prolonged use of total parenteral nutrition (TPN) with insufficient magnesium, hyper- aldosteronism, and hypercalcemia. Symptoms are similar to those of hypocalcemia (hyperactive deep tendon reflexes, Chvostek sign, tremors, delirium, and seizures). 2. Treatment consists of replacing magnesium. Oral replacement is best. Intra- venous magnesium in the form of magnesium sulfate is often used, especially in more severe deficiencies. While replacing magnesium, the EKG should be moni- tored, and in renal failure, any magnesium must be given with great caution. I. Hypophosphatemia. This condition occurs in hyperparathyroidism and mal- nourished patients (for example, alcoholics). Neuromuscular effects (fatigue, weakness, convulsions, and even death) predominate when serum phosphorus levels fall below 1 mg/dL. Replacement is accomplished either orally or par- enterally (potassium phosphate). J. Hyperphosphatemia. This disorder occurs in severe trauma, muscle breakdown, and in severe renal failure. Elevated serum phosphorus decreases intravascular calcium. Phosphate-binding antacids (such as aluminum hydroxide) can be used, as well as diuretics to promote urinary excretion of phosphorus. In severe renal failure, hemodialysis may be necessary. IV. Acid–Base Disorders A. General principles 1. Hydrogen ions are generated in the body at a rate of about 70 mEq/kg/day. Carbon dioxide is formed from aerobic metabolism. The Henderson– Hasselbalch equation depicts the relationship of bicarbonate to carbonic acid and pH: pH ⫽ pK ⫹ log ([HCO3⫺] (0.03 p ⫻ CO2) A simpler form of this same equation is: [H⫹] ⫽ (24 ⫻ pCO2) [HCO3⫺] and it must be remembered that: H2O ⫹ CO2⫺ ⫽ H2CO3 ⫽ HCO3⫺ ⫹ H⫹ 2. The serum pH is a reflection of the amount of carbon dioxide that is pro- duced, the efficiency of elimination in the lung (ventilation), and the buffer- ing capability (in the serum, and either elimination or retention of bicarbonate by the kidney) according to the equations above. Hydrogen ion can also be excreted by the kidney in the form of ammonium ion. B. Respiratory disorders 1. Acidosis. Patients who inadequately eliminate CO2 develop respiratory aci- dosis. As a result, hydrogen ion accumulates as the equation above is forced to the “right.” Treatment acutely is to improve ventilation and elimination of CO2. Patients with a metabolic alkalosis (high HCO3⫺) drive the equation to the right, resulting in a compensatory respiratory acidosis. 2. Alkalosis. Patients may hyperventilate for many reasons, including anxiety, hypoxia, sepsis, and a mechanically induced small tidal volume. Elimination of excessive CO2 results in the equation being driven to the “left,” causing an alka- losis. Patients who have a metabolic acidosis (high H⫹) also drive the equation to the left, prompting hyperventilation and a compensatory respiratory alkalosis. C. Metabolic disorders 1. Acidosis. Excessive production of hydrogen ion or increased excretion of bicarbonate results in a metabolic acidosis. The decrease in bicarbonate is McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 7 S U R G I CAL P HYS I O LO GY 7 SURGICAL PHYSIOLOGY exchanged for an increase in serum chloride, maintaining a normal anion pap. The anion gap (AG) is simply measured by: [HCO3 ⫹ Cl⫺] ⫺ Na ⬍15 mEq/L If the AG is greater than 15, an unmeasured anion (such as lactate or ketoacid) is present. a. Distinguishing AGA (anion gap acidosis) from NAGA (non-anion gap acidosis) is critical in evaluating a patient with a metabolic acidosis. Treating the underlying cause of the acidosis is most relevant. In NAGA, bicarbonate depletion is primarily the cause. b. Example: In AGA, the presence of lactate may signify inadequate perfu- sion and anaerobic metabolism, generating lactate. In this case, treatment is directed at restoring perfusion. 2. Alkalosis. The kidneys play a significant role in acid–base homeostasis. Active hydrogen ion secretion occurs in response to acidosis, and bicarbon- ate combines with hydrogen ion to form carbonic acid and CO2, thereby facilitating reabsorption of bicarbonate. D. Mixed disorders. In the acute phase of injury or surgery, many acid–base disor- ders are purely respiratory or metabolic. However, patients with premorbidities and medical conditions, as well as those who are beyond the acute phase of their disease, often manifest mixed acid–base disorders. 1. Example: A patient who suffers an injury and is in shock develops lactic (metabolic) acidosis (AGA). The patient hyperventilates to remove CO2 and develops a compensatory respiratory alkalosis. However, it is uncommon for the compensation to ever exceed the primary process. Therefore, despite the patient’s best efforts, he or she remains acidotic with a primary metabolic acidosis and compensatory respiratory acidosis until the shock and poor perfusion are corrected with resuscitation. 