Anesthesiology Core Review Part Two-ADVANCED Exam 2016

Anesthesiology Core Review Part Two: ADVANCED Exam

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Anesthesiology Core Review Part Two: ADVANCED Exam

Brian S. Freeman, MD Associate Pro essor o Clinical Anesthesia Residency Program Director Department o Anesthesiology Georgetown University School o Medicine Washington, DC

Jef rey S. Berger, MD, MBA Associate Pro essor o Anesthesiology Residency Program Director Associate Dean or Graduate Medical Education and Designated Institutional Of cial T e George Washington University School o Medicine & Health Sciences Washington, DC

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Anesthesiology Core Review: Part 2, Advanced Exam Copyright © 2016 by McGraw-Hill Education. Inc. All rights reserved. Printed in China. 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. 1 2 3 4 5 6 7 8 9 0

DSS/DSS 20 19 18 17 16

ISBN 978-1-259-64177-0 MHID 1-259-64177-5 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 Richard Ruzycka. Project Management was provided by Vastavikta Sharma, Cenveo Publisher Services. T e cover designer was Dreamit, Inc. T e index was prepared by Alexandra Nickerson. RR Donnelley/Shenzhen was printer and binder. T is book is printed on acid- ree paper.

Library of Congress Cataloging-in-Publication Data Freeman, Brian S., author. Anesthesiology core review / Brian Freeman. p. ; cm. Includes index. ISBN 978-1-259-64177-0 (paperback : alk. paper)—ISBN 1-259-64177-5 (paperback : alk. paper) I. itle. [DNLM: 1. Anesthesia—Examination Questions. 2. Anesthetics—Examination Questions. WO 218.2] RD82.3 617.9′6076—dc23 2014003623

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DEDICATION

To my wi e Rebecca and son Alexander, or all o your support. To my colleagues and residents, or your hard work and dedication. (BF) --------To my GW community: aculty, residents, and students. Once again, you rose to the challenge and produced an outstanding work with the only incentive being a simple request—what an outstanding team! (JB)

Contents Contributors xv Pre ace xxiii

P A R T

BASIC SCIENCES 1 1. Invasive Arterial Blood Pressure Monitoring 1 Audrey Spelde and Christopher Monahan, MD

2. Central Venous Pressure 5 Gabriela Calhoun, MD, and James Gould, MD

3. Pulmonary Artery Catheterization 9 Adrian Ionescu, MD, and Johan Suyderhoud, MD

4. Mixed Venous Oxygen Saturation 13 Hannah Schobel, DO

5. Cardiac Output Monitors 15 Carlton Q. Brown, MD

6. Coagulation Monitors 19 Alan Kim, MD

7. Thromboelastography 23 Amanda N. Hopkins, MD, and Babak Sarani, MD

8. Pacemakers 25 Nilda E. Salaman, MD

9. Laser Sa ety 29 Christine Gerbstadt, MD, MPH

10. Pharmacogenetics 33

13. Peripheral Nerve Blocks: Head and Neck 45 Alan Kim, MD

14. Peripheral Nerve Blocks: Upper Extremity 51 Binoy Bhatt, MD, and Daniel Asay, MD

15. Peripheral Nerve Blocks: Trunk and Perineum 57 Brent Yeung, MD, and Joseph Mueller, MD 16. Peripheral Nerve Blocks: Lower Extremity 61 Binoy Bhatt, MD, and Christopher Monahan, MD

17. Use o Peripheral Nerve Stimulators 67 Brian S. Freeman, MD

18. Intravenous Regional Anesthesia 71 Omar Syed, MD, and Daniel Asay, MD

19. Controlled Hypotension 73 Curt Bergstrom, MD

20. Controlled Hypothermia 77 Mo ya S. Diallo, MD, MPH

21. Hyperbaric Oxygen and Anesthesia Care 79 Ti any Minehart, MD, and George Hwang, MD

22. High Altitude Anesthesia 83 Carlton Q. Brown, MD

Katie Tully and Je rey S. Berger, MD, MBA

11. Addiction 37 Hiep Dao, MD P A R T

ANESTHESIA TECHNIQUES 41 12. Autonomic Nerve Blocks 41 Janish J. Patel, MD

P A R T

III

ORGAN-BASED ADVANCED SCIENCES 87 23. Cerebral Metabolism 87 Janish J. Patel, MD

24. Intracranial Pressure 89 Christopher Monahan, MD vii

viii

Contents

25. Electroencephalography 91 Kumu Hendrix, MD

26. Evoked Potentials 95 Kumu Hendrix, MD

27. Anticonvulsant Therapy 99 Domiciano Santos Jr., MD

28. Antidepressant Drugs 103 Sandy Christiansen, MD, and Brian S. Freeman, MD

29. Anti Parkinson Drugs 107 Brendan Keen, MD, and Marian Sherman, MD

30. Chronic Opioid Dependence and Therapy 109 Sandy Christiansen, MD, and Brian S. Freeman, MD

31. Seizures 111 John Dun ord, MD

32. Coma 115 John Dun ord, MD

33. Central Nervous System Drug Intoxication 119 Charles Baysinger and Je rey Berger, MD, MBA

34. Spinal Cord Injury 125 Nathanael Leo and Palak Turakhia, MD

35. Tetanus 129 Caroll N. Vazquez-Colon, MD

36. Aneurysms and Arteriovenous Mal ormations 131 Vanessa Gluck, MD

37. Anesthesia or Interventional Neuroradiology 135 Audrey Spelde, Binoy Bhatt, MD, Anita Cucchiaro, MD, and Je rey S. Berger, MD, MBA

38. Transsphenoidal Hypophysectomy 139 Brian S. Freeman, MD

39. Fluid Management During Neurosurgery 143 Jacob J. Jones and Je rey S. Berger, MD, MBA

40. Ventilation and Per usion 147 Gabrielle Brown, MD, and Seol W. Yang, MD

41. Bronchial Anatomy 151 Brian A. Kim, MD, and Seol W. Yang, MD

42. Normal Acid–Base Regulation 155 Mona Rezai Rudnick, MD, and Johan Suyderhoud, MD

43. Strong Ion Di erence 159 John R. Benjamin, MD

44. Interpretation o Arterial Blood Gases 161 Kristen Carey Rock, MD, and Maurizio Cereda, MD

45. Obstructive Pulmonary Disease 167 M. Alexander Pitts-Kie er, MD, and Lorenzo De Marchi, MD

46. Restrictive Lung Disease 173 M. Alexander Pitts-Kie er, MD, and Lorenzo De Marchi, MD

47. Preoperative Pulmonary Evaluation 177 M. Alexander Pitts-Kie er, MD, and Lorenzo De Marchi, MD

48. One Lung Ventilation 181 Joseph Mueller, MD

49. Management o Respiratory Failure 185 Gurwinder Gill, MD

50. Anesthesia or Lung Transplantation 189 Wil redo Puentes, MD, and Massimiliano Meineri, MD

51. Echocardiographic Anatomy 193 Mona R. Rudnick, MD, and Lorenzo De Marchi, MD

52. Ischemic Heart Disease: Perioperative Risks 199 Tom Hayes, MD

53. Acute Coronary Syndromes 203 Tom Hayes, MD

54. Perioperative Myocardial Ischemia 207 Tom Hayes, MD

55. Coronary Artery Bypass Gra ting 209 Lisa A. Andersen, DO, Hanwool Ryan Choi, and Tricia Desvarieux, MD

56. Cardiopulmonary Bypass: Overview 211 James K. Kim, MD, and Johan Suyderhoud, MD

Contents

57. Cardiopulmonary Bypass: Anticoagulation 217 Hanwool Ryan Choi and Choy Lewis, MD

58. Cardiopulmonary Bypass: Anti ibrinolysis 221 Adam J. Rubinstein, MD

59. Cardiopulmonary Bypass: Anesthetic Considerations 223 John A. Hodgson, MD

60. Cardiopulmonary Bypass: Myocardial Preservation 225 John A. Hodgson, MD

61. Extracorporeal Membrane Oxygenation 227 Bryan Laliberte, MD

62. Deep Hypothermic Circulatory Arrest 233 Brian S. Freeman, MD

63. Intra aortic Balloon Pump 237 Andrew Winn, MD, and Brian S. Freeman, MD

64. Ventricular Assist Devices 241 Hiep Dao, MD

65. Stenotic Valvular Disease 245 Lauren Lobaugh, MD, and Brian S. Freeman, MD

66. Regurgitant Valvular Disease 249 Lauren Lobaugh, MD, and Brian S. Freeman, MD

67. Subacute Bacterial Endocarditis 253 Brian S. Freeman, MD

68. Perioperative Cardiac Dysrhythmias 257 Kasra Razmjou, MD, and Brian S. Freeman, MD

69. Management o Pacemakers and AICDs 263 Nilda E. Salaman, MD

70. Cardiomyopathies 267 Adrian M. Ionescu, MD, and Brian S. Freeman, MD

71. Cardiac Transplantation 271 Massimiliano Meineri, MD

72. Cardiac Tamponade 275 Andrew Winn, MD, and Brian S. Freeman, MD

73. Pulmonary Embolism 279 Raj N. Parekh, MD, and Hiep Dao, MD

74. Hypertension: Preoperative Evaluation 283 Hannah Schobel, DO

75. Hypertension: Perioperative Management 287 Hannah Schobel, DO

76. Anesthesia or Carotid Endarterectomy 289 Lakshmi Geddam, MD, and Tatiana N. Lutzker, MD

77. Peripheral Vascular Disease 291 Bahaa Daoud and Je rey S. Berger, MD, MBA

78. Aortic Aneurysms 295 Karen Halsted, MD, and Lorenzo De Marchi, MD

79. Cardiopulmonary Resuscitation 299 Kasra Razmjou, MD, and Brian S. Freeman, MD

80. Nutrition 303 Matthew de Jesus, MD

81. Morbid Obesity 305 M. Alexander Pitts-Kie er, MD, and Medhat Hannallah, MD

82. Anesthesia or Bariatric Surgery 307 Janelle D. Vaughns, MD

83. Hepatic Disease: Preoperative Evaluation 311 Je rey Huang and George C. Hwang, MD

84. Postoperative Hepatic Dys unction 315 Je rey Huang and George C. Hwang, MD

85. Liver Transplantation 319 Je rey Plotkin, MD

86. Intestinal Obstruction 323 Daniel Bassiri, MD, and Alessia Pedoto, MD

87. Pathophysiology o Renal Disease 327 Polyanna Silver, MD

88. Renal Failure: Anesthetic Considerations 333 Mo ya S. Diallo, MD, MPH

89. Renal Transplantation 337 Patrick Laughlin, MD, and Je rey Plotkin, MD

90. Perioperative Oliguria and Anuria 339 Mariam Salisu and Je rey S. Berger, MD, MBA

91. Dialysis and Hemo iltration 341 Jessica Reidy, MD, and Brian S. Freeman, MD

92. Lithotripsy 345 Alan Kim, MD

93. Transurethral Resection o Prostate 349 Brian S. Freeman, MD

Contents

94. Anemias 353 Christine Gerbstadt, MD, MPH

95. Polycythemia 357 Monica Passi and Michael J. Berrigan, MD, PhD

96. Thrombocytopenia and Thrombocytopathy 361 Jeremy Epstein, MD, and Vinh Nguyen, DO

97. Congenital and Acquired Factor De iciencies 363 Vinh Nguyen, DO

98. Disseminated Intravascular Coagulation 367 Christopher Potestio, MD, and Vinh Nguyen, DO

99. Fibrinolysis 371 Raj Parekh, MD, and Vinh Nguyen, DO

100. Hemoglobinopathies 375

111. Pheochromocytoma 411 Alan Kim, MD

112. Carcinoid Syndrome 415 Michael J. Berrigan, PhD, MD

113. Diabetes Mellitus 417 Matthew deJesus, MD

114. Demyelinating Diseases 421 Juanita M. Villalobos, MD

115. Primary Neuromuscular Diseases 427 Angela Lee, MD

116. Myasthenic Syndromes 429 Brian S. Freeman, MD

117. Ion Channel Myopathies 433 Kia Sedghi, Ramon Go, MD, and Je rey Berger, MD, MBA

Vinh Nguyen, DO

101. Porphyria 379 Bryan Laliberte, MD

102. Massive Trans usion Protocols 385 Samuel Gilliland, MD, and Rachel M. Kacmar, MD

103. Hypopituitarism 389 Alan Kim, MD

104. Hyperpituitarism 391 Alan Kim, MD

105. Hyperthyroidism 393 Caleb Awoniyi, MD, PhD

106. Hypothyroidism 397 Caleb Awoniyi, MD, PhD

107. Complications o Thyroid Surgery 399 Chukwudi Chiaghana, MD, and Caleb Awoniyi, MD, PhD

108. Hyperparathyroidism 401 Chukwudi Chiaghana, MD, and Caleb Awoniyi, MD, PhD

109. Hypoparathyroidism 405 Chukwudi Chiaghana, MD, and Caleb Awoniyi, MD, PhD

110. Adrenal Disease 407 Jeremy Epstein, MD, and Brian S. Freeman, MD

P A R T

CLINICAL SUBSPECIALTIES 437 118. Acute Pain Pathophysiology 437 James K. Kim, MD, and Lisa Bellil, MD

119. Chronic Lower Back Pain 441 James K. Kim, MD, and Lisa Bellil, MD

120. Complex Regional Pain Syndrome 445 Alyson Engle, Omar Syed, MD, and Palak Turakhia, MD

121. Postherpetic Neuralgia 449 Jessica Rodriguez, MD, and Palak Turakhia, MD

122. Phantom Limb Pain 451 Elvis W. Rema, MD, and Palak Turakhia, MD

123. Treatment o Cancer Pain 453 Elvis W. Rema, MD

124. Pediatric Anesthesia: Equipment 455 Sudha Ved, MD, FAAP

125. Pediatric Premedication 461 Ronak Patel, MD, and Srijaya K. Reddy, MD, MBA

126. Induction Techniques or Children 465 Sudha Ved, MD, FAAP

Contents

127. Pediatric Anesthetic Pharmacology 469 Alomi O. Parikh, and Sophie R. Pestieau, MD

128. Pediatric Airway Management 473 Sudha Ved, MD, FAAP

129. Pediatric Fluid Management 479 Sudha Ved, MD

130. Neonatal Respiratory Physiology 483 Nina Rawtani, MD, and Sudha Ved, MD, FAAP

131. Neonatal Cardiac Physiology 489 Nina Deutsch, MD

132. Retinopathy o Prematurity 493 George C. Hwang, MD

133. Apnea o Prematurity 495 Mohebat Taheripour, MD

134. Bronchopulmonary Dysplasia 499 Victor Leslie, MD, and Kuntal Jivan, MD

135. Cyanotic Congenital Heart Disease 501 Nina Deutsch, MD

136. Acyanotic Congenital Heart Disease 507 Nina Deutsch, MD

137. Anesthesia or Pediatric Cardiac Surgery 511 Nina Deutsch, MD

138. Diaphragmatic Hernia 515 Sudha Ved, MD, FAAP

139. Tracheoesophageal Fistula and Esophageal Atresia 519 Jamie Barrie, MD, and Kuntal Jivan, MD

140. Pyloric Stenosis 521 Binoy Bhatt, MD, and Srijaya K. Reddy, MD, MBA

141. Necrotizing Enterocolitis 525 Alomi O. Parikh, and Sophie R. Pestieau, MD

142. Omphalocele and Gastroschisis 527 Srijaya K. Reddy, MD, MBA

143. Neonatal Respiratory Distress Syndrome 529 Mohebat Taheripour, MD

144. Myelomeningocele 531 Andrew T. Waberski, MD, and Srijaya K. Reddy, MD, MBA

145. Pediatric Respiratory Diseases 533 Nina Rawtani, MD, and Mohebat Taheripour, MD

146. Malignant Hyperthermia 537 Vinh Nguyen, DO

147. Pediatric Otolaryngology 541 Sudha Ved, MD, FAAP

148. Scoliosis 547 Victor Leslie, MD, and Vinh Nguyen, DO

149. Strabismus 551 Lauren Lobaugh, MD, and Vinh Nguyen, DO

150. Pediatric Sedation and O site Anesthesia 553 Sudha Ved, MD, FAAP

151. Maternal Physiology 557 Elizabeth E. Holtan, MD

152. Placental Physiology 561 Amanda N. Hopkins, MD, and Je rey S. Berger, MD, MBA

153. Oxytocic Drugs 565 Emily Harmon, Mandeep Gauthier, MD, and Marianne David, MD

154. Tocolytic Drugs 567 Gregory Dudzik, Mandeep Gauthier, MD, Lakshmi Geddam, MD, and Marianne David MD

155. Magnesium Sul ate 571 Emily Harmon, Mandeep Gauthier, MD, and Marianne David, MD

156. Maternal–Fetal Pharmacology 573 Amanda N. Hopkins, MD, and Je rey S. Berger, MD, MBA

157. Amniotic Fluid 577 Amanda N. Hopkins, MD, and Je rey S. Berger, MD, MBA

158. Fetal Assessment 581 Brian S. Freeman, MD

159. Labor Analgesia 585 Medhat Hannallah, MD

160. Anesthesia or Cesarean Delivery 591 Medhat Hannallah, MD

xii

Contents

161. The Parturient or Nonobstetric Surgery 595 Elizabeth E. Holtan, MD

162. Ectopic Pregnancy 599 Mirza Baig, MD, and Alan Kim, MD

163. Gestational Trophoblastic Disease 603 Christopher Webb, MD, Paul Weyker, MD, and Matthew Haight, DO

164. Pre Eclampsia and Eclampsia 607 Ti any Minehart, MD, and Lisa Bellil, MD

165. Supine Hypotensive Syndrome o Pregnancy 613 Caitlin Sherman, Mandeep Gauthier, MD, and Marianne David, MD

166. Embolic Disorders in Pregnancy 615 Neil Ray, MD, and Matthew Haight, DO

167. Antepartum Hemorrhage 617 Elizabeth E. Holtan, MD

168. Postpartum Hemorrhage 621 Lisa Bellil, MD

169. Maternal Cardiopulmonary Resuscitation 625 Bahaa Daoud, Mandeep Gauthier, MD, and Marianne David, MD

170. Maternal Fever and In ection 627 Paul Weyker, MD, Christopher Webb, MD, and Matthew Haight, DO

176. Anesthesia or Ophthalmologic Surgery 651 Brendan Keen, MD, and Marian Sherman, MD

177. Anesthesia or Orthopedic Surgery 655 Ryan J. Keneally, MD

178. Evaluation o the Trauma Patient 657 Michael Best, MD and K. Grace Lim, MD

179. Burn Management 661 Karen Halsted, MD and George Hwang, MD

180. Mass Casualty and Crisis Management 665 Joseph Mueller, MD

181. Anesthesia or Ambulatory Surgery 667 G. Ryan Pomicter, MD

182. Geriatric Anesthesia 671 Matthew Glading, MD and George Hwang, MD

183. Shock States 675 Gurwinder Gill, MD

184. Poisoning 679 Jeremy Epstein, MD, and Matthew de Jesus, MD

185. Drowning 683 Caroll N. Vazquez-Colon, MD

186. In ection Control 687 Pamela Bland, MD

187. Antibiotics 689 Angela Lee, MD

171. Vaginal Birth a ter Cesarean Section 631 Janice Lee, MD and Lisa Bellil, MD

172. Neonatal Resuscitation 633 Ronak R. Patel, MD, and Rupa J. Dainer, MD

173. Intrauterine Surgery 637 Devon Smith, MD, Matthew U berg, MD, and Matthew Haight, DO

174. Anesthesia or Plastic Surgery 641 Brian S. Freeman, MD

175. Anesthetic Implications o Laparoscopic Surgery 645 Pamela C. Bland, MD

P A R T

SPECIAL ISSUES IN ANESTHESIOLOGY 691 188. Electroconvulsive Therapy 691 Graham Lubinsky, MD, and Michael J. J. Berrigan, MD, PhD

189. Obstructive Sleep Apnea 695 Arlene Hudson, MD

190. Organ Donation 701 Je rey Plotkin, MD

Contents

191. Anesthesia or Radiologic Procedures 703

194. Practice Management 715

Domiciano Santos, Jr, MD

192. Patient Privacy 707

Louis A. Damiano, MD

195. Patient Sa ety 721

Raymond Pla, MD

Matthew deJesus, MD

193. Malpractice 711 Hiep Dao, MD

Index

723

xiii

Contributors

Lisa A. Andersen, DO, JD

John R. Benjamin, MD

Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Daniel Blaine Asay, MD Clinical Instructor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Caleb A. Awoniyi, MD, PhD Adjunct Clinical Associate Pro essor o Anesthesiology University o Florida Health Science Center Gainesville, Florida

Mirza Baig, MD Resident Georgetown University School o Medicine Washington, DC

Daniel Bassiri, MD Resident Weill Cornell Medical College New York, New York

Charles W. Baysinger Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Lisa Bellil, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Jef rey S. Berger, MD, MBA Associate Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Curt Bergstrom, MD Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Michael J. Berrigan, MD, PhD Pro essor o Anesthesiology, Chair T e George Washington University School o Medicine & Health Sciences Washington, DC

Michael Best, MD Resident University o Pittsburgh School o Medicine Pittsburgh, Pennsylvania

Binoy Bhatt, MD Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Pamela Bland, MD Sta Anesthesiologist Walter Reed National Military Medical Center Washington, DC

xvi

Contributors

Carlton Q. Brown, MD

Louis A. Damiano, MD

Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Gabrielle Brown, MD

Hiep Dao, MD

Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Gabriela Calhoun, MD

Bahaa E. Daoud

Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Maurizio Cereda, MD

Marianne D. David, MD

Assistant Pro essor o Anesthesiology and Critical Care Medicine Perelman School o Medicine at the University o Pennsylvania Philadelphia, Pennsylvania

Chukwudi Chiaghana, MD

Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Matthew deJesus, MD

Resident University o Florida College o Medicine Gainesville, Florida

Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Hanwool R. Choi

Lorenzo De Marchi, MD

Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Associate Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Sandy Christiansen, MD

Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident Georgetown University School o Medicine Washington, DC

Tricia Desvarieux, MD

Nina Deutsch, MD Anita Cucchiaro, MD Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Rupa J. Dainer, MD Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Associate Pro essor o Anesthesiology Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Mo ya S. Diallo, MD, MPH Assistant Pro essor o Anesthesiology Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Contributors

Gregory Douglas Dudzik

Samuel Gilliland, MD

Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident University o Colorado School o Medicine Denver, Colorado

John Dun ord, MD Clinical Associate in Anesthesiology T e Johns Hopkins University School o Medicine Baltimore, Maryland

Matthew Glading, MD Resident New York University School o Medicine New York, New York

Alyson M. Engle

Vanessa Gluck, MD

Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Ramon Christopher V. Go, MD Jeremy Epstein, MD Resident Georgetown University School o Medicine Washington, DC

Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Brian Freeman, MD

James Gould, MD

Associate Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Mandeep Gauthier, MD

Karen Halsted, MD

Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident Georgetown University School o Medicine Washington, DC

Matthew Haight, DO Lakshmi M. Geddam, MD Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Associate Clinical Pro essor o Anesthesiology University o Cali ornia San Francisco School o Medicine San Francisco, Cali ornia

Medhat Hannallah, MD, FFARCS Christine Gerbstadt, MD, MPH Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Gurwinder Gill, MD Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Emily Penn Harmon Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

xvii

xviii

Contributors

Tom Hayes, MD

Jacob J. Jones

Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Kumudhini Hendrix, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Rachel Kacmar, MD Assistant Pro essor o Anesthesiology University o Colorado School o Medicine Denver, Colorado

John A. Hodgson, MD Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Elizabeth Holtan, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Amanda N. Hopkins, MD Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Jef rey Huang Medical Student Georgetown University School o Medicine Washington, DC

Arlene J. Hudson, MD Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

George Hwang, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Adrian Ionescu, MD Fellow Harvard Medical School/Massachusetts General Hospital Boston, Massachusetts

Kuntal Jivan, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Brendan Keen, MD Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Alan Kim, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Brian A. Kim, MD Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

James Kim, MD Resident Georgetown University School o Medicine Washington, DC

Bryan Laliberte, MD Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Patrick Laughlin, MD Resident Georgetown University School o Medicine Washington, DC

Victor Leslie, MD Resident Georgetown University School o Medicine Washington, DC

Contributors

Angela C. Lee, MD

Tif any Minehart, MD

Assistant Pro essor o Anesthesiology & Pediatrics Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident Georgetown University School o Medicine Washington, DC

Janice Lee, MD Resident Georgetown University School o Medicine Washington, DC

Nathanael Leo Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Choy R. A. Lewis, MD Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Grace Lim, MD Clinical Assistant Pro essor o Anesthesiology University o Pittsburgh School o Medicine Pittsburgh, Pennsylvania

Lauren Lobaugh, MD Resident Georgetown University School o Medicine Washington, DC

Graham Trevor Lubinsky, MD, MA

Christopher Monahan, MD Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Joseph Mueller, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Vinh Nguyen, DO Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Raj Parekh, MD Resident Georgetown University School o Medicine Washington, DC

Alomi O. Parikh Student Intern T e George Washington University School o Medicine & Health Sciences Washington, DC

Monica Passi

Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Tatiana Lutzker, MD

Janish Jay Patel, MD

Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Assistant Pro essor in Anesthesiology & Pediatrics Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Massimiliano Meineri, MD Associate Pro essor University o oronto Department o Anesthesia oronto, Ontario

Ronak Patel, MD Fellow Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

xix

Contributors

Alessia Pedoto, MD

Nina Rawtani, MD

Associate Pro essor o Anesthesia and Critical Care Medicine Memorial Sloan-Kettering Medical Center New York, New York

Resident Georgetown University School o Medicine Washington, DC

Sophie R. Pestieau, MD

Kasra Razmjou, MD

Associate Pro essor in Anesthesiology Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident Georgetown University School o Medicine Washington, DC

M. Alexander Pitts-Kie er, MD Resident Georgetown University School o Medicine Washington, DC

Raymond A. Pla, Jr, MD Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

G. Ryan Pomicter, MD Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Srijaya K. Reddy, MD, MBA Assistant Pro essor o Anesthesiology Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Jessica Reidy, MD Resident Georgetown University School o Medicine Washington, DC

Elvis W. Rema, MD Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Kristen Carey Rock, MD Wil redo Puentes, MD Fellow University o oronto Department o Anesthesia oronto, Ontario

Fellow Hospital o the University o Pennsylvania Philadelphia, Pennsylvania

Jessica Rodriguez Jef rey Plotkin, MD Associate Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Chris Potestio, MD Resident Georgetown University School o Medicine Washington, DC

Neil Ray, MD Fellow Stan ord University School o Medicine San Francisco, Cali ornia

Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Adam Rubinstein, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Mona Rudnick, MD Resident Georgetown University School o Medicine Washington, DC

Contributors

Nilda E. Salaman, MD

Devon Smith, MD

Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident University o Cali ornia San Francisco School o Medicine San Francisco, Cali ornia

Mariam B. Salisu, MPH Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Domiciano Jerry Santos, MD Assistant Pro essor o Anesthesiology Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Babak Sarani, MD Associate Pro essor o Surgery T e George Washington University School o Medicine & Health Sciences Washington, DC

Hannah Schobel, DO Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Kia Sedghi Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Caitlin M. Sherman Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Marian Sherman, MD Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Polyanna Silver, MD Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Audrey Spelde Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Johan P. Suyderhoud, MD Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Omar A. Syed, MD Resident T e George Washington University School o Medicine & Health Sciences Washington, DC

Mohebat Taheripour, MD Assistant Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Katherine M. Tully Medical Student T e George Washington University School o Medicine & Health Sciences Washington, DC

Palak Turakhia, MD Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Matthew U berg, MD Resident University o Cali ornia San Francisco School o Medicine San Francisco, Cali ornia

Janelle D. Vaughns, MD Assistant Pro essor o Anesthesiology Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

xxi

xxii

Contributors

Caroll N. Vazquez-Colon, MD

Paul Weyker, MD

Assistant Pro essor o Anesthesiology Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident University o Cali ornia San Francisco School o Medicine San Francisco, Cali ornia

Sudha Ved, MD Pro essor o Clinical Anesthesia Georgetown University School o Medicine Washington, DC

Juanita M. Villalobos, MD

Andrew Winn, MD Resident Georgetown University School o Medicine Washington, DC

Seol W. Yang, MD

Assistant Pro essor o Anesthesiology Uni ormed Services University o Health Sciences Bethesda, Maryland

Assistant Pro essor o Anesthesiology T e George Washington University School o Medicine & Health Sciences Washington, DC

Andrew T. Waberski, MD

Brent Yeung, MD

Fellow Children’s National Health System T e George Washington University School o Medicine & Health Sciences Washington, DC

Resident Georgetown University School o Medicine Washington, DC

Christopher Webb, MD Resident Stan ord University School o Medicine San Francisco, Cali ornia

Preface

T e year 2014 marked the beginning o a new phase in board certi cation or anesthesiology residents. Previously, all residents had to pass one written and one oral examination, both taken a er the completion o residency training. Now the American Board o Anesthesiology has increased the stakes. T e Part I examination has been split into two written examinations: “Basic” (administered at the beginning o the third postgraduate year) and “Advanced” (administered the summer a er graduation). Understandably, a new clinically based examination a er the completion o residency training creates stress and anxiety. his is where Anesthesiology Core Review comes in. he organization o the second volume o this review book conorms to the newly revised content outline issued by the American Board o Anesthesiologists or the “Advanced” examinations. Each chapter succinctly summarizes key concepts or each topic rom the new content outline. his review book should serve as the “core” o your study preparation. As program directors with many years

o board examination advising experience, we recommend supplementing Anesthesiology Core Review with multiplechoice practice questions, keyword reviews, and re erences to major anesthesiology textbooks. Space is provided throughout this book to add notes rom other sources. Anesthesiology Core Review represents the success ul collaboration between the three academic anesthesiology departments located in our nation’s capitol: Georgetown University, George Washington University, and the Uni ormed Services University o the Health Sciences. ogether we challenge you to recognize your assets and de ciencies, work collaboratively, and use this book to pass the new ABA “Advanced” Examination with f ying colors! Best regards or a productive career in this dynamic specialty, Brian S. Freeman, MD Jef rey S. Berger, MD, MBA Washington, DC

xxiii

PART I BASIC SCIENCES

Invasive Arterial Blood Pressure Monitoring Audrey Spelde and Christopher Monahan, MD

Arterial cannulation with continuous pressure transduction allows or moment-to-moment monitoring o blood pressure changes. In addition, it permits detection o intraoperative hypotension earlier than indirect monitoring techniques and provides reliable vascular access or blood sampling. Invasive arterial blood pressure monitoring allows pressure monitoring in situations when noninvasive blood pressure monitoring is not possible, such as during nonpulsatile cardiopulmonary bypass. Invasive monitoring also allows or the analysis o arterial pressure wave orms, which can be utilized to better understand clinical scenarios. However, invasive monitoring is not without its disadvantages: it requires technical expertise; it is costly; and it has the potential or serious complications when compared to noninvasive techniques.

OVERVIEW Indications Indications or invasive arterial blood pressure monitoring include: • • • • •

Induced, on-going or anticipated hypotension, or wide variations in blood pressure End-organ disease requiring precise pressure regulation T e need or requent or multiple blood gas measurements T e need or continuous monitoring o cardiac output and stroke volume, where the placement o a pulmonary artery catheter is impractical Situations when noninvasive methods o blood pressure monitoring are unreliable or di cult, such as with burns, trauma, or dysrhythmias

1 A

E R

Contraindications A ew absolute contraindications to invasive pressure monitoring exist. Catheterization should be avoided in smaller end-arteries with inadequate collateral blood ow. o prevent ischemia, invasive monitoring should also be avoided in extremities with suspected or preexisting vascular insu ciency.

Complications Complications associated with arterial cannulation include hematoma ormation, thrombosis with distal ischemia, air or catheter embolism, blood loss, arterial drug administration, vasospasm, pseudoaneurysm, systemic in ection, and inadvertent nerve damage or damage to adjacent structures. However, data suggest that the majority o complications can be attributed to equipment misuse, such as incorrect calibration or incorrect interpretation o the pressure display. Overall, there is a very low incidence o long-term complications associated with invasive arterial blood pressure monitoring. For example, the risk o distal ischemia is estimated to be less than 0.1%. T ere are several risk actors that can potentially contribute to complications with arterial cannulation, including prolonged cannulation, repeated insertion attempts, highdose vasopressor administration, and the use o large-bore catheters. Additional risk actors include hyperlipidemia, anticoagulation, vasospastic arterial disease, previous arterial injury, thrombocytosis, and protracted shock.

Best Practice Several steps can be taken to minimize the risk o complications. Small catheters and continuous saline in usion at 2–6 mL/h help 1

PART I Basic Sciences

reduce the risk o thrombosis and disruption o the arterial wall. Using exible guidewires may reduce the risk o traumatic cannulation, especially in tortuous vessels. Monitoring with a pulse oximeter on the ipsilateral side o the catheter helps to detect decreased per usion to distal tissues. Additionally, minimizing the cannulation time and insertion attempts, and limiting ushing can help to decrease complication rates. Finally, an aseptic technique and early discontinuation o unnecessary catheters reduces the risk or catheter-associated in ections. Femoral catheters should be discontinued within 5 days and catheters at other sites should not be changed or discontinued within 7 days.

