105530__MedicalBooksStore_2016_Schwartz.pdf

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SCHWARTZ’S

PRINCIPLES OF SURGERY ABSITE and Board Review

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NOTICE Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. T e authors and the publisher o this work have checked with sources believed to be reliable in their e orts to provide in ormation that is complete and generally in accord with the standards accepted at the time o publication. However, in view o the possibility o human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication o this work warrants that the in ormation contained herein is in every respect accurate or complete, and they disclaim all responsibility or any errors or omissions or or the results obtained rom use o the in ormation contained in this work. Readers are encouraged to con rm the in ormation contained herein with other sources. For example and in particular, readers are advised to check the product in ormation sheet included in the package o each drug they plan to administer to be certain that the in ormation contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications or administration. T is recommendation is o particular importance in connection with new or in requently used drugs.

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SCHWARTZ’S

PRINCIPLES OF SURGERY ABSITE and Board Review 10th Edition Edited by F. Charles Brunicardi, MD, FACS

Moss Foundation Chair in Gastrointestinal and Personalized Surgery Pro essor and Vice Chair Surgical Services Chie o General Surgery, UCLA Santa Monica Medical Center Department o Surgery David Gef en School o Medicine at UCLA Los Angeles, Cali ornia

Associate Editors Dana K. Andersen, MD, FACS

Program Director Division o Digestive Diseases and Nutrition National Institute o Diabetes and Digestive and Kidney Diseases National Institutes o Health Bethesda, Maryland

Timothy R. Billiar, MD, FACS

George Vance Foster Pro essor and Chairman Department o Surgery University o Pittsburgh School o Medicine Pittsburgh, Pennsylvania

David L. Dunn, MD, PhD, FACS

Executive Vice President or Health Af airs Pro essor o Surgery, Microbiology and Immunology University o Louisville Louisville, Kentucky

John G. Hunter, MD, FACS Mackenzie Pro essor and Chair Department o Surgery Oregon Health &Science University Portland, Oregon

Jef rey B. Matthews, MD, FACS Surgeon-in-Chie and Chairman Department o Surgery Dallas B. Phemister Pro essor o Surgery Chicago, Illinois

Raphael E. Pollock, MD, PhD, FACS

Pro essor and Director Division o Surgical Oncology Chie o Surgical Services The James Comprehensive Cancer Center The Ohio State University Wexner Medical Center Columbus, Ohio

James X. Wu, MD

General Surgery Resident Department o Surgery UCLA David Gef en School o Medicine Los Angeles, Cali ornia

New York Chicago San Francisco Athens London Milan New Delhi Singapore Sydney

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Madrid oronto

Mexico City

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Schwartz’s Principles of Surgery: ABSITE and Board Review, 10th Edition Copyright © 2016 by McGraw-Hill Education. All rights reserved. Printed in the United States o America. Except as permitted under the United States Copyright Act o 1976, no part o this publication may be reproduced or distributed in any orm or by any means, or stored in a data base or retrieval system, without the prior written permission o the publisher. Previous editions copyright 2011, 2007 by T e McGraw-Hill Companies, Inc. 1 2 3 4 5 6 7 8 9 0 ROV/ROV 20 19 18 17 16 ISBN 978-0-07-183891-7 MHID 0-07-183891-0 T is book was set in Minion Pro by Cenveo®Publisher Services. T e editors were Brian Belval and Christie Naglieri T e production supervisor was Catherine Saggese Project management was provided by anya Punj, Cenveo Publisher Services. RR Donnelley was the printer and binder. T is book is printed on acid- ree paper.

Library of Congress Cataloging-in-Publication Data Schwartz’s principles o surgery. ABSI E and board review / edited by F. Charles Brunicardi ; associate editors, Dana K. Andersen, imothy R. Billiar, David L. Dunn, John G. Hunter, Raphael E. Pollock, Je rey B. Matthews.— enth edition. p. ; cm. Principles o surgery. ABSI E and board review Should be used in conjunction with the tenth edition o Schwartz’s principles o surgery. Includes index. ISBN 978-0-07-183891-7 (pbk., alk. paper)—ISBN 0-07-183891-0 I. Brunicardi, F. Charles, editor. II. Schwartz’s principles o surgery. enth edition. Complemented by (expression): III. itle: Principles o surgery. ABSI E and board review. [DNLM: 1. Surgical Procedures, Operative—Examination Questions. WO 18.2] RD31 617.0076—dc23 2015020914 International Edition. ISBN 978-1-259-25124-5; MHID 1-259-25124-1. Copyright 2016 by McGraw-Hill Education. Exclusive rights by McGraw-Hill Education or manu acture and export. T is book cannot be re-exported rom the country to which it is consigned by McGraw-Hill Education. T e International Edition is not available in North America. McGraw-Hill Education books are available at special quantity discounts to use as premiums and sales promotions or or use in corporate training programs. o contact a representative, please visit the Contact Us pages at www.mhpro essional.com

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CONTENTS

Contributors

vii

PART II

Introduction

ix

Specif c Considerations

105

Acknowledgments

xi

16 The Skin and Subcutaneous Tissue

107

17 Breast

115

18 Disorders o the Head and Neck

121

19 Chest Wall, Pleura, and Mediastinum

125

20 Congenital Heart Disease

135

21 Acquired Heart Disease

143

22 Thoracic Aneurysms and Aortic Dissection

151

23 Arterial Disease

159

24 Venous and Lymphatic Disease

179

25 Esophagus and Diaphragmatic Hernia

189

26 Stomach

203

27 The Surgical Management o Obesity

215

28 Small Intestine

219

29 Colon, Rectum, and Anus

225

30 The Appendix

237

31 Liver

241

32 The Gallbladder and Extrahepatic Biliary System

253

33 Pancreas

261

34 Spleen

275

35 Abdominal Wall, Omentum, Mesentery, and Retroperitoneum

283

PART I Basic Considerations

1

1 Leadership

3

2 Systemic Response to Injury and Metabolic Support

5

3 Fluid and Electrolyte Management o the Surgical Patient

9

4 Hemostasis, Surgical Bleeding, and Trans usion

17

5 Shock

25

6 Surgical In ections

33

7 Trauma

41

8 Burns

55

9 Wound Healing

61

10 Oncology

69

11 Transplantation

73

12 Patient Sa ety

81

13 Physiologic Monitoring o the Surgical Patient

87

14 Minimally Invasive Surgery

93

15 Molecular and Genomic Surgery

97

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vi 36 So t Tissue Sarcomas

287

44 Surgery o the Hand and Wrist

335

37 Inguinal Hernias

289

45 Plastic and Reconstructive Surgery

341

38 Thyroid, Parathyroid, and Adrenal

299

46 Anesthesia or the Surgical Patient

343

39 Pediatric Surgery

305

47 Surgical Considerations in the Elderly

347

40 Urology

315

48 Ethics, Palliative Care, and Care at the End o Li e

351

49 Global Surgery

353

41 Gynecology

319

42 Neurosurgery

323

43 Orthopedic Surgery

331

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Ind ex

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357

CONTRIBUTORS

Dana K. Andersen, MD, FACS Program Director Division o Digestive Diseases and Nutrition National Institute o Diabetes and Digestive and Kidney Diseases National Institutes o Health Bethesda, Maryland Timothy R. Billiar, MD, FACS George Vance Foster Pro essor and Chairman Department o Surgery University o Pittsburgh School o Medicine Pittsburgh, Pennsylvania F. Charles Brunicardi, MD, FACS Moss Foundation Chair in Gastrointestinal and Personalized Surgery Pro essor and Vice Chair Surgical Services Chie o General Surgery, UCLA Santa Monica Medical Center Department o Surgery David Ge en School o Medicine at UCLA Los Angeles, Cali ornia Mary Condron, MD Resident Department o Surgery Oregon Health & Science University Portland, Oregon Christopher Connelly, MD Resident Department o Surgery Oregon Health & Science University Portland, Oregon Mackenzie Cook, MD General Surgery Resident Department o Surgery Oregon Health & Science University Portland, Oregon David L. Dunn, MD, PhD, FACS Executive Vice President or Health A airs Pro essor o Surgery, Microbiology and Immunology University o Louisville Louisville, Kentucky

John G. Hunt er, MD, FACS Mackenzie Pro essor and Chair Department o Surgery Oregon Health & Science University Portland, Oregon Scott Louis, MD Surgery Resident Oregon Health & Science University Portland, Oregon Jef rey B. Matthews, MD, FACS Surgeon-in-Chie and Chairman Department o Surgery Dallas B. Phemister Pro essor o Surgery Chicago, Illinois Fernando Mier, MD Advanced GI and Bariatric Surgery Fellow Department o General and Gastrointestinal Surgery Oregon Health and Science University Portland, Oregon Alexis Moren, MD General Surgery Resident Oregon Health & Science University Portland, Oregon Raphael E. Pollock, MD, PhD, FACS Pro essor and Director Division o Surgical Oncology Chie o Surgical Services T e James Comprehensive Cancer Center T e Ohio State University Wexner Medical Center Columbus, Ohio Tana Lynn Repella, MD, PhD General Surgery Resident Department o Surgery Oregon Health & Science University Portland, Oregon Julia C. Swanson, MD Congenital Cardiac Surgery Fellow Department o Surgery exas Children’s Hospital Houston, exas

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viii Erica Swenson, DO General Surgery Resident Department o Surgery Oregon Health & Science University Portland, Oregon

James X. Wu, MD General Surgery Resident Department o Surgery UCLA David Ge en School o Medicine Los Angeles, Cali ornia

Patrick R. Varley, MD Resident Department o General Surgery University o Pittsburgh Medical Center Pittsburgh, Pennsylvania

Estin Yang, MD, MPH Resident Physician Department o Surgery Oregon Health & Science University Portland, Oregon

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INTRODUCTION

T is 10th edition o Schwartz’s Principles of Surgery: ABSITE and Board Review marks a milestone o excellence in surgical education or the betterment o cra , quality o care, and the edi cation o surgical students and colleagues alike. With 842 questions spanning the 49 updated chapters o this edition, including two new chapters, Fundamental Principles o Leadership raining in Surgery and Global Surgery, this is the comprehensive companion text or reviewing and assessing the in ormation compiled in the main book and or preparation or the American Board o Surgery In- raining Examination (ABSI E). Contributors o the primary book have updated the questions or each chapter since the last edition in an e ort to continue to provide

a high level o review on the most up-to-date in ormation and techniques currently taught and employed in the operating theater. We have maintained the proven ormat o providing the answerbearing portion o the text immediately ollowing the question and answer as an ef cient method or rein orcement and recall. T e user may read the question ollowed by the answer as a orm o review, or by covering the right-hand column o the page, the user can complete the questions in a more authentic test ormat and uncover the answers or review/scoring.

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ACKNOWLEDGMENTS

o Brian Belval, Christie Naglieri, and all at McGraw-Hill, we are thank ul or the continued belie in and support o this book. We

wish to thank Katie Elsbury or her dedication to the organization and editing o this book. F. Charles Brunicardi, MD, FACS

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PART I Basic Considerations

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CHAPTER

1

Leadership

1. T e undamental principles o leadership are A. Vision and willingness B. Command and control C. ime management and mentoring D. Coaching, pacesetting, and democratic

Answer: A Vision and willingness are the two undamental principles o leadership. Command and control is a colloquial term or the previously predominant style o leadership in surgery based on ear and intimidation. ime management and mentorship are key leadership skills. Coaching, pacesetting, and democratic are leadership styles. (See Schwartz 10th ed., p. 3.)

2. E ective communication is a key component o leadership, given that miscommunication is a leading cause o medical errors. Which o the ollowing statements is FALSE regarding communication? A. To Err Is Human, a publication by the US Institute o Medicine, identi ed medical errors as the eighth leading cause o death in the United States, causing 100,000 deaths annually. B. E ective communication that ensures all team members understand daily goals o care or an ICU patient can signi cantly decrease patient’s length o stay in the ICU. C. Communication errors are o en simply due to negligence and ailure to transmit in ormation. D. In ormation trans er and communication errors cause delays in patient care and can cause serious adverse events. E. Improved communication in OR among the cardiac surgery patients is associated with decreased adverse outcomes.

Answer: C Communication errors are o ten caused by miscommunication due to hierarchical di erences, concerns with upward in luence, con licting roles and role ambiguity, and interpersonal con lict. (See Schwartz 10th ed., p. 6.)

3. Daniel Goleman o the Harvard Business Review described six key leadership styles. Which o the ollowing statements is FALSE regarding leadership styles? A. T e coercive style o leadership is antiquated and is no longer e ective in surgery. B. Democratic leadership is use ul or building team consensus and minimizing conf ict, but may rustrate team members i there is no clear, uni ying vision. C. T e pacesetter leads by example and sets high standards or his team, but typically takes over the tasks o something alling behind instead o building them up. D. T e authoritative leader is o en the most e ective, and ocuses on directing the team toward a common vision, allowing team members to give room or innovation and experimentation, and supporting their e orts.

Answer: A hough it is no longer appropriate as the predominant leadership style, during times o duress when a clear, single leader is needed, a coercive leadership style may be prudent. his is most appropriate in emergency trauma settings. Excessive coercive leadership can erode team members’ sense o responsibility, motivation, sense o participation in a shared vision, and ultimately, per ormance. (See Schwartz 10th ed., p. 9.)