2. Example: A patient suffers acute respiratory distress syndrome, and this results in the inability of the lungs to ventilate adequately. Therefore, the PaCO2 rises, resulting in a respiratory acidosis. Over time (more than 24 hours), the kidneys respond and excrete hydrogen ion and chloride in order to retain bicarbonate. This results in a compensatory metabolic alkalosis. However, until the lung condition improves, the compensation is partial, and the patient remains slightly acidotic. 3. Example: A patient who has diarrhea and chronic obstructive pulmonary dis- ease may have a high respiratory rate and therefore a respiratory alkalosis. However, the diarrhea causes loss of fluid and bicarbonate, and results in a metabolic acidosis. 4. Example: A patient with vomiting may present with a metabolic alkalosis. The patient may also be breathing rapidly due to abdominal pain, and may also have a respiratory alkalosis. E. Arterial blood gas and interpretation 1. Co-oximeter analyzer separately can measure oxyhemoglobin, methemoglo- bin, and carboxyhemoglobin. A normal ABG is: PaO2 ⫽ 100 mm Hg, PaCO2 In pure respiratory ⫽ 40 mm Hg, pH ⫽ 7.40, bicarbonate ⫽ 24 mEq/L, base excess/deficit ⫽ 0, disorders, a rise in and HbO2 ⫽ 100%. PaCO2 by 10 lowers the pH by 0.08. Therefore, in respiratory 2. In a pure metabolic condition, the PaCO2 remains normal at 40, but acidosis, a PaCO2 ⫽ 50 results in the pH is low (in a metabolic acidosis) or high (in a metabolic alkalosis). a pH ⫽ 7.32. In respiratory The calculated base deficit or excess, respectively, reflects the degree alkalosis, a PaCO2 ⫽ 30 results in of metabolic derangement. It is important to remember that base a pH ⫽ 7.48. In both cases, the deficit and excess are a reflection of the metabolic acidosis or calculated bicarbonate is still alkalosis, respectively, and not a reflection of respiratory acid–base 24 and the base excess/deficit is conditions. still 0. 3. In mixed acid–base disorders, the base deficit/excess as seen on an ABG helps sort out the primary disorder. With metabolic acidosis, the AG further helps sort out the abnormality and direct treatment. McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 8 8 STE P-U P TO S U R G E RY SURGICAL PHYSIOLOGY T A B L E 1-3 Solute Concentrations of Standard Crystalloid Solution Naⴙ Clⴙ Kⴙ HCO3ⴚ Caⴙ Crystalloid (mEq/L) (mEq/L) (mEq/L) (mEq/L) (mEq/L) Glucose Lactate Normal saline (0.9%) 154 154 Lactated Ringers 130 109 4 28 2.7 D51/2NS 77 77 50 D51/2NS ⫹ 20KCl 77 97 20 50 V. Fluid Therapy A. Crystalloids. The solute concentrations of four typical crystalloids are presented in Table 1-3. 1. Normal saline is ubiquitously used for dehydration and hypovolemia. It is compatible with blood product transfusion and most medications. It is the most commonly used fluid in trauma resuscitation. 2. Lactated Ringers provides less sodium than normal saline and offers a small amount of other solutes as well. Some studies suggest that lactated Ringers stimulates the immune system. In severely underperfused patients, the increase in circulating lactate may exacerbate an acidosis. Lactated Ringers is not compatible with blood product transfusions and with some medications. Despite these considerations, lactated Ringers is widely used and has equal efficacy in most circumstances to normal saline. The L-lactate is converted to bicarbonate in the perfusing liver, thereby helping to resolve acidosis. 3. D51/2 NS. a. This mildly hypotonic fluid provides a small amount of dextrose along with hypotonic salt. Adding 20 mEq/L of KCl results in an almost iso- tonic solution whose solute concentrations approach that of stomach fluid. The small amount of dextrose helps decrease the hypotonicity and may help with minimizing ketoacidosis. However, the dextrose is not a nutritional substrate in this setting. b. Example: Initially in the resuscitative management of the patient with emesis, normal saline should be used. Once stabilized, maintenance with D51/2 NS with 20 KCl is often used as the replacement fluid. 4. Other crystalloids. Another crystalloid solution is 3% NaCl, which can be used as a resuscitation fluid (for example, with burns), as well as occasion- ally in traumatic brain injury and intracranial hypertension. Hypertonic saline solutions of various concentrations have been studied. B. Colloids 1. Plasmanate is a dilute colloid consisting of 5% albumin in saline. It is occa- sionally used in anesthesia but is not common in other settings. 