Collaterals T e Allen test was designed to examine the integrity o the ulnar collateral circulation. It is per ormed by rst having the patient make a st to exsanguinate the hand. T e operator then occludes both the radial and ulnar arteries while the patient relaxes the blanched hand. Pressure on the ulnar artery is released and a positive ow through the ulnar collaterals is con rmed by ushing o the thumb or palm within 5 seconds o release. An equivocal test is indicated by delayed ushing o 5–10 seconds. Insu cient collateral circulation is indicated by ushing a er >10 seconds. However, it should be noted that this is not considered to be a reliable predictor o ischemic complications or sa ety or radial artery cannulation.

ARTERIAL SITE SELECTION Sites commonly selected or cannulation include the radial, emoral, brachial, posterior tibial, dorsalis pedis, and axillary arteries. T e posterior tibial and dorsalis pedis arteries are typically used only or the pediatric population. T e temporal and umbilical arteries can also be used in pediatric patients, i necessary. •

•

Radial—T e most popular site used is the radial artery due to its accessibility and typically robust collateral blood supply. However, the radial artery is subject to inaccuracies due to its distal location and may lead to peripheral neuropathy. Following cardiopulmonary bypass, increased pressure gradients between the aorta and radial arteries may exist. Ulnar—T e ulnar artery, though deeper and typically more tortuous in its path, may be cannulated as an alternative to the radial artery, even when the ipsilateral radial artery has been unsuccess ully cannulated. T e most common complications at these sites are occlusion and hematoma, which rarely result in permanent injury. Axillary—T e axillary artery permits patient mobility and com ort as well as a wave orm resembling central arterial pressure. However, this site is associated with the potential or brachial plexopathy. Furthermore, more centrally located catheters lead to an increased risk o cerebral air or emboli with vigorous retrograde ushing.

•

Brachial—T e brachial artery also provides a less distorted wave orm than more peripheral vessels. Disadvantages o this site are its proximity to the elbow, making it more prone to kinking. T ere is also the potential or median nerve injury. Femoral—T e emoral artery is the largest artery that is routinely selected. T is site is desirable because the emoral wave orm more closely resembles aortic pressure than peripheral sites such as the radial artery. Distal ischemia is less likely to occur at this site. Femoral artery cannulation is associated with the potential or atherosclerotic plaque embolization, pseudoaneurysm, in ection, and retroperitoneal hematoma or hemorrhage i punctured above the inguinal ligament.

Direct arterial pressure monitoring involves introducing a catheter into an arterial vessel. T e catheter connects to an electromechanical transducer via uid- lled tubing. T ere are our techniques that are commonly used or cannulation: direct arterial puncture, guidewire-assisted cannulation, also known as the Seldinger technique, the trans xion-withdrawal method, and more recently, the ultrasound guided technique. Regardless o the chosen technique, when cannulating the radial artery, the wrist and hand should be immobilized in slight dorsi exion. Extreme dorsi exion should be avoided to prevent attenuation o blood ow and median nerve injury. o begin, the artery is palpated and the skin prepared with an antiseptic. Local anesthetic may be injected or patient comort and may additionally reduce vasospasm. T e needle and catheter are then introduced into the vessel. Once the catheter is in place, the artery is occluded proximally, the tubing is connected to the catheter, and a sterile dressing is applied.

CLINICAL CONSIDERATIONS A system’s requency response, or dynamic response, is characterized by its natural requency and damping coe cient. Natural requency re ers to how rapidly the system oscillates, while the damping coe cient re ers to how rapidly the system comes to rest. Variations in either o these actors will af ect the recorded pressure wave orm. I the natural requency is too low, the displayed wave orm will be exaggerated or amplied, resulting in an overestimation o intra-arterial pressure. T is is due to overlap between requencies in the monitored pressure wave orm and the natural requency o the system, resulting in resonance or ringing. Overdamping o the system results in a slurred upstroke, absent dicrotic notch, loss o ne detail, and ultimately narrowed pulse pressure. Conversely, underdamping results in systolic pressure overshoot and additional arti acts. A system will have the most avorable response i its natural requency is as high as possible, at which point damping will have a minimal ef ect on the recorded wave orm. Several dif erent actors af ect the natural requency o a system and there ore the displayed pressure signal, including

CHAPTER 1

arterial catheter size, length o tubing, number o stopcocks, ush devices, transducer, ampli er, and recorder. T e highest natural requency is best achieved by using short, stif pressure tubing and limiting the number o stopcocks and other connections to the system. In short, any increase in system damping (e.g., air bubbles and blood clots) is ollowed by a decrease in natural requency. Accuracy o the pressure transducer depends on zeroing, calibrating, and leveling to the appropriate position on the patient. he midchest position in the midaxillary line (or 5 cm posterior to the sternal border) is most commonly used in the supine patient as the point o measurement or leveling, assigning a speci c point on the patient’s body as the zero re erence point. However, in a seated patient, the level o the ear is used, which approximates the circle o Willis and there ore cerebral pressure. A er leveling the transducer, a stopcock at the desired level is opened and the zero trigger is activated on the monitor. T is exposes the transducer to atmospheric pressure, which is then established as the zero pressure re erence value. As the patient’s position is altered, the transducer must be moved with the patient or zeroed at the new level o the zero re erence point. Zero dri occasionally occurs and the transducer’s zero should be checked regularly. Calibration is no longer routinely per ormed; however, this historically involved calibrating the transducer against a mercury manometer and should be considered i blood pressure values seem inaccurate despite transducer zeroing.

WAVEFORM ANALYSIS Analysis o the arterial pressure wave orm gives a great deal o clinical in ormation. For example, identi cation o the arterial dicrotic notch can guide timing or intra-aortic balloon counterpulsations. Hypovolemia can also be detected by excessive variations in systolic blood pressure during the respiratory cycle. In addition, the slope o the upstroke indicates

Invasive Arterial Blood Pressure Monitoring

contractility and the slope o the downstroke indicates peripheral vascular resistance. Normal physiologic phenomena cause subtle dif erences in the arterial pressure wave orm when measured at dif erent sites throughout the body. wo o these phenomena are distal pulse ampli cation and pressure wave re ection. With distal pulse ampli cation, changes can be seen in the arterial pressure wave orm when traveling rom central to peripheral arteries. In peripheral compared to central arterial waveorms, there is a steeper arterial upstroke, a higher systolic peak, a later dicrotic notch, a more prominent diastolic wave, and a lower end-diastolic pressure. T e overall ef ect results in a higher systolic pressure, a lower diastolic pressure, and a wider pulse pressure in the periphery. Pressure wave re ection occurs due to the sudden increase in vascular resistance at the arteriolar level, which causes diminished pressure pulsations in more distal vessels and augments upstream arterial pressure. T is causes dif erences in the shape o the arterial pulse wave at dif erent sites in the body (Figure 1-1). As arteries become stif er with age, pulse pressure increases, the systolic pressure peaks occurs later, and the diastolic pressure wave disappears. Abnormal arterial pressure gradients can also be caused by pathophysiologic conditions, such as vascular compression during surgery due to patient position or surgical retraction. T e operative procedure (e.g., cardiopulmonary bypass and surgical site) and pathophysiologic disturbances (e.g., shock, patient temperature, vasoactive drugs, and anesthetics) should be considered when choosing a cannulation site. Particular conditions also produce characteristic changes in the arterial pressure wave orm. For example, aortic stenosis results in a reduced stroke volume, a slowly rising arterial pressure, a late systolic peak (pulsus tardus), and a small amplitude (pulsus parvus) due to the xed obstruction to le ventricular out ow. An anacrotic notch (notch in the upstroke) o en distorts the pressure upstroke and the dicrotic notch (notch in

Circula tion ce ntra l Aortic root S ubcla via n a rte ry Axilla ry a rte ry

Bra chia l a rte ry Ra dia l a rte ry P e riphe ra l

FIGURE 1-1

Changes in arterial waveform from central to peripheral sites. (Reproduced with permission from Lake CL, Hines RL, Blitt CD. Clinical Monitoring: Practical Applications in Anesthesia and Critical Care Medicine. Philadelphia, PA: Saunders; 2001.)

PART I Basic Sciences

Bis fe rie ns puls e

FIGURE 1-2

Pulsus bisferiens. (Reproduced with permission from Fuster V, Walsh RA, and Harrington RA (eds). Hurst’s The Heart, 13th ed. McGraw-Hill Education, Inc., 2011: Fig. 14-43B.)

the downstroke) may be lost, causing the wave orm to appear overdamped. T e characteristic wave orm in aortic regurgitation is called bis erious (“beating twice”). T is is due to the two systolic peaks produced rom the large stroke volume ejected rom the le ventricle, causing a normal systolic peak and a second peak, which is re ected rom the periphery. In addition, the wave orm in this condition has a sharp rise, a wide pulse pressure, and a low diastolic pressure (Figure 1-2). Hypertrophic cardiomyopathy is associated with a “spike-and-dome” appearance. T e spike is caused by rapid le ventricular ejection ollowed by a le ventricular out ow obstruction and subsequent rapid decrease in arterial pressure. T e dome is created by a re ected wave rom the periphery, similar to the bis eriens pulse seen in aortic regurgitation. Pulsus alternans is a beat-to-beat variation in systolic pressures (Figure 1-3). Le ventricular alternans indicates severe le ventricular systolic impairment due to cardiomyopathy, coronary artery disease, systemic hypertension, or aortic stenosis. Pulsus alternans has a regular rhythm,

P uls us a lte rna ns

FIGURE 1-3

Pulsus alternans. (Reproduced with permission from LeBlond RF, Brown DD, Suneja M, and Szot JF (eds). DeGowin’s Diagnostic Examination, 10th ed. McGraw-Hill Education, Inc., 2015: Fig. 8-42E.)

distinguishing it rom ventricular bigeminy, which also displays an alternating pulse pressure. Pulsus paradoxus is de ned as a all in systolic arterial pressure o greater than 10 mmHg during inspiration, which is an exaggeration o the normal inspiratory decrease (Figure 1-4). It is characteristically seen in cardiac tamponade, but may also be observed in conditions with large swings in intrathoracic pressure or distension o the right ventricle, such as in severe acute asthma or chronic obstructive pulmonary disease exacerbations.

P uls us pa ra doxus Ins pira tion

FIGURE 1-4

Pulsus paradoxus. (Reproduced with permission from LeBlond RF, Brown DD, Suneja M, and Szot JF (eds). DeGowin’s Diagnostic Examination, 10th ed. McGraw-Hill Education, Inc., 2015: Fig. 8-42G.)

Central Venous Pressure Gabriela Calhoun, MD, and James Gould, MD

T e central venous compartment corresponds to the volume enclosed by the right atrium and the great veins in the thorax. Central venous pressure (CVP) is the intravascular pressure in the great thoracic veins, measured relative to atmospheric pressure. It is conventionally measured at the right atriumsuperior vena cava junction and provides an estimate o the right atrial pressure.

PHYSIOLOGY CVP is primarily in uenced by blood volume and compliance in the central venous compartment. T e interaction o cardiac unction and the physiologic components that in uence venous return to the heart determine the nal CVP. Multiple actors in uence CVP measurements, including total blood volume, blood volume distribution between vascular compartments, cardiac inotropic state, right ventricle compliance, and an imbalance between cardiac output and venous return. Intrathoracic pressure changes also a ect CVP, particularly in consideration o mechanical respiratory support with positive end-expiratory pressure (PEEP). A normal CVP wave orm consists o ve phasic events: three peaks (a, c, v) and two descents (x, y) (Figure 2-1). T e most prominent wave is the a wave, resulting rom atrial contraction ollowing the ECG P wave at the end-diastole

y de s ce nt a c

S ys tole

QRS

FIGURE 2-1

E R

(ventricular diastole). Atrial pressure decreases ollowing the a wave, as the atrium relaxes. T is decline in atrial pressure is interrupted by the c wave at the beginning o ventricular systole. T is wave is a transient increase in atrial pressure produced by isovolumic right ventricular contraction. T e ventricular contration closes the tricuspic valve and displaces it toward the right atrium in early systole, producing an increase in atrial pressure. As an early systolic event, the c wave must ollow onset o the QRS or R wave on the ECG. Atrial pressure continues its decline during ventricular systole as a consequence o continued atrial relaxation and changes in atrial geometry produced by ventricular contraction and ejection. T is is the x descent or systolic collapse in atrial pressure. T e x descent is considered to be the systolic decline, or collapse, in atrial pressure. T e x descent can be divided in two segments: x be ore the c wave and x′ af er the c wave. T e last atrial pressure peak is the v wave, caused by venous lling o the right atrium during late systole while the tricuspid valve remains closed. T e v wave peaks just af er the ECG wave. Atrial pressure then decreases as the tricuspid valve opens and blood ows rom atrium to ventricule. T is is the y descent or diastolic collapse in atrial pressure ( able 2-1). I the CVP is to be used as an index o cardiac preload, then the pressure just prior to c wave onset is most relevant

Event

Cardiac Cycle

Mechanical Event

a wave

End diastole

Atrial contraction

c wave

Early systole

Isovolumic ventricular contraction, tricuspid motion toward right atrium

v wave

Late systole

Systolic f lling o atrium

x descent

Mid systole

Atrial relaxation, descent o the base, systolic collapse

y descent

Early diastole

Early ventricular f lling, diastolic collapse

Dia s tole

ECG T

Central Venous Pressure Waveform Phasic Events and Corresponding Description

CVP

2 A

TABLE 2-1

x de s ce nt

T QRS

CVP tracing. (Modif ed with permission rom Mark JB. Central venous pressure monitoring: clinical insights beyond the numbers. J Cardiothorac Vasc Anesth. 1991;5:163–173.)

PART I Basic Sciences

to measure. Immediately be ore c wave onset, the measured pressure should be equivalent to the right ventricular enddiastolic pressure (RVEDP) in the absence o tricuspide disease. T e CVP measured in the superior vena cava (SVC) should be equivalent to the right atrium pressure; accordingly, the RVEDP equals CVP. Note that the RVEDP only predicts preload, or right ventricular end-diastolic volume, when right ventricular compliance is normal.

HR ~ 150

150

Part

0 Pra 30 0

“Canno n a wave s ”

CARDIAC ABNORMALITIES

FIGURE 2-2

Atrio-ventricular dissociation. (Reproduced with permission from Hall JB, Schmidt GA, and Kress JP (eds). Principles of Critical Care, 4th ed. McGraw-Hill Education, Inc., 2015. Fig. 28-29, left side.)

T e CVP tracing di erentiates and diagnoses various cardiac arrythmias, valvular abnormalities, and disease states: 1. Atrial f brillation—T e a wave is lost and the c wave becomes more prominent. Fibrillation waves can be visible in the CVP wave orm. 2. Atrio-ventricular dissociation or junctional rhythm— Atrial contraction may occur during ventricular systole. Cannon a waves occur due to atrial contraction against a closed tricuspid valve (Figure 2-2). 3. Tricuspid regurgitation—Blood ejects backwards during ventricular systole rom the right ventricle into the right atrium. T is e ect produces a large used c–v wave on the CVP tracing (Figure 2-3). 4. Tricuspid stenosis—Forward movement o blood rom the right atrium into the ventricule occurs against greater than normal resistance, leading to an accentuated a wave and an attenuated y descent (Figure 2-4). 5. Pericardial constriction—A short, steep y descent characterized by a dip and plateau pattern or square root sign. Prominent a and v waves and steep x and y decents produce an “M” or “W” pattern (Figure 2-5). 6. Cardiac tamponade—Equalization o pressures in cardiac chambers during diastole produce a monophasic CVP wave with a single x descent (Figure 2-6).

Pra

30 –

Y INS P

INS P

0–

FIGURE 2-3

Tricuspid regurgitation. (Reproduced with permission from Hall JB, Schmidt GA, and Kress JP (eds). Principles of Critical Care, 4th ed. McGraw-Hill Education, Inc., 2015. Fig. 28-26, bottom image.)

O.S.

FIGURE 2-4

O.S.

aa wave wave

a a wave wave

Tricuspid stenosis. (Reproduced with permission from Crawford MH (ed). Current Diagnosis &Treatment Cardiology, 4th ed. McGraw-Hill Education, Inc., 2014. Fig. 21-3.)

CHAPTER 2

Central Venous Pressure

Pressure inter erence is minimized by measuring CVP at endexpiration, when the pleural pressure best approximates atmospheric pressure.

Guiding Fluid Therapy

a RA

v x y

FIGURE 2-5

Pericardial constriction. (Reproduced with permission from Hall JB, Schmidt GA, Kress JP, eds. Principles of Critical Care. 4th ed. New York, NY: McGraw-Hill Education, Inc.; 2015: Fig. 40-6 [right side].)

ECG

Alone, CVP neither indicates adequacy o vascular volume nor indicates accuracy o cardiac preload. A direct measurement or clinical prediction o cardiac output is additionally required. Increase in CVP only increases cardiac output when cardiac unction is normal. T e cardiac unction curve has a steep ascending portion and a plateau phase. T e plateau phase is due to the constraint on cardiac lling by pericardium, cytoskeleton, and mediastinal structures. In the plateau phase, increase in CVP contributes to peripheral edema, renal, and hepatic congestion, and distortion o the intraventricular septum, which can impede le heart unction. Elevated CVP means that increases in intravascular volume alone will unlikely increase cardiac output. CVP measurement may be utilized or volume responsiveness. I a suf cient uid bolus is given to increase cardiac output, then there will be adequate ventricular lling pressure. T ere is no convincing evidence that CVP monitoring improves outcome in critically ill patients, particularly when other variables are being assessed. However, CVP may aid volume assessment in anesthetized patients whose vasoconstrictor re exes are pharmacologically impaired by the anesthetic agents.

Complications Pa rt

100

Pra 30 x

FIGURE 2-6

Cardiac tamponade. (Reproduced with permission from Hall JB, Schmidt GA, and Kress JP (eds). Principles of Critical Care, 4th ed. McGraw-Hill Education, Inc., 2015. Fig. 28-27, left side.)

LIMITATIONS OF CENTRAL VENOUS PRESSURE MEASUREMENTS Cardiac Preload Assessment CVP is measured relative to atmospheric pressure. T e transmural pressure, that is, the intracardiac pressure relative to extracardiac pressure, actually determines cardiac preload.

T ere is a signi cant morbidity and possibly mortality associated with obtaining central venous access. Central cannulation can result in complications with a range o 5%–19%, even when per ormed by experienced pro essionals. However, most critically ill patients require central venous access or other aims, such as measurement o venous oxygen saturation, adminstration o drugs, or parental nutrition; consequently, CVP is an adjunct measure with minimal additional risk. Alternatively, non-invasive CVP measurement with ultrasound-guided determination o the in erior vena cava index estimates CVP without cannulation risks.

SUGGESTED READINGS Pinsky MR, Payen D. Functional hemodynamic monitoring. Crit Care. 2005;9(6):566. Magder S, Ba aqeeh F. T e clinical role o central venous pressure measurements. J Intensive Care Med. 2007;22(1):44–51. Marik PE, Cavallazzi R. Does the central venous pressure predict uid responsiveness? An updated meta-analysis and a plea or some common sense. Crit Care Med. 2013;41(7):1774–1781.

Pulmonary Artery Catheterization Adrian Ionescu, MD, and Johan Suyderhoud, MD

T e rst peer-reviewed, journal publication describing the clinical utility o the pulmonary artery catheter (i.e., PA catheter, Swan–Ganz catheter) dates its roots to H. J. Swan’s original publication in the New England Journal of Medicine in 1970, although the experimental concept o the catheter was described much earlier by Lategola and Rahn in 1953. Since its inception, the clinical use o the PA catheter has become a prevalent intra-operative monitoring modality during complex cardiovascular, thoracic, and organ transplant operations, as well as during the postoperative period in the management o critically ill patients. T e PA catheter allows clinicians to easily and rapidly transduce a patient’s central venous pressure (CVP), pulmonary artery pressure (PAP), as well as measure a patient’s temperature, pulmonary capillary wedge pressure, mixed venous oxygen saturation (MVO2), systemic and pulmonary vascular resistance (SVR and PVR), and calculate a patient’s cardiac output (CO) and cardiac index (CI).

E R

The rmis tor P ulmona ry a rte ry dis ta l port P roxima l infus ion port Right a tria l port Ba lloon

PULMONARY ARTERY CATHETER ANATOMY T e modern PA catheter is 7.5 FR, 110 cm long, typically made o polyvinylchloride and consists o multiple ports to access the central venous and pulmonary artery circulation. ypically, a thermistor (located 4 cm rom the most distal port, tip o the catheter) acilitates the continuous measurement o the core blood temperature and also serves as the basis or the calculation o a patient’s CO and CI via the thermodilution technique (Figure 3-1). T e distal port (located at 0 cm, tip o the catheter) allows the clinician to directly transduce the PAP, while assessing the le ventricular unction indirectly based on the le ventricular end-diastolic pressure (LVEDP) and pulmonary capillary wedge pressure. T e proximal port (located 30 cm rom the most distal port, tip o the catheter) acilitates the continuous administration o uids and medications at the level o the right atrium (RA), while transducing a patient’s right atrial pressure (RAP) as well as CVP. T e proximal injectate lumen also marks the exit point or the cold injectate used in the determination o a patient’s CO and CI via the thermodilution technique.

3 A

P roxima l infus ion

FIGURE 3-1

Anatomical representation of the PA catheter. (Reproduced with permission from Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 5-20.)

CLINICAL INDICATIONS Possible clinical indications or the placement o a PA catheter include: 1. Neurological a. Posterior ossa surgery (i.e., sitting craniotomy) b. Venous air embolism 2. Cardiovascular a. Impaired le ventricular systolic unction (ejection raction < 35%) 9

PART I Basic Sciences

b. Hemodynamically signi cant cardiac valvular disease c. Intraoperative management o surgical patients requiring the application o an aortic clamp/cardiac pulmonary bypass/deep hypothermic circulatory arrest d. Signi cant coronary artery disease/unstable angina e. Recent myocardial in arction . Congestive heart ailure, cardiomyopathy or cor pulmonale g. T oraco-abdominal aneurysm repair h. Liver/multivisceral transplantation 3. Pulmonary a. Severe chronic obstructive pulmonary disease b. Acute respiratory distress syndrome c. Lung transplantation 4. Complex Fluid Management a. Burns b. Shock physiology 5. High-Risk Obstetrical Care a. Placental abruption b. oxic shock syndrome (i.e., toxemia)

may produce a temporary complete heart block requiring subsequent pacing. However, studies have shown this to be a rare complication, especially when the LBBB has been present or more than six months. Also, placement o a PA catheter is relatively contraindicated in patients with Wol Parkinson White (WPW) Syndrome and in patients with Ebstein’s Anomaly due to the risk o eliciting a malignant ventricular tachyarrhythmia.

INSERTION TECHNIQUE Prior to insertion o the PA catheter, the clinician must ensure that all lumens are primed with saline, that the catheter balloon is ully unctional, and that the distal port is zeroed at the level o the mid-axillary line. T e placement o a PA catheter requires access to the central venous circulation, which is generally established via Seldinger’s technique. T e PA catheter is systematically advanced through the pulmonary artery access port on the central venous catheter (Figure 3-2). T e catheter is advanced beyond the tip o the introducer, typically 17–20 cm, the balloon is care ully in ated, and the catheter then urther advanced. Generally, at approximately 20–25 cm, the tip o the PA catheter should enter the right atrium and a recognizable right atrial wave orm should be observed. Under normal physiologic conditions, the mean right atrial pressure

CLINICAL CONTRAINDICATIONS One potential contraindication to the insertion o a PA catheter includes the presence o a le bundle branch block (LBBB) as the placement o a PA catheter in this patient population

135 80 PA

SVC

25 10 8

5 Corona ry s inus

Pa pilla ry mus cle

130 8

Inte rve ntricula r s e ptum

IVC

10 0

25 5 5

11 20

(P 1 ) PA

10 0

FIGURE 3-2

LA (P 1 )

Waveform measurements during PA catheterization. (Reproduced, with permission, from Soni N. Practical Procedures in Anaesthesia and Intensive Care. Boston, MA: Butterworth-Heinemann; 1994.)

CHAPTER 3

TABLE 3-1

Normal Pressure Values Obtained by a

PA Catheter Mean

Range

3 mm Hg

1–5 mm Hg

Peak-systolic

25 mm Hg

15–30 mm Hg

End-diastolic

9 mm Hg

4–12 mm Hg

Pulmonary capillary wedge pressure

9 mm Hg

4–12 mm Hg

Systemic vascular resistance

1100 dyne-sec·cm –5

700–1600 dyne-sec·cm –5

Pulmonary vascular resistance

70 dyne-sec·cm –5

20–130 dyne-sec·cm –5

Right atrium Right ventricle

is 3 mmHg with a range o 1–5 mmHg ( able 3-1). As the catheter is urther advanced, an increase in the peak-systolic pressure (usually to 30 mm Hg) is noted when the tip o catheter reaches the right ventricular cavity. Further advancement will place the tip in the pulmonary artery at a distance o 35–45 cm, noted by the stepwise increase in the diastolic pressure (usually to 12 mm Hg). Further advancement o the catheter (usually 40–50 cm) will generate the pulmonary capillary wedge pressure wave orm. Following wedging, the balloon should be de ated and the catheter withdrawn 1–2 cm in order to measure the PAP as well as ensure a sa e proximal location o the catheter tip so as not to lodge in a terminal pulmonary artery, which could lead to pulmonary ischemia/in arction or pulmonary artery rupture.

COMPLICATIONS Numerous complications associated with the use o PA catheters have been described in the literature and these can be grouped into procedural or cognitive complications. Procedural complications include (1) ventricular dysrhythmias; (2) complete heart block in patients with a le bundle branch block; (3) bacteremia and endocarditis; (4) thrombogenesis; (5) valve injury (tricuspid and pulmonic); (6) pulmonary ischemia and in arction; (7) air emboli; and (8) pulmonary artery rupture (rare [< 0.005% incidence], but carries a >50% mortality). Problems with estimating le ventricular preload probably constitute the bulk o complications with PA catheters and hence may contribute to many o the controversies about its clinical use ulness. PA catheters measure pulmonary artery occlusion pressure (PAOP) as a surrogate measurement o le ventricular end-diastolic pressure and hence le ventricular preload. However, the relevant measurement should be le ventricular end-diastolic volume and its relationship to the Frank–Starling principle. Measurements o pressure as a surrogate o volume thus depend on several actors: whether there is relative linearity in the pressure–volume relationship o the le ventricle, whether there is a continuous column o

Pulmonary Artery Catheterization

blood rom the tip o the PA catheter to the le ventricle at the time o measurement, where the catheter tip is located in the pulmonary artery anatomy, and whether there are anatomic or physiologic actors that would alter those measurements. T us, actors that may lead to arti actual or real increases in the PAOP but would then overestimate the true LVEDP (and hence LVEDV [le ventricular end-diastolic volume]) are: • • • • • • • •

Positive pressure ventilation PEEP Mitral stenosis COPD Le -to-right cardiac shunt Increased PVR achycardia Non-West Zone III placement o the tip o the PA catheter

Conversely, actors that may underestimate the LVEDP include: • • •

Decreases in LV compliance (aortic valve stenosis) Pulmonary vascular dilation Aortic valve regurgitation

Outcome studies on patients with PA catheters have been equivocal as to the utility in their routine use or high-risk patients. T e SUPPOR rial posited increased harm in a heterogeneous group o critically ill patients managed with PA catheters versus CVP catheters, but there were methodological problems in the study’s design that may have biased the study’s conclusion (retrospective, unblinded, lack o standard treatment algorithms, etc.). More recent and improveddesign studies have demonstrated nonin eriority when comparing care o homogenous patient groups with PA catheters versus CVP catheters. In 1991, the American Society o Anesthesiologists (ASA) established a ask Force on Pulmonary Artery Catheterization and subsequently issued a set o Practice Guidelines based on the bene ts and risks associated with the clinical use o PA catheters in the various settings encountered by anesthesiologists: •

•

With respect to the patient, according to the guidelines, routine pulmonary artery catheterization is considered inappropriate in low-risk or in moderate-risk patients (ASA 1–3 patients in which hemodynamic perturbations are unlikely/occasionally produce hemodynamic variations leading to end-organ dys unction). T e use o a PA catheter should be considered in high-risk (ASA 4 and 5) patients undergoing surgery since signi cant hemodynamic variations are likely to produce end-organ dysunction in this patient population. With respect to the procedure, and according to the guidelines, patients undergoing heart, lung, liver, kidney, or brain operations have a higher probability to bene t rom pulmonary artery catheterization since

•

PART I Basic Sciences

interventional procedures on these organs are more likely to produce signi cant variations in multiple hemodynamic parameters. With respect to the practice setting, the clinician must care ully consider the catheter-skill, level o training, and clinical experience o the physicians and nurses in the recovery room (or intensive care unit) in order to be able to rapidly and e ectively manage the complications that are detected by the PA catheter.

In summary, incorrectly obtained or interpreted values rom a PA catheter will lead to the wrong treatment. Studies have demonstrated that even in the hands o experienced clinicians, such as board-certi ed intensivists, such errors occur at a signi cant rate.

CARDIAC OUPUT: THERMODILUTION Cardiac output is the total amount o blood ow (L/min) generated during cardiac systole. Mathematically, CO is the product o heart rate (beats/min) and stroke volume (mL/beat), represented by the ormula: CO = HR × SV. T e normal range or CO in a healthy adult is 4.0–6.5 L/min. T e thermodilution technique is considered the clinical gold standard or measuring CO using the thermistor unction o the PA catheter. In order to calculate the CO, a xed volume (usually 10 mL) o cold or room temperature saline is injected through the proximal port o the catheter and the subsequent temperature change in the pulmonary artery blood is detected by the thermistor located at the tip o the PA catheter. T e

temperature change recorded by the thermistor is plotted (on the Y-axis) as a unction o time (on the X-axis) in order to generate a thermodilution curve. Calculating the integral o the area under the curve (AUC) generates the measured CO. T e degree o change in the temperature o the pulmonary artery blood is inversely proportional to the CO. T us, highCO states correlate with a smaller change in the pulmonary blood temperature, while low-CO states correlate with a higher change in the pulmonary blood temperature. T e accurate determination o the CO via the thermodilution technique is based on the ollowing assumptions: (1) the ow o blood, the blood volume, and the pulmonary artery temperature are constant; (2) absence o intracardiac shunts; (3) absence o tricuspid or pulmonary insuf ciency; and (4) the temperature as well as the volume o the injectate must be programmed accurately. T ere ore, a alsely elevated CO will be obtained i a smaller injectate volume is utilized or i the temperature o the injectate is higher than anticipated. Conversely, a alsely diminished CO will be obtained i a larger injectate volume is utilized or i the temperature o the injectate is colder than anticipated.

SUGGESTED READINGS American Society o Anesthesiologists ask Force on Pulmonary Artery Catheterization. Practice Guidelines For Pulmonary Artery Catheterization: an updated report by the American Society o Anesthesiologists ask Force on Pulmonary Artery Catheterization. Anesthesiology. 2013;99(4):988–1014. Whitener S, Konoske R, Mark JB. Pulmonary artery catheter. Best Pract Res Clin Anaesthesiol. 2014;28(4):323–335.

Mixed Venous Oxygen Saturation Hannah Schobel, DO

Mixed venous oxygen saturation (SvO2) is a measurement o whole body oxygenation. Mixed venous blood in measured in the pulmonary artery to sample deoxygenated blood entering the pulmonary artery be ore passing through the lungs. T e pulmonary artery receives a mixture o blood rom the superior vena cava, in erior vena cava, and coronary sinus. It serves as a sample o whole body oxygen utilization. Pulmonary artery blood can be sampled periodically by withdrawing blood through a pulmonary artery catheter or continuously with an oximetric Swan–Ganz catheter. T e normal mixed venous oxygen saturation is about 70%–75%. T is value re ects the act that the body normally extracts only 25%–30% o oxygen carried in the blood. Mixed venous oxygen saturation can be explained using the modi ed Fick equation: SvO 2 = SaO 2 − (VO 2 /Q × 1.34 × Hgb), where SaO2 is the arterial Hgb saturation (%),VO2 is the oxygen consumption (mL/min), Q is the cardiac output (L/min), and Hgb is hemoglobin (g/dL). T e majority o oxygen in blood in bound to hemoglobin. A very small amount in dissolved in the blood as indicated by the arterial oxygen content equation CaO 2 = (1.34 × Hgb × SaO 2 ) + (0.003 × PaO 2). T e Fick equation can be rewritten to express the relationship between oxygen consumption, oxygen content, and cardiac output. T e di erence between CaO 2 and CvO 2 is the amount o oxygen utilized by the tissues: VO 2 = Q × (CaO 2 − CvO 2 ), where CaO2 is the arterial oxygen content (mL/dL) and CvO2 is the mixed venous oxygen content (mL/dL). When oxygen delivery is reduced, oxygen consumption remains constant by increasing oxygen extraction as well as cardiac output. T is mechanism is protective until tissues extract about 50%–60% o oxygen rom the blood. Once oxygen extraction reaches this maximum, oxygen consumption is supply-dependent and lactic acidosis due to

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cellular hypoxia develops. SvO 2 can be used as an indirect indicator o cardiac output in the presence o constant SaO 2 , VO 2 , and Hgb.

DECREASED MIXED VENOUS OXYGEN SATURATION A decrease in SvO2 signi es insuf cient oxygen delivery or increased oxygen consumption ( able 4-1). T is problem occurs in low cardiac output, anemia, hypoxemia, or hypermetabolic states. T e body compensates to maintain aerobic respiration by increasing oxygen extraction rom hemoglobin. T e body can maximally extract 50%–60% o oxygen carried in the blood, decreasing SvO2 to 40%–50%. Once the tissues reach maximal oxygen extraction, urther reduction in oxygen delivery results in anaerobic metabolism, acidosis, and multiorgan ailure.