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4 4. Which is FALSE regarding modern conf ict resolution techniques? A. Based upon objectivity and willingness to listen. B. Should seek a solution that bene ts all involved and which is based upon core values o the organization. C. raditional command-and-control technique based on ear and intimidation can lead to sanctions and lawsuits. D. Conf ict resolution is more success ul when both sides can admit they share some ault.

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Answer: D Modern con lict resolution techniques are based upon objectivity, willingness to listen, and pursuit o principle-based solutions. For example, an e ective style o con lict resolution is the utilization o the “abundance mentality” model, which attempts to achieve a solution that bene its all involved and is based upon core values o the organization, as opposed to the utilization o the traditional ault- inding model, which identi ies sides as right or wrong. Application o the abundance mentality in surgery elevates the con lict above the a ected parties and ocuses on the higher uni ying goal o improved patient care. Morbidity and mortality (M&M) con erences are managed in this style and have the purpose o practice improvement and improving overall quality o care within the system, as opposed to placing guilt or blame on the surgeon or surgical trainees or the complication being reviewed. he traditional style o command-and-control technique based on ear and intimidation is no longer welcome in any health care system and can lead to sanctions, lawsuits, and removal o hospital privileges or position o leadership. (See Schwartz 10th ed., p. 7.)

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CHAPTER

2

Systemic Response to Injury and Metabolic Support 1. C-reactive protein (CRP) A. Is secreted in a circadian rhythm with higher levels in the morning B. Increases a er eating a large meal C. Does not increase in response to stress in patients with liver ailure D. Is less sensitive than erythrocyte sedimentation rate as a marker o in ammation

Answer: C he acute phase proteins are nonspeci ic biochemical markers produced by hepatocytes in response to tissue injury, in ection, or in lammation. Interleukin (IL)-6 is a potent inducer o acute phase proteins that can include proteinase inhibitors, coagulation and complement proteins, and transport proteins. Clinically, only C-reactive protein (CRP) has been consistently used as a marker o injury response due to its dynamic re lection o in lammation. Importantly, CRP levels do not show diurnal variations and are not a ected by eeding. Only pre-existing liver ailure will impair CRP production. here ore, it has become a use ul biomarker o in lammation as well as response to treatment. Its accuracy surpasses that o the erythrocyte sedimentation rate. (See Schwartz 10th ed., p.17.)

2. Which o the ollowing is true regarding the in ammatory response ollowing traumatic injury? A. T ere is an acute proin ammatory response caused by stimulation o the adaptive immune system. B. T ere is an anti-in ammatory response that leads to a return to homeostasis accompanied suppression o the innate immune system. C. T e degree o in ammation is proportional to injury severity. D. Systemic in ammation ollowing trauma is related to the immune response to microbes.

Answer: C he degree o the systemic in lammatory response ollowing trauma is proportional to injury severity and is an independent predictor o subsequent organ dys unction and resultant mortality. Recent work has provided insight into the mechanisms by which immune activation in this setting is triggered. he clinical eatures o the injury-mediated systemic in lammatory response, characterized by increased body temperature, heart rate, respirations, and white blood cell count, are similar to those observed with in ection. While signi icant e orts have been devoted to establishing a microbial etiology or this response, it is now widely accepted that systemic in lammation ollowing trauma is sterile. (See Schwartz 10th ed., p.14.)

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6 3. High-mobility group protein B1 (HMGB1) A. Is associated with the best-characterized damageassociated molecular pattern (DAMP), detectable in the circulation within 30 minutes o trauma B. Is a protein secreted by immune-competent cells stimulated by pathogen-associated molecular patterns (PAMPs) or in ammatory cytokines C. Is also secreted by endothelial cells, platelets, and also as a part o cell death D. All o the above

Answer: D he best-characterized DAMP in the context o the injuryassociated in lammatory response is high-mobility group protein B1 (HMGB1), which is rapidly released into the circulation within 30 minutes ollowing trauma. Subsequent studies have proven, however, that HMGB1 is actively secreted rom immune-competent cells stimulated by PAMPs (eg, endotoxin) or by in lammatory cytokines (eg, tumor necrosis actor and interleukin-1). Stressed nonimmune cells, such as endothelial cells, and platelet also actively secrete HMGB1. Finally, passive release o HMGB1 can occur ollowing cell death, whether it is programmed or uncontrolled (necrosis). he diverse proin lammatory biological responses that result rom HMGB1 signaling include: (1) the release o cytokines and chemokines rom macrophage/monocytes and dendritic cells; (2) neutrophil activation and chemotaxis; (3) alterations in epithelial barrier unction, including increased permeability; and (4) increased procoagulant activity on platelet suraces; among others. (See Schwartz 10th ed., p.15.)

4. T e most abundant amino acid in the human body is A. Carnitine B. Arginine C. Glutamine D. Methionine

Answer: C Glutamine is the most abundant amino acid in the human body, comprising nearly two-thirds o the ree intracellular amino acid pool. (See Schwartz 10th ed., p. 53.)

5. What is the role o mitochondrial DAMPs in the injurymediated in ammatory response? A. Mitochondrial DNA induces production o HMGB1. B. Mitochondrial DNA and peptides rom damaged mitochondria activate the macrophage in ammasome. C. Mitochondrial DNA and peptides modulate the antiin ammatory response that suppresses the adaptive immune system. D. Mitochondrial DNA is directly toxic to the liver and lung in high amounts.

Answer: B Mitochondrial proteins and/or DNA can act as DAMPs by triggering an in lammatory response to necrosis and cellular stress. Speci ically, the release o mitochondrial DNA (mtDNA) and ormyl peptides rom damaged or dys unctional mitochondria has been implicated in activation o the macrophage in lammasome, a cytosolic signaling complex that responds to cellular stress. With stress or tissue injury, mtDNA and peptides are released rom damaged mitochondria where they can contribute to a sterile in lammatory response. From an evolutionary perspective, given that eukaryotic mitochondria derive rom bacterial origin, it would make sense that they retain bacterial eatures capable o eliciting a strong response that is typically associated with a pathogen trigger. (See Schwartz 10th ed., p. 16.)

6. Which is FALSE regarding the hypothalamic-pituitaryadrenal (HPA) axis and injury-associated stress? A. T e HPA is initiated by the hypothalamus producing corticotropin-releasing hormone (CRH) in response to in ammatory cytokines. B. CRH acts on the anterior pituitary to stimulate adrenocorticotropin hormone (AC H) secretion. C. CRH simulates the zona asciculata o the adrenal gland to synthesize and secrete glucocorticoids. D. Insuf cient cortisol in response to critical illness can lead to tachycardia, hypotension, weakness, hypoglycemia, hyponatremia, and hyperkalemia.

Answer: C CRH acts on the anterior pituitary to stimulate the secretion o adrenocorticotropin hormone (AC H) into the systemic circulation. AC H acts on the zona asciculata o the adrenal glands to synthesize and secrete glucocorticoids. Cortisol is the major glucocorticoid in humans and is essential or survival during signi icant physiologic stress. he resulting increase in cortisol levels ollowing trauma has several important anti-in lammatory actions. Adrenal insu iciency represents a clinical syndrome highlighted largely by inadequate amounts o circulating cortisol and aldosterone. Classically, adrenal insu iciency is described in patients with atrophic adrenal glands caused by exogenous steroid administration who undergo a stressor such as surgery. hese patients subsequently mani est signs and symptoms such as tachycardia, hypotension, weakness, nausea, vomiting, and ever. (See Schwartz 10th ed., p. 20.)

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7 7. Nutritional ormulas used to treat pulmonary ailure typically increase the at intake o a patient’s total caloric intake to A. 50% B. 20% C. 80% D. 10%

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Answer: A In pulmonary ailure ormulas, at content is usually increased to 50% o the total calories, with a corresponding reduction in carbohydrate content. he goal is to reduce carbon dioxide production and alleviate ventilation burden or ailing lungs. (See Schwartz 10th ed., p. 54.)

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CHAPTER

3

Fluid and Electrolyte Management of the Surgical Patient urs

Answer: C Metab li a id sis with a n rmal ani n gap (AG) results r m either a id administrati n (HCl r NH 4+) r a l ss bi arb nate r m gastr intestinal (GI) l sses, su h as diarrhea, istulas (enteri , pan reati , r biliary), ureter sigm id st my, r r m renal l ss. he bi arb nate l ss is a mpanied by a gain hl ride, thus the AG remains un hanged. (See S hwartz 10th ed., p. 74.)

2. All are p ssible auses p st perative hyp natremia EXCEP A. Ex ess in usi n n rmal saline intra peratively. B. Administrati n antipsy h ti medi ati n. C. ransient de rease in antidiureti h rm ne (ADH) se reti n. D. Ex ess ral water intake.

Answer: C Hyp natremia is aused by ex ess ree water (diluti n) r de reased s dium (depleti n). hus, ex essive intake ree water ( ral r IV) an lead t hyp natremia. Als , medi ati ns an ause water retenti n and subsequent hyp natremia, espe ially in lder patients. Primary renal disease, diureti use, and se reti n antidiureti h rm ne (ADH) are mm n auses s dium depleti n. ADH an be released transiently p st peratively, r less requently, in syndr me inappr priate ADH se reti n. Lastly, pseud hyp natremia an be seen n lab rat ry testing when high serum glu se, lipid, r pr tein levels mpr mise s dium measurements. (See S hwartz 10th ed., p. 69.)

3. Whi h the ll wing is an early sign A. Peaked waves B. Peaked P waves C. Peaked (sh rtened) QRS mplex D. Peaked U waves

Answer: A Sympt ms hyperkalemia are primarily GI, neur mus ular, and ardi vas ular. GI sympt ms in lude nausea, v miting, intestinal li , and diarrhea; neur mus ular sympt ms range r m weakness t as ending paralysis t respirat ry ailure; while ardi vas ular mani estati ns range r m ele tr ardi gram (ECG) hanges t ardia arrhythmias and arrest. ECG hanges that may be seen with hyperkalemia in lude

1. Metab li a id sis with a n rmal ani n gap (AG) with A. Diabeti a id sis B. Renal ailure C. Severe diarrhea D. Starvati n

hyperkalemia?

Peaked waves (early hange) Flattened P wave Pr l nged PR interval ( irst-degree bl k) Widened QRS mplex Sine wave rmati n Ventri ular ibrillati n (See S hwartz 10th ed., p. 71.)

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10 4. Hyp al emia may ause whi h A. C ngestive heart ailure B. Atrial brillati n C. Pan reatitis D. Hyp parathyr idism

the ll wing?

5. T e next m st appr priate test t rder in a patient with a pH 7.1, Pco 2 40, s dium 132, p tassium 4.2, and hl ride 105 is A. Serum bi arb nate B. Serum magnesium C. Serum ethan l D. Serum sali ylate

Answer: A Mild hyp al emia an present with mus le ramping r digital/peri ral paresthesias. Severe hyp al emia leads t de reased ardia ntra tility and heart ailure. ECG hanges hyp al emia in lude pr l nged Q interval, -wave inversi n, heart bl k, and ventri ular ibrillati n. Hyp parathyr idism and severe pan reatitis are p tential auses hyp al emia. (See S hwartz 10th ed., p. 72.) Answer: A Metab li a id sis results r m an in reased intake a ids, an in reased generati n a ids, r an in reased l ss bi arb nate. In evaluating a patient with a l w serum bi arb nate level and metab li a id sis, irst measure the AG, an index unmeasured ani ns. AG = [Na] – [Cl + HCO3] Metab li a id sis with an in reased AG urs r m either ex gen us a id ingesti n (ethylene gly l, sali ylate, r methan l) r end gen us a id pr du ti n β-hydr xybutyrate and a et a etate in ket a id sis, la tate in la ti a id sis, r rgani a ids in renal insu i ien y. (See S hwartz 10th ed., p. 74.)

6. Whi h the ll wing is FALSE regarding hypert ni saline? A. Is an arteri lar vas dilat r and may in rease bleeding B. Sh uld be av ided in l sed head injury C. Sh uld n t be used r initial resus itati n D. In reases erebral per usi n

Answer: B Hypert ni saline (7.5%) has been used as a treatment m dality in patients with l sed head injuries. It has been sh wn t in rease erebral per usi n and de rease intra ranial pressure, thus de reasing brain edema. H wever, there als have been n erns in reased bleeding be ause hypert ni saline is an arteri lar vas dilat r. (See S hwartz 10th ed., p. 76.)

7. N rmal saline is A. 135 mEq NaCl/L B. 145 mEq NaCl/L C. 148 mEq NaCl/L D. 154 mEq NaCl/L

Answer: D S dium hl ride is mildly hypert ni , ntaining 154 mEq s dium that is balan ed by 154 mEq hl ride. he high hl ride n entrati n imp ses a signi i ant hl ride l ad up n the kidneys and may lead t a hyper hl remi metab li a id sis. It is an ideal s luti n, h wever, r rre ting v lume de i its ass iated with hyp natremia, hyp hl remia, and metab li alkal sis. (See S hwartz 10th ed., p. 76.)

8. Fluid resus itati n using albumin A. Is ass iated with agul pathy B. Is available as 1% r 5% s luti ns C. Can lead t pulm nary edema D. De reased a t r XIII

Answer: C Albumin is available as 5% ( sm lality 300 mOsm/L) r 25% ( sm lality 1500 mOsm/L). Due t in reased intravas ular n ti pressure, luid is drawn int the intravas ular spa e, leading t pulm nary edema when albumin is used r resus itati n r hyp v lemi sh k. Hydr xyethyl star h s luti ns are ass iated with p st perative bleeding in ardia and neur surgery patients. (See S hwartz 10th ed., p. 77.)