2. A solution of 25% albumin (formerly called salt-poor albumin) is a concen- trated form of albumin derived from human serum. Albumin has limited indica- tions. When colloid osmotic pressure is low, albumin can be used in some circumstances. Associated irradiation and infectious complications are very rare. C. Synthetic colloids 1. The hetastarch (Hespan) synthetic colloids have the greatest application in surgery and trauma. They are excellent volume expanders; the volume infused remains intravascularly longer than crystalloids. In addition, there are few side effects. However, large quantities of hetastarch can interfere with coagulation, and therefore its use must be limited in the trauma patient. 2. Dextran 40 and 70. These two synthetic colloids were once popular as both volume expanders and as hemorheologic modifiers (making the blood less vis- cous and promoting perfusion). They are still used in some vascular situations. 3. Gelatin synthetic colloids are available in Europe and Asia, but not in the United States. McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 9 S U R G I CAL P HYS I O LO GY 9 SURGICAL PHYSIOLOGY D. Blood products. U.S. blood banks provide an array of blood products, and transfusion is based on clinical need. Although viral and other infections are well-known transmissible complications of blood product transfusions, they occur rarely (1 in 200,000 units for hepatitis B, and 1 in 1.6 million units for hepatitis C or human immunodeficiency virus (HIV)). Transfusion reactions are significantly more common (1 in 200 units), can be morbid, and on rare occasion, anaphylaxis can be life threatening. Judicious transfusion with a clear clinical indication is always warranted. 1. Whole blood is not approved in the United States by the American Red Cross. In the United States, blood component therapy is the standard. Inter- estingly, the U.S. military has used whole blood transfusions overseas in combat, with excellent results. 2. Each unit of packed red blood cells (PRBCs) is a volume of approximately 550 mL and weighs 400 g. Generally speaking, one unit of transfused blood equates to a patient hemoglobin rise of 1 g/dL, but depends on the donor’s initial hemoglobin. 3. Platelets are pooled from multiple donors and generally are provided in a six-pack. Because the platelets are pooled from multiple donors, their trans- fusion must be for clinically appropriate reasons only. 4. Fresh frozen plasma (FFP) is rich in fibrinogen, coagulation factors, and protein. When there is a need for a colloid, as well as to reverse a coagu- lopathy, FFP is transfused. Often, the amount is determined by the clinical appearance of bleeding and the prothrombin time (PT). 5. Cryoprecipitate is pooled from multiple donors, and similarly to platelets, its administration must be guided by a true need. Cryoprecipitate is especially rich in fibrinogen. 6. Recombinant factor VIIa (rFVIIa) is a U.S. Food and Drug Administration (FDA)-approved agent for hemophilia. However, its use has recently gained popularity in bleeding patients. Some data exist regarding its utility in car- diac surgery. There are no conclusive studies in trauma and in surgery, but rFVIIa appears promising as an adjunct in the bleeding patient, especially one who is already acidotic from hypoperfusion. It is sometimes adminis- tered at a dose of 90 µg/kg body weight. rFVIIa currently is quite expensive. E. Blood substitutes have been investigated for 40 years. At the moment, there is no FDA-approved blood substitute. HEMOSTASIS/COAGULATION I. General Principles. Hemostasis is a complex interaction of multiple components in the body. Usually, it occurs in an ordered way as the body’s response to injury, but can also occur in a dysfunctional manner, leading to significant morbidity. A. Vasoconstriction is the initial response to injury. It occurs as a reflex to most stimuli. B. Platelet aggregation results from the release of platelet factors and fibrin. This leads to formation of a platelet plug that acts as a physical barrier to further bleeding. C. Coagulation is an interaction of factors that leads to the formation of a fibrin and platelet plug. It is a series of enzymatic reactions that can be slowed with hypothermia or a deficiency of factors. D. Fibrinolysis is the final step in the coagulation cascade. Its main effect is to pre- vent the thrombosis from going unchecked. It also helps break down the clot once bleeding has been controlled and leads to improved blood flow in the vessel. II. Testing the Surgical Patient for Hemostatic Risk Factors A. For minor surgical procedures, all that is needed is a thorough history and physical. It is especially important to ask about excessive