INCREASED MIXED VENOUS OXYGEN SATURATION An increase in SvO2 signi es decreased oxygen consumption ( able 4-2). T is situation occurs commonly in vasodilatory shock. T e oxygenated blood is not circulating normally throughout the body. T e majority o oxygenated blood is diverted away rom the core to the periphery. T e blood supply and oxygen carried to vital organs such as the brain, heart, and kidneys is insuf cient. T ough the mechanism is di erent

TABLE 4-1

Cause of Decreased SvO2

Decreased Oxygen Delivery

Increased Oxygen Consumption

Hypoxia

Fever

Decreased cardiac output

Shivering

Anemia

Exercise

Abnormal Hgb (e.g., CO)

Hyperthyroid/thyroid storm Malignant hyperthermia

PART I Basic Sciences

TABLE 4-2

SvO 2 can be measured to help guide resuscitation. It is used as one variable in addition to blood pressure, pulse pressure variation, labs, urine output, as well as physical exam in diagnosing and treating the unstable patient.

Causes of Increased SvO2

Decreased oxygen consumption Left to right shunt Impaired tissue uptake, e.g., CN and CO Hypothermia Sepsis Increased cardiac output Sampling error, e.g., wedged PA catheter

SUMMARY

rom those in states o low SvO2, the result o anaerobic respiration and multiorgan ailure is the same. Severe hypotension and shock are the clinical scenarios where O 2 is most commonly measured in the critical care setting. Shock is de ned as a condition where oxygen delivery does not meet the demands or aerobic metabolism o the tissues. T ere are three commonly de ned types o shock: Shock

CVP

CI/CO

SVR

SvO2

Cardiogenic

High

Low

High

Low

Hypovolemic

Low

High

Low

Vasodilatory

Low

High

Low

High

Mixed venous oxygen saturation needs to be used as one monitor in a larger assessment o tissue oxygen and hemodynamic stability. SvO2 measures global oxygenation and may not re ect tissue hypoxia o individual organs and extremities. In these cases, a patient may exhibit lactic acidosis in the presence o normal SvO2. In addition, increased cardiac output can compensate or decreased Hgb or increased VO2, rendering a normal SvO2.

Cardiac Output Monitors Carlton Q. Brown, MD

Since pulmonary artery (PA) catheters were introduced in the early 1970s, cardiac output (CO) measurement has become a readily available clinical tool or the diagnosis o hemodynamic disturbances in critically ill patients. Randomized studies have not proven that PA catheters yield improved outcomes; thereore, caution should be used prior to clinical application. As an alternative, less invasive technologies to provide CO monitoring are now available.

PHYSICAL PRINCIPLES In 1870, Adol Fick observed that CO could be calculated rom whole-body oxygen uptake and the di erence in the amount o oxygen between arterial and venous blood. T e Fick equation is CO = MVO2/(CaO2 – CvO2) × 10, where CO is the cardiac output (o en denoted as “Q”) (L/min), MVO2 is the minute oxygen consumption (mL/min), CaO2 is the arterial oxygen content (mLO2/100 mL blood), and CvO2 is the mixed venous oxygen content (mLO2/100 mL blood). T e content o oxygen in blood is quanti ed as CaO2 = Hb × 1.36 × SatO2 – (PaO2 × 0.003), where CaO2 is the content o oxygen in blood (mL O2/100mL), Hb is the hemoglobin concentration (gm/100 mL), SatO2 is the oxygen saturation (%), PaO2 is the partial pressure o oxygen (mmHg), and the dissolved (unbound) oxygen = PaO2 × 0.003, approximately 0. T is arterial–venous content di erence can be rewritten within the Fick equation as CO = MVO2/([Hb × 1.36 × [SaO2 – SvO2]] × 10).

TECHNIQUES TO MEASURE CO T e Fick principle is simple, but the need or the actual measurement o oxygen consumption and sampling arterial and mixed venous blood limit clinical utility. An arterial line and

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PA catheter are required to measure the di erence in wholebody blood oxygen content. Spirometric, calorimetric, or other measures o oxygen uptake are required or an accurate MVO2. Attempts to estimate MVO2 introduce error as the demographic calculation o MVO2 to roughly 250–300 mL/ min produces inaccurate estimates in perioperative or critically ill patients. Multiplying inspired minus expired oxygen (FIO2 – FEO2) by MVO2 and other indirect measurements o MVO2 have had mixed success. Fiber-optic PA catheters (“oximetric”), which obtain continuous colorimetric PA saturation, track relative changes in CO, but still require oxygen consumption and arterial data to be ully quantitative. T e Fick principle can be practically applied by measuring short-term uptake o gases other than oxygen. T ese marker gases include xenon, nitrous oxide, anesthetic vapors, helium, carbon dioxide, and others. By using uptake during short time periods, venous concentration approximates zero, the arterial concentration is close to end-tidal, and the equation avoids arterial–venous data. A transient carbon dioxide rebreathing method has been commercially developed or clinical use.

Thermodilution and Dye Dilution T ermodilution CO measurement is a orm o “indicator dilution” ow measurement. Quickly injecting a known amount o an indicator into the circulation and measuring downstream dilution over time allows or quantitative CO calculation. Indocyanine green and other vital dyes, lithium, radioactive tracers, and other substances that can be quantitatively measured in blood have been used as dilution markers. T ermodilution uses the injection o a known number o “calories” in the orm o a cold solution into the blood. All dilution markers allow calculation o CO using the Stewart–Hamilton equation. Vital dyes and other molecular markers are uncommon clinically due to repeated blood sampling requirements and tissue accumulation. A lithium ion injection technique has been developed or commercial clinical use. It uses a selective intra-arterial lithium electrode to overcome the need or repeated arterial sampling. wo distinct principles allow PA catheters to measure cardiac output without the limitations o molecular markers. 15

PART I Basic Sciences

T e concept that calories could be used as an indicator and measured as a change in temperature permits use o nontoxic solutions. Quanti cation o calories injected involves multiplying thermal capacitance o an injectate solution (expressed as calories per gram per degree) times the volume o the solution. Additionally, the inclusion o a thermistor downstream rom the injection port on a PA catheter allows direct measurement o changes in blood temperature a er injection. T e measured change in blood temperature at the distal thermistor is converted back into cal/mL using the thermal capacitance or blood. Practical aspects o thermodilution include using adequate injectate volumes and temperature di erences to provide a good signal-to-noise ratio or the measured blood temperature. Di erences in accuracy between iced-saline and room temperature injectates appear to be minimal. ypically, 10 mL o injectate is used or adult patients and

three measurements are averaged to reduce errors caused by uneven injection, changes in CO with ventilation, and other sources o variance to 10% compared to re erence injections. Sources o error or thermodilution measurements include intracardiac shunts, tricuspid or pulmonic valve regurgitation, incomplete delivery o the injectate into the right heart, unintended warming o the injectate by syringe handling, temperature measurement errors caused by brin or clot on the thermistor at the distal PA catheter, a wedged catheter, and unexpected acute changes in patient blood temperature. Unexpected changes in patient blood temperature are common immediately a er cardiac bypass, and may also result rom either rapid peripheral IV uid injection or uid injections directly through the PA catheter or its introducer. Measurements made at the same time relative to cyclic ventilation, particularly with positive pressure ventilation, will have the least variance (Figure 5-1).

D Inte rrupte d inje ction

A Norma l the rmodilution curve

Tim e

Tim e E Tric u s p id re g u rg ita tio n

B Hig h c a rd ia c o u tp u t

Tim e

Tim e Ba s e line te mpe ra ture drift F (e .g., following ca rdiopulmona ry bypa s s )

C Low ca rdia c output

Tim e

FIGURE 5-1

Tim e

Thermodilution curves. (Reproduced with permission rom Longnecker DE, Brown DL, Newman MF, Zapol WM, eds. Anesthesiology. 2nd ed. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig. 30-14, p. 420.)

CHAPTER 5

Doppler and Ultrasound ransesophageal echocardiography ( EE) and transthoracic echocardiography ( E) provide anatomic and unctional evidence o cardiac per ormance. T e minimally invasive nature o ultrasound, the availability o Doppler ow measurements, and new computational packages allowing or the calculation o stroke volume (SV) and CO o en make these devices pre erable to invasive monitoring. Measurement o CO by ultrasound is done either by calculating SV rom anatomic imaging o the le ventricle or by integration o Doppler ow velocities across a major artery. Anatomic EE or E CO calculation involves estimating both the le ventricular end-diastolic (LVEDV) and le ventricular end-systolic volumes (LVESV), subtracting to obtain SV, and then multiplying SV × HR to calculate CO. Several models or estimating le ventricular contractile geometry are used, typically using Simpson’s rule. Measurements are o en limited by anatomy, surgical site, or other constraints on imaging. T ese devices also obtain Doppler ows and in that manner calculate quantitative CO. Doppler calculation o CO relies on a requency shi when emitted ultrasound pulses re ect o moving red cells. T e Doppler principle states that the requency shi o a re ected pulse is proportional to the velocity o the re ecting object. Sampling and compiling re ected requencies rom a major blood vessel permits compilation o a ow pro le or the cross-sectional area and blood velocities within the vessel. aking the integral o those instantaneous velocities yields a computation o ow through that vessel. T ese calculations are now largely automated and may be displayed as interval or continuous values. Esophageal Doppler CO enjoys considerable enthusiasm or measuring relative CO and guiding goal-directed uid management. Responsiveness o measured SV to small uid boluses is re ected quickly and may provide insight into le ventricular per ormance with additional uids. Similar to an esophageal Doppler probe, a EE probe can be aligned rom the esophagus with major thoracic vessels to measure CO. However, EE placement is not nearly as technically acile as the esophageal Doppler device.

NONINVASIVE CO MEASUREMENT Noninvasive CO measurement, using substantively sur ace EKG leads, is based on cardiac cycle changes in thoracic and aortic blood volume, altering electrical impedance across the chest wall. Changes in electrical conductance are proportional to changes in blood volume and can be used to calculate an SV. T oracic impedance and bioreactance provide continuous measurement o CO. Bioreactance, a modi cation o thoracic impedance, has several advantages in calibration and stability.

Impedance Impedance across the thorax is measured by inserting a low-intensity, high- requency (75 kHz) current across pairs

Cardiac Output Monitors

o electrodes placed on the chest wall. T oracic impedance includes an element o ordinary resistance in the chest wall electrodes. Hence, i electrodes lose conductivity, any calibration done at the outset o monitoring will be rendered inaccurate. Continuity o sur ace electrodes is problematic. Several considerations degrade device output, including electrocautery inter erence, increased lung water, sepsis, aortic regurgitation, and cardiac pacing. Recent increases in computational analysis o thoracic impedance have improved accuracy and increased arti act rejection; however, electrode continuity remains elusive.

Reactance T e human thorax can be electrically modeled as a combination o a resistor and a capacitor. Changes in blood volume with each cardiac cycle cause a change in impedance. In bioreactance CO measurement, the voltage applied across the chest electrodes alternates in polarity and there is a time lag between the ow o current and the applied voltage. T e lag is determined by the requency o the applied current and the capacitance o the thorax. Since it is dependant on time rather than electrode continuity, bioreactance is a superior measure o intrathoracic blood volume compared to simple thoracic impedance. A commercial device has been developed that accurately detects relative changes in CO; however, the device exhibits electrocautery inter erence, which may be problematic.

Pulse Wave Analysis Pulse wave analysis attempts minimally invasive CO measurement with computerized analysis o the pressure waveorm generated in the arterial system (aorta, radial, emoral arterial lines) or rom a noninvasive nger pulse wave orm. High- delity transducers placed near an arterial catheter measure dP/dt or arterial pulse waves and derive SV based on a “conservation o energy” theory. T e larger the pulse wave, the larger the SV. Quanti cation o SV requires dividing the cardiac cycle into systolic and diastolic blood ows and assuming that total CO equals the sum o systolic and diastolic blood ows. Pulse wave devices analyze blood pressure, pulse pressure, arterial compliance, and systemic vascular resistance to calculate SV, then CO = SV × HR. At least our commercial systems are currently available. T ey all share in common pressure–volume measurement o the arterial pressure pulse, but di er in their algorithms and calibration. Pulse contour methods are based on solid physical principles and o er beat-to-beat monitoring. However, these methods are highly computational and rely on the number o assumptions that may not remain true in anesthetized or critically ill patients. Nonlinearity o aortic compliance, delity o peripheral arterial pressure waves (resonance and damping), the relationship between peripheral and aortic pulse waves, aortic insuf ciency, intra-aortic balloon pumps, and

PART I Basic Sciences

150 140 Arte ria l blood pre s s ure

130 120 110

100 90 80 70 60 50 40

Thre e me cha nica l bre a ths with gra dua lly incre a s ing paw

30 20 10

Paw

0 –10

FIGURE 5-2

Stroke volume variation. (Reproduced with permission rom Preisman S, Kogan S, Berkenstadt H, Perel A. Predicting f uid responsiveness in patients undergoing cardiac surgery: unctional haemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators. Br J Anaesth. 2005;95(6):746–755.)

interbeat SV variation with atrial brillation all skew data quality. T e disparity o peripheral and central wave orms is particularly problematic a er cardiac bypass, in patients with septic shock, and in patients with reper usion a er liver transplantation. High levels o vasoconstrictors con ound pulse wave computations as they modi y aortic elastance with a disproportional change in peripheral wave orm. All pulse wave analyzers su er these limitations based on the basic physical principles o pulse wave analysis, regardless o the initial calibration method or proprietary algorithms. It remains to be seen i pulse wave analysis is clinically use ul.

Stoke Volume Assessment Although not a ully quantitative measurement o CO, pulse pressure volume (PPV) and stroke volume variation (SVV)

represent short-term changes in le ventricular per ormance rom periodic increases in preload due to mechanical ventilation. PPV is de ned as pressure di erences between systole and diastole with respiratory unction. SVV is de ned as the di erence in stroke volume with the same respiratory cycling (Figure 5-2). While PPV is seen as a variation in the height o the arterial wave orm, SVV is seen as a change in the area under the wave orm. Some CO monitors calculate SVV by dividing CO by HR, yet others do not have a short enough time domain resolution to accurately re ect periodic SVV and PPV changes rom ventilation. CO measures that display real-time wave orms are more use ul or PPV and SVV. Newer pulse wave analyzers automatically compute PPV and SVV. PPV and SVV derived rom the pulse oximeter wave orm can be use ul, but that wave orm is more complex in its capacitance than an arterial wave orm and may be misleading.

Coagulation Monitors Alan Kim, MD

An accurate assessment o a patient’s hemodynamic status is crucial to a sa e anesthetic plan. In the presence o ongoing blood loss, one must quickly distinguish between surgical bleeding and coagulation derangements. Initially, this risk is assessed preoperatively with several tests assessing di erent stages o the clotting cascade. However, given the potential or evolving intraoperative derangements, the clotting ability should also be assessed perioperatively as well. Certain surgical procedures require the induction o a coagulopathic state, such as necessitating the use o extracorporeal blood ow machines. Coagulopathies result rom three etiologies: a ailure in primary hemostasis, an incompetent coagulation cascade, and excessive brinolysis. Primary hemostasis encompasses platelet plug ormation. T is process requires unctional, circulating platelets and an endothelial de ect that exposes platelet-binding receptors. T e coagulation cascade rein orces this platelet plug and simultaneously begins the process o deactivating itsel . T is cascade consists o two pathways, the intrinsic and the extrinsic, that overlap in a common pathway. Fibrinolysis is the process through which the clot breaks down a er serving its unction in hemostasis.

Complete Blood Count (CBC) Measurement o the CBC provides a platelet count but does not assay the unctional status o each platelet. Perioperatively, both quantitative and qualitative de cits in platelets contribute to coagulopathies. T ese de cits are especially prevalent in surgeries involving signi cant uid shi s and requiring extracorporeal blood ow such as in extracorporeal

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membrane oxygenation or cardiopulmonary bypass. Distinguishing between these etiologies aids in identi ying the appropriate intervention. Qualitative de cits have a variety o causes: decreased production, splenic sequestration, increased destruction, or dilution. When splenic sequestration is the underlying cause, platelet levels will o en increase in the presence o stressors. In disseminated intravascular coagulation, the platelets will be rapidly consumed, and provide minimal bene t. T e risk-to-bene t ratio o administering these products must be weighed. Repeated platelet trans usions run the risk o sensitizing a patient to platelet ragments, impeding uture transusions. As such, platelet trans usions should be reserved or patients with less than 10,000/uL platelets, ongoing blood loss, or invasive procedures.

Bleeding Time Bleeding time is an older test that can be per ormed in the absence o a laboratory. T ere are two variants to this method: •

TESTS OF PRIMARY HEMOSTASIS T e essential elements o primary hemostasis include the concentration and quality o platelets as well as important components that lead to platelet plug ormation. Some have a more historical context and are not easily or commonly employed in perioperative use, while others are a part o a standard preoperative workup. Platelet unction tests are usually employed when there is evidence o coagulopathies.

•

T e Ivy bleeding time is determined by placing a blood pressure cu on the upper arm and in ated to 40 mmHg. A cut is made on the volar sur ace o the arm. T e cut is blotted every 30 seconds until the bleeding stops. T ere are devices that standardize the depth and size o the cut. A normal range is between 2–9 minutes. T e time it takes or the bleeding to stop can also be assessed against a nomogram. T e time period is assessed as prolonged, normal, or shortened. T e Duke method changes the location o the cut by using the earlobe. T is location is used as the head is more accessible during surgery. However, the depth and width o the cut cannot be standardized. Bleeding time may be elevated due to platelet de cit, dys unction, or vascular abnormalities. A platelet de cit should be investigated as with CBC. Platelet dys unction can be acquired (medication-induced) or hereditary (von Willebrand de ciency) and should be urther elucidated.

Perioperatively, bleeding time has a limited utility. Studies comparing bleeding time changes to the increased 19

PART I Basic Sciences

postoperative bleeding risk have been unable to demonstrate a strong association. Bleeding time thus is not use ul or identi ying underlying platelet de ects.

Platelet Function Analyzer (PFA-100) T e PFA-100 runs resh blood run through a sample tube coated with two platelet activating mediums: collagen with epinephrine and collagen with adenosine diphosphate. It tracks how long it takes or the sample tube to completely occlude rom clotting. T is test has a high negative predictive value, is airly rapid, and does not require any specialized training to run. However, it does have a ew limitations. T ese include the variable responses due to citrate concentration, collection time, hematocrit level, platelet counts, drug e ects, and abnormal von Willebrand actor levels. Patients with a normal PFA-100 will generally have an intact primary hemostasis. I this test is abnormal, a ormal platelet aggregation test is required. T e PFA-100 is used to identi y patients with an aspirin resistance. In patients with aspirin resistance, some respond to higher doses.

Platelet Aggregation Tests Activated platelets aggregate in two stages. Initially, alpha and dense platelet granules release a host o actors that spur platelet aggregation. Further aggregation promotes a second irreversible phase o coagulation that utilizes energy-dependent actors such as thromboxane. T ese two phases are assessed with the use o a photooptical instrument that measures the degree o light transmittance through a blood sample. Each coagulation phase is associated with a relative increase in light transmittance. T is is due to the decreased turbidity o the sample when platelet components aggregate. Since there is more “empty” space in the blood sample, the light is able to transmit more. De-aggregation results in an increase in platelet particles and increases the turbidity.

TESTS OF THE COAGULATION CASCADE Standard Coagulation Tests T e coagulation cascade consists o two main tracks: extrinsic and intrinsic. T ese two tracks measure very di erent aspects o coagulation, although they overlap in a common pathway. rauma triggers the tissue actor pathway (i.e., extrinsic pathway), which in turn provides a sharp increase in thrombin levels. When the vasculature is damaged, actor VII leaves the circulation and encounters tissue actor ( F) bearing cells. Factor VII orms a complex with F, initiating the extrinsic coagulation pathway. T is process is very quick, taking only a ew seconds to nish. T e contact activation pathway (i.e., intrinsic pathway) has a minor role in initial clot ormation. Instead, it plays a signi cant part in provoking in ammation. T e nal common pathway is the continuation o the prothrombotic state, promoted by activated actors VIII and IX, until negative eedback curtails these e ects. Prothromboplastin (P ) values track the intrinsic coagulation cascade. Normal P values are in the range o 28–32 seconds. T e test uses a phospholipid matrix to emulate the interaction o actor XII and the platelet membrane. P values are extremely sensitive to even small amounts o heparin. As a result, it is o en used as a way to track the ef cacy o a heparin dose. Given the variable responses to heparin dosing, a patient’s response to standard dosing is actored into urther titrating to a therapeutic level. Prothrombin time (P ) values re ect the extrinsic pathway. P values are measured by adding recombinant tissue actor ( actor III) to a sample o plasma. T e speed at which this sample coagulates is the P value. Factor VII has the greatest e ect on the speed at which this occurs. P values can di er signi cantly based on the speci c system used to calculate its value. As such, the international normalized ratio (INR) value is calculated to standardize the values across di erent systems. INR = (P sample/P normal)ISI, where ISI is the international sensitivity index that will vary depending on the system employed in its measurement.

Anti-Xa Activity Platelet-Mediated Force Transduction T is device assesses both platelet concentration and unction. It consists o a sample cup with a tightly tting upper plate. T e upper plate is attached to a device that senses orces exerted on the plate. A blood sample is placed in between the plate and the cup. As the blood clots, it exerts a orce on the upper plate that is sensed by the device and transduced. T e normal values have been established by the device manu acturers. It has shown that high doses o heparin remove the retraction orces that clotting causes. Furthermore, i protamine is applied to reverse the anticoagulant e ects o heparin, it does not necessarily remove its antiplatelet e ects.

Anti-Xa activity is ordered to track the e ects o low molecular weight heparin (LMWH) or un ractionated heparin (UFH). T e e ect o LMWH such as enoxaparin is lost in the P /P / INR tests. It requires a separate test o the heparin Xa levels to judge its e ects. As such when giving a therapeutic dose o enoxaparin, heparin Xa levels can be ollowed closely.

Reptilase Time Reptilase time measures de ciencies in brinogen. Reptilase mimics thrombin activity in cleaving brinopeptides, but only cleaves the A variant, while thrombin cleaves both A and B variants to release brin. Unlike thrombin, reptilase is poorly inhibited by antithrombin III (A -III). As such, anticoagulants

CHAPTER 6

that rely on A -III activity, such as heparin, hirudin, and argatroban, do not prolong reptilase time.

Ecarin Clotting Time Ecarin clotting time (EC ) is used to track hirudin-based anticoagulant e ects. Ecarin activates prothrombin. Direct thrombin inhibitors such as hirudin inhibit this activation pathway. EC is una ected by war arin administration.

•

Specif c Factor Testing In the presence o speci c actor de ciencies such as hemophilia A ( actor VIII) and hemophilia B ( actor IX), these actors can have their levels tested directly. Hemophiliac A patients require at least 30% actor VIII activity prior to proceeding to a minor surgery. T ese same patients require 100% actor VIII levels when undergoing major surgeries. T ese levels should be assessed shortly prior to the start o surgery. I levels are de cient, surgeries should be delayed until restored. In an emergency, they should be run through the case. Disseminated intravascular coagulation (DIC) is another test in which speci c actor levels, as well as actor degradation byproducts, are indicative o a pathologic state. T e assessment o brinogen levels and brin split products, coupled with clinical signs o excessive bleeding, are hallmarks o ongoing DIC.

Activated Coagulation Time (ACT) AC is a widely used assay o heparin activity. Whole blood is added to an activator that triggers the intrinsic coagulation pathway. T ere is a manual and automated version o this test. T e manual version relies on the visual con rmation o clot ormation as the endpoint. T e automated version relies on the clot retracting orce to trigger the endpoint. A normal time is generally between 80 and 120 seconds. T ere are two main automated AC machines (Hemochron and Hemo ec systems). Although the individual mechanics di er, the objective is the same. When a reliable clot orms, the machine triggers a time. T e results o the two tests are not interchangeable as statistically di erent measurements have been conducted at both low and high heparinization levels. A single type should be used over the duration o a case. T is test is o en used to con rm adequate heparinization prior to initiating cardiopulmonary bypass. A level o 300– 400 seconds is generally considered sa e or cardiopulmonary bypass. Institution- and service-dependent thresholds may vary. A level o 400 and above is considered adequate in an emergency situation as long as additional anticoagulation is administered and assessed over the course o the surgery. T ere are several limitations with the use o AC : •

AC levels do not correlate with plasma heparin levels. In cardiopulmonary bypass, the addition o an extracorporeal circuit causes hemodilution, which can

Coagulation Monitors

theoretically lower AC values. Hypothermia increases AC in a dose-dependent ashion. T ese two e ects are limited to heparinized blood samples. T e AC values o unheparinized samples are not a ected by hypothermia or hemodilution. Platelet levels and unction in uence AC as well. T rombocytopenia with platelet levels below 50,000/uL can prolong AC . Platelet unction inhibitors such as aspirin and prostacyclin will also prolong AC times. Platelet lysis will actually shorten AC values by releasing platelet actor 4 (PF-4). PF-4 neutralizes heparin which in turn shortens the AC time. Both anesthesia and surgery will cause a hypercoagulable state, shortening the AC as well.

Inadequate rises in AC in response to therapeutic doses o heparin should be investigated thoroughly. However, the most likely etiology is a de ciency in unctional A -III levels. Heparin activates A -III as the initial step o its anticoagulant activity. Although it also neutralizes several coagulation actors, the bulk o its unction relies upon the presence o unctional A -III. When adequate AC levels are not achieved, even a er signi cant heparin doses, A -III de ciency should be considered as a possible etiology. Patients will have a wide range o responses to the same heparin dose, depending on the levels o innate antiheparin actors that are present in them. Heparin dose response (HDR) curves are used to account or this variability. T us, based on the patient’s initial response to the heparin bolus, the automated HDR curves will in orm the need or any additional heparin.

TESTS OF FIBRINOLYSIS T e thromboelastogram (Chapter 7) is one o the most commonly used perioperative assays to assess both coagulation and brinolysis. Alternative measurements o brinolysis are discussed below.

Fibrin Degradation Products Fibrin degradation products are various byproducts o brin breakdown by plasmin. Antibody assays detect their presence, and any elevation in their levels is indicative o increased brinolytic activity. T e D-dimer is one o these brin degradation products. Although its presence is o en sought during a diagnosis o deep vein thrombosis, pulmonary embolism, or disseminated intravascular coagulation, they can be elevated in a variety o other conditions.

Euglobulin Lysis Time T e euglobulin lysis time measures the time it takes or the euglobulin raction o a plasma sample to break down a clot. T e time is shorter when brinolysis is more active, longer when not. As with other tests, there are both automated and manual versions o this test.

T romboelastography Amanda N. Hopkins, MD, and Babak Sarani, MD

Normal physiologic hemostasis is achieved through the interplay o pro- and anti-coagulant properties o the vascular endothelium, platelets, and the coagulation cascade. Conventional laboratory tests look at this system in a piecemeal ashion and give a limited indication o in vivo unctionality. T ese tests take signi cant time or results, urther limiting real-time use ulness. o address these limitations, anesthesiologists have adopted the use o thromboelastography ( EG). EG provides a rapid point-o -care assessment o the coagulation process, with initial results available within 5 minutes. EG measures viscoelastic changes o clot ormation through clot lysis, evaluating the integrity o the coagulation system, platelet unction, brin polymerization, clot strength, and brinolysis. Results o EG permit targeted trans usion. EG is used in liver transplant, cardiac bypass, and, increasingly, trauma and general surgery.

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cuvette. A 0.36-mL whole blood sample is mixed with an activator, such as kaolin or celite, to trigger clot ormation. T e sample is pipetted into the cup, and the cup begins to oscillate slowly through an angle o 4° at a temperature o 37°C. Initially, the movement o the cup does not a ect the pin, but as the blood thickens, the pin becomes entangled in the developing clot, coupling the motion o the cup to the pin. T e movement o the pin is trans erred through the torsion wire to the electronic recorder, and the analyzer produces a tracing (Figure 7-1). Several parameters are presented on the tracing: •

TECHNIQUE AND INTERPRETATION T e EG analyzer consists o an electronic recorder attached to a torsion wire that suspends a plastic pin into a plastic cup or

•

Reaction time—T e time in minutes elapsed rom the start o the test until the clot moves the pin enough to produce a 2-mm amplitude on the tracing is de ned as the reaction time (R). R re ects the activity o the coagulation cascade; a coagulation actor de ciency produces a prolonged R and hypercoagulability yields a shortened R time. T e normal values or R depend on the type o clotting activator used. Alpha angle—T e alpha angle (α) is a measure in degrees o the speed o clot ormation. It is de ned as the angle

B Coa gula tion

Fibrinolys is

Ma ximum a mplitude (mm) α

P la te le ts (MA)

TEG ACT Enzyma tic

Fibrinoge n (K,α )

Thrombolys ins (Ly30, EP L) Time (s )

FIGURE 7-1

Thromboelastogram tracing. (Reproduced, with permission, rom Kashuk JL, Moore EE, Sawyer M, et al. Postinjury coagulopathy management: goal directed resuscitation via POC thrombelastography. Ann Surg. 2010;251:604.)

PART I Basic Sciences

TABLE 7-1

•

TEG Tracing Parameters and Suggested Therapy for Abnormal Values

Parameter

Abnormality

Interpretation

Suggested Therapy

Reaction time (R, minutes)

↑

Coagulation actor def ciency

Fresh rozen plasma

Clot ormation time (K, minutes)

↑

Low f brinogen

Cryoprecipitate

Alpha angle (α, degrees)

↓

Low f brinogen

Cryoprecipitate

Maximum amplitude (MA, millimeters)

↓

Thrombocytopenia and/or platelet dys unction

Platelets and/or DDAVP

Clot lysis (Ly30, %)

↑

Hyperf brinolysis

Antif brinolytic (e.g., Amicar)

between the horizontal axis o the tracing and the tangent to the tracing at 20-mm amplitude. Decreased angles indicate a slower rate o clot strengthening, as seen with low brinogen levels. Normal values are in the range o 45°–55°. Coagulation time—T e coagulation time (K) is measured in minutes rom the end o R to when the tracing amplitude reaches 20 mm. Like the alpha angle, K is determined by the rate at which the clot strengthens and is a actor o thrombin’s cleaving o available brinogen into brin. Low brinogen levels produce greater K values. T e normal values or K depend on the type o clotting activator used. Maximum amplitude—Maximum amplitude (MA) is the point o maximum clot strength in millimeters. T e amplitude o MA is determined primarily by the unctional contribution o platelets to the clotting process, re ecting the end result o platelet– brin interaction. Normal values are in the range o 50–60 mm. Lysis index 30—T e lysis index at 30 minutes (Ly30) is the percentage reduction in MA af er 30 minutes. Higher brinolytic activity produces a greater Ly30. Normal values are not higher than 7.5%–8%.

T romboelastography is use ul or directing therapy in patients with coagulopathic bleeding ( able 7-1). However, EG has not proven reliable in identi ying patients who are going to bleed, so abnormal EG tracings should not be used to guide therapy in the absence o bleeding.

CHARACTERISTIC TEG TRACINGS Speci c derangements in coagulation produce characteristic EG tracings (Figure 7-2). Platelet dys unction or severe thrombocytopenia produces a tracing with a decreased MA, indicating reduced clot strength. Coagulation actor de ciency, whether innate or due to anticoagulants such as heparin or wararin, gives a tracing with a prolonged R time. Hypercoagulable states yield a tracing with decreased R and K times along with an increased alpha angle and MA, re ecting an increased speed o clotting (R, K, α) and increased clot strength (MA). Excess brinolysis is noted by a tracing with an increased clot lysis (Ly30). A

FIGURE 7-2

Characteristic TEG tracings. (Reproduced, with permission, rom Johansson PI, Stissing T, Bochsen L, et al. Thrombelastography and thromboelastometry in assessing coagulopathy in trauma. Scand J Trauma Resusc Emerg Med. 2009;17:45.)

Pacemakers Nilda E. Salaman, MD

A cardiac pacemaker (PM) is an electronic device that provides electrical stimuli or myocardial contraction when indicated. Current PM devices are used to treat bradyarrhythmias, tachyarrhythmias, and resynchronization, and, in some cases, are combined with implantable de brillators. T e rst permanent cardiac PM was implanted in a human in 1958. echnological advances have since revolutionized the unction o the PM and expanded therapeutic indications. T e device has evolved rom simple, single-chamber, xed-rate PMs to multichamber, rate-responsive units with the capability o pacing, cardioversion, and de brillation.