9. Water nstitutes what per entage A. 30–40% B. 40–50% C. 50–60% D. 60–70%

t tal b dy weight?

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Answer: C Water nstitutes appr ximately 50 t 60% t tal b dy weight. he relati nship between t tal b dy weight and t tal b dy water ( BW) is relatively nstant r an individual and is primarily a re le ti n b dy at. Lean tissues, su h as mus le and s lid rgans, have higher water ntent than at and b ne. As a result, y ung, lean men have a higher pr p rti n b dy weight as water than elderly r bese individuals. An average y ung adult male will have 60% his t tal b dy

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11 weight as BW, while an average y ung adult emale’s will be 50%. he l wer per entage BW in w men rrelates with a higher per entage adip se tissue and l wer per entage mus le mass in m st. Estimates BW sh uld be adjusted d wn appr ximately 10 t 20% in bese individuals and up by 10% in maln urished individuals. he highest per entage BW is und in newb rns, with appr ximately 80% their t tal b dy weight mp sed water. his de reases t ab ut 65% by 1 year and therea ter remains airly nstant. (See S hwartz 10th ed., p. 65.) 10. I a patient’s serum glu se in reases by 180 mg/dL, what is the in rease in serum sm lality, assuming all ther lab rat ry values remain nstant? A. D es n t hange B. 8 C. 10 D. 12

Answer: C Osm ti pressure is measured in units sm les ( sm) r milli sm les (mOsm) that re er t the a tual number sm ti ally a tive parti les. F r example, 1 millim le (mm l) s dium hl ride ntributes t 2 mOsm ( ne r m s dium and ne r m hl ride). he prin ipal determinants sm lality are the n entrati ns s dium, glu se, and urea (bl d urea nitr gen [BUN]): Cal ulated serum sm lality = 2 s dium + glu se/18 + BUN/2.8 (See S hwartz 10th ed., p. 67.)

11. What is the a tual p tassium and serum p tassium 2.2? A. 2.2 B. 2.8 C. 3.2 D. 3.4

a patient with pH

7.8

Answer: D he hange in p tassium ass iated with alkal sis an be alulated by the ll wing rmula: P tassium de reases by 0.3 mEq/L r every 0.1 in rease in pH ab ve n rmal (See S hwartz 10th ed., p. 71.)

12. T e ree water de it 154 is A. 0.1 L B. 0.7 L C. 1 L D. 7 L

a 70 kg man with serum s dium

Answer: D his is the rmula used t estimate the am unt required t rre t hypernatremia

water

serum sodium − 140 Water deficit L = × TBW 140 Estimate BW (t tal b dy water) as 50% lean b dy mass in men and 40% in w men. (See S hwartz 10th ed., p. 69.)

13. A patient with serum al ium a rre ted al ium A. 7.7 B. 8.0 C. 8.6 D. 9.2

6.8 and albumin

1.2 has

Answer: D When measuring t tal serum al ium levels, the albumin nentrati n must be taken int nsiderati n. Adjust t tal serum al ium d wn by 0.8 mg/dL r every 1 g/dL de rease in albumin. (See S hwartz 10th ed., p. 72.)

14. All the ll wing treatments r hyperkalemia redu e serum p tassium EXCEP A. Bi arb nate B. Kayexalate C. Glu se in usi n with insulin D. Cal ium

Answer: D When ECG hanges are present, al ium hl ride r al ium glu nate (5–10 mL 10% s luti n) sh uld be administered immediately t untera t the my ardial e e ts hyperkalemia. Cal ium in usi n sh uld be used auti usly in patients re eiving digitalis, be ause digitalis t xi ity may be pre ipitated. Glu se and bi arb nate shi t p tassium intra ellularly. Kayexalate is a ati n ex hange resin that binds p tassium, either given enterally r as an enema. (See S hwarz 10th ed., p. 77.)

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12 15. An al h li patient with serum albumin 3.9, K 3.1, Mg 2.4, Ca 7.8, and PO4 3.2 re eives three b luses IV p tassium and has serum p tassium 3.3. Y u sh uld A. C ntinue t b lus p tassium until the serum level is >3.6. B. Give MgSO4 IV. C. Che k the i nized al ium. D. Che k the BUN and reatinine.

Answer: B Magnesium depleti n is a mm n pr blem in h spitalized patients, parti ularly in the ICU. he kidney is primarily resp nsible r magnesium h me stasis thr ugh regulati n by al ium/magnesium re ept rs n renal tubular ells that sense serum magnesium levels. Hyp magnesemia results r m a variety eti l gies ranging r m p r intake (starvati n, al h lism, pr l nged use IV luids, and t tal parenteral nutriti n with inadequate supplementati n magnesium), in reased renal ex reti n (al h l, m st diureti s, and amph teri in B), GI l sses (diarrhea), malabs rpti n, a ute panreatitis, diabeti ket a id sis, and primary ald ster nism. Hyp magnesemia is imp rtant n t nly r its dire t e e ts n the nerv us system but als be ause it an pr du e hyp alemia and lead t persistent hyp kalemia. When hyp kalemia r hyp al emia exist with hyp magnesemia, magnesium sh uld be aggressively repla ed t assist in rest ring p tassium r al ium h me stasis. (See S hwartz 10th ed., p. 73.)

16. Cal ulate the daily maintenan e uids needed r a 60-kg emale A. 2060 B. 2100 C. 2160 D. 2400

Answer: B A 60-kg emale w uld re eive a t tal 2100 mL luid daily: 1000 mL r the irst 10 kg b dy weight (10 kg × 100 mL/kg/ day), 500 mL r the next 20 kg (10 kg × 50 mL/kg/day), and 80 mL r the last 40 kg (40 kg × 20 mL/kg/day). (See S hwartz 10th ed., p. 78.)

17. A patient wh has spasms in the hand when a bl sure u is bl wn up m st likely has A. Hyper al emia B. Hyp al emia C. Hypermagnesemia D. Hyp magnesemia

d pres-

Answer: B Asympt mati hyp al emia may ur with hyp pr teinemia (n rmal i nized al ium), but sympt ms an devel p with alkal sis (de reased i nized al ium). In general, sympt ms d n t ur until the i nized ra ti n alls bel w 2.5 mg/dL, and are neur mus ular and ardia in rigin, in luding paresthesias the a e and extremities, mus le ramps, arp pedal spasm, strid r, tetany, and seizures. Patients will dem nstrate hyperre lexia and p sitive Chv stek sign (spasm resulting r m tapping ver the a ial nerve) and r usseau sign (spasm resulting r m pressure applied t the nerves and vessels the upper extremity, as when btaining a bl d pressure). De reased ardia ntra tility and heart ailure an als a mpany hyp al emia. (See S hwartz 10th ed., p. 72.)

18. T e a tual AG a hr ni al h li with Na 133, K 4, Cl–101, HCO3 – 22, albumin 2.5 mg/dL is A. 6 B. 10 C. 14 D. 15

Answer: D he n rmal AG is 100 mg/dL B. Hyp kalemia C. Severe a id sis D. Uremi peri arditis E. Uremi en ephal pathy

ndings

Answer: A Hyperkalemia, severe a id sis, uremi en ephal pathy, and uremi peri arditis are all indi ati ns li e-threatening pr blems, and urgent rre ti n is mandat ry. Elevati n BUN is mm nly seen as well, but is n t itsel an indi ati n r dialysis. (See S hwartz 10th ed., p. 81.)

27. An elderly diabeti patient wh has a ute h le ystitis is und t have a serum s dium level 122 mEq/L and a bl d glu se 600 mg/dL. Af er rre ting the glu se n entrati n t 100 mg/dL with insulin, the serum s dium n entrati n w uld A. De rease signi antly unless the patient als re eived 3% saline B. De rease transiently but return t appr ximately 122 mEq/L with ut spe i therapy C. Remain essentially un hanged D. In rease t the n rmal range with ut spe i therapy

Answer: D A rise in the extra ellular luid n entrati n a substan e that d es n t di use passively a r ss ell membranes (eg, gluse r urea) auses an in rease in e e tive sm ti pressure, a trans er water r m ells, and diluti nal hyp natremia. F r ea h 100 mg/dL rise in bl d glu se ab ve n rmal, the serum s dium level alls appr ximately t 3 mEq/L. Alternatively, the serum s dium level w uld in rease by ab ut 15 mEq/L i the bl d glu se level ell r m 600 t 100 mg/dL. (See S hwartz 10th ed., p. 69.)

28. Ex essive administrati n n rmal saline r uid resusitati n an lead t what metab li derangement? A. Metab li alkal sis B. Metab li a id sis C. Respirat ry alkal sis D. Respirat ry a id sis

Answer: B S dium hl ride is mildly hypert ni , ntaining 154 mEq s dium that is balan ed by 154 mEq hl ride. he high hl ride n entrati n imp ses a signi i ant hl ride l ad n the kidneys and may lead t a hyper hl remi metab li a id sis. S dium hl ride is an ideal s luti n, h wever, r rre ting v lume de i its ass iated with hyp natremia, hyp hl remia, and metab li alkal sis. (See S hwartz 10th ed., p. 74.)

29. T e rst step in the management a ute hyper al emia sh uld be A. C rre ti n de it extra ellular uid v lume B. Hem dialysis. C. Administrati n ur semide. D. Administrati n mithramy in.

Answer: A Patients with a ute hyper al emia usually have either a ute hyperparathyr idism r metastati breast ar in ma with multiple b ny metastases. hese patients devel p severe heada hes, b ne pain, thirst, emesis, and p lyuria. Unless treatment is instituted pr mptly, the sympt ms may be rapidly atal. Immediate rre ti n the ass iated de i it extraellular luid v lume is the m st imp rtant step in treatment. When e e tive, this results in the l wering the serum al ium level by diluti n. On e extra ellular luid v lume has been repla ed, ur semide is e e tive treatment. Hem dialysis may als be empl yed, but its e e t is less rapid. Mithramyin is very use ul in ntr lling metastati b ne disease, but its e e t is sl w, and it ann t be depended up n when the patient has a ute hyper al emia. (See S hwartz 10th ed., p. 72.)

30. A vi tim a m t r vehi le a ident arrives in hem rrhagi sh k. His arterial bl d gases are pH, 7.25; Po 2, 95 mm Hg; Pco 2, 25 mm Hg; HCO3–, 15 mEq/L. T e patient’s metab li a id sis w uld be treated best with A. Ampule s dium bi arb nate B. S dium bi arb nate in usi n C. La tated Ringer s luti n D. Hyperventilati n

Answer: C In patients su ering r m hem rrhagi sh k, the presen e a metab li a id sis early in the p stresus itative peri d is indi ative tissue hyp xia due t persistent inadequate tissue per usi n. Attempts t rre t this pr blem by administering an alkalizing agent will n t s lve the basi pr blem.

hara teristi

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15 H wever, pr per v lume repla ement by means a balan ed salt s luti n su h as la tated Ringer s luti n will rest re perusi n and rre t the metab li a id sis by ending anaer bi metab lism. (See S hwartz 10th ed., p. 79.) 31. T ree days af er surgery r gastri ar in ma, a 50-yearld al h li male exhibits delirium, mus le trem rs, and hypera tive tend n re exes. Magnesium de ien y is suspe ted. All the ll wing statements regarding this situati n are true EXCEP A. A de isi n t administer magnesium sh uld be based n the serum magnesium level. B. Adequate ellular repla ement magnesium will require 1 t 3 weeks. C. A n mitant al ium de ien y sh uld be suspe ted. D. Cal ium is a spe i antag nist the my ardial e e ts magnesium.

Answer: A Magnesium de i ien y sh uld be suspe ted in any maln urished patient wh exhibits disturbed neur mus ular r erebral a tivity in the p st perative peri d. Lab rat ry n irmati n ten is n t reliable, and the syndr me may exist in the presen e a n rmal serum magnesium level. Hyp al emia ten exists, parti ularly in patients wh have lini al signs tetany. Intraven us magnesium an be administered sa ely t a well-hydrated patient r initial treatment a severe de i it, but n mitant ele tr ardi graphi m nit ring is essential. he ele tr ardi graphi hanges ass iated with a ute hypermagnesemia resemble th se hyperkalemia, and al ium hl ride r glu nate sh uld be readily available t untera t any adverse my ardial e e ts ex ess magnesium i ns. Partial r mplete relie sympt ms may ll w the initial in usi n magnesium, alth ugh ntinued repla ement r a peri d 1 t 3 weeks is ne essary t replenish ellular st res. (See S hwartz 10th ed., p. 78.)

32. Re eeding syndr me an be ass iated with all ll wing EXCEP A. Respirat ry ailure B. Hyperkalemia C. C n usi n D. Cardia arrhythmias

Answer: B With re eeding, a shi t in metab lism r m at t arb hydrate substrate stimulates insulin release, whi h results in the ellular uptake ele tr lytes, parti ularly ph sphate, magnesium, p tassium, and al ium. H wever, severe hypergly emia may result r m blunted basal insulin se reti n. (See S hwartz 10th ed., p. 81.)

the

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CHAPTER

4

Hemostasis, Surgical Bleeding, and Transfusion

1. Which o the ollowing is NO one o the our major physiologic events o hemostasis? A. Fibrinolysis B. Vasodilatation C. Platelet plug ormation D. Fibrin production

Answer: B Hemostasis is a complex process and its unction is to limit blood loss rom an injured vessel. Four major physiologic events participate in the hemostatic process: vascular constriction, platelet plug ormation, ibrin ormation, and ibrinolysis. hough each tend to be activated in order, the our processes are interrelated so that there is a continuum and multiple rein orcements. (See Schwartz 10th ed., p. 85.)