bruising after minor injuries or significant bleeding after small cuts or abrasions. Medications are also an important factor. McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 10 10 STE P-U P TO S U R G E RY SURGICAL PHYSIOLOGY B. If the history and physical are unrevealing, but the patient is to undergo a major surgical procedure (one that involves a large part of the body), or the operation is to involve a part of the body where even a small amount of exces- sive bleeding would have disastrous complications (that is, involving the eye or brain), then additional tests need to be ordered. In most circumstances, check- ing a prothrombin time (PT), prothromboplastin time (PTT), and platelets suf- fices. However, if these are normal, but the history or physical suggest some bleeding abnormalities, then tests such as bleeding time can be ordered. C. Other tests that are useful include a hematocrit and a platelet count (although this gives no information on the function of the platelets). III. Tests of Hemostasis and Coagulation A. PT measures mostly the extrinsic factors that lead to clotting. Extrinsic refers to the interaction between platelets, and specifically, factors outside the blood vessel, leading to initiation of the clotting cascade. It is also used as a surrogate to reflect the function of the liver. B. PTT refers to the function of the intrinsic pathway. C. Bleeding time is not useful as an initial screening test because it is labor inten- sive, and the results can be subjective. It is useful though when the bleeding disorder is caused by factors that are not measured by the PT or PTT. IV. Congenital Defects A. Hemophilia A, or classic hemophilia, is caused by an abnormality in factor VIII. It occurs as a sex-linked recessive trait that occurs almost exclusively in males. Although history may lead to the diagnosis, levels of factor VIII confirm it. Patients also have an elevated PTT, with a normal PT. Treatment is with factor VIII or cryoprecipitate. B. Hemophilia B, or Christmas disease, is caused by a factor IX abnormality. It is also sex-linked and recessive, and so occurs exclusively in males. The disease has a similar presentation to classic hemophilia. Treatment is with factor IX concentrate. C. Von Willebrand disease is secondary to abnormalities with von Willebrand factor (vWF). Normally vWF helps in platelet adhesion to collagen and cross- linking platelets in clot aggregation. It is commonly inherited in an autosomal dominant pattern with variable penetrance. Affected people usually have episodes of mucocutaneous bleeding. Bleeding time is commonly prolonged, although the PTT can also be prolonged. Treatment is with cryoprecipitate. V. Acquired Defects A. Platelet defects can occur secondary to drugs, uremia, or thrombocytopenia (which may be related to massive blood transfusion or platelet destruction). B. Fibrinogen deficiency usually occurs with disseminated intravascular coagula- tion (DIC). DIC can be brought on by multiple causes, including retained pla- centa, sepsis, or amniotic fluid embolism. Treatment is to remove the underlying cause, if possible. VI. Hepatic and Renal Disease A. Liver disease, especially if severe, can lead to depletion in coagulation factors by a decrease in production. All factors, except for factor VIII and von Willebrand factor, Low platelets can which are produced by the endothelium, are produced by the liver. This can lead to also be an indicator a severe coagulopathy that is difficult to correct. Vitamin K should be administered that significant liver disease first. If that fails, then FFP may be necessary. Platelet transfusion may be warranted exists. if concomitant thrombocytopenia is present. A prolonged PT is usually present. B. Renal failure leads to a uremic state. This occurs typically when the patient has not undergone dialysis and the blood urea nitrogen has increased significantly. The uremia interferes with the aggregation of platelets and leads to a diffuse bleeding diathesis. The best way to correct this is through dialysis. If that is not immediately available, then intravenous 1-deamino-8-D-arginine vasopressin or conjugated estrogens have been shown to work. McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 11 S U R G I CAL P HYS I O LO GY 11 SURGICAL PHYSIOLOGY VII. Anticoagulation A. Heparin is a naturally occurring heterogeneous mixture of glycosaminoglycans with differing molecular weights. It accelerates the effect of antithrombin III, leading to a systemically anticoagulated state. It is given intravenously or sub- cutaneously. The heparin antithrombin III complex inactivates several factors The half-life of in the anticoagulant