OVERVIEW A cardiac pacing system consists o a pulse generator (battery), pulse-sensing elements, timing, and output circuitry lead(s) or signal transmission. T e pulse generator is placed subcutaneous or submuscular in the chest wall. Pacing energy is delivered rom a pulse generator to a single chamber (atrium or ventricle), dual chambers (atrium and ventricle), or multiple chambers (in biventricular pacing) using either unipolar or bipolar leads. Bipolar leads have been most commonly used due to the decreased susceptibility to electromagnetic inter erence (EMI). Cardiac pacing can be achieved in several ways, transcutaneous (by the application o external pacing pads), esophageal, transvenous (insertion o a pacing lead via central venous access), and intracardiac via implantation o endocardial or epicardial leads. Symptomatic bradycardia is an indication or a PM. T e most common reason or symptomatic bradycardia is sinus node dys unction due to degeneration o the conduction system. Pacemakers can be temporary or permanently implanted devices ( able 8-1). emporary cardiac pacing can serve as therapy or transient bradyarryhthmias or as a bridge or permanent generator placement. T e Class I indications (i.e., the bene t greatly outweighs the risk, and the treatment should be administered) or temporary pacing include: • • •

Sinus node dys unction Acquired atrioventricular block in adults Chronic bi ascicular block

TABLE 8-1

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Permanent Pacemaker Indications

Symptomatic diseases o impulse ormation (sinus node disease) Symptomatic diseases o impulse conduction (disease o the atrioventricular node) Long QT syndrome Hypertrophic obstructive cardiomyopathy (HOCM) Dilated cardiomyopathy (D-CMP)

• • • • •

A er acute myocardial in arction Hypersensitive carotid sinus syndrome and neurocardiogenic syncope A er cardiac transplantation Pacing to prevent tachycardia Patients with congenital heart disease

PACEMAKER CODES T e PM code o the North American Society o Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) or Generic Pacemaker NBG Code describes the pacing behavior ( able 8-2). T ere are ve positions. In any o the positions, O indicates that pacing, sensing, or a unction is not present. • • •

•

T e rst position indicates the chamber(s) paced: A (atrium), V (ventricle), or D (dual chamber, both A and V). T e second position re ers to the chamber where the PM senses native cardiac electrical activity: A, V, or D. T e third position indicates the response to the sensed native cardiac activity: I (inhibition), (triggered), or D (a dual unction o atrial tracking and ventricular inhibition). T e ourth position o the code indicates that rate modulation is present by the letter R. Rate modulation is the use o a sensor to meet the patient’s metabolic demands, independent o intrinsic cardiac activity. PM manu acturers have devised a number o mechanisms to detect “patient exercise,” such as sensors that detect vibration, respiration, and pressure. Pacing rate is increased with increased exercise. As the exercise tapers, this sensorindicated rate returns to the programmed lower rate. 25

PART I Basic Sciences

TABLE 8-2

Generic Pacemaker Code (NBG)

Position I: Chamber(s) Paced

Position II: Chamber(s) Sensed

Position III: Response(s) to Sensing

Position IV: Programmability

Position V: Multisite Pacing

O, none; A, atrium; V, ventricle; D, dual (A + V); I, inhibited; T, triggered; R, rate modulation.

•

T e h position indicates whether multisite pacing is present: A, V, or D. Multisite pacing is de ned as more than one stimulation site in any single chamber. Biventricular (BiV) pacing (cardiac resynchronization therapy [CR ]) or multisite ventricular pacing involves simultaneous pacing o the right ventricle (RV) and the le ventricle (LV). T e goal is to restore LV synchrony in the treatment o dilated cardiomyopathy. A lead is advanced to the coronary sinus or le ventricular epicardial pacing in addition to single- or dual-chamber right heart pacing leads. T e LV and RV are paced and the activation sequence o the ventricles is timed to “resynchronize” RV and LV ejection. Atrial-synchronized biventricular pacing is said to improve cardiac output, hemodynamics, heart ailure symptoms, and quality o li e in patients with progressive heart ailure symptoms. CR through biventricular pacing is currently indicated or reduction in symptoms o moderate to severe heart ailure in those patients who remain symptomatic, despite stable, optimal medical therapy with an LV ejection raction (LVEF) less than or equal to 35% and wide QRS complex greater than 120 milliseconds. T is device can be used with or without the use o an implantable cardioverter-de brillator (ICD). BiV pacing can lengthen the Q– interval in some patients, producing torsade-de-pointes. T e most common pacing modes are DDD and VVI:

1. DDD ([synchronous-demand] dual-chamber pacing, sensing, and dual response [inhibited or triggered])— Every atrial event is ollowed by a ventricular event. It inhibits itsel i a native QRS is detected. I there is no atrial activity, it will be paced, and a er any sensed or paced atrial event, a ventricular event will either be allowed to occur within the allowed time rame or, i it has not occurred, it will be paced. T is setting ensures that an atrial contraction occurs; thus, its advantage over VDD is that it guarantees atrial kick. DDD may resemble AAI, VA , VDD, and DVI modes. Four distinct patterns can be observed with DDD pacing: • •

Sensing in the atrium and sensing in the ventricle; Pacing in the atrium and sensing in the ventricle;

• •

Sensing in the atrium and pacing in the ventricle (“P” wave tracking); Pacing in the atrium and pacing in the ventricle.

2. VVI (only ventricular pacing and sensing)—T e ventricle is sensed, and i there is no event within the predetermined time rame, the ventricle is paced. I ventricular activity is sensed, the pacemaker is inhibited. T e VVI is a step up rom the VOO in that it prevents R-on- phenomena. When the atria is beating above the lower rate interval (LRI) and producing a ventricular contraction, this PM will inhibit and allow AV synchrony. When the atria is not beating above the LRI, this PM will re a er the LRI has occurred, leading to loss o AV synchrony—this loss o AV synchrony can lead to PM syndrome. Pacemaker syndrome is characterized by nonspeci c signs and symptoms o low cardiac output, hypotension, near syncope, heart ailure, cannon A waves, or neck vein distention. Pacemaker syndrome occurs in ~25% o VVI patients, and produces severe symptoms in 5%. 3. VOO—T is is a xed-rate or asynchronous mode. T ere is ventricular pacing only, with no regard or the underlying rhythm.

ANESTHETIC CONSIDERATIONS Magnets T e magnet-activated switches in the PM generator were incorporated to produce pacing behavior that demonstrates the remaining battery li e and sometimes pacing threshold sa ety actors. Not all PMs revert to an asynchronous mode with the application o a magnet. Not all models rom a particular company behave the same way. For all generators, contacting the manu acturer remains the most reliable method or determining the magnet response.

Pacemaker Failure or Malfunction 1. Failure to capture can result rom acid–base disturbances, electrolyte abnormalities, myocardial ischemia, myocardial in arction, or abnormal antiarrhythmic drug levels. 2. Lead or generator ailure events are rare.

CHAPTER 8

TABLE 8-3

Perioperative Factors Associated with Electromagnetic Interference of Pacemakers Electrosurgery (monopolar causes the most inter erence) Evoked potential monitors Nerve stimulators Transcutaneous electrical stimulation (TENS) Fasciculations Shivering Large tidal volumes External def brillation Magnetic resonance imaging Radio requency ablation Extracorporeal shock wave lithotripsy Electroconvulsive therapy

3. EMI can result in sensing abnormalities, alteration o rate, or reprogramming. Radio requency waves between 0 and 109 Hz can generate sources o EMI. T e most common result is pacing inhibition due to ventricular oversensing. Prolonged exposure to EMI can cause the PM to initiate a noise reversion mode, which triggers asynchronous pacing until the noise stops. 4. able 8-3 lists actors associated with generation o EMI in the perioperative setting. 5. Medications a. Succinylcholine ( asciculations can inhibit PM; not an absolute contraindication) b. Cardiac medications modi ying detection or stimulation thresholds (e.g., sotalol, verapamil) c. Sympathomimetic drugs can decrease pacing threshold

Magnetic Resonance Imaging Magnetic resonance imaging (MRI) has been shown to pose serious risks, including li e-threatening arrhythmias and death. Magnetic resonance imaging is generally contraindicated in patients with PMs. T e American Heart Association (AHA) guidelines recommend consideration o MRI only in exceptional circumstances.

Perioperative Management • •

A ocused preoperative evaluation should establish whether the patient has a PM (or ICD), type, dependence, and unction. Evaluate and optimize the coexisting disease.

• •

• • •

•

Pacemakers

Consider a secondary method or pacing the patient should a PM ailure occur. Determine whether signi cant EMI will be present during the planned procedure that might af ect the programmed behavior o the device. Advise the operator about minimizing the use o monoplar electrosurgery unit (ESU) bursts to 5 seconds or less, and consider using a bipolar ESU or harmonic scalpel. Assure that the electrosurgical receiving plate is positioned so the current pathway does not pass through or near the device system. Determine whether reprogramming pacing unction to an asynchronous mode or disabling the rate responsive unction is advantageous. Have a magnet available. Anesthetic technique/agents should be dictated by the patient’s underlying physiology and surgical procedure. Maintain vigilance in accordance with the ASA standards, monitoring o pulse, rate, and rhythm intraoperative and throughout the immediate postoperative period. T e PM device that was reprogrammed or the operating room should be reset in the immediate postoperative period.

SUGGESTED READINGS American Society o Anesthesiologists. Practice advisory or the perioperative management o patients with cardiac implantable electronic devices: PMs and implantable cardioverter-de brillators: an update report by the American Society o Anesthesiologists task orce on perioperative management o patients with cardiac implantable electronic devices. Anesthesiology. 2011;114:247–261. Atlee JL, Bernstein AD. Cardiac rhythm management devices (Part II): perioperative management. Anesthesiology. 2001;95:1492–1506. Stone M, Salter B, Fischer A. Perioperative management o patients with cardiac implantable devices. Br J Anaesth. 2011;107(S1):i16–i26.

Laser Safety Christine Gerbstadt, MD, MPH

PRINCIPLES OF LASER ENERGY Laser (light ampli cation by stimulated emission o radiation) di ers rom common light in that it emits a more ocused, or coherent beam. T is specialized beam transmits energy, potentially use ul to cut or vaporize tissue in surgery. Additionally, because laser beams remain compact over distances or which regular light would di use, lasers can be pointed precisely. Furthermore, compared to solid scalpels, laser light does not need to be sterilized, disposed, or ordered rom central supply. Surgeons value lasers because they cut clean, precise, rom a distance, and with depth control. However, like many powerul tools, lasers are potentially dangerous. Lasers contain three structural components: a power source (pump), a gain medium (tube), and an optical resonator (o en two parallel mirrors or optical bers). T e power supplied to a laser may directly stimulate the population o atoms in the gain medium, thereby raising the electrons to a higher energy level, producing the traditional laser energy. T e gain medium can be in any physical state; medical lasers commonly utilize gas (argon, carbon dioxide, helium) or solid-state elements (ruby, garnet). It is the gain medium that determines the wavelength emitted, thus de ning the applications and risks. T e wavelength emitted may be in the visible light spectrum (385–760 nm), or beyond visible light, in wavelengths rom ultraviolet (200–400 nm) to in rared and ar-in rared (700–10,600 nm). Laser energy travels as monochromatic (single wavelength), synchronous (in phase), parallel (collimated) beams deliverable to a small target. Since energy density is inversely proportional to the square o the spot size radius, halving the spot size o a laser beam, with energy constant, increases energy density by a actor o 4. Variables that relate to the degree o therapeutic e ect or damage to tissue are the power density, duration o exposure, and photon wavelength. In addition to laser variables, tissue characteristics also modulate biologic e ects o laser. T ese include (1) absorption, the magnitude by which excited electrons increase energy in cells, (2) scatter, the degree by which atoms disperse or remain localized, (3) thermal conductivity, how heat transmits outwardly or remains contained, and (4) local circulation,

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the movement o surrounding cells. As an example, the commonly used medical CO 2 laser is completely absorbed by tissue water within the top ew layers o skin cells. T is results in vaporization o sur ace cell layers with minimal or no damage to the underlying layers. In comparison, the Nd:YAG (neodymium-doped yttrium aluminum garnet) laser is less absorbed by water such that the beam di uses through several millimeters, dispersing energy to produce more coagulation or “cooking” and less vaporization. A summary o types o lasers is given in able 9-1.

SAFETY STANDARDS AND LASER HAZARD CLASSIFICATION T e American National Standards Institute’s (ANSI) Z136 series classi es lasers into one o our hazard categories. •

•

Class 1—A Class 1 laser is sa e to view, and does not emit levels o optical radiation above the normal exposure limits or the eye. An example is the laser in a CD/DVD drive. Light rom the subclass 1M is similarly sa e or viewing with the naked eye, but may be unsa e i viewed through optical devices such as microscopes, o en used in surgical procedures, and binoculars. Class 2—Class 2 lasers emit a visible laser beam that would be considered hazardous or extended viewing, but human aversion and blink re exes to the brightness o this light energy encourage avoidance, o ering some protection. Many point-o -sale barcode scanners are in this category. Class 2M lasers are not sa e with optic modi cations as in class 1M. Class 3—Class 3R and 3B lasers may emit any wavelength, but cannot produce a di use, nonmirror-like re ection hazard, unless ocused or viewed or extended periods at a close range. T e power output rating o class 3R, 0.5 W or less, is not considered a re hazard or serious skin hazard. Currently popular or use in public speaking, laser presentation pointers are class 3R devices. Class 3B lasers, containing devices with higher power outputs, are treated similarly to class 4 devices. 29

PART I Basic Sciences

TABLE 9-1 LASER TYPES Laser Type

Uses

Penetration Depth

Absorbed by/Eye Safety

Carbon dioxide (CO2) (mirror system)

Good or cutting, low coagulation; ablating benign raised lesions

1 mm (0.1 mm thermal necrosis)

Water/clear plastic or glass eyewear to protect cornea

Argon (f ber optic)

Vascular, pigmented lesions; poor cutting

2–3 mm (6 mm scatter)

Hemoglobin, melanin/tinted eyewear*

Krypton

Pigmented lesions

KTP (potassium/titanyl/ phosphate)

Coagulation radiation hemorrhagic cystitis, incisions, ablation

Xenon

Cornea, angioplasty

V beam (pulsed dye laser)

Port wine stain, hemangioma removal

Femtosecond

Deep anterior lamellar keratoplasty

Thulium

Benign prostate hypertrophy vaporization

Alexandrite laser

Facial melasma, port wine stain, pigmented urologic stones, hair removal

Deep (Iris)

Melanin/metal eye shield or patient to prevent choroidal and retinal vasculature or retinal pigment

Holmium: yttrium–aluminum–garnet

Lithotripsy

1–2 mm

Water

Ruby

Tattoos, nevi, hair removal

Neodymium (Nd-YAG) (f ber optic)

Good coagulation; air cutting, oculodermal melanocytosis, hair removal

5–10 mm

Tissue protein/tinted eyewear,* metal eye shield or patient to prevent choroidal and retinal vasculature or retinal pigment when near eye

FREDDY ( requency doubled, double pulse Nd: YAG)

Lithotripsy (no so t tissue use)

Hemoglobin/tinted eyewear*

Water

*Tinted eyewear f ltering specif c wavelength o laser only.

•

Class 4—Stringent control measures are required or class 4 lasers, considering re, skin, and eye hazards rom both direct beam and di use re ection. Any acility using class 3B or class 4 lasers should designate a Laser Sa ety Of cer (LSO).

LASER SAFETY ANSI laser sa ety standards include control measures in two categories o (1) engineering controls, such as protective housings and interlocks, and also laser-protective endotracheal tubes, and (2) administrative and procedural controls, such as standard operating procedures and the use o personal protective equipment, including eye protection or class 4 lasers. Most injuries, including burns rom direct application and environmental res, can be traced to errors. It ollows that prevention o airway injury, and injury to the patient’s other tissues or to the operating room environment and sta , is best addressed by a combination o education, equipment maintenance, and error-reducing modi cations to the system.

Airway Fire Hazard reduction, both at the prevention stage and at the rescue stage, should address all three components o the re triad: oxidizer, uel, and ignition source. Fires and explosions involving an endotracheal tube in a person’s trachea during surgery are a major concern with operative lasers. T e ollowing summarizes current science about endotracheal tube res in acial and airway operation with laser. Attempting to “ ire-proo ” a conventional endotracheal tube by wrapping a re lective tape in spiral ashion is not advised. he use o a specially manu actured laser endotracheal tube is sa er than wrapping; however, the protection against combustion is only relatively reduced. A laser tube can combust directly by laser impacting the tube, or indirectly by something else in the airway combusting, and the tube ignites in the established ire. In late the endotracheal cu with water rather than air whenever possible or laser surgery o the airway. Some tubes have a sa ety pilot or methylene blue to identi y cu rupture via dye dispersion.

CHAPTER 9

Airway res during laser use are most common with an open breathing system such as nasal cannula in which the inspired oxygen is greater than 30%. T ere ore, use FiO 2 o less than 30% by adding air. Nitrous oxide is as ammable as oxygen; dilution o the inspired gas with nitrous oxide is not e ective in reducing combustion o the re triad and should there ore be avoided. Also, avoid use o alcohol-based solutions and ammable surgical drapes and paper products during airway and acial laser surgery. A backup endotracheal tube should be available or emergent reintubation. Should an airway re occur, the re triad can be disrupted by immediate discontinuation (disconnection o circuit) o oxygen ollowed by removal o any airway device.

Ocular Injury Anesthesia closed claims analysis o operating room res report incidences o 19% or eye damage, 14% or airway res, and 9% skin, tissue, and “other” burns. T e cornea transmits and ocuses visible and near-in rared energy to the back o the eye, but also absorbs the ultraviolet and arin rared energy. Imperative to eye sa ety is the understanding o optical density (OD), an expression o how much laser energy is ltered by a protective lens. Filters are rated or optical density on a logarithmic scale rom 0.0, providing no protection by permitting 100% light transmission, to an OD o 4.0, allowing only 0.01% o light transmission, there ore providing the greatest amount o protection. ANSI laser sa ety standards or personal protective equipment include eye protection or all class 4 lasers. Other eye sa ety practices include (1) never looking directly into a laser, (2) never shining a visible or invisible laser into another person’s eyes, (3) avoiding blinking with high brightness, which is help ul but not ully protective, (4) never using magni ying optics with laser energy, and (5) keeping a re ective object away rom the eld o laser operation.

Laser Sa ety

Visible and near-visible laser energy, ound in Nd:YAG, argon, and K P lasers, can burn the retina, whereas arin rared energy o CO 2 lasers will burn the cornea. T e cornea transmits and ocuses visible and near-in rared energy to the back o the eye, but also absorbs the ultraviolet and ar-in rared energy. All persons, including the patient, must wear protective eyewear that speci cally lters the laser wavelength in use.

Skin Injury T e re ection o laser rom surgical instruments may cause harm to intestines and intra-abdominal tissue in laparoscopic surgeries, since laser may injure by re ection, transmission, or absorption. Gloves and covering o skin are recommended. Other skin complications include hyperpigmentation, hypopigmentation, erythema, blistering, milia, purpura, and scarring. Properly installed, operated, and maintained laser units can reduce the risk o electric shock due to the high voltage o this equipment.

Infection Sa ety in laser operation must always consider particulate contamination risks, in addition to the emphasis on risks o wave physics or this high-energy medium. In ections such as human papillomavirus may in theory spread to another part o the body or another human, via smoke plume and splatter. T ese hazards can be reduced using a smoke evacuator and laser surgical masks ltered to 0.3 µm. Gloves, antisplash eye protection, and masks should always be worn during laser surgery.

SUGGESTED READINGS Mehta SP, Bhananker SM, Posner KL, Domino KB. Operating room res: a closed claims analysis. Anesthesiology. 2013;118(5): 1133–1139.

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Pharmacogenetics Katie Tully and Jef rey S. Berger, MD, MBA

Pharmacogenetics is the study o inherited and acquired genetic variations in metabolic pathways responsible therapeutic responses and adverse reactions to pharmacotherapy. Pharmacogenomics encompasses pharmacogenetics and investigates the genetic basis or variations in drug metabolism, e cacy, and targeting using techniques such as DNA sequencing and mapping. Ideally, prospective genotype determinations permit individualized therapies that are e ective without harm ul side e ects. Perioperative pharmacogenetic considerations include genetic susceptibility to risk actors and also potential adverse reactions to physiologic disturbances. T e eld o perioperative genomics seeks to understand the connection between genetic variations and di erences in anesthetic responses and outcomes.

GENETIC FACTORS IN DRUG DOSE– RESPONSE RELATIONSHIPS A wide variety o genetic polymorphisms, or changes that result in phenotype variation, occur with genetic promoter, coding, insertion, or deletion alterations. Most genetic polymorphisms only modestly impact drug action relative to the more signi cant nongenetic e ects. Furthermore, most phenotypic traits are multigenetic, decreasing their utility in describing genetic variation. Individual responses to drugs may be based on genetic variability in both pharmacokinetics and pharmacodynamics. Pharmacokinetic variability re ects the di erences in absorption, distribution, metabolism, and excretion. T is variability is due to genetic variations in transport molecules that mediate a drug’s uptake and excretion and in drug metabolizing enzymes such as cytochrome P450 liver enzymes. Pharmacodynamic variability re ers to phenotypic drug variability despite equivalent delivery to sites o action, re ecting molecular di erences in target unctions or receptors. A clinical example o genetic variation in pharmacodynamics is the OPRM1 receptor or morphine. A certain percentage o the population exhibit a single nucleotide polymorphism (SNP) on the gene or the OPRM1 receptor that encodes a resistance to the drug morphine.

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MALIGNANT HYPERTHERMIA (MH) MH is a very rare (1/10,000), li e-threatening, autosomal dominant, genetic disorder characterized by a metabolic state in which a patient exposed to a triggering agent may develop multisystem organ damage and death.

Pathophysiology MH results rom abnormal excitation–contraction (EC) coupling in skeletal muscle, leading to the uncontrolled release o calcium (Ca2+) rom the sarcoplasmic reticulum (SR). T is massively increases intracellular calcium and causes sustained muscle contractions. T e ensuing hypermetabolic state produces tachypnea, tachycardia, hyperthermia, and metabolic acidosis. During typical EC coupling, the skeletal muscle membrane depolarizes to induce a con ormational change in the DHPR (voltage-gated Ca2+ channel dihydropyridine receptor). T is activates the ryanodine receptor type 1 (RYR1) protein to release Ca2+ rom the SR. Ca2+ travels rom a high concentration in the lumen o the SR to the skeletal muscle cytosol where it binds troponin C. Ca2+-bound troponin C causes tropomyosin to move away rom thin- lament myosin-binding sites, resulting in muscle contractions. Contractions are terminated as Ca2+ is pumped back into the SR by the sarco/endoplasmic reticulum Ca2+–A Pase (SERCA), an A P-dependent Ca2+ pump. Mutations in the RYR1 and the α-1 subunit o the DPHR (CACNA1s) genes are associated with MH. RYR1 genetic mutations result in hypersensitive RYR1 channels, permitting greater Ca2+ release compared to normal channels. Additionally, a mutation in the DHPR inhibits RYR1 rom closing, maintaining increased intracellular Ca2+ levels and sustained muscle contractions.

Triggers Agents that trigger MH include succinylcholine and/or the halogenated volatile anesthetics (i.e., halothane, iso urane, sevo urane, and des urane). T ough all depolarizing muscle relaxants and halogenated anesthetics have the potential to trigger MH, it does not always occur ollowing exposure to 33

PART I Basic Sciences

these agents, re ecting the variable expression and penetrance o the gene mutations o the RYR1 gene. T e ollowing agents do not cause MH: propo ol, ketamine, nitrous oxide, xenon, etomidate, barbituates, narcotics, benzodiazepines, nondepolarizing muscle relaxants, local anesthetics, or phenothiazines.

Signs and Symptoms T e earliest signs o MH include hypercarbia, sinus tachycardia, and possible masseter spasm, ollowing the administration o succinylcholine. Other cardiac arrhythmias include ventricular tachycardia and ventricular brillation with uctuations in blood pressure. Rhabdomyolysis causes elevations in serum creatinine kinase (CK > 10,000 – 20,000 IU) and dark colored urine rom myoglobin (>60 µg/L). Respiratory acidosis presents with rising end-tidal CO2. During controlled ventilation, an end-tidal CO2 > 55 mg and arterial CO2 > 60 mmHg is signi cant, and spontaneous ventilation values or end-tidal CO2 > 60 mg and arterial CO2 > 65 mmHg should raise concern. Lactic acidosis leads to metabolic acidosis with an arterial pH < 7.25 and base excess > –8 mEq/L. Hyperthermia ensues with b > 38.8°C, increasing 1°C–2oC every 5 minutes; however, hyperthermia is typically a late sign.

Diagnosis History should include obtaining in ormation about perioperative deaths or unexplained high evers in the patient or rst degree relative, or a history o Duchene muscular dystrophy, central core disease, Becker dystrophy, cardiac arrest during strenuous activity, or exercise-induced rhabdomyolysis. Pertinent ndings in personal or amily history warrant a trigger- ree anesthetic, and perhaps genetic testing or mutations in the RYR1 and CACNA1S genes, though a negative screen does not exclude MH susceptibility. Alternatively, a skeletal muscle biopsy can be taken or in vitro ca eine and halothane contracture testing.

Treatment MH requires an emergent response. It is important to rst call or assistance, including a call to the MH hotline: 1-800644-9737, and halt administration o the triggering agent. Dantrolene (2.5 mg/kg IV mixed in sterile water) is the treatment o choice and works by decreasing skeletal myoplasmic Ca2+. Improved intravenous access or uid delivery and arterial access or hemodynamic and laboratory monitoring is essential. Respiratory acidosis can be managed by hyperventilating the patient with high- ow oxygen and metabolic acidosis can be treated with a bicarbonate (0.5–1 mEq/kg). Hyperthermia can be managed by actively cooling the patient to reduce the core temperature. Bladder catheterization should be per ormed or monitoring urine output and isotonic uids with or without diuretics should be given as goaldirected therapy. Patients should be monitored or 24 hours or until stable.

PSEUDOCHOLINESTERASE (PCE) DEFICIENCY PCE de ciency is an autosomal recessive disorder caused by atypical or absent pseudocholinesterase enzymes. De cient PCE leads to decreased metabolism o neuromuscular blocking agents, such as succinylcholine and mivacurium, resulting in prolonged apnea and paralysis.

Pathophysiology Cholinesterase enzymes hydrolyze the ester o acetylcholine, whereas PCE has a lower a nity or acetylcholine and a higher a nity or other esters such as succinylcholine. In people with typically unctioning PCE, administered succinylcholine levels rapidly decline because o the rapid action o PCE; however, in patients with mutated PCE, the e ects o succinylcholine can last up to 10 hours. Pharmacogenetic testing is not currently recommended to the population at large.

Signs and Symptoms Cardiac signs include arrhythmia, ventricular brillation, or cardiac arrest, and neurological signs include seizures and a rare case o coma. Laboratory tests utilize the property o dibucaine to con rm atypical PCE enzymes. T e local anesthetic dibucaine typically inhibits PCE up to 80% in vitro but has minimal e ect on mutated PCE with only 20% inhibition ( able 10-1).

Diagnosis Patients should be asked about the personal and amily history o anesthesia-related problems. Physiologic states associated with decreased PCE activity include in ancy, pregnancy, advanced age, liver disease, acute myocardial in arction, myxedema, acute in ections, and patients undergoing plasmaphoresis. PCE de ciency is asymptomatic prior to the use o succinylcholine and should be suspected in any patient with prolonged paralysis (>10 minutes) af er administration o succinylcholine. T ere are two di erent clinical presentations with nerve stimulation that can occur ollowing administration o a triggering neuromuscular blocking agent in patients with PCE de ciency: (1) depolarizing block with tetanus that

TABLE 10-1

Dibucaine Number (DN) Ranges

DN*

Genetic Mutation

70–83

None (normal genetics)

40–60

Heterozygous (Dd)

470 milliseconds or males or 480 milliseconds or emales). Congenital PQ S has been identi ed with seven di erent genetic de ects in the structure o sodium and potassium channels. PQ S is associated with syncope and documented ventricular arrhythmia, orsades de Pointes, ventricular tachycardia, and sudden death. Preoperative interview should elicit the patient or amily history o syncope episodes, ascertain current medications, and con rm illicit drug usage. It is also important to correct any electrolyte abnormalities preoperatively. Forty percent o patients with PQ S are asymptomatic and 10% will have cardiac arrest as their rst clinical sign. Symptoms include syncope, epilepsy, and palpitations precipitated by stress ul events, especially swimming. EKG ndings include prolonged Q c in lead II or V5—a corrected Q (Q c) greater than 0.46 s has a positive predictive value > 90%, abnormal wave, ventricular dysrhythmia, torsades de pointes, and ventricular tachycardia. Medical management involves suppressing sympathetic nervous system activation using beta-adrenergic receptor antagonists. Implantable cardiac de brillator placement may be warranted in symptomatic patients.

Addiction Hiep Dao, MD

In 2010, nearly 12 million Americans reported nonmedical use o prescription painkillers in the past year. As the use and abuse o opioids increases, the likelihood o an anesthesiologist these patients during clinical practice also will increase. As both illegal and prescription use o opioids increases, anesthesiologists will encounter more patients exhibiting opioid tolerance. Secondly, as abusers o opioids seek treatment or their addiction, the numbers o patients receiving long-term opioid therapy or their addiction also will increase. All anesthetic plans can be divided into preoperative considerations, intraoperative management, and postoperative recovery and analgesia. For patients with known or suspected opioid abuse, this strategy is no di erent. T e interviewing clinician will bene t rom realizing that many patients with a history o abuse or dependence on prescription opioids will be evasive about that history or will attempt to minimize their use o these drugs. A help ul strategy when collecting the patient history is to ocus on speci c questions while preserving a nonjudgmental environment. When possible, the interviewer should determine the time o the last dose o opioids and, i applicable, who is prescribing these medications. Drug screening, speci cally urine drug screening, is an important tool in obtaining objective in ormation about a patient’s use o opioids. However, these tests have several important limitations. Immunoassay screening, which is the most common urine drug screen, can detect the presence o speci c opioids and their metabolites but requently returns alse-positive results and typically ndings must be conrmed by gas chromatography—a time-consuming process. Drug testing can provide use ul objective in ormation as long as clinicians are aware o these limitations. T e clinician will likely encounter patients who have been taking opioids chronically. T ese include the opioid agonists methadone and buprenorphine-naloxone, as well as the opioid antagonist naltrexone. Having a working knowledge o these medications is help ul in understanding their anesthetic and analgesic implications.

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OPIOID ADDICTION Patients on long-standing prescription opioids can be directed to take these medications as they normally would on the morning o surgery. Patients at risk or or entering withdrawal can have their symptoms managed. Clonidine is commonly used to treat symptoms o opioid withdrawal and can be given as a starting dose o 0.1 mg twice daily. Other medications, such as loperamide, also can be administered to target speci c withdrawal symptoms. Intraoperative management o patients with opioid dependence or abuse relies heavily on three areas: managing intoxication, preventing or treating withdrawal, and achieving e ective analgesia. Although many patients will not present or elective surgery when they are acutely intoxicated, urgent or emergent situations involving these patients o en occur. In these incidents, monitoring respiratory rate and oxygen saturation is critical. Antagonist therapy should be reserved or patients with potentially li e-threatening respiratory depression, as precipitating withdrawal in such a patient may make both anesthetic and analgesic management more di cult. Analgesia strategies or patients with signi cant histories o opioid use should ocus less on opioids as a oundational, single-agent therapy and more on opioid-sparing or multimodal techniques with non-opioid agents such as intravenous (IV) acetaminophen or liposomal bupivacaine. Many o these agents can be initiated in the preoperative or intraoperative phases and continued into the postoperative period. Nonopioid analgesics such as acetaminophen and nonsteroidal antiinf ammatory drugs, regional anesthesia and, when possible, alpha-2 agonists, and ketamine can have pro ound analgesic e ects, particularly when used in combination. Pregabalin and gabapentin also can be use ul or managing neuropathic pain, which o en is poorly controlled by opioids in general. Goals or the postoperative period can be divided into two main objectives: com ort and sa ety. Patient com ort consists o providing adequate analgesia and continued prevention or management o opioid withdrawal. Patient sa ety

PART I Basic Sciences

is equally important, as this population typically mani ests signi cant opioid tolerance. Patients with opioid tolerance generally will require at least two to three times more opioids than an opioid-naïve patient. Yet despite their analgesic tolerance, they appear to be at risk or respiratory side e ects. Opioid withdrawal, either real or potential, can complicate pain assessments; patients may over-report pain to obtain increased opioid dosages. Even patients on high doses o opioids in the postoperative period may su er intermittent withdrawal symptoms, given the waxing and waning e ects o short-acting opioids. I appropriate, combining a long-acting opioid analgesic with shorter-acting agents, such as hydromorphone, by patientcontrolled analgesia during periods o breakthrough pain may help to alleviate patients’ withdrawal ear or symptoms.

Methadone Methadone is by ar the most commonly used long-term opioid treatment and has been widely available since the 1960s. Methadone is a long-acting opioid agonist with some activity as an N-methyl-D-aspartate antagonist. T e major unction o methadone is suppression o withdrawal symptoms. Clinicians should veri y the dose by contacting the methadone clinic by telephone. reating opioid withdrawal with opioids is against the guidelines rom the Drug En orcement Administration; there ore, the use o methadone is reserved exclusively or treating pain and must be thoroughly documented in the patient’s medical records. For those patients receiving methadone maintenance, management is relatively straight orward. A er veri ying the dose with a methadone clinic, the drug can be continued during the postoperative period. T e dose can be divided into a three-times-daily regimen to take advantage o methadone’s analgesic properties, which are much shorter than its withdrawal-preventing e ects.

e ects will plateau. At this point, urther doses will have no e ect on widening the drug’s therapeutic window by broadening its sa e dosing range. Coupled with its long hal -li e, these attributes help to make buprenorphine both relatively sa e and e ective in managing long-term opioid dependence. T e drug has a high a nity or mu-receptors, about 1000 times higher than that o morphine. With its long hal -li e and high receptor a nity, buprenorphine will persist on the receptor even when more potent, short-acting opioids are introduced in an attempt to provide analgesia. And because buprenorphine is only a partial agonist, e ective analgesia will be di cult to provide. Several recommendations or acute pain generally exist when dealing with buprenorphine. First, maintenance therapy can be continued and short-acting opioids can be titrated to e ect. One must recognize that with buprenorphine present on the receptor sites, the patient likely will require higher than usual doses o a short-acting opioid to achieve an expected e ect. A second option is to divide buprenorphine into threetimes-daily dosing to take advantage o its inherent analgesic properties in much the same way as methadone. T is strategy may be help ul i the surgery or procedure is not likely to be particularly invasive or pain ul. A third option is to discontinue buprenorphine therapy and treat the patient with ull opioid analgesics, while being mind ul o potential withdrawal. T e clinician must be mind ul that buprenorphine can continue to be present on the receptor up to 5 days a er the last dose. Finally, the ourth option with buprenorphine is to convert to methadone at 30–40 mg per day. T is total daily dose is usually su cient to prevent withdrawal symptoms. However, because methadone cannot be prescribed or withdrawal outside a methadone clinic, this strategy requires the standard three-times-daily dosing o methadone, and its primary purpose would need to be documented as treating pain, not managing withdrawal.