2. Which is required or platelet adherence to injured endothelium? A. T romboxane A2 B. Glycoprotein (GP) IIb/IIIa C. Adenosine diphosphate (ADP) D. Von Willebrand actor (vWF)

Answer: D Platelets do not normally adhere to each other or to the vessel wall but can orm a plug that aids in cessation o bleeding when vascular disruption occurs. Injury to the intimal layer in the vascular wall exposes subendothelial collagen to which platelets adhere. his process requires von Willebrand actor (vWF), a protein in the subendothelium that is lacking in patients with von Willebrand disease. vWF binds to glycoprotein (GP) I/IX/V on the platelet membrane. Following adhesion, platelets initiate a release reaction that recruits other platelets rom the circulating blood to seal the disrupted vessel. Up to this point, this process is known as primary hemostasis. Platelet aggregation is reversible and is not associated with secretion. Additionally, heparin does not inter ere with this reaction and thus hemostasis can occur in the heparinized patient. Adenosine diphosphate (ADP) and serotonin are the principal mediators in platelet aggregation. (See Schwartz 10th ed., p. 85.)

3. Which o the ollowing clotting actors is the rst actor common to both intrinsic and extrinsic pathways? A. Factor I ( brinogen) B. Factor IX (Christmas actor) C. Factor X (Stuart-Prower actor) D. Factor XI (plasma thromboplasma antecedent)

Answer: C he intrinsic pathway begins with the activation o actor XII that subsequently activates actors XI, IX, and VII. In this pathway, each o the primary actors is “intrinsic” to the circulating plasma, whereby no sur ace is required to initiate the process. In the extrinsic pathway, tissue actor ( F) is released or exposed on the sur ace o the endothelium, binding to circulating actor VII, acilitating its activation to VIIa. Each o these pathways continues on to a common sequence that begins with the activation o actor X to Xa (in the presence o VIIIa). Subsequently, Xa (with the help o actor Va) converts actor II (prothrombin) to thrombin and then actor I ( ibrinogen) to ibrin. Clot ormation occurs a ter ibrin monomers are cross-linked to polymers with the assistance o actor XIII. (See Schwartz 10th ed., p. 87.)

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18 4. Which congenital actor de ciency is associated with delayed bleeding a er initial hemostasis? A. Factor VII B. Factor IX C. Factor XI D. Factor XIII

Answer: D Congenital actor XIII (FXIII) de iciency, originally recognized by Duckert in 1960, is a rare autosomal recessive disease usually associated with a severe bleeding diathesis. he male-to- emale ratio is 1:1. Although acquired FXIII de iciency has been described in association with hepatic ailure, in lammatory bowel disease, and myeloid leukemia, the only signi icant association with bleeding in children is the inherited de iciency. Bleeding is typically delayed because clots orm normally but are susceptible to ibrinolysis. Umbilical stump bleeding is characteristic, and there is a high risk o intracranial bleeding. Spontaneous abortion is usual in women with FXIII de iciency unless they receive replacement therapy. Replacement can be accomplished with resh rozen plasma(FFP), cryoprecipitate, or a FXIII concentrate. Levels o 1 to 2% are usually adequate or hemostasis. (See Schwartz 10th ed., p. 89.)

5. In a previously unexposed patient, when does the platelet count all in heparin-induced thrombocytopenia (HI )? A. 19 IU/L

Alkaline phosphatase level

>2 IU/L

>2 IU/L

Bilirubin level

>0.01 mg/dL

>0.01 mg/dL

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46 11. A er an automobile accident, a 30-year-old woman is discovered to have a posterior pelvic racture. Hypotension and tachycardia respond marginally to volume replacement. Once it is evident that her major problem is ree intraperitoneal bleeding and a pelvic hematoma in association with the racture, appropriate management would be A. Application o medical antishock trousers with in ation o the extremity and abdominal sections. B. Arterial embolization o the pelvic vessels. C. Celiotomy and ligation o the internal iliac arteries bilaterally. D. Celiotomy and pelvic packing. E. External xation application to stabilize the pelvis.

Answer: D Severe pelvic bleeding is a major problem in the trauma patient. Neither external ixation nor the use o medical antishock trousers control ree intra-abdominal hemorrhage regardless o its source. In the unstable patient, celiotomy is mandatory. I there is a ruptured retroperitoneal hematoma bleeding into the peritoneal cavity, control is a major problem. Internal iliac artery ligation has been abandoned as it is rarely e ective. Angiography and arterial embolization may be e ective with an arterial bleeding problem, but most severe pelvic hemorrhage is venous in origin. I the hematoma is stable, it is best to leave it undisturbed. However, i the hematoma has ruptured into the peritoneal cavity, pelvic packing o ers the best hope o control. (See Schwartz 10th ed., p. 181.)

12. Which is true o vascular injuries o the extremities? A. In the absence o hard signs o vascular injury, i the dif erence between SBP in an injured limb is within 15% o the uninjured limb, no urther evaluation is needed. B. Occult pro unda emoris injuries can result in compartment syndrome and limb loss. C. All patients with signi cant hematoma should be surgically explored. D. Vascular injury repair should be per ormed prior to realignment o bony ractures or dislocations.

Answer: B Physical examination o ten identi ies arterial injuries, and indings are classi ied as either hard signs or so t signs o vascular injury ( able 7-3). In general, hard signs constitute indications or operative exploration, whereas so t signs are indications or urther testing or observation. Bony ractures or knee dislocations should be realigned be ore de initive vascular examination. In management o vascular trauma, controversy exists regarding the treatment o patients with so t signs o injury, particularly those with injuries in proximity to major vessels. It is known that some o these patients will have arterial injuries that require repair. he most common approach has been to measure SBP using Doppler ultrasonography and compare the value or the injured side with that or the uninjured side, termed the A-A index. I the pressures are within 10% o each other, a signi icant injury is unlikely and no urther evaluation is per ormed. I the di erence is >10%, C A or arteriography is indicated. Others argue that there are occult injuries, such as pseudoaneurysms or injuries o the pro unda emoris or peroneal arteries, which may not be detected with this technique. I hemorrhage occurs rom these injuries, compartment syndrome and limb loss may occur. Although busy trauma centers continue to debate this issue, the surgeon who is obliged to treat the occasional injured patient may be better served by per orming C A in selected patients with so t signs. (See Schwartz 10th ed., able 7-8, pp. 181 and 185.)

TABLE 7-3

Signs and symptoms o peripheral arterial injury

Hard Signs (Operation Mandatory)

Soft Signs (Further Evaluation Indicated)

Pulsatile hemorrhage

Proximity to vasculature

Absent pulses

Signif cant hematoma

Acute ischemia

Associated nerve injury A-A index o 110 s e c 2 units tha we d pla s ma P la te le t count 20 mm Hg. Indications or operative intervention to remove space-occupying hematomas are based on the clot volume, amount o midline shi t, location o the clot, GCS score, and ICP. A shi t o >5 mm typically is considered an indication or evacuation, but this is not an absolute rule. (See Schwartz 10th ed., p. 195.)

18. Cerebral per usion pressure (CPP) A. Equals the SBP minus ICP B. Should be targeted to be greater than 100 mm Hg C. Is lowered with sedation, osmotic diuresis, paralysis, ventricular drainage, and barbiturate coma D. Can be increased by lowering ICP and avoiding hypotension

Answer: D he goal o resuscitation and management in patients with head injuries is to avoid hypotension (SBP o 1500 mL (blunt injury) • Ongoing tube thoracostomy drainage o >200 mL/h or 3 consecutive hours in noncoagulopathic patients • Caked hemothorax despite placement o two chest tubes • Selected descending torn aortas • Great vessel injury (endovascular techniques may be used in selected patients) • Pericardial tamponade • Cardiac herniation • Massive air leak rom the chest tube with inadequate ventilation • Tracheal or main stem bronchial injury diagnosed by endoscopy or imaging • Open pneumothorax • Esophageal per oration • Air embolism

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51 22. A er sustaining a gunshot wound to the right upper quadrant o the abdomen, the patient has no signs o peritonitis. Her vital signs are stable, and C scan shows a grade III liver injury. What is the next step in management? A. Exploratory laparotomy with control o hepatic parenchymal hemorrhage. B. Admission to SICU with serial complete blood count. C. Admission to SICU with repeat C in 24 hours. D. Hepatic angiography.

Answer: B he liver’s large size makes it the organ most susceptible to blunt trauma, and it is requently involved in upper torso penetrating wounds. Nonoperative management o solid organ injuries is pursued in hemodynamically stable patients who do not have overt peritonitis or other indications or laparotomy. Patients with more than grade II injuries should be admitted to the SICU with requent hemodynamic monitoring, determination o hemoglobin, and abdominal examination. he only absolute contraindication to nonoperative management is hemodynamic instability. Factors such as high injury grade, large hemoperitoneum, contrast extravasation, or pseudoaneurysms may predict complications or ailure o nonoperative management. Angioembolization and endoscopic retrograde cholangiopancreatography (ERCP) are use ul adjuncts that can improve the success rate o nonoperative management. he indication or angiography to control hepatic hemorrhage is trans usion o 4 units o RBCs in 6 hours or 6 units o RBCs in 24 hours without hemodynamic instability. (See Schwartz 10th ed., p. 203.)

23. A 25-year-old man has multiple intra-abdominal injuries a er a gunshot wound. Celiotomy reveals multiple injuries to small and large bowel and major bleeding rom the liver. A er repair o the bowel injuries, the abdomen is closed with towel clips, leaving a large pack in the injured liver. Within 12 hours, there is massive abdominal swelling with edema uid, and intra-abdominal pressure exceeds 35 mm Hg. T e immediate step in managing this problem is to A. Administer albumin intercavernously B. Give an IV diuretic C. Limit IV uid administration D. Open the incision to decompress the abdomen

Answer: D Cardiac, pulmonary, and renal problems develop when invasive ascites compresses the diaphragm and the in erior vena cava. Dialysis, diuresis, and increasing serum oncotic pressure will not correct this problem rapidly enough to save the patient’s li e. Opening the incision relieves the intra-abdominal pressure. here are ew reports o sudden hypotension a ter this maneuver, but volume loading has largely eliminated this problem. (See Schwartz 10th ed., p. 217.)

24. Which o the ollowing statements is correct regarding traumatic spleen injury? A. An elevation in WBC to 20,000/mm 3 and platelets to 300,000/mm 3 on postoperative day 7 is a common benign nding in postsplenectomy patients. B. Delayed rebleeding or rupture will typically occur within 48 hours o injury. C. Common complications a er splenectomy include subdiaphragmatic abscess, pancreatic tail injury, and gastric per oration. D. Postsplenectomy vaccines against encapsulated bacteria is optimally administered preoperatively or immediately postoperative.

Answer: C Unlike hepatic injuries, which usually rebleed within 48 hours, delayed hemorrhage or rupture o the spleen can occur up to weeks a ter injury. Indications or early intervention include initiation o blood trans usion within the irst 12 hours and hemodynamic instability. A ter splenectomy or splenorrhaphy, postoperative hemorrhage may be due to loosening o a tie around the splenic vessels, an improperly ligated or unrecognized short gastric artery, or recurrent bleeding rom the spleen i splenic repair was used. An immediate postsplenectomy increase in platelets and WBCs is normal; however, beyond postoperative day 5, a WBC count above 15,000/mm 3 and a platelet/WBC ratio o 4 mm) and calci ication, dilation o the in erior vena cava, de ormed ventricular contours, and lattening or le tward shi t o the ventricular septum. Pericardial adhesions may also be seen on tagged cine MRI studies. As discussed, it is most important to distinguish pericardial constriction rom restrictive cardiomyopathy, which is best done with either echocardiography or right heart catheterization. Findings avoring constriction on echocardiography include respiratory variation o ventricular septal motion and mitral in low velocity, preserved or increased mitral annulus early diastolic illing velocity, and increased hepatic vein low reversal with expiration. Cardiac catheterization will show increased atrial pressures, equalization o end-diastolic pressure, and early ventricular diastolic illing with a subsequent plateau, called the square-root sign. Additional indings upon catheterization that would avor constriction include respiratory variation in ventricular illing and increased ventricular interdependence, mani est as a discordant change in the total area o the LV and RV systolic pressure curve with respiration. (See Schwartz 10th ed., pp. 773–774.)

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148 17. Each o the ollowing e ects is anticipated a er insertion o an intra-aortic balloon pump EXCEP A. Preload decrease B. Increased total myocardial oxygen consumption C. Improvement in cardiac index D. Coronary blood ow increase

Answer: B he intra-aortic balloon pump (IABP) is the most commonly used device or mechanical circulatory support, and it may be easily deployed in the catheterization laboratory, in the operating room or at the bedside. he device is inserted percutaneously through the emoral artery into the thoracic aorta. It is synchronized so that the balloon is in lated during diastole and de lated during systole, resulting in augmentation o diastolic per usion o the coronary arteries and decreased a terload. ypically, this improves cardiac index and decreases both preload and myocardial oxygen consumption. (See Schwartz 10th ed., p. 768.)

18. Pericarditis is usually treated with A. A short course o nonsteroidal anti-in ammatory drugs (NSAIDs). B. Use o steroids or intravenous antibiotics. C. Surgical exploration and drainage. D. Observation.