cascade, especially thrombin and factor X. The level of heparin is just anticoagulation achieved can be measured by checking the PTT. over 1 hour. B. Low-molecular-weight heparin (LMWH), which is made by fractionating heparin into its lower-weight molecules, acts primarily by inhibiting factor X. It is always administered subcutaneously. The lower-weight molecule is incapable of inacti- The efficacy of vating thrombin or antithrombin. Because of this, LMWH does not prolong PTT. LMWH can be mea- C. Warfarin leads a deficiency of vitamin K, resulting in a decrease in production sured by checking anti-Xa levels. by the liver of factors II, VII, IX, X, protein C, and S. The drug is given orally, with a half-life of about 1.5 days, and so it takes a few days to take effect and to reverse. The level of anticoagulation can be measured by checking the PT Because proteins C and S lead to sys- (the international normalized ratio [INR] is an indirect measure of the PT). temic anticoagulation, their D. Heparin-induced thrombocytopenia (HIT) occurs in two forms: deficiency can lead to a pro- 1. HIT type I, which occurs frequently. It usually occurs with a drop in platelet thrombotic state if the patient is count of more than 100,000. It occurs by a nonimmune-mediated phenome- given warfarin compounds. For non. There is no risk of thrombosis, and discontinuation of heparin is not this reason, heparinization should necessary. always be performed prior to 2. HIT type II, which occurs far less frequently (in 2–10% of all exposed administering warfarin. patients). It should be suspected when the platelet count drops by more than 50% from baseline, or to a total less than 100,000. The diagnosis can be confirmed by checking for antibodies to HIT antibody. The cause is an immune-mediated reaction against heparin-platelet factor antibodies. This results in aggregation of platelets, leading to thrombocytopenia and possibly HIT is also possible arterial and venous thrombosis. Because up to 30% of patients with HIT with LMWH (at a type II develop thrombosis even after discontinuation of heparin, anticoagu- lower incidence than with lation with a nonheparinoid product is essential. regular heparin). VIII. Management of Bleeding. Local control of bleeding is especially important during, and sometimes after, surgical procedures. The most frequent cause of sur- gical bleeding is inadequate hemostasis in the wound. Less likely causes include coagulopathies. A. Direct pressure is a very effective way to control and slow most bleeding. Liga- ture of vessels also controls most surgical bleeding. Tourniquets can be used for small periods of time under dire circumstances. B. Electrocautery leads to hemostasis by the denaturation of proteins, resulting in coagulation over a large surface area, secondary to the diffusion of the electrical current. C. Chemical agents can act as procoagulants and vasoconstrictors (epinephrine). New agents are being tested; they lead to a mild thermal burn, resulting in coagulation. IX. Replacement Therapy A. Typing and cross-matching is performed to establish serologic compatibility— to establish A, B, O, and the Rh status of the patient. This may take upward of an hour or so to do. If no knowledge about the patient’s blood type is available, but PRBCs are urgently needed, then type O Rh-negative blood can be given to women, and type O Rh-positive can be given to men. If time permits, a type- and-screen can be done, and type-specific blood can be infused. B. Component therapy has mostly replaced fresh whole blood because of cost and efficiency; the American Red Cross does not approve of its usage. C. Platelet concentrates are given for either a significant deficiency in platelet function or quantity. Each unit raises the count by about 10,000/µL. D. Volume expanders are isotonic or hypertonic crystalloid products, such as lactated Ringers, 0.9% normal saline, or 3% normal saline. Artificial colloids such as het- astarch, or natural ones such as albumin, are also useful for volume expansion. McFadden_CH01_001-016.qxd 6/5/08 12:12 PM Page 12 12 STE P-U P TO S U R G E RY SURGICAL PHYSIOLOGY E. Concentrates of factors such as FFP, or concentrates of specific factors such as factor VIII, are useful for replacement of deficiencies or dysfunction. X. Indications for Replacements of Blood and Its Substitutes A. Volume replacement is best performed based on amount of blood loss. Initially, isotonic crystalloid solutions are best. As significant amounts of blood are lost, replacement should be completed using a combination of PRBCs and crystal- loid solutions. If massive bleeding is occurring, and large amounts of transfu- sions are ne