Buprenorphine Unlike methadone, buprenorphine is a partial opioid agonist. Buprenorphine relieves drug cravings without producing the “high” and dangerous side e ects o other opioids. Suboxone is a combination o buprenorphine and naloxone that received FDA approval in 2002. I Suboxone is injected intravenously, the naloxone component will precipitate withdrawal symptoms. Its increased therapeutic window and deterrence o IV use allow Suboxone to be prescribed by certi ed physicians outside the context o a specialized treatment clinic and without the need or daily supervision. Management can be signi cantly more complicated or patients receiving buprenorphine–naloxone therapy. As a partial mu-opioid agonist, buprenorphine has a ceiling e ect. Similar to ull agonists, morphine, or methadone, initially increasing buprenorphine dosage will heighten both its analgesic properties and its unwanted side e ects. Unlike ull agonists, as the dose o buprenorphine increases, the

COCAINE ADDICTION Cocaine is an extremely addictive local anesthetic, which can produce stimulation o the sympathetic nervous system due to the inhibition o catecholamine reuptake at the synaptic junction. Because o the rapid metabolism o cocaine, the probability o a patient presenting to the operating room with acute intoxication is unlikely. However, the physiological e ects o chronic cocaine abuse on various organ systems have an impact on anesthesia management. Cocaine is an alkaloid extract rom the leaves o the Erythroxylon coca bush. For centuries, the natives o Bolivia and Peru have chewed the leaves or their stimulant e ect. In 1868, cocaine was recognized or its local anesthetic e ects. By the 1880s, physicians became aware o the addictive properties o cocaine through sel -experimentation. Cocaine produces a euphoria that is ollowed by depression

CHAPTER 11

and craving or more cocaine, resulting in psychological addiction. Cerebral e ects, called a “rush” or “f ash,” occur within 6–8 seconds a er smoking cocaine and last 20 minutes. Intravenous cocaine reaches the brain in 15 seconds. Smoking cocaine produces peak blood levels that are 60% o the same dose given IV. T e elimination hal -li e o cocaine is approximately 30–60 minutes a er IV use and 60–90 minutes a er nasal administration.

Preoperative Considerations

Since polysubstance abuse is common, a drug history should include speci c questioning about the timing, amount, requency, and route o all drugs taken in the last 24 hours, as well as length o addiction. In orming the abuser o potential drug interactions with anesthetics may prompt honest reporting o drug use. Drug testing, although not required, may help identi y what drugs are present. T e use ulness o blood testing is limited because o the rapid metabolism o cocaine. Urine testing or cocaine metabolites is much more use ul with 99.2% accuracy, 96% sensitivity, and 100% speci city. Urine testing can detect cocaine metabolites up to 6 days a er a single dose and up to 10–20 days a er high-dose, long-term use. T e cardiovascular e ects o cocaine are signi cant. Cocaine blocks the reuptake o norepinephrine, dopamine, and serotonin at the synaptic junctions producing an excess o transmitter at the postsynaptic receptor sites. T e e ects that occur are due to sympathetic stimulation. Cardiovascular e ects o acute cocaine use mani est as hypertension, tachycardia, dysrhythmias, myocardial in arction, cardiomyopathy, or aortic rupture. Cocaine-induced myocardial in arction may mani est within minutes a er cocaine use or up to 18 hours later.

Intraoperative Concerns Following a thorough preoperative assessment, attempts should be made to stabilize the altered hemodynamics prior to induction. Premedication or surgery should provide enough sedation and anxiolysis while taking into account the patient’s potential or increased tolerance to sedatives and narcotics. Cocaine-induced hypertension results rom vasoconstriction rom alpha stimulation. Reduced intravascular volume may be masked by sympathetic vasoconstriction. Assessment o intravascular volume or blood loss should not be based solely on a normal blood pressure. Controversy exists regarding the management o cocaine-induced hypertension and tachycardia. Various pharmacologic interventions have been used which include the ollowing: 1. Propranolol—A nonselective beta adrenergic blocker, it was advocated at one time or use to treat tachycardia because o its beta blockade. However, propranolol was ound to worsen the myocardial depressant e ect o

Addiction

cocaine on the le ventricle and allow unopposed alphaadrenergic stimulation mani ested as increased peripheral and coronary vascular resistance due to blockade o beta 2 receptors. Labetalol—Having selective alpha 1 and nonselective beta 1 and beta 2 antagonist properties, it has been used success ully to manage hypertension. However, it has been suggested that the use o labetalol could result in an unopposed alpha e ect since the nonselective beta-blocking e ects are as much as seven times more potent than the alpha-blocking e ects. Phentolamine—An alpha antagonist, it has been used to treat hypertension. Phentolamine inhibits vasoconstriction in response to endogenous catecholamines via the blockage o alpha 1 receptors. However, it has an equal a nity or blockage o alpha 2 receptors. T is results in signi cant tachycardia caused by release o norepinephrine with its corresponding stimulation o beta 1 receptors. Nitroprusside—It has also been documented or use in hypertension related to cocaine abuse. Vasodilation occurs in response to the release o nitric oxide as the drug decomposes. T is vasodilation is associated with a reduction in arterial pressure, a modest baroreceptor-mediated increase in heart rate, and a decrease in myocardial oxygen consumption. Nitroprusside is superior to other hypotensive drugs due to its rapid onset o action, easily titratable dose to the desired e ect, and lack o tachyphylaxis seen with other drugs like phentolamine. Esmolol—It has been used success ully since it selectively blocks only beta 1 receptors. Esmolol appears to result in less incidence o hypertension rom unopposed alpha-agonist activity than does the nonselective beta antagonist, propranolol. In addition, the short duration o the action o esmolol allows or easy titration. itration o esmolol and nitroprusside in usions appears to be the optimum choice or the management o hypertension and tachycardia related to the hyperadrenergic state o cocaine abuse.

Regional anesthesia has been used success ully in the management o parturients who have a history o cocaine abuse. Prior to per orming the procedure, consideration should be given to the potential or coagulopathies, sepsis, HIV in ections, and hypovolemia. A platelet count should be evaluated be ore the procedure to rule out thrombocytopenia related to cocaine abuse. Uncorrected coagulation de ects are an absolute contraindication to epidural or spinal anesthesia. No adverse outcomes have been reported when regional anesthesia was per ormed on HIV patients, suggesting that the presence o HIV in ection is not an absolute contraindication to regional anesthesia. Epidural anesthesia should be used with caution in parturients who used cocaine during their pregnancy. T ese patients have a signi cant increase in the incidence o hypotension and need or supplemental IV narcotics. It has been suggested that the segmental level o epidural anesthesia

PART I Basic Sciences

should be raised gradually by titration o the local anesthetic dose and by hydration to prevent hypotension. Anesthesiologists should also consider the risks o potentiation o sympathomimetic e ects o cocaine by the use o epinephrine and the reduction in the seizure threshold by the use o additional local anesthetics. At times, the bene ts o regional anesthesia may outweigh the risks. Chronic use o cocaine may also deplete the central nervous system stores o dopamine and serotonin. In the event o catecholamine depletion, there may be a decreased minimum alveolar concentration requirement or volatile agents and

hypotension may be mani ested. Direct acting sympathomimetics such as phenylephrine or epinephrine are recommended to treat hypotension in these patients. T e incidence o extrapyramidal side e ects o dopaminergic antagonists, such as methyldopa, haloperidol, droperidol, and metoclopramide, may be increased because o the dopamine depletion that may occur with chronic cocaine use. T ese agents should be used with caution. However, haloperidol continues to be recommended as the rst choice in managing psychotic symptoms. Diphenhydramine may be used to treat dystonic reactions that occur.

PART II

ANESTHESIA TECHNIQUES

Autonomic Nerve Blocks Janish J. Patel, MD

Interruption o autonomic nerve transmission at the spinal nerve roots or sympathetic ganglion can produce autonomic nerve block, providing treatment or severe pain and visceral pain syndromes. Block o spinal nerve roots with subarachnoid, epidural, or paravertebral blocks results in the blockade o somatic, sympathetic-mediated, and psychogenic pain origins. Sympathetic ganglion blocks can be used to help di erentiate pain that arises rom sympathetic origins. T ey are widely used or both diagnostic and therapeutic purposes. Pain syndromes responsive to initial sympathetic blocks are then treated with repeated blocks or ollowed up with surgical, chemical, or radio requency sympathectomy.

E R

white rami communicans, which synapses with sympathetic ganglia located along the anterolateral sur ace o the vertebral bodies. Preganglionic bers may transverse variable distances cephalad and caudad, orming synapses with many postganglionic neurons in di erent ganglia at other levels in the chain. Postganglionic axons exit the ganglia as gray rami communicans, which join the spinal nerve to their peripheral targets.

STELLATE GANGLION BLOCK Indications

AUTONOMIC NERVOUS SYSTEM ANATOMY T e sympathetic chain receives a erent visceral bers that conduct pain rom the head, neck, abdominal and pelvic viscera, and extremities. T e sympathetic nervous system (SNS) is part o the autonomic nervous system (ANS), which innervates a variety o visceral organs, smooth muscle and glandular tissues, mediating a variety o re exes. In certain pathologic pain states, neuronal hyperactivity in the SNS may be involved in the maintenance o chronic pain. T e peripheral sympathetic system arises rom the intermediolateral column o the spinal cord. T e axons o these cells leave the spinal cord via the ventral nerve roots o 1 to L2. T e ventral nerve root initially proceeds as part o a spinal nerve, separates rom the somatic motor neuron, orming

Pain ul syndromes that may bene t rom stellate ganglion blocks include those that cause ace, neck, arm, and upper chest pain. Stellate blocks may also be used or vasospastic disorders causing vascular insu ciency o the arm.

Anatomy In the cervical and thoracic regions, the sympathetic chain lies anterolateral to the vertebral body, just anterior to the transverse processes. T e cervical sympathetic chain is composed o a superior, middle, and in erior cervical ganglion. T e in erior cervical ganglion and rst thoracic ganglion use to orm the stellate ganglion. T e stellate ganglion receives preganglionic sympathetic bers via white rami communicans rom the intermediolateral cell column o 1 to 6 in the spinal cord. 41

PART II Anesthesia echniques

T e ganglion resides within a ascial space, anterior to the rst rib along the anterior tubercle o C7. T e dome o the pleura binds it in eriorly. Anterior to the ganglion lies the carotid sheath and vertebral artery. Posterior to the ganglion lies the transverse process o C7 and 1. Superior to the stellate ganglion is the transverse process o the C6 vertebrae, or Chassaignac’s tubercle, a prominence that is palpable along the paratracheal region o the neck. While Chassaignac’s tubercle is the major landmark or blocking the stellate ganglion, the location o the ganglion itsel is in erior to the tubercle.

Clinical Assessment Sympathetic block may take 20 minutes to mani est ollowing local injection. Clinical signs o success ul blockade include sympathectomy o the ace and arms: nasal congestion, ushing o skin and conjunctiva, and Horner’s syndrome (ptosis, miosis, enophthalmos, anhidrosis). Venodilation in the hand causing an increase in temperature o the ipsilateral arm is strongly suggestive o a success ul sympathetic block o the arm.

Complications Technique While there are many techniques or stellate blockade, the anterior paratracheal approach is the easiest to per orm, involves least risk, and is also least pain ul compared to posterior and lateral approaches. T e patient is positioned supine and the head is kept midline with slight extension. T e stellate ganglion can be blocked at the C6 or C7 level, but due to the risk o pleural puncture, the block is of en made slightly superior to the ganglion by palpating Chassaignac’s tubercle at the C6 vertebral level between the trachea and sternocleidomastoid muscle and major vessels (Figure 12-1). When the needle tip reaches the optimal ascial plan, ollowing negative aspiration or blood or cerebrospinal uid, 1 mL o local anesthetic is injected as a test dose. Intravertebral arterial injection can result in seizure. Following a negative test dose, local anesthetic is injected.

Many important structures lie in close proximity to the stellate ganglion. Recurrent laryngeal nerve block occurs in approximately 60% o stellage ganglion blocks, resulting in hoarseness and dysphagia. Superior laryngeal nerve block, identi ed by inability o patient to say “ee,” may also complicate the stellate ganglion block. Bilateral stellate ganglion block should not be per ormed because bilateral recurrent laryngeal nerve blocks may lead to loss o laryngeal re exes and respiratory compromise. T e phrenic nerve is also commonly blocked by direct spread o local anesthetic and leads to unilateral diaphragmatic paresis. Other rare but serious complications include pneumothorax, puncture o esophagus or trachea, cerebrospinal uid, epidural, or intra-arterial injection. Injection o local anesthetic along the nerve root may intrude into the epidural space, causing pro ound neuraxial block, including high spinal or epidural block with loss o consciousness and apnea. Intravascular injection into the carotid artery or vertebral artery likely will result in immediate onset o generalized seizures.

CELIAC PLEXUS BLOCK Tra che a

Es opha gus

Ca rotid a rte ry

Sympa the tic cha in Longus colli mus cle

Cha s s a igna c’s tube rcle

C-6 ve rte bra l body

Ve rte bra l a rte ry

FIGURE 12-1

Stellate ganglion block at the level o the cricothyroid cartilage. (Reproduced with permission rom Warf eld CA, Bajwa ZH, eds. Principles &Practice of Pain Medicine. 2nd ed. New York, NY: McGraw-Hill, Inc.; 2004: Fig. 69-2.)

Indications Celiac plexus block is indicated or patients in pain rom upper abdominal viscera or tumors such as pancreatic cancer, acute and chronic pancreatitis, or intra-abdominal metastatic disease. Pain rom intra-abdominal tumors can be severe and opioid therapy is limited by sedation and constipation. emporary diagnostic blockade can di erentiate visceral pain rom somatic pain, while neurolytic celiac plexus blocks can provide long-lasting analgesia or up to 3–4 months.

Anatomy T e celiac plexus is a dense sympathetic ganglia located anterior to the aorta near the celiac arterial trunk at the 12 to L1 vertebral level. T ere are sympathetic, parasympathetic, and visceral a erent contributions to the celiac plexus. Sympathetic bers originate at 5 to 12 and combine to orm the splanchnic nerve. T e splanchnic nerve joins the parasympathetic vagus nerve to orm the celiac plexus.

CHAPTER 12

Autonomic Nerve Blocks

Ere ctor s pina e mus cle s P s oa s mus cle Crus of dia phra gm Infe rior ve na cava

Kidney

Porta l ve in

Adre na l gla nd

Right ce lia c plexus

Le ft ce lia c plexus Pa ncre a s Aorta a nd ce lia c trunk

S pre a d of a ne s the tic

FIGURE 12-2

Celiac plexus block. (Reproduced with permission rom Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. McGraw-Hill Education, Inc.; 2013: Fig. 47-21.)

Technique

Complications

T e classic posterior approach is a two-needle technique commonly practiced by anesthesiologists. With the patient in the prone position, utilizing uoroscopy, landmarks such as the 12th rib, 12 and L1 spinous process are marked. A spinal needle is advanced caudal to the 12th rib and cephalad to the transverse process o L1, about 8–10 cm until contacting the anterolateral sur ace o the L1 vertebral body. T e needle is withdrawn to skin and redirected laterally by 10° and re-advanced until the needle is “walked o ” the lumbar body. T e nal placement o the needle tip is 1.0–1.5 cm anterolateral to the L1 vertebrae (Figure 12-2). T e second needle is placed on the contralateral side using the same technique. Once positioned, the needle is aspirated to exclude vascular or intrathecal placement. Radiographic contrast under live uoroscopy should layer over the anterior sur ace o the aorta and appear pulsatile. Diagnostic celiac plexus block be ore neurolysis is per ormed using 10–15 mL o local anesthetic per side, with or without methylprednisolone or triamcinolone. For celiac plexus neurolysis, 10–15 mL o 50%–100% ethyl alcohol is injected per side. Because o intense burning pain on injection, alcohol is best diluted with local anesthetic prior to injection or injected af er placing a small volume o local anesthetic.

Due to the proximity o celiac plexus to aorta, vascular injury is possible, including hematoma, intravascular injection, or hematuria. Pneumothorax and spinal block by unintentional intrathecal or epidural spread are also possible complications. Neurolytic celiac plexus block carries signi cant additional risks, such as permanent block o an unintended nerve resulting in paraplegia.

Clinical Assessment Following celiac plexus block, sympathectomy o abdominal viscera results in unopposed parasympathetic innervation to the intestinal tract. Several physiologic side e ects are expected, including diarrhea, abdominal cramping, and orthostatic hypotension.

LUMBAR SYMPATHETIC BLOCK Indications Lumbar sympathetic blockade can be used or the diagnosis and treatment o sympathetically mediated pain syndromes and vascular insu ciency involving the lower extremities. Common indications include compromised circulatory insu ciency and lower extremity claudication. T e block can also be used to treat pain syndromes caused by renal colic, herpes zoster, postherpetic neuralgia, phantom limb pain, amputation or stump pain, and complex regional pain syndrome (CRPS) o the lower extremity.

Anatomy T e lumbar sympathetic ganglia lie between the L2 and L4 vertebrae and commonly the ganglia lie over the in erior portion o L2. T e chain resides anterolateral to the L2 vertebrae, inside a ascial sheath. T e chain is bound posteriorly by the psoas muscle, which separates the sympathetic chain rom the somatic lumbar plexus. T e psoas muscle minimizes local anesthetic spread, minimizing side e ects.

PART II Anesthesia echniques

7 cm

is recommended to ensure the characteristic longitudinal spread o contrast. Once veri ed, diagnostic blocks are perormed with the injection o local anesthetic. T is procedure is repeated at L3 and L4. I diagnostic block with local anesthetic improves blood ow and reduces pain, the patient may bene t rom surgical or chemical sympathectomy with phenol under direct uoroscopy visualization. Alternatively, a single injection technique can be used with the same approach.

10 cm

Sympa the tic ga nglia

Aorta

P s oa s ma jor mus cle

Clinical Assessment

FIGURE 12-3

Lumbar sympathetic block. (Reproduced with permission rom Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 47-22.)

Contrast injection under lateral uoroscopy is used to conrm the block. Spread o contrast agent along the anterolateral vertebral bodies in a cranio-caudal direction indicates correct injection. Signs o success ul sympathetic blockade include venodilation and skin temperature rise in the lower extremities. A rise in temperature o at least 1°C should occur with success ul sympathetic block in the ipsilateral leg.

Technique

Complications

T e patient is positioned lateral or prone. Landmarks indicating spinous processes o L2 to L4 are marked and a local anesthetic skin wheel is made 6–10 cm rom the midline. A spinal needle is inserted at a 45°60° angle toward the midline (Figure 12-3). T e needle is advanced between the transverse processes, through the psoas muscle and toward the anterolateral aspect o the vertebral body. Needle position is adjusted to walk o the vertebral body and veri ed using a loss o resistance technique or uoroscopy. As long as the needle is within the psoas muscle, there will be some resistance to injection. Once positioned, the needle is aspirated or blood, CSF, or urine. Screening with contrast injection and uoroscopy

T e lumbar sympathetic chain is blocked with relatively ew complications compared to other levels o the sympathetic chain due to the prevertebral position o the sympathetic chain and relative separation rom somatic nerves by the psoas muscle. T e most common complaint is backache rom multilevel needle trauma. Following neurolytic blockade, a 20% incidence o genito emoral neuralgia is a possible complication. Symptoms o genito emoral neuralgia include burning groin pain, perhaps lasting 6–8 weeks. Other more serious complications o lumbar sympathetic block include somatic nerve damage, kidney puncture, hematoma, and subarachnoid injection.

Infe rior ve na cava

Sympa the tic ga nglia

Peripheral Nerve Blocks: Head and Neck Alan Kim, MD

Regional anesthesia in the head and neck can supplement or serve as the main anesthetic plan or a variety o surgeries. T ese techniques can also aid in di cult airway management.

SCALP BLOCK Craniotomies provide a unique challenge in that the majority o sensory innervation is present on the scalp, with very little within the cranial vault. As such, the analgesic needs o a craniotomy are o en bimodal, markedly elevated at the beginning o and at the end o a case. Scalp blocks reduce the analgesic and sedative requirements by blocking sensation to the heavily innervated scalp. Historically, scalp blocks were commonly used when earlier general anesthetic agents had deleterious perioperative e ects. With the advent o sa er agents such as propo ol, these blocks have been employed less. In cases that require skull immobilization, a scalp block reduces hemodynamic increases seen with pin application. Although local in ltration by the surgeon can be used as well, a scalp block has a longer duration. T is preemptive blockade o a signi cant pain stimulus provides several bene ts. It reduces the cardiovascular lability seen with abrupt stimulation. It also reduces the general anesthetic requirements during the surgery. Furthermore, there are several types o neurosurgeries (deep brain stimulator, mass resections) that require the patient to be awake and interact with the neurosurgeon, neurologist, and anesthesiologist. T e scalp block is especially use ul in these patients, as it negates pain ul stimuli rom the pins and allows the patient to wake up in a controlled ashion.

Anatomy T e scalp is innervated by two nerve groups: the trigeminal nerve and the cervical spinal nerves. T e trigeminal nerve is responsible or the innervation o the anterior scalp and ace. It has three main branches: the ophthalmic (V1), maxillary (V2), and mandibular (V3). V1 splits into the supraorbital and supratrochlear nerves. T ese two branches innervate the majority o the anterior scalp and orehead. T e V2 and V3 components contribute the zygomaticotemporal and auriculotemporal nerves, respectively, innervating the temporal scalp.

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T e posterior scalp is innervated by the greater occipital nerve and to a lesser extent the lesser occipital nerve. T e greater occipital nerve is derived rom the posterior ramus o the second cervical nerve root. T e lesser occipital nerve is derived rom the ventral rami o C1 and C2. T e entire scalp can be blocked by addressing these two nerve groups. In unilateral surgical approaches, the operative side can be avored when depositing local anesthetics. I pinning is required, a bilateral block is pre erred.

Technique T ere are six sites (supraorbital, supratrochlear, auriculotemporal, zygomaticotemporal, and lesser and greater occipital nerves) to block on each side. Local in ltration at so many sites can be pain ul, and patients o en require sedation. T e exact level o sedation should be tailored to the patient’s desired level o sedation, coupled with the risks o sedation with a general emphasis on shorter acting agents. T e choice o local anesthetic and adjunct medications varies with the patient, anticipated duration o surgery, and operative approach. A common ormulation is 0.75% ropivicaine with epinephrine 1:200,000. A max o 35 mL is used in a normal adult male patient, although the exact maximum dose should be calculated according to the patient’s weight. T e distribution should be tailored to the operative approach. In addition to the location, the depth at which the local is deposited is important. T e supraorbital nerve is blocked as it exits rom the orbit. T e supraorbital notch can be palpated at the medial third o the orbit. Right above the notch, the needle is inserted to orm a wheel. It is then advanced until it hits bone, retracted slightly, and the remainder o the local injected in that site. T e supratrochlear nerve is blocked near the supraorbital notch. One centimeter medial to the supraorbital notch, the needle is inserted perpendicularly until it hits bone, then withdrawn slightly. Local should be deposited just super cial to the periosteum a er care ul aspiration. T e auriculotemporal nerve is injected at the level o the auditory meatus, immediately posterior to the super cial temporal artery. T e injection should be per ormed supercially to avoid acial nerve injection and subsequent acial nerve blockade. 45

PART II Anesthesia echniques

T e zygomaticotemporal nerve exits rom a oramen o the orbital ossa. It has many deep branches that help innervate the temporal region. o block this nerve, the lateral orbital rim is identi ed. One centimeter lateral to this rim, the needle is inserted acing in eriorly and anteriorly. T e needle is walked down into the space at the level o the lateral canthus and then aspirated. Local should be deposited throughout this area. T e lesser occipital nerve can be blocked at the upper, posterior border o the sternocleidomastoid muscle at the level o the in erior border o the mandible. T e local should be injected both super cially and deeply. o nd the greater occipital nerve, a line is drawn between the mastoid process and the external occipital protuberance. T e intersection o a line drawn through the middle third o this line and the superior nuchal ridge is the site o injection. T is local should be deposited deep at this site. As the local anesthetic distributes super cially, it will rein orce the lesser occipital nerve.

As with most regional blocks, there is a risk o direct nerve injury, in ection, intravascular injection, and bleeding. As such, care should always be taken to properly identi y the anatomic landmarks, to aspirate requently, and to stop and reassess i paresthesias increase with injection.

CERVICAL PLEXUS BLOCK Cervical plexus blocks provide anesthesia and analgesia to the neck. T ey are o en utilized or carotid endarterectomy, neck dissection, tracheostomy, thyroidectomy, and other surgeries o the neck. T ey can be used as either the primary anesthetic technique, or as an adjunctive technique. T e cervical plexus is composed o the anterior rami o the C1 to C4 nerve roots, orming the ollowing ve main branches (Figure 13-1): 1. T e cutaneous branches supply the lesser occipital, greater auricular, transverse cervical, and supraclavicular nerves.

C1 C2 C3

Thyrohyoid mus cle

C4 C5

Ans a ce rvica lis

Omohyoid mus cle P hre nic ne rve

S te rnothyroid mus cle

FIGURE 13-1

Cervical plexus. (Reproduced with permission from Hadzic A, ed. Hadzic’s Peripheral Nerve Blocks and Anatomy for UltrasoundGuided Regional Anesthesia. 2nd ed. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig. 1-9.)

CHAPTER 13

2. T e ansa cervicalis innervates the geniohyoid and in rahyoid muscles. 3. T e phrenic nerve innervates the diaphragm. 4. Components o the accessory nerve innervate the sternocleiodomastoid and trapezius muscles. 5. Direct muscular branches innervate the prevertebral muscles o the neck. For both blocks, the relevant anatomy should be identied rst, and the patient’s head turned away rom the surgical side. For carotid endarterectomy or in any patients in whom carotid atherosclerosis is suspected, the head should not be excessively hyperextended or turned aggressively due to concerns or cerebral ischemia or embolic stroke rom a dislodged clot. T e sternocleidomastoid (SCM) muscle can be more easily identi ed in patients who are li ing their head.

Superf cial Cervical Plexus Block T e patient’s head is turned to the nonoperative side. T e posterior border o the SCM is identi ed rst and outlined. A line is drawn between the mastoid process and the clavicular head o the SCM. T e midpoint o this line is the injection site. A er thorough cleaning, a needle is inserted perpendicular to the skin. A er aspiration, the local is injected at the midpoint up to hal the muscle’s depth. Five to ten milliliters o local anesthetic can be deposited. T e needle is retracted to the skin and redirected in both the cephalad and the caudad directions along the posterior border o the SCM. T e block should take e ect in 10–15 minutes, and can be supplemented with local in ltration. T ese blocks rarely provide enough coverage to unction as the sole anesthetic. T e maximum local anesthetic dose should be calculated and strictly adhered to. Mild sedation can be given to help the patient tolerate the procedure. Phrenic nerve blockade is possible but not likely with this block.

Deep Cervical Plexus Block With the head turned to the nonoperative side, the transverse process ( P) o C6 (Chassaignac’s tubercle) needs to be identied. It should be palpable at the level o the cricoid cartilage. A line is drawn rom this point to the mastoid process. T e P o the cervical vertebrae should be palpable along this line. T e rst palpable P located immediately below the mastoid is the C2 P. By palpating in erior to this position along the drawn line, both C3 and C4 are identi ed as well. I palpation o the Ps is di cult, an alternative technique is to mark positions at 2 cm intervals rom the mastoid down along the drawn line. T e rst mark should be C2, with the next two being C3 and C4. Both techniques require the correct identi cation o Chassaignac’s tubercle. Once the three sites have been identi ed, a 5 cm needle is inserted in a slightly caudad orientation until the P is contacted within 2–3 cm. Once contacted, the needle is withdrawn slightly and a er con rming negative blood or CSF

Peripheral Nerve Blocks: Head and Neck

aspiration, the local injected. Given the proximity to both the vertebral vessels and dura, requent, care ul aspiration should be employed prior to and during injections. Intraneural injection will result in notable pain. I pain is present, the injection is stopped, needle withdrawn, and redirected. Potential complications include ipislateral phrenic nerve blockade, recurrent laryngeal nerve blockade, intravascular injection, intrathecal injection, vagal nerve blockade, hematoma, and in ection. Given that the phrenic nerve blockade is very likely, patients with underlying respiratory concerns should be care ully considered.

RETROBULBAR AND PERIBULBAR BLOCKS With the advent o newer surgical techniques, routine ophthalmic surgeries do not require the same level o akinesia they used to. T is has led to a marked increase in the use o regional anesthesia as the primary technique in simple eye surgeries like cataract surgeries. wo blocks (retrobulbar and peribulbar) are employed most requently (Figure 13-2). raditionally, retrobulbar blocks were considered to be more e ective than peribulbar blocks due to their direct placement o anesthetic. However, comparisons when a higher volume o local anesthetic was used demonstrate comparable rates o e cacy between retrobulbar and peribulbar blocks.

Retrobulbar Block T is block is primarily employed or surgeries in the anterior chamber o the eye, like cataract surgeries. It directly blocks cranial nerves II, III, and VI and di uses out to block cranial nerve IV. Blockade o the ciliary nerves provides anesthesia o the conjunctiva, cornea, and uvea. It is generally per ormed by the surgeon. A supplemental block o the acial nerve is required to prevent blinking. T e block is per ormed with the patient in a sitting or a supine position, with or without sedation. raditionally, awake patients were told to look upwards and inwards with the operative eye during the block. However, research shows that this movement increased the potential risk to the optical nerve. As a result, patients are now told to keep their eyes in a neutral position. T e needle is inserted perpendicularly at the junction o the lateral third and medial two-thirds o in erior orbital rim and then aimed in a slightly cephalad and medial direction. It is walked in this direction to a depth o 25–35 mm. O en a “pop” is elt, indicating the needle’s passage through the muscle cone. A er aspiration to avoid intervascular injection, 3–5 mL o local anesthetic is injected into this place.

Peribulbar Block Peribulbar blocks are placed in the extraconal space. As such, they require an additional volume. With enough volume, their

PART II Anesthesia echniques

Re la tions hips to cone of re ctus mus cle s Extra cona l (pe ribulba r)

Intra cona l (re trobulba r)

FIGURE 13-2

Retrobulbar vs peribulbar blocks. (Reproduced with permission from Longnecker DE, Brown DL, Newman MF, Zapol WM, eds. Anesthesiology. 2nd ed. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig. 66-4, p. 1209.)

rate o e cacy is similar to that o retrobulbar blocks. T ese blocks are per ormed in the supine state. T is block consists o two injections. T e rst is injected in the in erior and temporal regions, inserted in the same location as with the retrobulbar block, but with a smaller cephalad and medial adjustment than with the retrobulbar block. No pop is indicated, as the needle should not pass the muscle cone. T e second injection is between the medial third and lateral two-thirds o the orbital roo edge. T ese two injections consist o 6–12 mL, as opposed to the 3–5 mL, or the retrobulbar block. T is increased volume is required so that the local anesthetic seeps into the intraconal space.

Sedation T ese blocks can be per ormed under a short-acting sedative like propo ol to avoid the pain elt with local anesthetic injection or the anxiety produced by needles. Once the block is per ormed, the patient is o en awake or the duration o the procedure. Some patients, however, may not tolerate the claustrophobic nature o the surgical setup (drapes, head xation, arm straps). T ese patients may request sedation through the remainder o the procedure. Although regional anesthesia is o en employed as the primary and sole technique in these patients, they still require a thorough preoperative workup or this very reason. Progression o sedation can easily convert to general anesthesia, and a thorough understanding o the patient’s medical history and potential airway risks should be attained prior to beginning the procedure. Furthermore, an obtunded or uncooperative patient who moves during the surgery is one o the most signi icant causes o intraoperative complications. As such, e orts made to reduce these risks should be employed judiciously.

Complications Most complications associated with these blocks are due to needle misplacement. T e complications have a wide range o mani estations, depending on exactly where the needle is placed. A physician’s level o amiliarity with the block is the largest contributor to the potential or a complication. Serious complications include retrobulbar hemorrhage, globe per oration, optic nerve damage, intra-arterial injection (leading to retrograde f ow to the anterior cerebral or internal carotid artery, allowing small volumes o local anesthetic to cause seizures), optic nerve sheath injection (causing a high spinal), and oculocardiac ref ex (leading to bradydysrhythmias with hypotension). O these, a retrobulbar hemorrhage is the only complication that occurs at a similar rate regardless o the level o experience. Given that the complication rate relies heavily on the level o experience o the user, the block should be administered by either the surgeon or the anesthesiologist who has the most experience with the block. Regardless o who perorms the block, an anesthesia provider should be present to address the potentially catastrophic complications that are possible with these blocks.