Answer: A he pre erred treatment depends on the underlying cause o the pericarditis. he disease usually ollows a sel -limited and benign course and can be success ully treated with a short course o nonsteroidal anti-in lammatory drugs (NSAIDs). Some patients may require judicious use o steroids or IV antibiotics. In cases o purulent pyogenic pericarditis, surgical exploration and drainage are occasionally necessary. Rarely, accumulation o luid in the pericardium may lead to tamponade, requiring prompt evacuation o the pericardial space. While pericardiocentesis will typically su ice, surgical drainage may be required or thick, viscous, or clotted luid or in patients with signi icant scarring rom previous surgeries. More commonly, surgical intervention is required to manage recurrent disease. (See Schwartz ed., p. 773.)

19. T e most common cause o isolated aortic in AI suf ciency in patients undergoing AVR is A. Congenital abnormalities o the aortic valve B. Systemic hypertension C. Aortic root disease D. Calci c degeneration

Answer: C he most common cause o isolated AI in patients undergoing AVR is aortic root disease, and represents over 50% o such patients in some studies. Other common causes o AI include congenital abnormalities o the aortic valve, such as bicuspid aortic valve, calci ic degeneration, rheumatic disease, in ective endocarditis, systemic hypertension, myxomatous degeneration, dissection o the ascending aorta, and Mar an syndrome. Less common causes o AI include traumatic injuries to the aortic valve, ankylosing spondylitis, syphilitic aortitis, rheumatoid arthritis, osteogenesis imper ecta, giant cell aortitis, Ehlers-Danlos syndrome, Reiter syndrome, discrete subaortic stenosis, and ventricular septal de ects with prolapse o an aortic cusp. Although most o these lesions produce chronic aortic insu iciency, rarely acute severe aortic regurgitation can result, o ten with devastating consequences. (See Schwartz 10th ed., p. 758.)

20. During cardiopulmonary bypass (CPB) anticoagulation, the range o heparin needed to increase the activated clotting time to greater than 450 seconds is A. 200 to 300 B. 300 to 400 C. 400 to 500 D. 450 to 550

Answer: B he basic cardiopulmonary bypass (CPB) circuit consists o the venous cannulae, a venous reservoir, pump, oxygenator, ilter, and the arterial cannula. Anticoagulation is required during CPB, and 300 to 400 units/kg o heparin is given to increase the activated clotting time (AC ) to greater than 450 seconds. Once adequate anticoagulation is achieved, arterial cannulation is per ormed through a purse-string suture, or through a side gra t which is sewn on to the native artery. (See Schwartz 10th ed., p. 740.)

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149 21. Eligibility criteria or mechanical support as destination therapy includes all o the ollowing EXCEP A. Medically re ractory NYHA class III B. Peak oxygen consumption 25% D. Age >65

Answer: C Current eligibility criteria or mechanical support as destination therapy include: (a) medically re ractory NYHA class III or IV heart ailure or at least 60 days, (b) peak oxygen consumption 10 cm in diameter) tumors that usually occur in children and do not have a predilection or any particular chamber. hey requently invade nearby cardiac structures and are multicentric in 60% o cases. (See Schwartz 10th ed., p. 776.)

23. Age-related calci c AS causes some degree o AI in approximately A. 55% B. 65% C. 75% D. 85%

Answer: C here are also many primary valvular diseases that cause AI, generally in association with AS. One such disorder is agerelated calci ic AS, which causes some degree o AI in up to 75% o patients. In ective endocarditis may involve the aortic valve apparatus and cause AI through direct destruction o the valve lea lets, per oration o a lea let, or ormation o vegetations that inter ere with proper coaptation o the valve cusps. Rheumatic disease causes ibrous in iltration o the valve cusps and subsequent retraction o the valve lea lets, inhibiting apposition o the cusps during diastole and producing a central regurgitant jet. Patients with large ventricular septal de ects or membranous subaortic stenosis may develop progressive AI, owing to a Venturi e ect that results in prolapse o the aortic valve lea lets. (See Schwartz 10th ed., p. 760.)

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CHAPTER

22

Thoracic Aneurysms and Aortic Dissection

1. T e type o thoracic aortic aneurysm characterized by an outpouching o the aorta is A. Fusi orm B. Saccular C. Pseudoaneurysm D. None o the above

Answer: B Aortic aneurysms can be either “true” or “ alse.” rue aneurysms can take two orms: usi orm and saccular. Fusi orm aneurysms are more common and can be described as symmetrical dilatations o the aorta. Saccular aneurysms are localized outpouchings o the aorta. False aneurysms, also called pseudoaneurysms, are leaks in the aortic wall that are contained by the outer layer o the aorta and/or the periaortic tissue; they are caused by disruption o the aortic wall and lead blood to collect in pouches o ibrotic tissue. (See Schwartz 10th ed., p. 785.)

2. Which o the ollowing is the most common cause o thoracic aortic aneurysms? A. Atherosclerosis B. Mar an syndrome C. akayasu arteritis D. Nonspeci c medial degeneration

Answer: D Nonspeci ic medial degeneration is the most common cause o thoracic aortic disease. Histologic indings o mild medial degeneration, including ragmentation o elastic ibers and loss o smooth muscle cells, are expected in the aging aorta. However, an advanced, accelerated orm o medial degeneration leads to progressive weakening o the aortic wall, aneurysm ormation, and eventual dissection, rupture, or both. he underlying causes o medial degenerative disease remain unknown. (See Schwarz 10th ed., p. 787.)

3. T e most common complication o extensive repair or distal aortic aneurysms is A. Spinal cord ischemia B. Renal ailure C. Pulmonary dys unction D. Le recurrent laryngeal nerve injury

Answer: C Although spinal cord ischemia and renal ailure receive the most attention, several other complications warrant consideration. he most common complication o extensive repairs is pulmonary dys unction. With aneurysms adjacent to the le t subclavian artery, the vagus and le t recurrent laryngeal nerves are o ten adherent to the aortic wall and thus are susceptible to injury. (See Schwartz 10th ed., p. 802.)

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152 4. Mar an syndrome is caused by an abnormality in which o the ollowing proteins? A. Elastin B. Metalloproteinase C. Collagen D. Fibrillin

Answer: D Mar an syndrome is an autosomal-dominant genetic disorder characterized by a speci ic connective tissue de ect that leads to aneurysm ormation. he phenotype o patients with Mar an syndrome typically includes a tall stature, high palate, joint hypermobility, eye lens disorders, mitral valve prolapse, and aortic aneurysms. he aortic wall is weakened by ragmentation o elastic ibers and deposition o extensive amounts o mucopolysaccharides (a process previously called cystic medial degeneration or cystic medial necrosis). Patients with Mar an syndrome have a mutation in the ibrillin gene located on the long arm o chromosome 15. he traditionally held view is that abnormal ibrillin in the extracellular matrix decreases connective tissue strength in the aortic wall and produces abnormal elasticity, which predisposes the aorta to dilatation rom wall tension caused by le t ventricular ejection impulses. More recent evidence, however, shows that the abnormal ibrillin causes degeneration o the aortic wall matrix by increasing the activity o trans orming growth actor-beta ( GF-β). Between 75 and 85% o patients with Mar an syndrome have dilatation o the ascending aorta and annuloaortic ectasia (dilatation o the aortic sinuses and annulus). Such aortic abnormalities are the most common cause o death among patients with Mar an syndrome. Mar an syndrome also is requently associated with aortic dissection. (See Schwartz 10th ed., p. 787.)

5. T e ollowing is NO true regarding anastomotic pseudoaneurysms A. Can arise rom deterioration o aortic tissue due to in ection B. Have increased in incidence with an in ux o cardiovascular surgery C. Commonly occur in patients with Mar an syndrome D. Are associated with high incidence o morbidity and rupture

Answer: B Anastomotic pseudoaneurysms can be caused by technical problems or by deterioration o the native aortic tissue, gra t material, or suture. Commonly, they occur in patients with Mar an syndrome. issue deterioration usually is related to either progressive degenerative disease or in ection. Improvements in sutures, gra t materials, and surgical techniques have decreased the incidence o thoracic aortic pseudoaneurysms. Should thoracic aortic pseudoaneurysms occur, they typically require expeditious surgical or other intervention because they are associated with a high incidence o morbidity and rupture. (See Schwartz 10th ed., p. 788.)

6. T e most common cause o death in patients with type IV Ehlers-Danlos syndrome is A. Myocardial in arction B. Aortic dissection C. Ruptured visceral artery D. Pulmonary emboli

Answer: C Ehlers-Danlos syndrome includes a spectrum o inherited connective tissue disorders o collagen synthesis. he subtypes represent di ering de ective steps o collagen production. Vascular type Ehlers-Danlos syndrome is characterized by an autosomal dominant de ect in type III collagen synthesis, which can have li e-threatening cardiovascular maniestations. Spontaneous arterial rupture, usually involving the mesenteric vessels, is the most common cause o death in these patients. horacic aortic aneurysms and dissections are less commonly associated with Ehlers-Danlos syndrome, but when they do occur, they pose a particularly challenging surgical problem because o the reduced integrity o the aortic tissue. An Ehlers-Danlos variant o periventricular heterotopia associated with joint and skin hyperextensibility and aortic dilation has been described as being caused by mutations in the gene encoding ilamin A (FLNA), an actin-binding protein that links the smooth muscle cell contractile unit to the cell sur ace. (See Schwartz 10th ed., p. 787.)

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153 7. T e most common presenting symptom in patients with an ascending thoracic aneurysm is A. Anterior chest pain B. Posterior chest pain C. Aortic valve insuf ciency D. Sudden death

Answer: A Initially, aneurysmal expansion and impingement on adjacent structures causes mild, chronic pain. he most common symptom in patients with ascending aortic aneurysms is anterior chest discom ort; the pain is requently precordial in location but may radiate to the neck and jaw, mimicking angina. Aneurysms o the ascending aorta and transverse aortic arch can cause symptoms related to compression o the superior vena cava, the pulmonary artery, the airway, or the sternum. Rarely, these aneurysms erode into the superior vena cava or right atrium, causing acute high-output ailure. (See Schwartz 10th ed., p. 789.)

8. Endoleaks A. ype I and type IV generally require early and aggressive intervention B. Are uncommon C. Can occur during the initial procedure or over time D. Are benign

Answer: A Another signi icant complication o descending thoracic aortic stent gra ting is endoleak. An endoleak occurs when there is a persistent low o blood (visible on radiologic imaging) into the aneurysm sac, and it may occur during the initial procedure or develop over time. Although endoleaks are a relatively common complication, they are not benign, because they lead to continual pressurization o the sac, which can cause expansion or even rupture. hese complications are categorized ( able 22-1) according to the site o the leak. Although all endoleaks may progress such that they can be considered li e-threatening, type I and type III endoleaks generally necessitate early and aggressive intervention. Recently published reporting guidelines aid standardized reporting. (See Schwartz 10th ed., able 22-4, p. 806.) TABLE 22-1

Classif cation o and common treatment strategies or endoleak

Type I • Incomplete seal between stent gra t and aorta at the proximal landing site (Type Ia), the distal landing site (Type Ib), or branch module, enestration, or plug (Type Ic) • Early reintervention to improve seal or conversion to open surgery Type II • Retrograde per usion o sac rom excluded collateral arteries • Surveillance; as-needed occlusion with percutaneous or other interventions Type III • Incomplete seal between overlapping stent gra t or module (Type IIIa), or tear in gra t abric (Type IIIb) • Early reintervention to cover gap or tear or conversion to open surgery Type IV • Per usion o sac due to porosity o material • Surveillance; as-needed reintervention to reline stent gra t Type V • Expansion o sac with no identi able source • Surveillance; as-needed reintervention to reline stent gra t

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154 9. T e most use ul imaging study or thoracic aneurysms is A. Echocardiography B. Computed tomography (C ) scan C. Magnetic resonance angiography D. Aortography

Answer: B Computed tomographic (C ) scanning is widely available, provides visualization o the entire thoracic and abdominal aorta, and permits multiplanar and 3-dimensional aortic reconstructions. Consequently, C is the most common— and arguably the most use ul—imaging modality or evaluating thoracic aortic aneurysms. In addition to establishing the diagnosis, C provides in ormation about an aneurysm’s location, extent, anatomic anomalies, and relationship to major branch vessels. C is particularly use ul in determining the absolute diameter o the aorta, especially in the presence o a laminated clot, and also detects aortic calci ication. (See Schwartz 10th ed., pp. 790–791.)

10. A patient with Mar an syndrome who has undergone “aortic surgery” most likely had A. Aortic valve annuloplasty (annular plication) B. Aortic root replacement (valve and ascending aorta) C. otal arch replacement with reattachment o the brachiocephalic branches D. Elephant trunk repair o thoracic aneurysm

Answer: B Mechanical prostheses necessitate ollowing a li elong anticoagulation regimen. Separate replacement o the aortic valve and ascending aorta is not per ormed in patients with Mar an syndrome, because progressive dilatation o the remaining sinus segment eventually leads to complications that necessitate reoperation. here ore, patients with Mar an syndrome or those with annuloaortic ectasia require some orm o aortic root replacement. (See Schwartz 10th ed., p. 793.)

11. In the case o aortic dissection A. Choice o initial treatment is the dependent on dissection local. B. Diagnostic delays are common. C. T ey are categorized as chronic a er 14 days. D. Contrast-enhanced C is the diagnostic o choice.