AIRWAY BLOCKS Regional blockade o the airway can help supplement di cult airway management. T ese blocks are most requently employed during awake beroptic intubations. T ree nerves comprise the bulk o the innervation: the trigeminal, glossopharyngeal, and vagus nerve, with minor contributions rom the ol actory nerve. T ese nerves can be blocked individually,

CHAPTER 13

or en masse. Depending on the route o intubation, di erent combinations o nerves need to be addressed. No single block is adequate or intubation. Given the multiple routes o administration, it can be easy to lose track o the quantity o local anesthetic used. Each additional aliquot o local should be care ully documented and the total kept under the maximum sa e dose.

Anatomy T e trigeminal nerve contributes the greater and lesser palantine nerves, which innervate the nasal turbinates and posterior two-thirds o the nasal septum. T e anterior ethmoidal branches rom the ol actory nerve and innervates the nasal nares and the anterior third o the nasal septum. T e glossopharyngeal nerve innervates the posterior third o the tongue, vallecula, anterior sur ace o the epiglottis, pharyngeal walls, and tonsils. Vagal nerve branches innervate the posterior epiglottis and distal airway structures. T e superior laryngeal nerve is split into an internal and external branch. T e internal branch innervates the base o the tongue, posterior epiglottis, aryepiglottic old, and arytenoids. T e external branch innervates the cricothyroid muscle. T e recurrent laryngeal nerve innervates the trachea and the vocal cords. Although the anterior two-thirds o the tongue are controlled by the lingual branch o the mandibular division o the trigeminal nerve, the lingual branch does not contribute to the gag or cough ref ex. As such, it does not have to be blocked or the purposes o an oral beroptic intubation. T ese blocks can be blocked individually, or en masse. Less invasive measures include topical and aerosolized ormulations o local anesthetics. T e individual block techniques will be discussed rst ollowed by more generalized block techniques.

Trigeminal Nerve Block I a nasal intubation is selected, the trigeminal nerve branches must be addressed. T e ethmoidal branches can be blocked by direct in ltration, gel application, swab application, or aerosolized local administration. At our institution, lidocaine gel coats the outside o nasal trumpets that serially dilate the selected nare. Oxymetazoline 0.05% or phenylephrine 1% in the lidocaine gel provides local vasoconstriction to minimize nasal bleeding. Long cotton-tipped applicators or pledgets are soaked in local anesthetic and a vasoconstrictor. T ree applicators are employed or each nare. T e in erior, middle, and superior turbinates each have a single applicator placed. Applicators are le or 5 minutes, and pledgets or 2–3 minutes. Both nares should be prepped, as the posterior nasopharynx joins both sides and remains sensitive i both are not addressed. A popular technique is to administer pledgets or wide cotton swabs soaked in lidocaine and phenylephrine and

Peripheral Nerve Blocks: Head and Neck

place them deep in turbinates. Both nares are anesthetized since the posterior pharynx can react bilaterally.

Glossopharyngeal Block T is block inhibits the gag ref ex associated with direct laryngoscopy. T e glossopharyngeal nerve travels along the lateral sur ace o the pharynx. T ere are two ways to approach this nerve: perioral or peristyloid. T e perioral approach consists o having the patient open their mouth, pushing their tongue to the side with a tongue depressor, then injecting 5 mL o local anesthetic in the submucosal region. Both topical spray application and direct application o soaked pledgets can substitute or in ltration with the perioral approach. For the peristyloid approach, the patient is placed in a supine position. A line is drawn between the angle o the mandible and the mastoid process. Deep pressure is used to identi y the styloid process, which should be located directly posterior to the angle o the jaw. T e needle is inserted until it rests on the styloid process. T e needle tip is then walked o the styloid process until bony contact is lost and 5–7 mL o local anesthetic injected a er care ul aspiration. Both approaches will place the needle in close proximity to the carotid artery. Care ul aspiration prior to injection is crucial to avoid accidental intravascular injection.

Superior Laryngeal Block Mucosal absorption o local anesthetics by either inhalation or direct application can block the superior laryngeal nerve. However, both these techniques require time to absorb and can be impaired by mucosal drainage. In a more urgent situation, this nerve can be blocked with direct in ltration. T e patient is placed in a supine position, with the head extended. T e thyroid cartilage and the hyoid bone above are identi ed. T e hyoid bone is palpated to identi y the greater cornu, as well as to displace the bone towards the anesthesiologist. T is allows palpation o the carotid pulse and also provides counterpressure or the injection. T e needle is inserted until the greater cornu is contacted. T e needle is retracted by 2 cm and 2 mL o local anesthetic is injected. Care ul aspiration is required to avoid intravascular injection or inadvertent transtracheal injection. T is block is repeated or the contralateral side.

Recurrent Laryngeal Block T e recurrent laryngeal nerve can be blocked with the inhalational technique. However, the inhalational technique does not always provide an adequate level or intubation. A transtracheal approach indirectly blocks the nerve, but in a more acute ashion than the inhalational technique. Direct recurrent laryngeal nerve blockade is avoided, as it innervates most o the laryngeal muscles. I blocked, signi cant airway obstruction occurs.

PART II Anesthesia echniques

T e patient is supine with their head extended. T e thyroid cartilage and the cricoid cartilage in erior to it are palpated. T e cricothyroid membrane is palpated and a small wheel o local anesthetic is placed. A 20 or 22 gauge needle attached to a 10 mL syringe is inserted perpendicularly through the wheel. T e syringe is kept on continuous aspiration, and the needle advanced until an air bubble is noted, indicating a tracheal position o the needle tip. Four to ve milliliters o local anesthetic is subsequently injected, a er in orming the patient that they are going to cough. T e coughing will disperse the local anesthetic. o avoid needlerelated injuries during coughing, a rapid injection o the local anesthetic is recommended.

General Blockade T e alternatives to individual nerve blockade have been mentioned piecemeal, but consist o two main techniques:

aerosolized local anesthetic administration and direct administration via an epidural catheter. T e rst technique consists o nebulized lidocaine (4 mL o 4% lidocaine) administered to the patient, well in advance o coming into the OR. T e even distribution o local anesthetic can be di cult in patients with a lot o secretions. As such, glycopyrrolate is administered early in the preoperative bay to decrease airway secretions. Intramuscular administration o glycopyrrolate can attenuate some o tachycardia associated with intravenous administration o glycopyrrolate. T e second technique consists o a direct visualization technique. An epidural catheter may be threaded through the working port o the bronchoscope and attached to a syringe o local anesthetic. As the bronchoscope is passed via the oral/nasal passageways, key structures are topicalized directly.

Peripheral Nerve Blocks: Upper Extremity Binoy Bhatt, MD, and Daniel Asay, MD

Peripheral nerve blocks o the upper extremity may be used or anesthesia, postoperative analgesia, and the diagnosis and treatment o chronic pain syndromes. Preoperative analgesia may be obtained, and catheter techniques enable postoperative pain management with continuous in usions o local anesthetic, with or without an opioid. Such in usions can improve per usion to the operative extremity, reduce pain with movement, acilitate early joint mobilization, and improve the quality o li e weeks a er discontinuation o the in usion. T e types o upper extremity nerve blocks are listed in able 14-1.

BRACHIAL PLEXUS ANATOMY Success ul regional anesthesia o the upper extremity requires knowledge o the brachial plexus (Figures 14-1 and 14-2). Brachial plexus nerve roots arise rom the ventral rami rom C5 to 1, and course anterolaterally and in eriorly to orm three

TABLE 14-1

Examples of Peripheral Nerve Blocks of the Upper Extremities Peripheral Nerve Block

Nerve Involved

Surgical Indication

Interscalene

Rotator cuf Total shoulder arthroplasty Proximal humerus

Supraclavicular

Mid-humerus

In raclavicular

Elbow

Axillary

Elbow

Forearm block

Median Ulnar Radial

Distal orearm Hand

Digital nerves

Branches o the median, ulnar, and radial

Amputation Trauma*

Brachial plexus

*Do not use epinephrine-containing local anesthetics in digital blocks as vasoconstriction o digital arteries may lead to necrosis.

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trunks between the anterior and middle scalene muscles. T e trunks orm three anterior and three posterior divisions at the lateral edge o the rst rib at the midportion o the clavicle, which recombine to create lateral, middle, and posterior cords named or their relationship with the second part o the axillary artery. At the lateral border o the pectoralis minor muscle, the cords urther divide into terminal branches that supply all motor and sensory innervation o the upper extremity except (1) the skin over the shoulders, which is supplied by the cervical plexus; and (2) the medial aspect o the arm, which is supplied by the intercostobrachial branch o the second intercostal nerve.

INTERSCALENE BLOCK Local anesthetic solution is injected into the interscalene groove adjacent to the transverse process o C6. T is provides nerve blockade at the level o the superior and middle trunks. Brachial plexus nerve roots emerge between the anterior and middle scalene muscles. Anesthetizing this region allows or surgery on or manipulation o the shoulder and more distal upper extremity. Nerve stimulation o 0.2–0.5 mA o the pectoralis, deltoid, triceps, biceps, hand, or orearm is acceptable, with the goal to stimulate trunks and divisions. T e patient is supine with the head turned contralaterally to accentuate the posterior border o the sternocleidomastoid muscle. T e arm should lie at the patient’s side to relax the shoulder, and high- requency ultrasound can be used to image the brachial plexus within the posterior triangle o the neck where connective tissue is less abundant (Figure 14-3). However, it is o en easier to obtain a view o the subclavian artery and brachial plexus at the level o the clavicle and ollow the brachial plexus upward. Rare risks associated with an interscalene block include intraspinal or vertebral artery injection. Diaphragmatic hemiparesis secondary to blockade o the ipsilateral phrenic nerve is an expected side e ect o the interscalene block, as the phrenic nerve lies on the anterior scalene muscle. T e phrenic nerve contains branches o the third to h cervical nerves. T us, patients with severe respiratory insu ciency or

PART II Anesthesia echniques

Five ro o ts (ve ntral rami) Thre e trunks

Dorsal scapular ne rve (C5)

S ix divis io ns

Contribution to phrenic nerve (C5)

Suprascapular ne rve (C5 to C6)

Thre e c o rds

st e

Lateral pectoral ne rve (C5 to C7)

ri o

r io r e nt A

Subclavius ne rve (C5) d le Mid

Five branc he s

pe Up

An te rio r al er t La

Musculocutaneous ne rve (C5 to C7)

r io er t An

Long thoracic nerve (C5 to C7)

Medial pectoral nerve (C8 to T1) Medial cutaneous nerve of arm (C8 to T1)

Radial ne rve (C5 to T1)

Ulnar ne rve (C7 to T1)

ia l

Axillary ne rve (C5 to C6)

Median ne rve (C6 to T1)

r we Lo

P os te rior

r rio e st

d Me

io r r e st

Medial cutaneous nerve of forearm (C8 to T1) Subscapular nerves: Lower (C5 to C6) Middle (C6 to C8) Upper (C5 to C6)

FIGURE 14-1

Brachial plexus. (Reproduced with permission rom Morton DA, Foreman KB, Albertine KH, eds. The Big Picture: Gross Anatomy. 1st ed. New York, NY: McGraw-Hill Education, Inc.; 2011: Fig. 29-4.)

contralateral phrenic nerve palsy should not be o ered this block. Patients may develop a hoarse voice with the blockade o the recurrent laryngeal nerve. In addition, mild ipsilateral ptosis, miosis, nasal congestion, anhidrosis, enophthalmous, and ushing can occur due to sympathetic chain blockade. T ese phenomena are collectively known as “Horner’s syndrome.” Although pneumothorax occurs in requently, the diagnosis should be considered i cough or chest pain is elicited. Rarely, bilateral blockade o the recurrent laryngeal nerve can occur, leading to complete airway obstruction. A preoperative history o hoarseness, known contralateral vocal cord palsy, or neck surgery should alert the clinician to this possibility and warrants urther investigation prior to interscalene blockade. Although the interscalene approach can be used or orearm and hand surgery, the blockade o the in erior trunk is o en incomplete and must be supplemented at the ulnar nerve or adequate surgical anesthesia.

SUPRACLAVICULAR BLOCK Supraclavicular block is per ormed by injecting local anesthetic around the divisions o the brachial plexus adjacent to the subclavian artery. T is block is used or operations on the elbow, orearm, and hand. In the supraclavicular region, the brachial plexus is compact, nerve visibility is good, and structures are shallow. A small volume o solution produces a rapid onset o reliable nerve blockade, and the patient’s arm can be in any position. T e technique o the block is similar to the interscalene approach. T e arm to be anesthetized should be adducted, and the hand should be extended along the side as ar towards the ipsilateral knee as possible. T e neurovascular bundle lies in erior to the clavicle at roughly its midpoint. T e rst rib acts as a medial barrier to the needle. T e ultrasound probe is moved closer to the clavicle and aces caudally to visualize the brachial plexus super cial and lateral to the subclavian artery and superior to the rst rib and pleura (Figure 14-4).

CHAPTER 14

Ante rio r (palmar) vie w

Peripheral Nerve Blocks: Upper Extremity

Po s te rio r (do rs al) view

S upra clavicula r ne rve s (from ce rvica l plexus )

Axilla ry ne rve S upe rior la te ra l bra chia l cuta ne ous ne rve

S upra s ca pular ne rve

Ra dia l ne rve Infe rior la te ra l bra chia l cuta ne ous ne rve

Ra dia l ne rve Pos te rior bra chia l cuta ne ous ne rve , infe rior la te ra l bra chia l cuta ne ous ne rve , a nd pos te rior a nte bra chial cuta ne ous ne rve

Inte rcos tobra chia l a nd me dia l bra chia l cuta ne ous ne rve

La te ra l a nte bra chia l cuta ne ous ne rve (te rmina l pa rt of mus culocuta ne ous ne rve )

Me dia l a nte bra chia l cuta ne ous ne rve

Ra dia l ne rve S upe rficia l bra nch

Ulna r ne rve Pa lma r a nd pa lma r digita l bra nche s

Me dia n ne rve Pa lma r a nd pa lma r digita l bra nche s

La te ra l a nte bra chial cuta ne ous ne rve (te rmina l pa rt of mus culocuta ne ous ne rve )

Ulna r ne rve Dors a l bra nch, dors a l digita l bra nche s, a nd prope r pa lma r digita l bra nche s

Ra dia l ne rve S upe rficia l bra nch a nd dors a l digita l bra nche s Me dia n ne rve P rope r pa lma r digita l bra nche s

FIGURE 14-2

Cutaneous innervations o the upper extremity. (Reproduced with permission rom Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 46-7.)

S CM N AS M

MS M

N R

FIGURE 14-3

Interscalene approach to the brachial plexus. (Reproduced with permission rom Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 46-12.)

FIGURE 14-4

Supraclavicular approach to the brachial plexus. (Reproduced with permission rom Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 46-15.)

PART II Anesthesia echniques

T e in-plane approach allows or visualization o the pleura, which is important since pneumothorax is the most common serious complication o a supraclavicular block (1% incidence). Severe respiratory compromise should be taken into consideration prior to per orming a supraclavicular block. Phrenic nerve block incidence is 40%–60%. Horner’s syndrome and neuropathy are in requent complications.

INFRACLAVICULAR BLOCK In raclavicular block is used or procedures on the hand, orearm, and elbow. It is a secure, clean site that is stable or placement o a continuous brachial plexus catheter due to its depth. T e three cords o the brachial plexus are blocked where they tightly surround the axillary artery, just distal to the clavicle. T e risk o pneumothorax and spinal injection is less compared to the supraclavicular block; however, the risk o pneumothorax is still higher than with an interscalene block. T e patient is supine and the arm is abducted and externally rotated. T e ultrasound transducer is placed 2 cm below the midpoint o the in erior clavicular border to visualize the subclavian artery deep to the pectoralis major and minor muscles where the three cords o the brachial plexus lie adjacent to the artery (Figure 14-5). T e needle is advanced caudally in-plane until its tip lies within the ascial sheath that surrounds the brachial plexus. Potential disadvantages o an in raclavicular block include the risk o vascular puncture and patient discom ort associated with traversing the pectoralis major and minor muscles with the block needle. In addition, it is a deep block, and needle manipulation is necessary with steep angles, which may result in di culty with needle tip visualization.

AXILLARY BLOCK Axillary blocks can be used or anesthesia o the hand, orearm, and elbow. T e axillary artery is the most important landmark, as the nerves maintain a predictable orientation to the artery. At the level o the axilla, the terminal branches o the brachial plexus lie within the axillary sheath and in the tissue that immediately surrounds it. T e terminal branches can be remembered with the mnemonic “MARMU”— musculocutaneous, axillary, radial, median, and ulnar. T e median nerve lies superior to the axillary artery, radial nerve posterior and in erior, the ulnar nerve in erior, and the axillary vein anterior (Figure 14-6). Blocking the musculocutaneous nerve, which supplies sensation to the lateral aspect o the orearm, requires a separate injection site. T us, with an axillary block, the musculocutaneous nerve may not be blocked because it exits proximal to where the axillary nerve is blocked and can be supplemented at either the coracobrachialis muscle or the elbow. T e axillary nerve block’s onset progresses rom proximal to distal, as the outside o the nerve innervates the proximal region and the inside innervates the distal region. T e arm is abducted to 90° and externally rotated. T e ultrasound transducer is placed in the axilla, showing the brachial artery and surrounding nerves o the brachial plexus. T e needle is advanced rom superior to in erior and passes deep to the axillary artery within the axillary sheath. T e medial, ulnar, and radial nerves lie close to the axillary arterial wall, and the musculocutaneous nerve has a characteristic medial to lateral course within the axilla. T us, the musculocutaneous nerve is usually blocked within the coracobrachialis muscle, where its at shape gives a large amount o sur ace area or rapid block. T e intercostobrachial nerve is usually blocked via a 5 mL skin cu injection overlying the axillary artery.

PMa U

PMi

N N AA N N

AV TM

M AA

BM MC CB

FIGURE 14-5

In raclavicular approach to the brachial plexus. (Reproduced with permission rom Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 46-18B.)

FIGURE 14-6

Axillary approach to the brachial plexus. (Reproduced with permission rom Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 46-22.)

CHAPTER 14

Nerve injury with high volume blocks, due to compression o nerves within the axillary sheath, is a major risk with the axillary approach.

DISTAL BLOCKS T e median, ulnar, and radial nerves can be blocked at the level o the orearm. T is is use ul or hand surgery when a tourniquet is not used or surgical hemostasis. In addition, distal nerve blocks are use ul when limited anesthesia is required, when contraindications to a brachial plexus block exist (i.e., in ection, bilateral surgery, coagulation abnormalities, bleeding diathesis, or di cult anatomy). Nerve blocks at the orearm can also supplement any o the brachial plexus blocks with incomplete sensory distribution. T e median nerve innervates the palmar aspects o the thumb and index nger, middle nger, radial hal o the ring nger, and the nail beds o the same digits. Motor block includes the muscles o the thenar eminence, lumbrical muscles o the rst and second digits, and the wrist exor muscles o the orearm. It has a ne ascicular appearance and can be visualized while scanning the orearm. T e median nerve lies medial to the brachial artery, which is ound medial to the biceps tendon within the antecubital ossa. Blockade o the median nerve leads to inability to ex digits 2–3 at the

Peripheral Nerve Blocks: Upper Extremity

MCP joints and inability to ex and extend at the proximal interphalangeal and distal interphalangeal joints leading to the “hand o benediction.” T e ulnar nerve innervates the dorsal and palmar sides o the ulnar aspect o the hand, and classically the lateral side o the ourth and the entire h digits o the hand. T e ulnar nerve also innervates all the small muscles o the hand, except those o the thenar eminence and irst and second lumbricals. T us, the ulnar block produces the inability to adduct the thumb. he ulnar ner ve can be blocked in between the olecranon and medial epicondyle o the humerus above the elbow, where the ulnar nerve is not in direct contact with the ulnar artery. T e super cial radial nerve ollows the radial artery along its course through the orearm. It is normally blocked at the level o the elbow as it passes between the brachioradialis and biceps tendon. It can also be blocked at the elbow as it passes over the anterior aspect o the lateral epicondyle or at the level o the anatomic snuf ox. Blockade o the radial nerve provides anesthesia to the lateral aspect o the dorsum o the hand, proximal thumb, index, middle, and lateral hal o the ring nger. With all the distal nerve blocks o the upper extremity, 3–5 mL o local anesthetic solution can be injected around the respective nerves. Blockade o the radial nerve leads to wrist drop.

Peripheral Nerve Blocks: Trunk and Perineum Brent Yeung, MD, and Joseph Mueller, MD

TRUNK T e peripheral nerves which innervate the chest and abdominal wall originate rom the thoracic and lumbar plexuses. Regional anesthesia o the trunk ocuses on the blockage o pain impulses rom these areas to their corresponding location within the spinal cord.

Intercostal Nerve Block T is block provides analgesia to the thoracic and upper abdominal areas and has been shown to be e cacious in a variety o surgeries such as thoracotomy, breast surgery, and video-assisted thoracoscopy. Intercostal nerve blocks may be indicated or rib ractures, herpes zoster, cancer pain, and thoracotomy pain. Anticoagulation is a strong contraindication to

15 H

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this block due to the nerve’s proximity to the intercostal artery and vein. Potential adverse side e ects include intravascular injection and pneumothorax due to the close proximity to the lung. T e technique ocuses on the intercostal nerves which arise rom the ventral rami o thoracic nerves 1 to 11 (Figure 15-1). T e patient position can be prone, seated, supine, or lateral in order to per orm the block. T e dermatome and rib level is identif ed and the rib is palpated to the posterior axillary line, which is then marked and prepped in a sterile ashion. A 22 or 25 gauge needle is attached to a syringe and advanced perpendicular to the skin, aiming or the middle o the rib. Bony contact should be made and the needle should be walked down the rib in eriorly until bone contact is lost. T is is where the intercostal groove containing the intercostal nerve, artery, and vein is located. T e needle

Ne e dle ins e rtion point

Inte rcos ta l ne rve, a rte ry, a nd ve in

FIGURE 15-1

Intercostal nerve block. (Reproduced with permission from Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology, 5th ed. McGraw-Hill Education, Inc., 2013, Fig. 46-61.)

PART II Anesthesia echniques

should be advanced approximately 2 mm while care ully aspirating to ensure that the needle is not within the lumen o the intercostal vein or artery. Injection o 3–5 mL o local anesthetic is su cient. T is block may be repeated at multiple levels to cover the anticipated pain area.

Paravertebral Nerve Block T is block provides analgesia to the thoracic and upper abdominal areas and is e ective or breast surgery, thoracic surgery, and the management o rib ractures. It is used or both acute and chronic pain management and provides ipsilateral motor, sensory, and sympathetic blockade. Several advantages o paravertebral block over epidural anesthesia include a lower incidence o hypotension, urinary retention, respiratory problems, and postoperative nausea and vomiting. T e paravertebral space is targeted adjacent to the vertebral bodies where the spinal roots exit the spinal canal. T e paravertebral space is bounded by the costotransverse ligament with the parietal pleura anteriorly and transverse process and ribs posteriorly. Laterally, the space is continuous with the intercostal space. T e vertebral body, intervertebral disc, and intervertebral oramen (which communicates with the epidural space) all lie medially. T e patient position is seated or lateral with the neck and back exed while the shoulders are relaxed orward. T e midpoint o the spinous process is marked and a 21 gauge needle is placed laterally and then advanced perpendicular to the back toward the transverse process. T e needle is walked up the transverse process in the caudad direction and advanced approximately 1 cm into the paravertebral space (Figure 15-2). A loss o resistance or “pop” is of en appreciated as the superior

costotransverse ligament is penetrated. Aspiration or blood and air is done to ensure the needle is not within the pleura o the lung or within a vascular structure be ore injecting 3–5 mL o local anesthetic into the space. Ultrasound guidance with a high- requency transducer can be utilized to better visualize the needle, the transverse process, the costotransverse ligament, and the pleura throughout the placement o the block to prevent adverse side e ects. T ese may include hypotension resulting rom epidural or intrathecal spread o local anesthetic. Less commonly, intravascular injection or pneumothorax may occur.

Ilioinguinal and Iliohypogastric Nerve Blocks Regional blockade o the ilioinguinal and iliohypogastric nerves has been shown to be e cacious in providing analgesia or patients undergoing inguinal hernia repair, abdominal hysterectomy, or cesarean section. T e blocks do not provide visceral anesthesia so they cannot be the sole anesthetic or these procedures. T e ilioingunal and iliohypogastric nerves arise rom the rst lumbar spinal root. T eir branches are superomedial to the anterior superior iliac spine and run through the transversus abdominis muscle, eventually piercing the external oblique to provide cutaneous sensation. T e ilioinguinal nerve provides sensation to the superomedial aspect o the thigh and the iliohypogastric nerve supplies the skin over the inguinal region. T e patient is placed in the supine position. Needle insertion is per ormed 2 cm medially and 2 cm superior to the anterior superior iliac spine (Figure 15-3). Ultrasound can assist with the location o these nerves as Exte rna l oblique mus cle (cut)

Ante rior s upe rior ilia c s pine

Inte rna l oblique mus cle

Iliohypoga s tric ne rve

Ilioinguina l ne rve S pina l ne rve s

FIGURE 15-2

Paravertebral nerve block. (Reproduced with permission from Greengrass R, Steele S. Paravertebral blocks for breast surgery. Tech Reg Anesth Pain Manage. 1998;2:8–12.)

Inguina l liga me nt

FIGURE 15-3

Ilioinguinal and iliohypogastric nerve blocks. (Reproduced from Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology. 4th ed. New York, NY: McGraw-Hill Education, Inc.; 2005: Figs 17–35.)

CHAPTER 15

they course through the transversus abdominis and internal oblique muscles. It is important to inject local anesthetic into two separate planes to have adequate analgesia. T ese planes include the layer between transversus abdominis and internal oblique muscles and the layer between internal and external oblique muscles. Needles blunt enough to appreciate loss o resistance are recommended. Examples include 18 gauge Whitacre, 21 gauge Stimuplex, or 22 gauge uohy needles. T e needle is advanced in three separate orientations and injections are made in both muscle planes or a total o six separate injections. T e rst orientation is perpendicular to the skin ollowed by 45° medial and 45° lateral orientations. In each o the three orientations, the needle is advanced until resistance is met, indicating the needle is adjacent to the external oblique ascia. T e needle is advanced urther until a “pop” or loss o resistance is elt. Af er aspiration is negative or blood, 2 mL o local anesthetic is injected. T e needle is then advanced urther until the internal oblique ascia is encountered and the needle is passed through with con rmatory tactile sensation o a second loss o resistance and then again 2 mL o local anesthetic is injected. T e total amount o local anesthetic used is 12 mL. Potential complications include intravascular injection, pelvic hematoma, and bowel per oration.

Transversus Abdominis Plane Block T is block is utilized or abdominal surgeries that include laparotomy, hernia repair, appendectomy, cesarean section, abdominal hysterectomy, and prostatectomy. T e sensory innervation o the anterior abdominal wall arises rom the anterior rami o spinal nerves 7 to L1. In order to block sensory stimuli, local anesthetic is injected between the transversus abdominis and internal oblique muscles. T is is best accomplished with ultrasound guidance to assist in proper needle placement while preventing potential adverse side e ects. While the patient is in supine position, the ultrasound probe is placed in the transverse plane against the lateral abdominal wall in the midaxillary line between the costal margin and the iliac crest. T e needle should be placed between the internal oblique (IO) and transversus abdominis ( A) muscles (Figure 15-4). Injection o 20 mL o local anesthetic produces a visual expansion o the transversus abdominis plane ( AP). T is may be repeated bilaterally depending on the nature o the surgery and the orientation o the planned incision. Potential side e ects include intravascular injection and bowel per oration.

PERINEUM Anesthetic blocks o the perineum are most of en used in obstetrics and gynecology to provide analgesia or pain ul uterine contractions during active labor and as adjunctive analgesia or uterine procedures. T ese blocks are achieved through local in ltration o peripheral nerve endings that help preserve progression o labor. T e pudendal and paracervical nerve block techniques may be help ul when neuraxial anesthesia is not a viable option.

Peripheral Nerve Blocks: runk and Perineum

EO IO TAP TA

FIGURE 15-4

Transversus abdominis plane block. (Reproduced with permission from Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Figs 46–64.)

Pudendal Nerve Block T is block is primarily used during the second stage o labor or to provide analgesia ollowing episiotomy and vaginal tears ollowing delivery. It can be utilized when other analgesic options such as neuraxial analagesia are unavailable or contraindicated. Sensory innervation to this area originates rom the anterior division o S2 to S4 and is peripherally represented by the pudendal nerve. While the patient is in the lithotomy position, an Iowa trumpet or Kobak needle guide may be used to prevent injury to the vagina and etus. T e needle and needle guide are introduced through the vaginal mucosa near the sacrospinous ligament, which is located just medial and posterior to the ischial spine. T e pudendal artery runs proximal to the pudendal nerve, so care must be taken to avoid intravascular injection o local anesthetic. Seven to ten milliliters o local anesthetic is injected bilaterally.

Paracervical Block T is block provides analgesia or the rst stage o labor when the dilation o the cervix and the distention o the lower uterine segment and upper vagina are the primary sources o pain. T is sensory impulse originates rom the spinal cord at the level o 10 to L1. T ese nerves join the sympathetic chain at L2 to L3 and provide the visceral a erent nerve bers. T e block targets the uterovaginal plexus, a division o the in erior hypogastric plexus. It is located lateral and posterior to the cervicouterine junction. T e patient is placed in the modied lithotomy position with lef uterine displacement. Again a needle guide is used to reduce the risk o vaginal or etal injury and the needle and guide are introduced at the lef or right lateral vaginal ornix, proximal to the ornix. T e needle is advanced through the vaginal mucosa approximately 2–3 mm and ollowing negative needle aspiration, 5–10 mL o local anesthetic is injected bilaterally.

16 C

Peripheral Nerve Blocks: Lower Extremity Binoy Bhatt, MD, and Christopher Monahan, MD

T e lower extremity is supplied by nerves that are widely separated rom each other as they enter the thigh. For this reason, lower extremity blocks are technically more di cult to perorm than those o the upper extremity. Major nerves to the lower extremity include the sciatic, posterior emoral cutaneous, emoral, lateral emoral cutaneous, and obturator nerves (Figure 16-1). Lower extremity blocks provide or superior postoperative pain relie and are ideal or patients with comorbidities that make an epidural or spinal anesthetic otherwise unsa e.

ANATOMY T e nerve supply to the lower extremity is derived rom the lumbar and sacral plexuses (Figure 16-2). T e lumbar plexus is ormed by the L1 to L4 anterior rami and it innervates the anterior aspect o the thigh. T e plexus lies between the psoas major and quadratus lumborum muscles within the psoas compartment. T e lower components o the plexus, L2 to L4, innervate the anterior and medial aspects o the thigh. T e anterior divisions o L2 to L4 orm the obturator nerve, and the posterior divisions o L2 to L4 orm the emoral nerve. T e lateral emoral cutaneous nerve is ormed rom posterior divisions o L2 and L3. T e sacral plexus gives rise to the posterior emoral cutaneous and the sciatic nerves. It innervates the rest o the lower extremity aside rom the anterior aspect o the thigh and medial aspect o the leg. T e posterior cutaneous nerve is derived rom S1 to S3, and the sciatic nerve is derived rom the anterior rami o L4 to L5. Both nerves pass through the pelvis and greater sciatic oramen, and are blocked via the same technique. At or above the popliteal ossa, the sciatic nerve separates into the tibial nerve, which passes medially, and the common peroneal nerve, which passes laterally down the leg.

LUMBAR PLEXUS BLOCK T e lumbar plexus block provides anesthesia to the hip and anterolateral and medial aspects o the thigh, and the saphenous nerve below the knee. T e block is use ul or hip

E R

procedures such as arthroplasty or open reduction internal xation (ORIF). In conjunction with a proximal sciatic block, this block can provide total anesthesia to the lower limb. T e patient is placed in the sitting position, or in the lateral position with the hips exed and operative extremity up. T e spinous processes should be used to determine midline. A line is drawn to connect the iliac crests to the midline, and the needle is inserted 3–4 cm lateral to the midline on the side to be blocked. T e needle is then advanced perpendicular to skin entry until it contacts the h lumbar transverse process, a er which it is redirected cephalad until it slides of the transverse process. T e lumbar plexus is identi ed by elicitation o a quadriceps motor response. Up to 30 mL o local anesthetic solution is injected. Lumbar plexus blocks carry a higher risk o local anesthetic toxicity than other nerve block techniques because o the deep location and the close proximity o muscles. Peripheral nerve damage is also a potential risk with this technique. In addition, injury to the kidney or ureter can in requently occur.

FEMORAL NERVE BLOCK T e emoral nerve emerges rom the lateral border o the psoas muscle, descends in the groove between the psoas and iliacus muscles, and enters the thigh by passing beneath the inguinal ligament lateral to the emoral artery. It is use ul to think o the mnemonic “NAVEL” (nerve, artery, vein, ‘empty,’ lymph node) when recalling the relationship o the emoral nerve to the vessels in the emoral triangle rom lateral to medial. T e emoral nerve supplies the anterior compartment muscles o the thigh and the skin o the anterior aspect o the thigh rom the inguinal ligament to the knee. T us, a emoral nerve block provides anesthesia to the anterior aspect o the thigh and most o the emur and knee joint. It is used or knee arthroscopies, quadriceps tendon repair, emoral sha ractures, ACL reconstruction, and total-knee arthroplasties. It is combined with the sciatic nerve block to provide complete anesthesia below the knee. T e use o emoral nerve blocks in complex knee operations has been associated with lower pain scores and ewer hospital admissions a er same-day surgery. 61

PART II Anesthesia echniques

T12

Ge nitofe mora l

Iliohypoga s tric N (IH)

Ge nitofe mora l N (GF)

Ilioinguina l

Ilioinguina l N (II)

Fe mora l N (F) (+ s a phe nous N) GF

La te ra l fe mora l cuta ne ous

LFC

La te ra l fe mora l cuta ne ous N (LFC)

S upe rior glute a l N (S G) Infe rior glute a l N (IG)

Obtura tor

Obtura tor N (O)

L5 F

Tibia l N (S )

Common pe rone a l N (S )

Ante rior fe mora l cuta ne ous

P = P ude nda l N S = S cia tic N

S P

FIGURE 16-2

Lumbosacral plexus. (Reproduced with permission from Atchabahian A, Gupta R, eds. The Anesthesia Guide. 1st ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 139-1.) S a phe nous

FIGURE 16-1

Cutaneous distribution of nerves of the lower extremity. (Reproduced with permission from Hadzic A, ed. Hadzic’s Peripheral Nerve Blocks and Anatomy for Ultrasound-Guided Regional Anesthesia. 2nd ed. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig. 18-4A.)

T e patient is in the supine position with the thigh slightly abducted and externally rotated to improve access. T e goal is to visualize the emoral artery by ultrasound, and then move the transducer laterally. Elicitation o a patellar stimulation veri es the correct needle position. Commonly, sartorius muscle contraction will be seen rst as the anterior branch o the emoral nerve is identi ed. T is should not be accepted, and the needle should be redirected slightly lateral and within a deeper direction to encounter the posterior branch o the emoral nerve. T e emoral nerve is appreciated on sonograms using a linear transducer as a attened bundle o ascicles lying between the hyperechoic subcutaneous tissue and the hypoechoic iliopsoas muscle (Figure 16-3). T e emoral nerve is broad and at in shape. It lies lateral to the emoral artery, just over the sur ace o the iliopsoas muscle, and under the ascia iliaca as it passes under the inguinal ligament. Although a longer needle path, the in-plane approach allows or visualization o the block needle rom lateral to medial until it punctures the ascia iliaca, with a distinct pop.

CHAPTER 16

Peripheral Nerve Blocks: Lower Extremity

It supplies an articular branch to the hip and anterior adductor muscles, and variable cutaneous branches to the lower medial portion o the thigh. An obturator nerve block can be use ul in treating or diagnosing the extent o adductor spasm in patients with cerebral palsy and other muscle or neurologic diseases af ecting the lower extremities be ore surgical intervention.

PARASACRAL BLOCK

FIGURE 16-3

Femoral nerve block. (Reproduced with permission from Hadzic A, ed. Hadzic’s Peripheral Nerve Blocks and Anatomy for Ultrasound-Guided Regional Anesthesia. 2nd ed. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig. 7.49.1C.)

T e perivascular approach (three-in-one block) to the emoral nerve is based on the premise that injection o a large volume o local anesthetic within the emoral canal while maintaining distal pressure will result in proximal spread o solution into the psoas compartment and consequently additionally achieve a lumbar plexus block. T e ascia iliaca approach to blocking the emoral nerve utilizes the double-pop technique, which re ers to the sensation elt as the needle traverses the ascia lata and then the ascia iliaca. Intravascular injection and hematoma are less likely with this block due to the increased distance o the needle to the emoral artery.

T e parasacral block anesthetizes both components o the sciatic nerve and posterior cutaneous nerve o the thigh (Figure 16-4). For knee procedures, a parasacral block provides an advantage over more distal approaches. T is approach is also use ul when immediate access to the individual nerves o the sacral plexus is not possible (i.e., trauma or in ection). T e patient is positioned laterally with the side to be blocked positioned up. T e most prominent aspects o the posterior superior iliac spine and the ischial tuberosity are identi ed, and a line is drawn joining these two points. T e needle insertion site is 6 cm in erior to the posterior superior iliac spine. Plantar exion o the oot (tibial nerve compartment) or dorso exion (common peroneal nerve) is an acceptable motor response. A hamstring motor response is also acceptable. Loss o parasympathetic innervation to the bowel, bladder, and sphincters may occur. Injection o local anesthetic into the subarachnoid or vascular compartments is a remote risk. An appreciation o the pelvic contents, especially the colon, rectum, and bladder, is important, as a deeply inserted needle may result in seeding ecal material into the sacral canals.

LATERAL FEMORAL CUTANEOUS NERVE BLOCK T is block is utilized or skin gra harvesting and can be used in concert with other peripheral nerve blocks or complete anesthesia o the lower extremity. T e nerve emerges at the lateral border o the psoas muscle immediately caudad to the ilioinguinal nerve. Its branches supply the innervation to the lateral portion o the thigh rom the hip to the midthigh (posterior) and the anterolateral aspect o the thigh to the knee (anterior). T e entry point is 2 cm medial and 2 cm caudad to the anterior superior iliac spine. T e needle is moved in a anlike pattern laterally and medially to provide local anesthetic above and below the ascia.

OBTURATOR NERVE BLOCK Rarely blocked on its own, the obturator nerve is usually blocked or knee surgery. It lies deep in the obturator canal a er descending rom the medial border o the psoas muscle.

Ne e dle ins e rtion P S IS IT

FIGURE 16-4

6 cm

Parasacral block. (Reproduced with permission from Hadzic A, ed. NYSORA Textbook of Regional Anesthesia and Acute Pain Management. New York, NY: McGraw-Hill Education, Inc.; 2007: Fig. 37-11.)

PART II Anesthesia echniques

SAPHENOUS NERVE BLOCK he saphenous nerve is the only branch o the emoral nerve to contribute to innervation below the knee. It can be blocked at the midthigh level where it lies anterior to the emoral artery. he medial thigh is scanned with the patient supine and leg externally rotated. he needle advances rom anterior to posterior within the plane o imaging. he saphenous nerve is not always visible, but it courses with the emoral artery, just deep to the sartorius muscle. his block is o ten combined with a popliteal block or ankle anesthesia.

SCIATIC NERVE BLOCK Classic Approach of Labat T e sciatic nerve is a large nerve that provides near-complete sensation o the oot and lower leg. T e classic approach o Labat to sciatic nerve block requires the patient to lie with the injured side up (Figure 16-5). A line is drawn rom the sacral hiatus to the greater trochanter on the side o the nerve to be blocked. T e location o the sciatic nerve is hal way along this line, roughly 5 cm caudad to the greater trochanter. At this point, the sciatic nerve is 2 cm wide as it leaves the pelvis, directly in erior to the piri ormis muscle. I another line is drawn rom the greater trochanter to the posterior superior

iliac spine on the ipsilateral side, the point o needle insertion should be along a perpendicular line connecting these two lines (Figure 15-10). Foot movement evoked by nerve stimulation is a satis actory endpoint or needle placement be ore injection o local anesthetic.

Popliteal Approach T e sciatic nerve can be blocked within the popliteal ossa where the sciatic nerve divides into the common peroneal and tibial nerves. T is block provides anesthesia or oot and ankle surgeries. T e patient is placed in the prone position, or supine with exion o the leg to 30°, allowing space or an ultrasound transducer to scan the posterior thigh just proximal to the knee crease. T e needle is advanced rom lateral to medial within the plane o imaging, through the biceps emoris muscle. Local anesthetic is injected around both the common peroneal and tibial nerves, which are typically super cial and lateral to the popliteal artery and vein (Figure 16-6).

Pos te rior s upe rior ilia c s pine 5 cm

S a cra l hia tus

FIGURE 16-5

Gre a te r trocha nte r

Sciatic nerve block—Labat approach. (Reproduced with permission from Butterworth JF, Mackey DC, Wasnick JD, eds. Morgan &Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill Education, Inc.; 2013: Fig. 46-51.)

FIGURE 16-6

Sciatic nerve block—popliteal approach. (Reproduced with permission from Longnecker DE, Brown DL, Newman MF, Zapol WM, eds. Anesthesiology. 2nd ed. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig. 49—49A&B, p. 845.)

CHAPTER 16

ANKLE BLOCK All ve peripheral nerves that supply the oot can be blocked. T us, a complete ankle block requires injection o local anesthetic at multiple locations. It is convenient to elevate the oot by supporting the cal . Systemic toxicity is rare rom ankle blocks because the oot does not have a generous blood supply (Figure 16-7). 1. Tibial nerve—It is a major nerve to the sole o the oot. T e nerve lies on the medial ankle posterior to the posterior tibial artery. T is nerve can be blocked by advancing the needle posterior to the posterior tibial artery at the

2. 3. 4.

5. A

Tibia lis a nte rior te ndon S a phe nous ne rve

De e p pe rone a l ne rve Exte ns or ha llucis longus te ndon S upe rficia l pe rone a l ne rve

Fibula Pos te rior tibia l ne rve Achille s te ndon

S ura l ne rve

FIGURE 16-7

Anatomy and approaches to ankle block. (Reproduced with permission from Morgan GE Jr, Mikhail MS, Murray MJ, eds. Clinical Anesthesiology. 4th ed. New York, NY: McGraw-Hill Education, Inc.; 2006: p. 352.)

Peripheral Nerve Blocks: Lower Extremity

level o the medial malleolus. A er bone is encountered, the needle is withdrawn slightly and the injection is made. Sural nerve—It innervates the lateral oot. It can be blocked in the groove between the lateral malleolus and calcaneus. Saphenous nerve—It innervates the medial oot. It can be blocked anterior to the medial malleolus near the saphenous vein. Deep peroneal nerve—It innervates the webbing between the rst and second toes. It can be blocked adjacent to the dorsalis pedis artery. I arterial pulsation is absent, the deep peroneal nerve can be blocked deep to the extensor halluces longus tendon and extensor retinaculum. Superf cial peroneal nerve—It innervates the dorsum o the oot. T is can be blocked by injecting a subcutaneous ridge o anesthetic solution between the medial and lateral malleoli over the anterior sur ace o the oot.

Use of Peripheral Nerve Stimulators Brian S. Freeman, MD

Peripheral nerve stimulation (PNS) is a technique designed to localize plexuses or other larger peripheral nerves. It acilitates the placement o a needle close to the target nerve in order to deposit local anesthetic or conduction blockade (anesthesia and/or analgesia). Until the use o nerve stimulation became widespread in the 1990s, peripheral nerve blocks were traditionally per ormed using a technique in which subjective paresthesias were intentionally elicited. In contrast, PNS does not depend on patient cooperation or e ective nerve localization. Direct electrical stimulation o the nerve produces a reliable and objective endpoint: an evoked motor response (muscle twitch). PNS can be used or both single-injection nerve blocks and insertion o continuous nerve block catheters. oday, it is usually combined with ultrasound guidance or the administration o regional anesthesia.

ELECTROPHYSIOLOGY T e neuronal membrane maintains a negative resting potential o approximately 90 mV due to the active transport o sodium and potassium ions. When depolarization o the membrane exceeds a prede ned threshold, the ow o sodium ions into the cell triggers an action potential which propagates along the nerve ber. Depolarization occurs rom within the nervous system. PNS utilizes extracellular stimulation to depolarize the nerve ber rom outside the neuron. T e negative polarity o the electrical stimulus (needle) removes positive charges rom outside the neuronal membrane. T is extracellular change enables the membrane potential to decrease towards the threshold level or generating an action potential. A peripheral nerve stimulator delivers square pulses o current rather than a single prolonged current. T e total electrical charge (Q) applied to a nerve is the product o the current intensity (I) and current duration (t): Q = I × t. T ere ore, in order to cause depolarization, the stimulus current must have both su cient strength and duration. A weak or brie current will not generate an action potential. T e current intensity (I) required to stimulate the nerve depends on three variables: rheobase (Ir), chronaxie (C), and

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stimulus duration (t). T ese variables are related by the ollowing equation: I = Ir (1 + C/t). 1. Rheobase— o reach the threshold potential or nerve excitation, a certain minimum level o current intensity is necessary. T e rheobase is the minimum threshold current (in amperes) required to stimulate a nerve when using long pulse durations. Current intensities below rheobase will not generate an action potential even i administered or a long time. 2. Chronaxie—T e chronaxie time is the minimum duration (in milliseconds) required to generate an action potential when the current is applied at two times the rheobase level. A current applied at twice the rheobase value needs less time to achieve stimulation. Reducing pulse duration to very short times diminishes current dispersion rom the needle tip, thereby requiring the tip to be placed very close to the nerve. Chronaxie times re ect the relative excitability o di erent peripheral nerve bers due to their physical properties (Figure 17-1). With the largest diameters and highest degree o myelinization o all peripheral nerves, the motor bers (Aα) have ast conduction speeds and short re ractory periods. T ey are the easiest bers to depolarize to threshold potential via external stimulation. As such, Aα bers have the shortest chronaxie times (50–100 ms). Sensory nerve bers (Aδ and C) have smaller diameters, very little to no myelinization (higher membrane capacitance), and slower conduction speeds. T ese bers have higher threshold levels to external stimulation and thereore require longer chronaxie times (150 ms or Aδ bers, 400 ms or C bers). T e goal o PNS is to excite motor nerve bers without stimulating sensory nerves. Pulse currents with short chronaxie will stimulate the Aα motor bers (causing a muscle twitch) but not the Aδ and C bers, which would otherwise make it a pain ul experience or the patient. However, i the current is too high (>1.0 mA), the PNS may no longer be able to di erentially stimulate motor nerve bers and may cause pain ul paresthesias. 67

PART II Anesthesia echniques

Low-s pe e d pa in fibe r (2)

3.0

(

)

4.0

2.0

Chrona xy

High-s pe e d motor fibe r (1)

Chrona xy (1) 1.0

2 × Rhe oba s e

2 × Rhe oba s e Rhe oba s e (2) Rhe oba s e (1)

0 0

0.5 tc (1)

1.0

1.5

2.0

2.5

tc (2) S timulus dura tion (ms )

FIGURE 17-1

Comparison o motor and pain f bers. (Reproduced with permission rom Hadzic A, ed). Hadzic’s Peripheral Nerve Blocks and Anatomy for Ultrasound-Guided Regional Anesthesia. 2nd ed. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig 4-3A.)

T e quality o the motor response induced by electrical stimulation depends on several actors: 1. Electrode-to-nerve distance—T e use o peripheral nerve stimulators is based on Coulomb’s law, which describes the relationship between the needle–nerve distance and current intensity: I = k(Q/r ), 2

where I is the current required to stimulate the nerve, k is a constant, Q is the minimal current needed or stimulation, and r is the distance rom the stimulus to the nerve. Because the current varies with the inverse o the square o the distance, a higher current intensity is required as the needle tip moves urther away rom the nerve. T ere ore, the ability to stimulate a nerve at low current strengths (e.g., 1 mA) to evoke a motor response. Once the needle tip passes the target nerve, uncoated needles are not very accurate. In contrast, insulated needles emit a ocused current rom the tip, the only part o the needle that lacks insulation. Since the current density is ocused into a sphere around the needle tip, the smaller conducting area enables lower currents to stimulate the nerve. Insulated needles have improved accuracy during PNS by providing a better sense o tip location. 6. Stimulating catheters—Stimulating catheters unction in a manner similar to those o insulated needles. Catheters are usually inserted through a specially designed continuous nerve block needle, which acts as an introducer needle. Nerve stimulation using the metal wire inside the catheter can be per ormed to recon rm the position o the catheter tip near the target nerve. In this situation, threshold currents are typically higher. T e injection o saline or local anesthetic to expand the perineural space can also increase the threshold current or prevent an evoked motor response.

LIMITATIONS OF PNS PNS is a blind technique that does not result in an evoked motor response every time the needle is placed adjacent to the nerve. In act, several studies using ultrasound and PNS together suggest that PNS is a rather insensitive method o determining the proximity o the needle to the target nerve. Potential reasons or its poor sensitivity include di erent impedances within neural tissues, the in uence o comorbid diseases, the type o injection solutions, and the nonuni orm distribution o motor and sensory ascicles within a mixed peripheral nerve. False-positive results can occur. Despite objective and viable evoked motor responses, ailed blocks are possible. In this situation, it is possible that a structural barrier is the cause. For example, the tenting o a tissue layer between the needle and the nerve can result in depolarization and muscle twitches, but actual deposition o local anesthetic occurs outside the neural sheath. False-negative results are also common. A patient may experience paresthesia without evidence o the corresponding evoked motor response. T is problem can result in unnecessary needle repositioning. T ere are a number o reasons why alse negatives occur with PNS. T e current may be channeled away rom the nerve in an asymmetric manner due to di erences in tissue impedance. T ere may be an actual physical barrier between the sensory and motor nerve bers. Interstitial uid or blood in the tissue can inter ere with needle conductance. With respect to patient sa ety and block success, the literature does not support peripheral nerve stimulation as a superior approach over other techniques such as ultrasound or paresthesia elicitation.

Intravenous Regional Anesthesia Omar Syed, MD, and Daniel Asay, MD

Intravenous regional anesthesia (IVRA) provides anesthesia to either the upper or lower extremity by means o local anesthetic introduction into a peripheral vein. Alternatively named the Bier block, this anesthetic is contraindicated or procedures requiring muscle paralysis, blockade o individual nerves, or prolonged surgical duration. Developed in 1908 by Dr August Bier, the Bier block remains popular due to its ease o use, reliability, and low incidence o complications. It is use ul in short, modestly invasive procedures such as carpel tunnel release and ganglionectomy. T e duration o the block is predicated on the duration o tourniquet in ation, limiting toxicity risk rom longer acting agents; however, tourniquet discom ort precludes Bier blocks or longer procedures. When employed care ully, the Bier block is a sa e and reliable method o producing anesthesia.

TECHNIQUE Application o the Bier block requires several steps that ultimately exsanguinate the extremity ollowed by delivery o local anesthetic into the exsanguinated vascular space. An IV cannula is placed in an extremity that the Bier block is not being per ormed on or administration o adjunctive medications. An IV cannula is also placed distally in the procedure limb. Next, a double tourniquet with clearly designated proximal and distal tourniquets is placed on the operative extremity proximal to the surgical site. T e extremity is elevated above the level o the heart or 1 minute, allowing or passive evacuation o blood. T en, an Esmarch bandage is applied to the limb in a spiral ashion, starting distally, to actively remove remaining blood rom the vascular space. T e double tourniquet is tested with the distal tourniquet rst in ated ollowed by the proximal tourniquet to 50–100 mmHg above systolic blood pressure. Once the unction is veri ed, the distal tourniquet is de ated. T e Esmarch bandage is removed and local anesthetic given to the operative extremity. ypically, 12–15 mL o preservative- ree 2% Lidocaine HCL or 30–50 mL o preservative- ree 0.5% Lidocaine HCL is slowly administered in adult patients. A er injection, the IV cannula is removed rom the operative extremity.

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Surgical anesthesia typically occurs immediately but may take up to 5 minutes. A er 20–30 minutes the patient may experience tourniquet pain; with pain, the distal tourniquet can be in ated ollowed by de ation o the proximal cuf . T is technique is applied within 40–60 minutes o surgical anesthesia and is less pain ul as the distal cuf tightens on an anesthetized portion o the extremity. Upon surgical completion, the distal cuf is de ated or 10 seconds ollowed by rein ation or 1 minute. T is slowly releases local anesthetic into circulation, minimizing toxicity risk. A er 1 minute, the cuf can be de ated completely and the tourniquet removed.

LOCAL ANESTHETICS Nearly all local anesthetics are used or IV regional anesthesia. Lidocaine is the most commonly used local anesthetic with the ewest side ef ects. A maximum o 3 mg/kg is generally considered sa e since epinephrine is not used. Additionally, preservative- ree solution prevents thrombophlebitis associated with preservatives. Although prilocaine has low systemic toxicity, there is concern or methemoglobinemia. Current research is exploring adjunctive medications such as clonidine, meperidine, and ketorolac; however, these have yet to be widely accepted.

QUALITY OF BLOCKADE T e nerve blockade o the Bier block develops within 5 minutes and includes the entire extremity below the level o the tourniquet. Progressive insensitivity develops rst ollowed by discoloration o the skin and possibly motor paralysis. T e exact mechanism o action is unknown; however, it is thought that local anesthetic dif uses to peripheral nerves. Ischemia and nerve compression by the tourniquet may also play a signi cant role.

RISKS T e primary concern with IV regional anesthesia is systemic local anesthetic toxicity. oxicity results rom a mal unctioning

PART II Anesthesia echniques

tourniquet or equipment at the outset o the procedure. In order to prevent this, precautions must be employed to assure tourniquet unctionality. Long-acting local anesthetics are more likely to contribute to toxic ef ects and should there ore be avoided. Additionally, or procedures shorter than 20 minutes, 2 minutes should pass between each de ation or several de ations. I signs o local anesthetic systemic toxicity present, lipid emulsion should be readily available as well as equipment or oxygen delivery via acemask or tracheal intubation. Other Bier block risks include hematoma, extremity engorgement, and subcutaneous hemorrhage and bruising. o minimize hematoma risk, 22 gauge needles should be used and prolonged pressure applied a er ailed IV cannula. Extremity engorgement occurs with severe arteriosclerosis. T is limits tourniquet occlusion o the blood supply to the extremity while preventing vascular return

rom compressed veins. Palpation o the artery and a unctional tourniquet prevent this complication. I vascular engorgement occurs, tourniquet removal and elevation is appropriate. In order to prevent against subcutaneous hemorrhage, adequate tourniquet padding is applied.

CONTRAINDICATIONS Contraindications to IV regional anesthesia are limited to contraindications o tourniquet placement and local anesthetic usage. ourniquets should not be applied on patients with ischemic vascular disease, sickle cell disease, or in ection. Fracture pain also limits tourniquet use and traumatic lacerations may allow a systemic leak o local anesthetic. Allergic reactions to local anesthetic should prompt an alternate technique.

Controlled Hypotension Curt Bergstrom, MD

Controlled or deliberate hypotension is practitioner-initiated reduction o an anesthetized patient’s blood pressure (BP) to achieve a speci c therapeutic purpose. T e hypotensive state under hypotensive anesthetic sustains tissue per usion with adequate blood ow.

INDICATIONS As shown in able 19-1, controlled hypotension can be useul in a variety o surgical situations. T e main indications are (1) decreasing blood loss and subsequent trans usion requirements; and (2) acilitating operative conditions by improving visualization o the operative eld. Controlled hypotension can be used alone or as part o a larger blood conservation regimen that may include RBC salvage, anti brinolytics, normovolemic hemodilution, and/or positioning to reduce blood loss and trans usion requirements. Controlled hypotension has a role in procedures not associated with signi cant blood loss through improved visualization. For example, during thoracic aortic endovascular interventions, brie periods o controlled hypotension may acilitate an accurate positioning o the endovascular gra . Hypotension at the time o gra deployment minimizes gra migration risk.

CONTRAINDICATIONS Patients at risk or ischemia or with impaired autoregulation are poor candidates or controlled hypotension. Frequently

TABLE 19-1

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excluded conditions listed in able 19-2 avoid exacerbating the patient’s pre-existing disease. Many conditions are relative contraindications, based on the patient’s condition, type o surgery, monitoring used, and the technique or achieving hypotension. A list o absolute contraindications might include cerebrovascular disease with severe carotid stenosis, symptomatic or severe aortic or mitral stenosis, and stage IV chronic kidney disease. Patients with less severe orms o these conditions may bene t rom controlled hypotension, but the decision to proceed with should be made with consideration or the heightened risk their comorbid conditions present and possible alternatives.

MONITORING In addition to standard monitors, the use o invasive BP monitoring is appropriate when providing controlled hypotension. Since hypocarbia decreases cerebral blood ow, maintenance o normocarbia is important or preserving cerebral per usion during hypotension. T e monitoring o BP in patients in nonhorizontal positions deserves special attention. T ere can be a signi cant discrepancy in height between the brain and the site o BP measurement, resulting in low cerebral per usion pressure. T is can be minimized by placing the transducer at the level o the external auditory meatus in patients whose BP is being monitored with an arterial line. I that is not possible or i a noninvasive BP monitoring is being used, a conversion actor o 10 cm H 2O = 7.4 mmHg should be used to correct or the di erence in pressure rom the site o measurement to the brain.

Uses for Controlled Hypotension

Major spine surgery Total hip arthroplasty Orthognathic surgery Middle ear surgery Radical neck dissection Endoscopic sinus surgery Partial nephrectomy Radical cystectomy Major abdominal surgery Endovascular aortic graft procedures Bloodless surgery

TABLE 19-2

Contraindications to Controlled

Hypotension

Coronary artery disease Severe valvular heart disease Congestive heart failure Poorly controlled hypotension Cerebrovascular disease Peripheral vascular disease Diabetes mellitus Chronic kidney disease

PART II Anesthesia echniques

For example, using a BP cu positioned on the upper extremity (which is roughly 20 cm below the external auditory meatus) means that the actual pressure within the Circle o Willis is 14.8 mmHg lower than the measured cu pressure. T ere ore, i the goal mean arterial pressure (MAP) is 60, an MAP o 75 should be sought. Maintaining euvolemia is important or preserving tissue per usion while in a hypotensive state and vigilant monitoring o the patient’s intravascular status is necessary. T e decision to utilize additional hemodynamic monitoring should be made with consideration o the patient’s comorbidities and magnitude o blood loss expected. Pulse pressure variation monitoring o the arterial wave orm may prove suf cient. Changes in hemodynamic parameters suggesting a need to reduce the dose o hypotensive agents or increase hemodynamic support should prompt an assessment o the patient’s volume status. In ormation on uids given, estimated blood loss, and urine output should be integrated with hemodynamic data and laboratory data such as pH, base de cit, or lactate to decide i additional uids or blood is needed.

manner that leaves the abdomen ree rom compression signi cantly reduces blood loss.

Neuraxial Anesthesia T e sympathectomy produced by spinal or epidural anesthesia can be used to provide controlled hypotension as well as anesthesia or appropriate procedures. One widely studied approach to using epidural anesthesia involves using a lumbar catheter to achieve a minimum 4 level along with a lowdose epinephrine in usion. Achieving a high-level ( 2 to 4) blockade blocks cardioaccelerator bers in the thoracic sympathic chain, reducing MAP while central venous pressure (CVP) and cardiac output are maintained using a low-dose epinephrine in usion. Intraoperative neurological assessments allow or the determination o the adequacy o cerebral per usion.

Potent Volatile Anesthetics Iso lurane, sevo lurane, and des lurane produce dosedependent decreases in systemic vascular resistance and arterial BP. However, the speed o washout limits the o set o e ects once hypotension is no longer desired.

TECHNIQUES An ideal technique is reliable and rapidly titratable with minimal side e ects. Controlled hypotension can be provided using neuraxial anesthesia, potent volatile anesthetics, or any o a number o intravenous drugs that reduce BP. With varying success, vasodilators, propo ol, opioids, beta blockers, calcium channel blockers, and milrinone have been used to provide controlled hypotension. Some o the more titratable intravenous drugs include sodium nitroprusside, nitroglycerin, remientanil, and esmolol. A reasonable approach is to select a technique that is reliable, has a avorable side e ect pro le or the speci c patient, and that the practitioner is amiliar with. In addition, surgical considerations such as the risk o rapid hemorrhage, which may require rapid reversal o hypotensive agents to acilitate resuscitation, may actor in the choice o technique. Agents rom di erent classes may be combined to ameliorate the side e ect pro le o individual agents used in larger doses. Drugs requiring continuous in usion should be administered on a pump via a dedicated line to minimize variation in dose delivery by boluses o other medications. Along with selecting a technique, it is necessary to select a BP target to guide therapy. T e lower limit o cerebral autoregulation is roughly 60 mmHg. A MAP goal o the greater o 65 mmHg or 30% below the patient’s BP baseline is typical. When possible, positioning the patient so the surgical eld is above the level o the heart promotes venous drainage and decreases bleeding. During prone spinal surgery, pressure on the abdomen can create backpressure on the in erior vena cava (IVC), distending veinous drainage o the vertebral column and increasing bleeding. Positioning the patient in a

Sodium Nitroprusside Sodium nitroprusside (SNP) is a direct vasodilator that has been widely studied or providing controlled hypotension. It produces arterial and venous dilation by reacting with oxyhemoglobin in erythrocytes to produce nitric oxide (NO). In vascular smooth muscle, NO increases guanylate cyclase activity, leading to an increase in cGMP, which induces smooth muscle relaxation, and a decrease in systemic vascular resistance. SNP acts rapidly and has a 2 minute hal -li e in the circulation, making it highly titratable. Side e ects o SNP include re ex tachycardia, an increase in plasma renin activity, which contributes to rebound hypertension, decreased platelet aggregation, tachyphylaxis, and cyanide toxicity. Combining SNP with a beta blocker or angiotensin converting enzyme inhibitor can control the re ex tachycardia, reduce rebound hypertension, and decrease the dose o SNP required to achieve the targeted decrease in BP. Signs o cyanide toxicity include tachyphylaxis, metabolic acidosis, and increased mixed-venous oxygen saturation.

Nitroglycerin Nitroglycerin is a direct vasodilator with greater e ect on veins than arteries. It is metabolized in the vascular smooth muscle to produce NO, which leads to vasodilation similar to SNP. At low doses, nitroglycerin acts primarily on venous capacitance vessels. Venous pooling decreases cardiac preload, which leads to decreased cardiac output. As the dose rises, arterial dilation increases while venodilation remains constant. Nitroglycerin

CHAPTER 19

is slower acting and less potent in producing hypotension compared to SNP but does not have the side e ects o rebound hypertension or cyanide toxicity. It can cause re ex tachycardia and methemoglobinemia at doses > 5 mg/kg/d; however, that is a much higher dose than is typically used or controlled hypotension.

Remifentanil Opioids decrease central sympathetic out ow and can cause hypotension and bradycardia. When combined with a volatile agent or propo ol, remi entanil can provide titratable hypotension without additional vasoactive medications. Remi entanil’s brie 3–10 minute hal -li e allows a deep plane o analgesia to be maintained during surgery without the delay in awakening that might be seen with the use o other opioids.

Controlled Hypotension

COMPLICATIONS Ischemic complications such as cerebrovascular accidents, myocardial in arction, renal injury, and hepatic injury are rare. Serious complications are o en due to controllable actors such as patient selection, provider amiliarity with the selected technique, and appropriate vigilance in monitoring the patient. While there have been reports suggesting an association between hypotension and postoperative visual loss, analysis o the ASA Postoperative Visual Loss Registry ailed to nd evidence to support this association. Reactionary hemorrhage and hematoma ormation caused by bleeding a er normalization o BP is a potential surgical complication. T is may be prevented by allowing the BP to normalize with surgical closure so appropriate detection o bleeding can achieve hemostasis.

Esmolol Esmolol o ers a titratable reduction BP without rebound hypertension or re ex tachycardia. T e hemodynamic e ects o esmolol observed during controlled hypotension include a reduction in cardiac output, heart rate, and plasma renin activity, and elevation in systemic vascular resistance. Esmolol promotes a avorable balance between myocardial oxygen supply and demand but it may cause signi cant myocardial depression. T is may limit the ability to use esmolol as a sole agent in patients with heart disease.

SUGGESTED READINGS Degoute CS. Controlled hypotension: a guide to drug choice. Drugs. 2007; 67:1053–1076. Dutton RP. Controlled hypotension or spinal surgery. Eur Spine J. 2004; 12(Suppl 1):S68–S71. ASA ask Force on Perioperative Visual Loss. Practice advisory or perioperative visual loss associated with spine surgery. Anesthesiology. 2011;116:274–282.

Controlled Hypothermia Mofya S. Diallo, MD, MPH

Controlled hypothermia is indicated or neuroprotection a er cardiac arrest, neonatal asphyxia, and neonatal encephalopathy, with improved outcome in the intensive care unit setting. It has been shown that decreasing core temperature is protective when there is a risk o ischemia and hypoxia. T e brain has high metabolic demands, requiring a constant glucose and oxygen supply, which make it highly vulnerable to injury. Hypothermia is applied intraoperatively in neurosurgical and cardiac surgeries, both o which are associated with high risk o tissue hypoxia and ischemia. Cardiac surgery requiring cardiopulmonary bypass (CPB) exposes multiple organ systems, including the brain, to the risk o hypoxia and ischemia. Hypothermia during CPB reduces whole body oxygen consumption. However, routine application o induced hypothermia continues to be controversial. When applied, the controlled hypothermia target temperature is usually 32–34°C. T ere are several ways to cool a patient, including the ollowing: 1. Endovascular cooling is accomplished by inserting a heat-exchanging catheter into the in erior vena cava via the emoral vein. T is can cool a patient at the rate o 4°C/h, and is the most rapid method available. CPB is a more sophisticated variation o endovascular cooling that allows or rapid cooling. 2. Administration o cold, intravenous uids peripherally is the second most e ective way to induce hypothermia. emperature can decrease at 0.5°/L. However, this risks uid overload as it requires 4 L to reach the goal temperature o 34°C. 3. Forced-air blankets are easily accessible to cool a patient but do not rapidly decrease the core body temperature. It can take up to 2.5 hours to cool a patient to 33°C. 4. Submersion in ice water or external ice bag application. 5. Passive cooling is the slowest method.

SYSTEMIC EFFECTS Hypothermia reduces the tissue metabolic rate by 8% per °C. T is change is benef cial when there is a risk or ischemia and hypoxia during surgery where the arterial blood ow is disrupted or surgical exposure.