Answer: B Because o the variations in severity and the wide variety o potential clinical mani estations, the diagnosis o acute aortic dissection can be challenging.141-143 Only 3 out o every 100,000 patients who present to an emergency department with acute chest, back, or abdominal pain are eventually diagnosed with aortic dissection. Not surprisingly, diagnostic delays are common; delays beyond 24 hours a ter hospitalization occur in up to 39% o cases (Fig. 22-1.) (See Schwartz 10th ed., Figure 22-20, p. 810.)

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155 Manag e me nt o f ac ute ao rtic dis s e c tio n S us pe cte d a cute dis s e ction Anti-impuls e the ra py (be ta blocke rs ), blood pre s s ure control He modyna mica lly s ta ble ? Ye s

No

Contra s t-e nha nce d CT s ca n

Tra ns fe r to ope ra ting room, intuba tion, dia gnos tic TEE

Aortic dis s e ction? As ce nding a ortic dis s e ction (S ta nford A or De Ba ke y I or II)?

No

Ye s

S e conda ry dia gnos tic s tudy (MRA, TEE, or a ortogra phy)

No

Ye s Eme rge ncy ope ra tion

Aortic dis s e ction? Ye s

No

As ce nding a ortic dis s e ction (S ta nford A or De Ba ke y I or II)?

Ye s

Tra ns fe r to inte ns ive ca re for furthe r s ta biliza tion a nd dia gnos tic work-up

Furthe r dia gnos tic work-up

No

Eme rge ncy ope ra tion

Ye s

Eme rge ncy e ndova s cula r (fe ne s tra tion, s te nt) or ope n inte rve ntion

No

Tra ns fe r to inte ns ive ca re unit for blood pre s s ure control, a nti-impuls e the ra py

Complica te d de s ce nding a ortic dis s e ction (ma lpe rfus ion, rupture )?

FIG. 22-1. Algorithm used to acilitate decisions regarding treatment o acute aortic dissection. CT = computed tomography; MRA = magnetic resonance angiography; TEE = transesophageal echocardiography.

12. Mortality rates or operative repair o an aortic arch aneurysm have been signi cantly reduced intraoperatively by A. Deep hypothermia to allow circulatory arrest B. Innominate and le carotid artery cannulation to permit oxygenation o the brain C. Right heart to le subclavian artery bypass to continue brain per usion D. Use o an intraaortic balloon pump to maintain distal circulation

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Answer: A Like the operations themselves, per usion strategies used during proximal aortic surgery depend on the extent o the repair. Aneurysms that are isolated to the ascending segment can be replaced by using standard cardiopulmonary bypass and distal ascending aortic clamping. his provides constant per usion o the brain and other vital organs during the repair. Aneurysms involving the transverse aortic arch, however, cannot be clamped during the repair, which necessitates the temporary withdrawal o cardiopulmonary bypass support; this is called circulatory arrest. o protect the brain and other vital organs during the circulatory arrest period, hypothermia must be initiated be ore pump low is stopped. However, hypothermia is not without risk, and coagulopathy is associated with deep

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156 levels o hypothermia (below 20°C), which have been traditionally used in open arch repair. Recently, more moderate levels o hypothermia (o ten between 22°C and 24°C) have been introduced that appear to decrease risks associated with deep hypothermia while still providing su icient brain protection. (See Schwartz 10th ed., p. 797.) 13. According to the Craw ord classi cation scheme, surgical repair o thoracoabdominal aortic aneurysms with repairs beginning near the le subclavian artery but extending distally into the in rarenal abdominal aorta, o en reaching the aortic bi urcation is classi ed as A. Extent I B. Extent II C. Extent III D. Extent IV

Answer: B Extent I thoracoabdominal aortic aneurysm repairs involve most o the descending thoracic aorta, usually beginning near the le t subclavian artery, and extend down to the suprarenal abdominal aorta. Extent II repairs also begin near the le t subclavian artery but extend distally into the in rarenal abdominal aorta, and they o ten reach the aortic bi urcation. Extent III repairs extend rom the lower descending thoracic aorta (below the sixth rib) and into the abdomen. Extent IV repairs begin at the diaphragmatic hiatus and o ten involve the entire abdominal aorta. (See Schwartz 10th ed., p. 801.)

14.

reatment o descending aortic dissection by nonoperative, pharmacologic management A. Has lower morbidity and mortality rates than traditional surgical treatment. B. Most common cause o death during nonoperative treatment is aortic rupture and end-organ malper usion. C. A C scan obtained on day 2 or 3, compared with the initial scan, is suf cient to rule out signi cant aortic expansion. D. Inadequate blood pressure control has been ound to be associated with late aneurysm ormation.

Answer: C Nonoperative, pharmacologic management o acute descending aortic dissection results in lower morbidity and mortality rates than traditional surgical treatment does. he most common causes o death during nonoperative treatment are aortic rupture and end-organ malper usion. here ore, patients are continually reassessed or new complications. At least two serial C scans—usually obtained on day 2 or 3 and on day 8 or 9 o treatment—are compared with the initial scan to rule out signi icant aortic expansion. Once the patient’s condition has been stabilized, pharmacologic management is gradually shi ted rom intravenous to oral medications. Oral therapy, which usually includes a beta antagonist, is initiated when systolic pressure is consistently between 100 and 110 mm Hg and the neurologic, renal, and cardiovascular systems are stable. Many patients can be discharged a ter their blood pressure is well controlled with oral agents and a ter serial C scans con irm the absence o aortic expansion. Long-term pharmacologic therapy is important or patients with chronic aortic dissection. Beta blockers remain the drugs o choice. In a 20-year ollowup study, DeBakey and colleagues ound that inadequate blood pressure control was associated with late aneurysm ormation. Aneurysms developed in only 17% o patients with “good” blood pressure control, compared with 45% o patients with “poor” control. (See Schwartz 10th ed., p. 815.)

15. Which o the ollowing is the most typical presenting symptom in a patient with an aortic dissection? A. “ earing” pain B. Paraplegia C. Abdominal pain D. Cold le arm

Answer: A he onset o dissection o ten is associated with severe chest or back pain, classically described as tearing, that migrates distally as the dissection progresses along the length o the aorta. he location o the pain o ten indicates which aortic segments are involved. Pain in the anterior chest suggests involvement o the ascending aorta, whereas pain in the back and abdomen generally indicates involvement o the descending and thoracoabdominal aorta. (See Schwartz 10th ed., p. 809.)

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157 16. Delayed treatment or ascending aortic dissection should be considered A. In patients who present with severe acute stroke or mesenteric ischemia. B. In patients who are elderly and have substantial comorbidity. C. In patients who are in stable condition and may benet rom trans er to specialized centers. D. In patients who have undergone a cardiac operation in the past 3 weeks.

Answer: D Because o the risk o aortic rupture, acute ascending aortic dissection is usually considered an absolute indication or emergency surgical repair. However, speci ic patient groups may bene it rom nonoperative management or delayed operation. Delayed repair should be considered or patients who (a) present with severe acute stroke or mesenteric ischemia, (b) are elderly and have substantial comorbidity, (c) are in stable condition and may bene it rom trans er to specialized centers, or (d) have undergone a cardiac operation in the remote past. Regarding the last group, it is important that the previous operation not be too recent; dissections that occur during the irst 3 weeks a ter cardiac surgery pose a high risk o rupture and tamponade, and such dissections warrant early operation. (See Schwartz 10th ed., p. 813.)

17. A patient with a subclavian artery malper usion as a complication o aortic dissection would most likely experience A. Paraplegia B. Cold, pain ul extremity C. Incontinence D. Shock

Answer: B See able 22-2. (See Schwartz 10th ed., able 22-5, p. 811.)

TABLE 22-2

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Anatomic complications o aortic dissection and their associated symptoms and signs

Anatomic Manifestation

Symptoms and Signs

Aortic valve insu ciency

Dyspnea Murmur Pulmonary rales Shock

Coronary malper usion

Chest pain with characteristics o angina Nausea/vomiting Shock Ischemic changes on electrocardiogram Elevated cardiac enzymes

Pericardial tamponade

Dyspnea Jugular venous distension Pulsus paradoxus Muf ed cardiac tones Shock Low-voltage electrocardiogram

Subclavian or ilio emoral artery malper usion

Cold, pain ul extremity Extremity sensory and motor de cits Peripheral pulse de cit

Carotid artery malper usion

Syncope Focal neurologic de cit (transient or persistent) Carotid pulse de cit Coma

Spinal malper usion

Paraplegia Incontinence

Mesenteric malper usion

Nausea/vomiting Abdominal pain

Renal malper usion

Oliguria or anuria Hematuria

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CHAPTER

23

Arterial Disease

1. An ankle-brachial index (ABI) that suggests increased risk o myocardial in arction would be A. 0.6

Answer: A here is increasing interest in the use o the ankle-brachial index (ABI) to evaluate patients at risk or cardiovascular events. An ABI less than 0.9 correlates with increased risk o myocardial in arction and indicates signi icant, although perhaps asymptomatic, underlying peripheral vascular disease. (See Schwartz 10th ed., p. 829.)

2. All o the ollowing are correct regarding abdominal aortic aneurysm (AAA) rupture EXCEP A. It is the 10th leading cause o death or men in the United States. B. Risk o rupture is low when below 5.5 cm. C. Overall mortality rate o AAA rupture is higher than 70%. D. Men have a higher risk o rupture than women.

Answer: D Despite more than 50,000 patients undergoing elective repair o abdominal aortic aneurysm (AAA) each year in the United States, approximately 15,000 patients die annually as a result o ruptured aneurysm, making it the 10th leading cause o death or men. he rupture risk is quite low below 5.5 cm and begins to rise exponentially therea ter. his size can serve as an appropriate threshold or recommending elective repair provided one’s surgical mortality is below 5%. For each size strata, however, women appear to be at higher risk or rupture than men, and a lower threshold o 4.5 to 5.0 cm may be reasonable in good-risk patients. Overall mortality o AAA rupture is 71 to 77%, which includes all out-o -hospital and in-hospital deaths, as compared with 2 to 6% or elective open surgical repair. Nearly hal o all patients with ruptured AAA will die be ore reaching the hospital. For the remainder, surgical mortality is 45 to 50% and has not substantially changed in the past 30 years. (See Schwartz 10th ed., pp. 850–851.)

3. T e compartment most commonly a ected in a lower leg compartment syndrome is the A. Anterior compartment B. Lateral compartment C. Deep posterior compartment D. Super cial posterior compartment

Answer: A he most commonly a ected compartment is the anterior compartment in the leg. Numbness in the web space between the irst and second toes is diagnostic due to compression o the deep peroneal nerve. Compartment pressure is measured by inserting an arterial line into the compartment and recording the pressure. Although controversial, pressures greater than 20 mm Hg are an indication or asciotomy. (See Schwartz 10th ed., p. 888.)

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160 4. Magnetic resonance angiography (MRA) is contraindicated in the ollowing patient groups EXCEP those with A. Pacemakers B. Intracerebral shunts C. Cochlear implants D. Metallic stents

Answer: D Magnetic resonance angiography (MRA) has the advantage o not requiring iodinated contrast agents to provide vessel opaci ication (Fig. 23-1). Gadolinium is used as a contrast agent or MRA studies, and because it is generally not nephrotoxic, it can be used in patients with elevated creatinine. MRA is contraindicated in patients with pacemakers, de ibrillators, spinal cord stimulators, intracerebral shunts, cochlear implants, and cranial clips. Patients with claustrophobia may require sedation to be able to complete the test. he presence o metallic stents causes arti acts and signal drop-out; however, these can be dealt with using alternations in image acquisition and processing. Nitinol stents produce minimal arti act. Compared to other modalities, MRA is relatively slow and expensive. However, due to its noninvasive nature and decreased nephrotoxicity, MRA is being used more requently or imaging vasculature in various anatomic distributions. (See Schwartz 10th ed., Figure 23-5, pp. 832–833.)

FIG. 23-1. Magnetic resonance angiogram (MRA) o aortic arch and carotid arteries. This study can provide a three-dimensional analysis o vascular structure such as aortic arch branches, carotid and vertebral arteries.

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161 5. T e pre erred procedure or treatment o typical occlusive disease o the aorta and both iliac arteries is A. Endovascular stenting B. Extra-anatomic bypass C. Aortoiliac endarterectomy D. Aortobi emoral bypass

Answer: D In most cases, aortobi emoral bypass is per ormed because patients usually have disease in both iliac systems. Although one side may be more severely a ected than the other, progression does occur, and bilateral bypass does not complicate the procedure or add to the physiologic stress o the operation. Aortobi emoral bypass reliably relieves symptoms, has excellent long-term patency (approximately 70–80% at 10 years), and can be completed with a tolerable perioperative mortality (2–3%). (See Schwartz 10th ed., p. 876.)

6. T e most common cause o ischemic stroke is A. Carotid artery disease B. Idiopathic C. Cardiogenic emboli D. Lacunar

Answer: C Ischemic strokes are due to hypoper usion rom arterial occlusion or, less commonly, to decreased low resulting rom proximal arterial stenosis and poor collateral network. Common causes o ischemic strokes are cardiogenic emboli in 35%, carotid artery disease in 30%, lacunar in 10%, miscellaneous in 10%, and idiopathic in 15%. he term cerebrovascular accident is o ten used interchangeably to re er to an ischemic stroke. (See Schwartz 10th ed., p. 838.)

7. T e treatment o acute embolic mesenteric ischemia is A. Observation B. Anticoagulation C. T rombolysis D. Operative embolectomy

Answer: D he primary goal o surgical treatment in embolic mesenteric ischemia is to restore arterial per usion with removal o the embolus rom the vessel. he abdomen is explored through a midline incision, which o ten reveals variable degrees o intestinal ischemia rom the mid-jejunum to the ascending or transverse colon. he transverse colon is li ted superiorly, and the small intestine is re lected toward the right upper quadrant. he superior mesenteric artery (SMA) is approached at the root o the small bowel mesentery, usually as it emerges rom beneath the pancreas to cross over the junction o the third and ourth portions o the duodenum. Alternatively, the SMA can be approached by incising the retroperitoneum lateral to the ourth portion o the duodenum, which is rotated medially to expose the SMA. Once the proximal SMA is identi ied and controlled with vascular clamps, a transverse arteriotomy is made to extract the embolus, using standard balloon embolectomy catheters. In the event the embolus has lodged more distally, exposure o the distal SMA may be obtained in the root o the small bowel mesentery by isolating individual jejunal and ileal branches to allow a more comprehensive thromboembolectomy. Following the restoration o SMA low, an assessment o intestinal viability must be made, and nonviable bowel must be resected. Several methods have been described to evaluate the viability o the intestine, which include intraoperative intravenous luorescein injection and inspection with a Wood’s lamp, and Doppler assessment o antimesenteric intestinal arterial pulsations. A second-look procedure should be considered in many patients and is perormed 24 to 48 hours ollowing embolectomy. he goal o the procedure is reassessment o the extent o bowel viability, which may not be obvious immediately ollowing the initial embolectomy. I nonviable intestine is evident in the secondlook procedure, additional bowel resections should be perormed at that time. (See Schwartz 10th ed., pp. 863–864.)

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162 8. T e correct classi cation or the degree o stenosis in the internal carotid artery o a patient with a luminal diameter o 69% is A. Mild B. Moderate C. Severe D. No stenosis

Answer: B Atherosclerotic plaque ormation is complex, beginning with intimal injury, platelet deposition, smooth muscle cell proli eration, and ibroplasia, and leading to subsequent luminal narrowing. With increasing degree o stenosis in the internal carotid artery, low becomes more turbulent, and the risk o atheroembolization escalates. he severity o stenosis is commonly divided into three categories according to the luminal diameter reduction: mild (90%) are due to embolic occlusion o the main artery or the upper or lower divisions. Monocular blindness progressing over a 20-minute period suggests a migrainous etiology. Occasionally, the patient will recall no visual symptoms while the optician notes a yellowish plaque within the retinal vessels, which is also known as Hollenhorst plaque. hese plaques are requently derived rom cholesterol embolization rom the carotid bi urcation and warrant urther investigation. (See Schwartz 10th ed., p. 839.) 11. T e most accurate diagnostic test with the lowest morbidity in the diagnosis o renal artery stenosis is A. Angiography B. Computed tomography (C ) scan C. MRA D. Renal systemic renin index

Answer: C MRA has the advantage o not requiring iodinated contrast agents to provide vessel opaci ication (see Fig. 23-1). Gadolinium is used as a contrast agent or MRA studies, and because it is generally not nephrotoxic, it can be used in patients with elevated creatinine. (See Schwartz 10th ed., p. 832.)

12. T e risk o a recurrent ipsilateral stroke in patients with severe carotid stenosis is approximately A. 20% B. 30% C. 40% D. 50%

Answer: C Currently, most stroke neurologists prescribe both aspirin and clopidogrel or secondary stroke prevention in patients who have experienced a transient ischemic attack ( IA) or stroke. In patients with symptomatic carotid stenosis, the degree o stenosis appears to be the most important predictor in determining risk or an ipsilateral stroke. he risk o a recurrent ipsilateral stroke in patients with severe carotid stenosis approaches 40%. (See Schwartz 10th ed., p. 841.)

13. Which o the ollowing statements concerning carotid body tumors is true? A. Over 50% are hereditary. B. Require resection o the underlying carotid artery with reconstruction or cure. C. Are associated with catecholamine release. D. Are usually benign.

Answer: D he carotid body originates rom the third branchial arch and rom neuroectodermal-derived neural crest lineage. he normal carotid body is located in the adventitia or periadventitial tissue at the bi urcation o the common carotid artery (Fig. 23-3). he gland is innervated by the glossopharyngeal nerve. Its blood supply is derived predominantly rom the external carotid artery but can also come rom the vertebral artery. Carotid body tumor is a rare lesion o the neuroendocrine system. Other glands o neural crest origin are seen in the neck, parapharyngeal spaces, mediastinum, retroperitoneum, and adrenal medulla. umors involving these structures have been re erred to as paraganglioma, glomus tumor, or chemodectoma. Approximately 5 to 7% o carotid body tumors are malignant. Although chronic hypoxemia has been invoked as a stimulus or hyperplasia o carotid body, approximately 35% o carotid body tumors are hereditary. he risk o malignancy is greatest in young patients with amilial tumors. (See Schwartz 10th ed., Figure 23-27, p. 849.)

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FIG. 23-3A & B. A. Carotid body tumor (arrow) located adjacent to the carotid bulb. B. Following periadventitial dissection, the carotid body tumor is removed.

A

B

14. T e ollowing are major risk actors associated with carotid stenosis disease progression EXCEP A. Diet B. Cigarette smoking C. Diabetes mellitus D. Age

Answer: A he presence o or progression to a greater than 80% stenosis correlated highly with either the development o a total occlusion o the internal carotid artery or new symptoms. he major risk actors associated with disease progression were cigarette smoking, diabetes mellitus, and age. his study supported the contention that it is prudent to ollow a conservative course in the management o asymptomatic patients presenting with a cervical bruit. (See Schwartz 10th ed., p. 842.)

15. Rest pain seen with occlusive peripheral vascular disease in the lower extremity most commonly occurs in A. T e buttock B. T e quadriceps C. T e cal muscles D. T e metatarsophalangeal joint

Answer: D Progression o the underlying atherosclerotic process is more likely to occur in patients with diabetes, those who continue to smoke, and those who ail to modi y their atherosclerotic risk actors. In comparison, rest pain is constant, and usually occurs in the ore oot across the metatarsophalangeal joint. It is worse at night and requires placing the oot in a dependent position to improve symptoms. (See Schwartz 10th ed., p. 890.)

16. Fibromuscular dysplasia (FMD) is A. More common in men than women in the ourth or h decade o li e. B. Commonly present bilaterally in the carotid artery. C. Surgical correction is o en indicated. D. Usually involves short vessels with many branches.

Answer: B Fibromuscular dysplasia (FMD) usually involves mediumsized arteries that are long and have ew branches (Fig. 23-4). Women in the ourth or i th decade o li e are more commonly a ected than men. Hormonal e ects on the vessel wall are thought to play a role in the pathogenesis o FMD. FMD o the carotid artery is commonly bilateral, and in about 20% o patients, the vertebral artery is also involved. An intracranial saccular aneurysm o the carotid siphon or middle cerebral artery can be identi ied in up to 50% o the patients with FMD. Four histologic types o FMD have been described in the literature. he most common type is medial ibroplasia, which may present as a ocal stenosis or multiple lesions with intervening aneurysmal outpouchings. he disease involves the media with the smooth muscle being replaced by ibrous connective tissue. Commonly, mural dilations and microaneurysms can be seen with this type o FMD. FMD should be suspected when an increased velocity is detected across a

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165 stenotic segment without associated atherosclerotic changes on carotid duplex ultrasound. Antiplatelet medication is the generally accepted therapy or asymptomatic lesions. Endovascular treatment is recommended or patients with documented lateralizing symptoms. Surgical correction is rarely indicated. (See Schwartz 10th ed., Figure 23-24, pp. 847–848.)

FIG. 23-4. A carotid ibromuscular dysplasia with typical characteristics o multiple stenoses with intervening aneurysmal outpouching dilatations. The disease involves the media with the smooth muscle being replaced by ibrous connective tissue.

17. T e best initial treatment or a groin pseudoaneurysm a er angiography is A. Surgical repair B. Ultrasound-guided compression C. Ultrasound-guided injection o thrombin D. Observation

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Answer: C Percutaneous catheter aspiration should be the initial treatment or cal vessel embolization, but, or larger emboli, such as those that lodge in the pro unda emoris or common emoral arteries, surgical embolectomy may be required because the embolic material contains atherosclerotic plaque, which is not amenable to transcatheter aspiration or catheter-directed thrombolysis. he incidence o pseudoaneurysm ormation at the puncture site is 0.5%. he treatment o choice or pseudoaneurysms larger than 2 cm in diameter is percutaneous thrombin injection under ultrasound guidance. Arterial rupture may complicate the procedure in 0.3% o cases.

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166 amponade o the ruptured artery with an occlusion balloon should be per ormed, and a covered stent should be placed. In case o ailure, surgical treatment is required. (See Schwartz 10th ed., p. 880.) 18. T e primary cause o renal artery occlusive lesions is A. Fibromuscular dysplasia B. Atherosclerosis C. Renal artery aneurysm D. akayasu arteritis

Answer: B Approximately 80% o all renal artery occlusive lesions are caused by atherosclerosis, which typically involves a short segment o the renal artery ostia and represents spillover disease rom a severely atheromatous aorta (Fig. 23-5). Atherosclerotic lesions are bilateral in two-thirds o patients. Individuals with this disease commonly present during the sixth decade o li e. Men are a ected twice as requently as women. Atherosclerotic lesions in other territories such as the coronary, mesenteric, cerebrovascular, and peripheral arterial circulation are common. When a unilateral lesion is present, the disease process equally a ects the right and le t renal arteries. he second most common cause o renal artery stenosis is FMD, which accounts or 20% o cases and is most requently encountered in young, o ten multiparous women. FMD o the renal artery represents a heterogeneous group o lesions that can produce histopathologic changes in the intima, media, or adventitia. he most common variety consists o medial ibroplasia, in which thickened ibromuscular ridges alternate with attenuated media producing the classic angiographic “string o beads” appearance. he cause o medial ibroplasia remains unclear. Most common theories involve a modi ication o arterial smooth muscle cells in response to estrogenic stimuli during the reproductive years, unusual traction orces on a ected vessels, and mural ischemia rom impairment o vasa vasorum blood low. Fibromuscular hyperplasia usually a ects the distal two thirds o the main renal artery, and the right renal artery is a ected more requently than the le t. Other less common causes o renal artery stenosis include renal artery aneurysm (compressing the adjacent normal renal artery), arteriovenous mal ormations, neuro ibromatosis, renal artery dissections, renal artery trauma, akayasu arteritis, and renal arteriovenous istula. (See Schwartz 10th ed., Figure 23-43, pp. 866–867.)

FIG. 23-5. Occlusive disease o the renal artery typically involves the renal ostium (arrow), as a spill over plaque extension rom aortic atherosclerosis.

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167 19. Carotid coiling A. Is associated with loss o elasticity B. Is more common in men than women C. Are most o en acquired in both children and adults D. Are most likely due to embolic episodes

Answer: A A carotid coil consists o an excessive elongation o the internal carotid artery producing tortuosity o the vessel (Fig. 23-6). Embryologically, the carotid artery is derived rom the third aortic arch and dorsal aortic root and is uncoiled as the heart and great vessels descend into the mediastinum. In children, carotid coils appear to be congenital in origin. In contrast, elongation and kinking o the carotid artery in adults are associated with the loss o elasticity and an abrupt angulation o the vessel. Kinking is more common in women than men. Cerebral ischemic symptoms caused by kinks o the carotid artery are similar to those rom atherosclerotic carotid lesions but are more likely due to cerebral hypoper usion than embolic episodes. Classically, sudden head rotation, lexion, or extension can accentuate the kink and provoke ischemic symptoms. Most carotid kinks and coils are ound incidentally on carotid duplex scan. However, interpretation o the Doppler requency shi ts and spectral analysis in tortuous carotid arteries can be di icult because o the uncertain angle o insonation. Cerebral angiography, with multiple views taken in neck lexion, extension, and rotation, is use ul in the determination o the clinical signi icance o kinks and coils. (See Schwartz 10th ed., Figure 23-23, p. 847.)

FIG. 23-6. Excessive elongation o the carotid artery can result in carotid kinking (arrow), which can compromise cerebral blood low and lead to cerebral ischemia.

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168 20. Complications o endovascular treatment or mesenteric ischemia A. O en become li e threatening. B. Can include distal embolization resulting in acute intestinal ischemia. C. Can include access-site thrombosis. D. Dissections never occur.

Answer: C Complications are not common and rarely become li e threatening. hese include access-site thrombosis, hematomas, and in ection. Dissection can occur during percutaneous transluminal angioplasty (P A) and is managed with placement o a stent. Balloon-mounted stents are pre erred over the sel expanding ones because o the higher radial orce and the more precise placement. Distal embolization has also been reported, but it never resulted in acute intestinal ischemia, likely due to the rich network o collaterals already developed. (See Schwartz 10th ed., p. 865.)

21. T e most common location or the development o atherosclerotic disease is A. T e renal artery. B. T e coronary arteries. C. T e abdominal aorta. D. T e arteries in the circle o Willis.

Answer: A Obstructive lesions o the renal artery can produce hypertension, resulting in a condition known as renovascular hypertension, which is the most common orm o hypertension amenable to therapeutic intervention, and a ects 5 to 10% o all hypertensive patients in the United States. Patients with renovascular hypertension are at an increased risk or irreversible end-organ dys unction, including permanent kidney damage, i inadequate pharmacologic therapies are used to control the blood pressure. he majority o patients with renal artery obstructive disease have vascular lesions o either atherosclerotic disease or ibrodysplasia involving the renal arteries. he proximal portion o the renal artery represents the most common location or the development o atherosclerotic disease. It is well established that renal artery intervention, either by surgical or endovascular revascularization, provides an e ective treatment or controlling renovascular hypertension as well as preserving renal unction. he decision or intervention is complex and needs to consider a variety o anatomic, physiologic, and clinical eatures, unique or the individual patient. (See Schwartz 10th ed., p. 866.)

22. Angiograph indications or renal artery revascularization include all o the ollowing EXCEP A. Documented renal artery stenosis B. FMD lesion C. A ected/una ected kidney renin ration >1.5 to 1 D. Pressure gradient >10 mm Hg

Answer: D See able 23-1. (See Schwartz 10th ed., able 23-12, p. 869.)

TABLE 23-1

Indications or renal artery revascularization

Angiography Criteria • Documented renal artery stenosis (>70% diameter reduction) • Fibromuscular dysplasia lesion • Pressure gradient >20 mmHg • A ected/una ected kidney renin ratio >1.5 to 1 Clinical Criteria • Re ractory or rapidly progressive hypertension • Hypertension associated with ash pulmonary edema without coronary artery disease • Rapidly progressive deterioration in renal unction • Intolerance to antihypertensive medications • Chronic renal insu ciency related to bilateral renal artery occlusive disease or stenosis to a solitary unctioning kidney • Dialysis-dependent renal ailure in a patient with renal artery stenosis but without another def nite cause o endstage renal disease • Recurrent congestive heart ailure or ash pulmonary edema not attributable to active coronary ischemia

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169 23. Aortoiliac disease represented by di use aortoiliac disease above the iliac artery is classi ed as A. ype 1 B. ype II C. ype III D. ype IV

Answer: B See Figure 23-7. (See Schwartz 10th ed., Figure 23-50, p. 873.) Type I

Type II

Type III

FIG. 23-7. Aortoiliac disease can be classi ied into three types. Type I represents ocal disease a ecting the distal aorta and proximal common iliac artery. Type II represents di use aortoiliac disease above the inguinal ligament. Type III represents multisegment occlusive diseases involving aortoiliac and in ra-inguinal arterial vessels.

24. T e treatment o choice or type B iliac lesions is A. Observation B. Endovascular therapy C. Surgery D. Intravenous (IV) antibiotics

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Answer: B he most commonly used classi ication system o iliac lesions has been set orth by the ransAtlantic Inter-Society Consensus ( ASC) group with recommended treatment options. his lesion classi ication categorizes the extent o atherosclerosis and has suggested a therapeutic approach based on this classiication ( able 23-2 and Fig. 23-8). According to this consensus document, endovascular therapy is the treatment o choice or type A lesions, and surgery is the treatment o choice or type D lesions. Endovascular treatment is the pre erred treatment or type B lesions, and surgery is the pre erred treatment or good-risk patients with type C lesions. In comparison to the 2000 ASC document, the commission has not only made allowances or treatment o more extensive lesions, but also takes into account the continuing evolution o endovascular technology and the skills o individual interventionalists when stating the patient’s comorbidities, ully in ormed patient pre erence, and the local operator’s long-term success rates must be considered when making treatment decisions or type B and type C lesions. (See Schwartz 10th ed., Figure 23-55 and able 23-14, p. 875.)

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170 TABLE 23-2

TASC classi cation o aortoiliac occlusive lesions

Type A lesions • Unilateral or bilateral stenoses o CIA • Unilateral or bilateral single short (≤3 cm) stenosis o EIA Type B lesions • Short (≤3 cm) stenosis o in rarenal aorta • Unilateral CIA occlusion • Single or multiple stenosis totaling 3–10 cm involving the EIA not extending into the CFA • Unilateral EIA occlusion not involving the origins o internal iliac artery or CFA Type C lesions • Bilateral CIA occlusions • Bilateral EIA stenoses 3–10 cm long not extending into the CFA • Unilateral EIA stenosis extending into the CFA • Unilateral EIA occlusion that involves the origins o internal iliac artery and/or CFA • Heavily calcif ed unilateral EIA occlusion with or without involvement o origins o internal iliac artery and/or CFA Type D lesions • In rarenal aortoiliac occlusion • Di use disease involving the aorta and both iliac arteries requiring treatment • Di use multiple stenoses involving the unilateral CIA, EIA, and CFA • Unilateral occlusions o both CIA and EIA • Bilateral occlusions o EIA • Iliac stenoses in patients with AAA requiring treatment and not amenable to endogra t placement or other lesions requiring open aortic or iliac surgery AAA = abdominal aortic aneurysm; CFA = common emoral artery; CIA = common iliac artery; EIA = external iliac artery.

Type A le s ions

Type C le s ions

Type B le s ions

Type D le s ions

FIG. 23-8. Schematic depiction o TASC classi ication o aortoiliac occlusive lesions.

25. Carotid bi urcation occlusive disease resulting in stroke is usually caused by A. Atheroemboli B. T rombosis C. Rupture D. Dissection

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Answer: A Stroke due to carotid bi urcation occlusive disease is usually caused by atheroemboli (Fig. 23-9). he carotid bi urcation is an area o low low velocity and low shear stress. As the blood circulates through the carotid bi urcation, there is separation o low into the low-resistance internal carotid artery and the high-resistance external carotid artery. (See Schwartz 10th ed., Figure 23-13, p. 838.)

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171

Exte rna l ca rotid a rte ry

Inte rna l ca rotid a rte ry

Emboli S upe rior thyroid a rte ry

Ulce r

P la que

Common ca rotid a rte ry

FIG. 23-9. Stroke due to carotid bi urcation occlusive disease is usually caused by atheroemboli arising rom the internal carotid artery which provides the majority o blood low to the cerebral hemisphere. With increasing degree o stenosis in the carotid artery, low becomes more turbulent, and the risk o atheroembolization escalates.

26. Crescendo IAs re ers to a syndrome comprising repeated IAs within A. A short period o time that is characterized by complete neurologic recovery in between. B. A lengthy time period that is characterized by complete neurologic recovery in between. C. A short period o time that is characterized by a partial neurologic recovery in between. D. A lengthy time period that is characterized by a partial neurologic recovery in between.

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Answer: A IA is a ocal loss o neurologic unction, lasting or less than 24 hours. Crescendo IAs re er to a syndrome comprising repeated IAs within a short period o time that is characterized by complete neurologic recovery in between. At a minimum, the term should probably be reserved or those with either daily events or multiple resolving attacks within 24 hours. Hemodynamic IAs represent ocal cerebral events that are aggravated by exercise or hemodynamic stress and typically occur a ter short bursts o physical activity, postprandially, or a ter getting out o a hot bath. It is implied that these are due to severe extracranial disease and poor intracranial collateral recruitment. Reversible ischemic neurologic de icits re er to ischemic ocal neurologic symptoms lasting longer than 24 hours but resolving within 3 weeks. When a neurologic de icit lasts longer than 3 weeks, it is considered a completed stroke. Stroke in evolution re ers to progressive worsening o the neurologic de icit, either linearly over a 24-hour period or interspersed with transient periods o stabilization and/or partial clinical improvement. (See Schwartz 10th ed., pp. 838–839.)

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172 27. Late postoperative complications o aortobi emoral bypass gra ing include all o the ollowing EXCEP A. Gra in ection B. Anastomotic stula C. Paraplegia D. Aortourinary stula

Answer: C See able 23-3. (See Schwartz 10th ed., able 23-15, p. 878.) TABLE 23-3

Perioperative complications o aortobi emoral bypass gra ting

Medical Complications • Perioperative myocardial in arction • Respiratory ailure • Ischemia-induced renal ailure • Bleeding rom intravenous heparinization • Stroke Procedure-Related Complications Early • Declamping shock • Gra t thrombosis • Retroperitoneal bleeding • Groin hematoma • Bowel ischemia/in arction • Peripheral embolization • Erectile dys unction • Lymphatic leak • Chylous ascites • Paraplegia Late • Gra t in ection • Anastomotic pseudoaneurysm • Aortoenteric f stula • Aortourinary f stula • Gra t thrombosis

28. T e best diagnostic imaging modality or identi ying lower extremity occlusive disease is A. MRA B. C angiography C. Ultrasound D. Contrast angiography

Answer: D Contrast angiography remains the gold standard imaging study. Using contrast angiography, interventionists can locate and size the anatomic signi icant lesions and measure the pressure gradient across the lesion, as well as plan or potential intervention. Angiography is, however, semi-invasive and should be con ined to patients or whom surgical or percutaneous intervention is contemplated. Patients with borderline renal unction may need to have alternate contrast agents, such as gadolinium or carbon dioxide, to avoid contrastinduced nephrotoxicity. (See Schwartz 10th ed., p. 882.)

29. According to the Fontaine classi cation system or lower extremity occlusive disease A. Patients with tissue loss are classi ed as stage II. B. Patients with rest pain are classi ed as stage III. C. Asymptomatic patients are classi ed as stage I. D. Patients with claudication are classi ed as stage IV.

Answer: B he Fontaine classi ication uses our stages: Fontaine I is the stage when patients are asymptomatic; Fontaine II is when they have mild (IIa) or severe (IIb) claudication; Fontaine III is when they have ischemic rest pain; and Fontaine IV is when patients su er tissue loss, such as ulceration or gangrene ( able 23-4). (See Schwartz 10th ed., able 23-17, pp. 883–884.)

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173

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174 30. T e most common source o distal emboli is A. T e heart B. Atherosclerotic lesions C. Dilated cardiomyopathy D. Diseased valves

Answer: A he heart is the most common source o distal emboli, which accounts or more than 90% o peripheral arterial embolic events. Atrial ibrillation is the most common source. Sudden cardioversion results in the dilated noncontractile atrial appendage regaining contractile activity, which can dislodge the contained thrombus. Other cardiac sources include mural thrombus overlying a myocardial in arction or thrombus orming within a dilated le t ventricular aneurysm. Mural thrombi can also develop within a ventricle dilated by cardiomyopathy. Emboli that arise rom a ventricular aneurysm or rom a dilated cardiomyopathy can be very large and can lodge at the aortic bi urcation (saddle embolus), thus rendering both legs ischemic. Diseased valves are another source o distal embolization. Historically, this occurred as a result o rheumatic heart disease. Currently, subacute endocarditis and acute bacterial endocarditis are the more common causes. In ected emboli can seed the recipient vessel wall, creating mycotic aneurysms. (See Schwartz 10th ed., p. 885.)

31. An absolute contraindication to thrombolytic therapy is A. Pregnancy B. Intracranial tumor C. Intracranial trauma within the past 3 months D. Cardiopulmonary resuscitation within the past 10 days

Answer: C Patients with small-vessel occlusion are poor candidates or surgery because they lack distal target vessels to use or bypass. hese patients should be o ered a trial o thrombolysis, unless they have contraindications to thrombolysis or their ischemia is so severe that the time needed to achieve adequate lysis is considered too long. he major contraindications o thrombolysis are recent stroke, intracranial primary malignancy, brain metastases, or intracranial surgical intervention. Relative contraindications or per ormance o thrombolysis include renal insu iciency, allergy to contrast material, cardiac thrombus, diabetic retinopathy, coagulopathy, and recent arterial puncture or surgery ( able 23-5). (See Schwartz 10th ed., able 23-21, p. 887.) TABLE 23-5

Contraindications to thrombolytic therapy

Absolute Contraindications Established cerebrovascular events (including transient ischemic attack) within last 2 months Active bleeding diathesis Recent (180 mmHg systolic or >110 mmHg diastolic) Puncture o noncompressible vessel Intracranial tumor Recent eye surgery Minor Contraindications Hepatic ailure, particularly with coagulopathy Bacterial endocarditis Pregnancy Diabetic hemorrhagic retinopathy

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175 32. T e term chronic limb ischemia (CLI) is reserved or patients with objectively proven arterial occlusive disease and symptoms lasting or more than A. 1 week B. 2 weeks C. 3 weeks D. 4 weeks

TABLE 23-6

Answer: B he term chronic limb ischemia (CLI) is reserved or patients with objectively proven arterial occlusive disease and symptoms lasting or more than 2 weeks. Symptoms include rest pain and tissue loss, such as ulceration or gangrene ( able 23-6). he diagnosis should be corroborated with noninvasive diagnostic tests, such as the ABI, toe pressures, and transcutaneous oxygen measurements. Ischemic rest pain most commonly occurs below an ankle pressure o 50 mm Hg or a toe pressure less than 30 mm Hg.2 Ulcers are not always o an ischemic etiology ( able 23-7). (See Schwartz 10th ed., ables 23-24 and 23-25, pp. 889–890.)

Clinical categories o chronic limb ischemia

Grade

Category

Clinical Description

Objective Criteria

0

0

Asymptomatic—no hemodynamically signif cant occlusive disease

Normal treadmill or reactive hyperemia test

1

Mild claudication

Able to complete treadmill exercise a ; AP a ter exercise >50 mmHg but at least 20 mmHg lower than resting value

2

Moderate claudication

Between categories 1 and 3

3

Severe claudication

Cannot complete standard treadmill exercise a and AP a ter exercise