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Glucose and insulin homeostasis is also altered during hypothermic therapy. T ere is decreased glucose consumption, decreased insulin secretion, and resistance to exogenous insulin therapy. Glucose should be monitored actively in this setting; however, glucose regulation typically resolves with normothermia. Shivering is a common side e ect o hypothermia that requires treatment. It is even more likely to occur a er hypothermic therapy. Shivering increases metabolic oxygen requirements by increasing the heart rate, blood pressure, and stress. T ere is a three old increase in myocardial ischemia with shivering. Forced-air warming blankets are use ul in this setting. Hypothermia has been ound to increase bleeding, as it a ects coagulation. Proteins necessary or coagulation are particularly sensitive to temperature, thus a ecting actors in the coagulation cascade. Mild hypothermia to temperatures < 35°C induces platelet dys unction. Consequently, the need or trans usion may increase during intraoperative hypothermia secondary to increased bleeding. In ections are a common complication o hypothermia. Immune unction and per usion are impaired, increasing the risk o wound in ection. Prolonged hypothermia in the ICU is associated with pneumonia. Drug metabolism is signif cantly altered during hypothermia. Proteins involved in drug metabolism, such as cytochrome P-450 enzymes, are temperature-sensitive, leading to impaired drug metabolism with accumulation. I possible, serum drug levels should be monitored to avoid unwanted e ects. Hypothermia a ects cardiac conduction, resulting in dysrhythmias. T e most common dysrhythmia is bradycardia, resulting in decreased cardiac output.

DEEP HYPOTHERMIC THERAPY During cardiac surgery requiring CPB, lower temperatures are required to prevent tissue ischemia and hypoxia. T e goal core temperature or cardiac surgery is usually 28–33°C. A temperature o 28°C signif cantly decreases tissue oxygen consumption and prevents tissue hypoxia. It is particularly protective 77

PART II Anesthesia echniques

or organs with higher metabolic requirements such as the brain and heart. In surgeries requiring complete circulatory arrest, the core temperature is lowered to 18°C, as at this temperature there is little cellular activity and patients can tolerate the arrest or up to 30 minutes without neurologic injury. T e complications associated with these lower temperatures include coagulopathy and cardiac dys unction, both o which have to be addressed intraoperatively. Ventricular f brillation is commonly seen as the myocardium is most susceptible to f brillation at temperatures below 22°C.

REWARMING Rewarming a er controlled hypothermia causes vasodilation, which can signif cantly decrease systemic vascular resistance and cause hypotension. T ere ore, slow rewarming is recommended to decrease the likelihood o acute hemodynamic instability. It may be necessary to treat the hypotension associated with rewarming with IV uids and vasopressors. Methods or rewarming are numerous; however, aggressive attempts can lead to burn injury. T e slowest methods to warm a patient include administering warm IV uids, humidi ying air or intubated patients, and applying heated

blankets and heat packs to skin. A moderately ast approach is to provide heated IV uids at 65°C, gastric lavage and peritoneal lavage. T e astest methods to warm a patient are via CPB, arteriovenous dialysis, thoracic lavage, whole-body submersion, and extracorporeal membrane oxygenation. Oxygen requirements increase as the patient is rewarmed and it is important to optimize oxygen carrying capacity by avoiding anemia and arterial oxygen desaturation. Oxygen consumption during rewarming can be reduced by maintaining sedation and paralysis to decrease the negative e ects o shivering. In patients receiving insulin therapy, it is important to taper doses as insulin sensitivity improves with rewarming. Gradual rewarming also prevents thrombus ormation as platelet unction and aggregation return to normal.

SUGGESTED READINGS Polderman KH. Mechanisms o action, physiological e ects, and complications o hypothermia. Crit Care Med. 2009;37(7): S186–S202. Mackensen GB, McDonagh DL, Warner DS. Perioperative hypothermia: use and therapeutic implications. J Neurotrauma. 2009;26(3):342–358. Conolly S, Arrowsmith JE, Klein AA. Deep hypothermic cardiac arrest. Contin Educ Anaesth Crit Care Pain. 2010;10(5):138–142.

Hyperbaric Oxygen and Anesthesia Care Tif any Minehart, MD, and George Hwang, MD

Anesthesia has been used in conjunction with hyperbaric oxygen therapy (HBO ) since the 1960s. Hyperbaric medicine was rst ound to be use ul in divers su ering rom decompression sickness. Since this time, increased ambient pressure has been used to treat a variety o clinical conditions, including carbon monoxide poisoning, arterial gas embolism, and decompression sickness.

PHYSIOLOGIC EFFECTS 1. Increased barometric pressure—According to Boyle’s law, pressure and volume are indirectly related. T ere ore, an increase in ambient pressure will result in a concurrent contraction o gas in the same chamber. For example, pockets o gas in the body (middle ear, paranasal sinuses, intestines, and pneumothorax) decrease in volume when exposed to increased altitude, increased water depth, or a hyperbaric oxygen chamber. T is principle also explains how hyperbaric oxygen can be used to treat an arterial gas embolism or decompression sickness. 2. Increased partial pressure o oxygen—HBO acilitates breathing oxygen at increased ambient pressure and results in an increased in arterial and tissue oxygenation (Po 2). T is increased oxygenation results in a reduction in cardiac output, an increase in systemic vascular resistance, and a decrease in pulmonary vascular resistance. T e resulting systemic vasoconstriction allows or the treatment o traumatic edema that occurs in crush injuries, but is inhibited by the presence o nitric oxide. HBO is typically delivered at 2–3 A A (absolute atmospheres). At these levels, renal, mesenteric, and hepatic blood ows are unchanged; however, cerebral blood ow decreases. 3. Increased partial pressure o nitrogen—According to the Meyer–Overton hypothesis, increasing the partial pressure o an inert gas (e.g., nitrogen, hydrogen, argon) in a mixture o inhaled gases results in a narcotic e ect. T is e ect is thought to be the result o increased GABAA receptors in the nigrostriatal pathway, resulting in the release o dopamine. At 3 A A, N2 has a mild euphoric e ect. At 6 A A, individuals may experience memory loss. Unconsciousness results at 10 A A.

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4. High-pressure nervous syndrome—At ambient pressures greater than 15–20 A A, high-pressure nervous syndrome (HPNS) can present as tremor, ataxia, nausea, and vomiting. HPNS can be prevented by slow compression and increasing the partial pressure o nitrogen or another narcotic gas to the breathing mix. 5. Pressure reversal o anesthesia—High pressures, in the absence o increased partial pressure o a narcotic gas, will decrease the e ectiveness o both inhaled and intravenous anesthetics. T e 50% e ective dose (ED 50) or most inhaled anesthetics is increased by 20% at 50 A A. Similarly, the ED50 or barbiturates, propo ol, and dexmedetomidine has been proven to increase in high pressure conditions. T is e ect is not seen at elevations used in HBO (3–6 A A). Regional anesthesia and intravenous agents are recommended rather than inhaled anesthetics. Gaseous anesthetics can in ltrate the chamber, potentially a ecting medical personnel. 6. E ects o hyperbaric exposure on drug disposition— T ere is no evidence o pharmacokinetic or pharmacodynamic alteration o anesthetics under hyperbaric conditions under 6 A A. T us, conventional dosing o parenteral anesthetics can be sa ely delivered during standard hyperbaric oxygen treatment schedules.

CLINICAL APPLICATIONS Hyperbaric oxygen was rst used to recompress divers su ering rom decompression sickness in the nineteenth century. In modern medicine, hyperbaric oxygen is utilized in a variety o clinical conditions and is reviewed regularly by the Undersea and Hyperbaric Medical Society. T is organization publicizes a comprehensive list o medical indications or hyperbaric medicine.

Carbon Monoxide Poisoning Hemoglobin binds with carbon monoxide with 250 times greater a nity than oxygen, orming carboxyhemoglobin (HbCO). T e result is a unctional anemia, lef shif in the oxygen–hemoglobin dissociation curve, and inactivation o 79

PART II Anesthesia echniques

cytochrome oxidase, leading to an increase in mixed venous oxygen saturation (SvO 2). Since PaO2 is normal, the carotid bodies do not increase minute ventilation until there is tissue hypoxia, which causes lactic acidosis, which eventually compensates with tachypnea. Symptoms include nausea, vomiting, headache, dizziness, myocardial ischemia, altered mental status, and most notably absence o cyanosis. Symptoms are worsened in older individuals and in prolonged carbon monoxide exposure. I these symptoms are reported in the setting o carbon monoxide exposure, elevated HbCO levels in arterial or venous blood gases, particularly co-oximetry, can be used to con rm the diagnosis. T e extent o HbCO elevation should not be the only actor in determining clinical severity. Also, HbCO can be alsely elevated in in ants secondary to the presence o HbF con ounding laboratory measurement. Oxygen supplementation is the treatment o choice. Increasing PaO 2 acilitates lowering levels o HbCO by reducing the HbCO hal -time in the blood and tissue. HBO reduces the HbCO hal -time to 15 minutes, versus 5 hours at room air and 1 hour at FIO2 = 1.0. HBO is indicated in cases o carbon monoxide poisoning when patients present with neurologic impairment, cardiac abnormalities (arrhythmias, ventricular dys unction, ischemic cardiomyopathy), or in HbCO greater than 25%. Women who are pregnant can present with symptoms o etal distress. T ese patients should receive HBO because the etuses have an increased susceptibility to carbon monoxide toxicity.

the lungs’ ability to exchange gases and should be avoided by monitoring the patient closely. HBO is the de nitive treatment or decompression sickness and arterial gas embolism. T e increase in ambient pressure results in a contraction o gases within the body. Neurologic impairment should improve with HBO i treatment is initiated promptly. Imaging is not always use ul in detecting intravascular gas and should not delay treatment i there is a high suspicion o air embolism.

Infections HBO has a direct antibacterial e ect on anaerobic bacteria. For example, the α-toxin production by the clostridium species is inhibited by increased PO 2. Additionally, HBO can reverse hypoxia-induced neutrophil unction, enhance macrophage expression, and also has anti-in ammatory e ects.

Arterial Oxygenation During therapeutic lung lavage, the gas exchange gradient on the a ected side is diminished. T us, O2 exchange is limited to the contralateral lung. HBO has been used to support arterial oxygenation o the contralateral lung during therapeutic lavage procedures.

Oxygen Transport in Severe Anemia Gas Embolism/Decompression Sickness Arterial gas embolism classically occurs in scuba divers during the ascent while breathing compressed gas. Iatrogenic causes that result in the introduction o air into arterial circulation include cardiopulmonary bypass, intra-arterial injection during diagnostic arteriogram, or during hemodialysis. Symptoms o arterial gas embolism include seizures, impaired consciousness, or hemiparesis. Venous gas embolism can also occur iatrogenically during surgical procedures, hemodialysis, hydrogen peroxide irrigation, or when central venous catheters are exposed to air openly. T ere are also cases reported in patients receiving high positive end expiratory pressure (PEEP). Venous gas emboli are typically ltered in pulmonary vasculature; however, in cases o large amounts o venous gas or in the presence o patent oramen ovale, patients can present with neurologic symptoms similarly to arterial gas embolism. T e bubbles increase endothelial permeability and promote the extravasation o uid. Decompression sickness results rom the ormation o bubbles in tissues, and presents with joint pain, bladder or bowel incontinence, vertigo, tinnitus, or hearing loss. Initial treatment includes oxygenation to enhance di usion o gases rom within the bubbles to the surrounding tissues and care ul uid resuscitation to replenish the intravascular volume in the setting o endothelial dys unction and extravasation o uid. Pulmonary edema would worsen

In cases o severe anemia when trans usion o blood products is not an immediate option, HBO can be used to increase arterial oxygen content to allow oxygenation o tissue. T is serves as a supportive option until trans usion becomes available.

THERAPEUTIC SYSTEMS Chambers 1. Multiplace chambers vary in size, but are generally large enough to accommodate multiple patients. T e entire chamber is lled with compressed air and the patient wears a ace mask or other delivery system breathing 100% oxygen . T is design allows immediate access to the patient because there is enough space or treatment personnel. 2. Monoplace chambers are single patient chambers made o plexiglass walls lled with compressed 100% oxygen. T ese chambers have a pressure limit o 3 A A and typically have limited treatment times. Because o their small size, providers do not have direct access to their patients in the rare instance o a severe complication. T e placement o an emergent airway is not possible in monoplace chambers. However, modern designs permit the use o intravenous uid administration, intravascular monitoring o hemodynamics, and mechanical ventilation.

CHAPTER 21

Treatment Schedules reatment schedules were developed to minimize side e ects o hyperbaric oxygen delivery. Limiting the dose and duration o hyperbaric oxygen exposure prevents oxygen toxicity, eliminates the need or medical sta to undergo decompression while caring or a patient, and improves patient monitoring. Overtime, patients can also develop aversion to con nement. T e original treatment tables were developed by navies to treat decompression sickness and gas embolism. T ese schedules include variations in partial pressure o O2, atmospheric pressure, and exposure time to optimize treatment while limiting adverse e ects. Each clinical indication has a preerred treatment approach. T e US Navy tables outline standard treatments o decompression sickness and occasionally gas embolism. T ese tables start with 2.8 A A with a gradual decompression to 1.9 A A while inspiring alterations in high Po 2 with air. Schedules used to treat li e-threatening anaerobic in ections are aimed at maximizing Pao 2 . T e Duke therapeutic protocol or clostridial myonecrosis has the patient at 3 A A or 85 minutes, then 33 minutes o decompression at 1.3 A A. Patients are given 100% O 2 with multiple 5 minute breaks to prevent toxicity. Carbon monoxide treatments vary, but typically involve the use o 3 A A (60 minutes) or the initial treatment ollowed by 2 A A or an additional 60 minutes.

ADVERSE REACTIONS Oxygen Toxicity Oxygen toxicity is directly related to the PO 2 o the inspired gas. T e lungs are not the only organ at risk during hyperbaric therapy; the eyes and central nervous system (CNS) are also prone to toxicity. Adverse pulmonary reactions can present as chest pain, cough, or throat irritation. In rare cases o prolonged exposure, patients can develop reductions in vital capacity and ARDS. oxicity is minimized by allowing 5 minute “air breaks” during HBO . CNS symptoms o toxicity include nausea, numbness, and twitching. Strange ol actory, acoustic, or gustatory sensations have also been reported. Severe cases can present as tonic-clonic seizures. T e risk or seizure increases when hyperbaric therapy is administered or acute carbon monoxide treatment. Initial treatment o hyperoxic seizures includes reducing PO 2 in the chamber until convulsions terminate.

Barotrauma T e expansion o air within the paranasal sinuses and middle ear during hyperbaric therapy can cause tissue disruption and hemorrhage i the air becomes entrapped. Maneuvers such as Valsalva and jaw thrust can help alleviate some o the discomort o the middle ear. Patients with past head and neck radiation exposure are at increased risk and may require topical

Hyperbaric Oxygen and Anesthesia Care

nasoconstrictors or tympanostomy tube placement or ongoing HBO . Pulmonary barotrauma during decompression can cause alveolar rupture, leading to pneumothorax or pneumomediastinum. T e practice o slow decompression has made pulmonary barotraumas during HBO exceedingly rare.

ANESTHETIC CONCERNS 1. Patient monitoring—While conventional sphygmomanometers can be used to accurately monitor a patient’s blood pressure while in a hyperbaric oxygen chamber, electrocardiogram (EKG) and invasive intravascular pressure transducers must be channeled to a preampli er outside o the chamber. Pressure bags must be repressurized during compression and vented be ore decompression. Also, pulmonary artery catheter balloon ports need to be opened to ambient air during compression and decompression. 2. Intravenous uid administration—Intravenous uids can be administered during HBO . In multiplace chambers, the gas within the drip chamber can expand or contract depending on the changes in ambient pressure within the chamber. During decompression, expanding air can be pushed into the intravenous line. Glass bottles can easily rupture during hyperbaric oxygen treatment, so they are avoided. In monoplace chambers, in usion pumps must be able to handle pressure gradients o 3 A A as the tubing is channeled through the chamber well. 3. Blood gas assessment—Arterial blood gas samples are typically inaccurate unless obtained rom within the hyperbaric oxygen chamber with appropriately calibrated analyzers. T us, venous blood gas samples are used to monitor tissue oxygenation during HBO . Low venous PO 2 (P VO 2), in the absence o a lef -to-right shunt, would indicate insu cient tissue per usion despite hyperbaric therapy. CO 2 does not typically change during HBO , unless the patient is receiving mechanical ventilation. 4. Ventilator management—Ventilator machines are compact in design with no electrical requirements or ammable components. T ese machines need to have the capability to deliver a wide range o volumes, respiratory rates, provide PEEP, and work on intermittent and ventilation assist modes. T e anesthesia provider must also adjust the endotracheal tube cu volumes to account or associated gas volume changes or ll the balloon with water. Increased gas density and decreased lung conductance results in increased pulmonary resistance and increased dead physiologic dead space. Ventilator settings must account or this dead space; otherwise, the patient will have increased PaCO 2 and subsequent respiratory acidosis. 5. Sa ety and f re control—Fires in the setting o elevated ambient pressure are devastating. Because o increased oxygen, a small spark can escalate quickly and almost always results in atality. Sources o heat or spark should

PART II Anesthesia echniques

be minimized or avoided when possible. De brillators can cause re i there are combustible materials near the paddles during use. o prevent this, conductive gel should always be used to reduce resistance between the skin and the electrodes. De brillation should never be used inside a monoplace chamber when compressed O 2 is present. Ventilators with high O 2 buildup or leakage can increase risk o re and should be purged with nitrogen or another inert gas. Other precautions include controlling multiplace chamber O 2 concentrations and having a chamber re extinguisher available. 6. Patient obstacles—I HBO is indicated, providers will need to assess each case to ensure that treatment is optimized or the patient. Patients with lung disease/injury (unable to reach therapeutic PaO 2), claustrophobia, or those unable to equalize middle ear pressures will need to be medically optimized be ore going orward with increased pressure treatment. Patients with pulmonary bullae or blebs could experience barotrauma, resulting in worsening o their disease. T ere ore, it is a relative contraindication to HBO . Visual acuity will need to be monitored

in patients undergoing 20–30 treatments as these patients are susceptible to hyperbaric induced myopia. 7. Delivery o anesthesia—Increased ambient pressure is a challenging setting or the delivery o anesthesia. When delivering inhaled anesthetics, the concentration may be variable but the partial pressure remains constant. T ere ore, there is no need to adjust the dose under conditions o changing ambient pressure. Fluorinated anesthetics can be combustible at 1 A A. Sevo urane and iso urane have been tested and are considered sa e rom combustion up to 3 A A in 100% O 2 . Inhaled anesthetics can escape the delivery system and pollute the chamber, endangering care personnel. Because o these problems, intravenous anesthetics and regional anesthesia are both recommended when possible. Intravenous anesthetics dosing does not need to be adjusted under conditions o usual increased pressure treatment tables (up to 3 A A) and regional anesthesia is also considered to be sa e and e ective under these conditions. T e use o regional anesthesia may also prevent the use o mechanical ventilation in certain patients.

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High-Altitude Anesthesia Carlton Q. Brown, MD

Decre sed tmospheric pressure t ltitude h s pro ound e ects on hum n physiology nd nesthetic delivery. Approxim tely 140 million people worldwide live t ltitudes bove 2500 m (8000 ). T ese residents h ve the usu l needs or surgic l nd nesthesi c re in their n tive loc lities. Addition lly, millions o people tr nsiently visit high ltitudes. Anesthesiology providers re sked to support milit ry oper tions, vi tion, mount in climbing expeditions, nd hum nit ri n missions t extreme ltitudes. S e nd e ective nesthesi c re t high ltitude requires n underst nding o the norm l nd p thologic l e ects o ltitude nd n ppreci tion or the nesthetic ch llenges in this environment.

PHYSIOLOGY Atmospheric pressure decre ses nonline rly with incre se in ltitude. H l o the tmosphere is below 18,000 t nd the rem inder is up to >100,000 t. Incre sed ltitudes re o ten c tegorized to denote their incre sing e ect o physiology: • • •

“High ltitude” begins t 1500 m (~5000 ) bove se level. “Very high ltitude” begins t 3500 m (~11,500 ) bove se level. “Extreme ltitude” begins t 5500 m (~18,000 ) bove se level.

Anesthetics delivered between 5000 nd 11,500 require only modest ch nges rom st nd rd se -level pr ctices. Anesthetic c re bove 11,500 . becomes incre singly problemtic. Fr ction l tmospheric oxygen concentr tion rem ins pproxim tely 21% t ll ltitudes. As tmospheric pressure decre ses with elev tion, the bsolute p rti l pressure o oxygen in ir declines ccording to D lton’s L w, which st tes the sum o ll p rti l pressures equ ls the tot l pressure. T e alveolar gas equation de nes p rti l pressure or lveol r oxygen b sed on b rometric pressure: Pa O2 = FiO2 (P tm – Ph 2o ) – (PaCO2/RQ)

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where PAO 2 is the p rti l pressure oxygen in the lveolus (mmHg), FiO 2 is the r ction l concentr tion o oxygen in inh led g s, Pat m is the b rometric ( tmospheric) pressure (mmHg), PH 2O is the v por pressure o w ter t body temper ture (47 mmHg), PaCO 2 is the p rti l pressure o CO 2 in the lveolus (mmHg), nd RQ is the respir tory quotient (moles CO 2 produced per moles O 2 consumed, which is typic lly bout 0.82 or norm l diet). Using the lveol r g s equ tion, the e ects o ltitude nd CO 2 on lveol r (PAO 2) nd rteri l oxygen (PaO 2) become very evident ( ble 22-1; Figure 22-1). With hyperventil tion resulting in P CO 2 = 20 mmHg, t 20,000 nd Pat m = 364 mmHg, PAO 2 is 42 mmHg nd S O 2 is 78%.

ADAPTATION R pid scent to high ltitude without dequ te cclim tiz tion ddition lly risks ltitude-rel ted illnesses. Acute d pt tion to high ltitude involves hyperventil tion nd incre sed c rdi c output (CO). As hyperventil tion is the prim ry me ns o cute d pt tion to scent, the bility to r pidly toler te hypob ric environments depends l rgely on su cient pulmon ry reserve. Symp thetic sign ling rom hypoxemi , p rticul rly through n incre sed he rt r te, incre ses CO. T is cute response m y be detriment l to individu ls with

TABLE 22-1

Altitude E ects on Partial Pressure o Oxygen and Saturation Altitude ( t)

Patm (mmHg)

PAO2 (mmHg)*

SaO2 (%)*

0 (at sea level)

760

101

5000

632

10,000

522

15,000

438

20,000

364

*Calculations assume no compensation with hyperventilation; hence, PaCO2 = 40 mmHg.

PART II Anesthesi

echniques

100

5000 ft 8000 ft 15,000 ft 20,000 ft

25,000 ft

29,029 ft

50 40

(

)

30 20 10 0 25

50 P O 2 (torr)

100

FIGURE 22-1

Hemoglobin saturation declines rapidly with increasing altitude. (Adapted with permission from Sutton JR, Reeves JT, Wagner PD, et al. Operation Everest II: Oxygen transport during exercise at extreme simulated altitude. J Appl Physiol (1985). 1988 Apr;64(4):1309-1321.)

ischemic or v lvul r c rdi c dise se or with preexisting pulmon ry hypertension. Longer term d pt tion occurs over d ys to weeks. Genetic di erences modi y d ptive responses. Mech nisms include the ollowing: • • • •

Incre sed 2,3-DPG levels due to hypoxic stress, shi ing the O 2 –Hgb dissoci tion curve tow rd the right, nd cilit ting O 2 unlo ding to tissues Incre sed erythropoiesis—polycythemi tow rd >50% Hct Incre sed CO second ry to hypoxemi Ren l compens tion or the lk losis o hypoc rbi — l rgely bic rbon te w sting to improve the le -shi ed O 2 –Hgb dissoci tion curve

PATHOPHYSIOLOGY Risk ctors th t m y contribute to cute hypob ric illnesses include overexertion, poor hydr tion, nd young ge, nd m y ect either the provider or the p tient. Prolonged emergence, re r ctory hypoxemi , nd other dverse nesthetic p tient outcomes m y be expl ined by these mech nisms. Providers imp ired by these conditions constitute subst nti l h z rd to their p tients s cerebr l hypoxi imp irs judgment. Acute high- ltitude exposure c n c use sever l orms o illness, overl pping in both p thophysiology nd clinic l present tion: 1. Acute mountain sickness (AMS)—AMS is the mildest mild orm o hypob ric illness. E rly symptoms (12–24 h): he d che re r ctory to st nd rd n lgesics,

n use , norexi , sleep disturb nces, nd peripher l edem . Judgment m y be imp ired. L te symptoms: shortness o bre th, snoring, vomiting, h llucin tions, nd cognitive imp irment. Adv nced symptoms include severe dyspne , cy nosis, decre sed S O 2 , nd t xi . I severe, de nitive tre tment is descent. O en, descent o only 500–1000 m le ds to complete symptom tic resolution. Most symptoms resolve in sever l d ys even t ltitude. Other recovery str tegies include rest, hydr tion, n lgesics, cet zol mide, dex meth sone, nd oxygen ther py. 2. High-altitude pulmonary edema (HAPE)—HAPE is m lign nt orm o AMS with simil r e rly symptoms nd is li e-thre tening. It m y occur in he lthy individu ls er r pid scent bove 2500 m (8200 ). It is thought to be orm o right-he rt ilure c used by ex gger ted hypoxemic pulmon ry v soconstriction nd high CO. Right tri l nd pulmon ry rtery pressures re elev ted. I PFO is present, tri l f ow revers l m y occur. Alter tions o pulmon ry c pill ry perme bility m y lso be involved. An individu l with previous episode o HAPE m y be p rticul rly susceptible to this condition. Signs nd symptoms include dyspne , t chypne , chest p in, r les, t chyc rdi , dry cough, ollowed by the production o pink rothy sputum. Respir tory ilure nd de th c n quickly ensue. CXR shows p tchy in ltr tes, which sp re lung b ses nd costophrenic ngles. Elev ted pulmon ry rtery pressure second ry to hypoxi is evident on echo. ECG shows the right he rt str in with norm l LV unction. re tment o HAPE requires r pid descent to lower ltitude, supplement l oxygen, nd PEEP or BiPAP, i v il ble. Sever l medic tions m y be help ul s well, such s morphine ( lthough controversi l due to depression o ventil tion), ni edipine, nitric oxide, hydr l zine, phentol mine, nd silden l. 3. High-altitude cerebral edema (HACE)—HACE is nother severe orm o AMS nd is li e-thre tening. It is thought to be due to incre sed cerebr l blood f ow nd lter tions in blood–br in b rrier perme bility due to severe hypoxemi . E rly symptoms re simil r to AMS but progress to gross CNS dys unction. Judgment is severely imp ired. E rly signs nd symptoms include he d che, norexi , n use , emesis, p pilledem , retin l hemorrh ge, photophobi , tigue, irrit bility, nd decre sed soci liz tion; nd l te signs nd symptoms include t xi , irr tion lity, h llucin tions, visu l disturb nces, oc l neurologic l de cits, nd bnorm l ref exes. Di gnosis m y be del yed due to concurrent HAPE symptoms nd de th m y be imminent when symptoms o HACE become severe. Lumb r puncture m y show m rkedly elev ted CSF pressure. C sc n m y be suggestive o br in edem , p rticul rly in the corpus c llosum. re tment requires n immedi te, r pid descent nd oxygen ther py i pulmon ry symptoms re present. Ph rm cologic options include dex meth sone nd diuretics ( lthough m y worsen dehydr tion).

CHAPTER 22

HYPOTHERMIC INJURIES AND COMPLICATIONS Ambient temper ture decre ses with ltitude. T e “st nd rd l pse r te” is 3.5°F per 1000 o ltitude. By ex mple, i n re is 72°F t se level, it will be simult neously 40°F colder (i.e., 32°F) t 11,500 . W rming o severely hypothermic p tients should be completed, i possible, be ore ttempting surgic l or nesthetic intervention. wo common cold-induced injuries include rostbite, or cold-induced tissue d m ge, nd hypothermi , de ned s the core temper ture below 35°C. Rew rming m y be p ssive or ctive. Active rew rming m y include extern l sources, such s w ter immersion, r di nt he t, orced w rm ir he ting bl nkets, nd intern l techniques, such s he ted IV f uids, body c vity l v ge, nd c rdiopulmon ry byp ss solution. Resuscit tion with norm l s line inste d o l ct ted ringers ccounts or the hypothermic liver’s ine cient met bolism o l ct te. R pid rew rming should be pursued with c rdiov scul r inst bility, moder te or severe hypothermi (13 Hz), Delta (75 pV

REM s le e p: low volta ge —ra ndom, fa s t with s awtooth wave s

S awtooth wave s

FIGURE 25-2

EEG wave orms. (Used with permission rom Lawrence W. Brown, MD., Pediatric Neuropsychiatry Program Co-Director, Pediatric Regional Epilepsy Program The Children’s Hospital o Philadelphia. Power point presentation, Sleep and Epilepsy in Childhood.)

PERIOPERATIVE EEG CHANGES Hypoxia and Ischemia As cellular oxygen supply to an area o the cortex is restricted, metabolic activity is also reduced. T is change is re ected in the reduction o the high- requency component o the EEG with a resultant increase in the low- requency component. T ere ore, occlusion o artery, hypotension, anemia, and metabolic inhibitions (such as cyanide poisoning) all will cause these EEG changes.

Hypothermia Although hypothermia reduces the cerebral metabolic rate o oxygen consumption at a rate o 7.5% or every 1°C, EEG changes does not correlate consistently with temperature changes.

TABLE 25-1

Components of the EEG

Rhythms

Alpha (8–13 Hz) Beta (>13 Hz) Delta (14 Hz beta waves. Within 2 seconds, 2–3 Hz delta waves appear and continue or 1–2 minutes. Finally, beta waves incompletely replace the delta waves in the next 5 minutes. Overall, a er induction, there is a marked depression o neuronal activity in the EEG. Subsequently, burst suppression and isoelectric EEG ollow with increased doses. T e dose to achieve burst suppression ranges rom 40 to 200 mg.

Nitrous Oxide Above 25% concentration, nitrous oxide produces dosedependent changes in the EEG. Alpha activity is diminished and then lost at 50% concentrations. At these levels, the EEG consists o 4–8 Hz waves with ast (20–30 Hz) superimposed activity. T ere is signi cant individual variation.

Opioids Fentanyl, su entanyl, and al entanyl produce progressive, dose-dependent slowing o EEG waves until large-amplitude, low- requency waves ( 33°C should not be rewarmed. Major surgery within 14 days, systemic in ection, coma rom other causes and known bleeding diathesis, or active ongoing bleeding are exclusion criteria or therapeutic hypothermia. reatment at 32–34°C or 24 hours should commence within 6 hours o arrest or those who have adequate, unsupported blood pressure and or those who are comatose. Rewarming should proceed over 8 hours at 0.3–0.5°C/h.

PROGNOSIS Prognosis depends upon the etiology o the impaired consciousness. Residual anesthesia or other sedatives, therapeutic hypothermia, neuromuscular blockers, and metabolic abnormalities such as hypoglycemia, uremia, and liver ailure can a ect the physical exam and make prognosis based on physical exam alone more dif cult. Predicting outcome based on physical exam or anoxic coma a er cardiac arrest has been studied. Myoclonic movements and seizures are common. Lack o pupillary re exes, corneal re exes, and no response to pain ul stimuli, GCS < 4, and neuron-speci c enolase level o > 33 µg/L at 72 hours are associated with a poor prognosis.

Central Nervous System Drug Intoxication

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Charles Baysinger and Jef rey Berger, MD, MBA

Acute poisoning is a common hospital emergency, accounting or 5%–10% o medical admissions. T ere are speci c antidotes to a variety o toxins available; however, limited evidence exists on the acute poisoning management. T is chapter seeks to summarize clinical presentations and proper management o patients who present obtunded, acutely poisoned, and in need o emergent medical treatment.

CLINICAL PRESENTATION T e basic steps or the management o a poison victim consist o initial resuscitation and stabilization, diagnosis, gastrointestinal (GI) decontamination and toxin elimination, initiation o antidotes and interventions, and supportive care. While management considerations are discussed separately, concurrent initiation is o en required. In acutely poisoned patients, advanced cardiac li e support (ACLS) protocols should be initiated, i necessary. When permitted, a complete history should be obtained ocusing on the substances involved, the route o administration, potential dosage used, and timing o exposure. Also, special attention should be paid to assess the chronicity o use prior to overdose, and whether the medication was an immediate or time-released ormulation. T e clinician should also assess the patient’s baseline mental and health status. A detailed review o the patient’s medications should be completed and corroborated. Physical exam should ocus on neurologic ndings that may reveal etiology o toxicity. Many substances a ect the autonomic nervous system, and may be responsible or hemodynamic instability. I possible, caution should be taken to avoid initiating therapeutic interventions that may change the neurologic examination. Frequent re-evaluation is necessary to determine the e cacy o interventions as well as to discover late sequelae o intoxication. Exam should include assessment o extraocular muscles, pupil reactivity, and motor ref exes to narrow down the di erential diagnosis o overdose. For example, pupils remain reactive to light with cocaine, but do not with diphenhydramine overdose. Multiple toxic ingestions complicate evaluation.

MANAGEMENT Gastrointestinal Decontamination Historically, Ipecac ormulations have been used to induce emesis. By inducing vomiting, patients evacuate undigested toxins. However, this is no longer done or multiple reasons. First, inducing prolonged bouts o emesis prevents the clinician rom administering activated charcoal early in treatment. Also, Ipecac is now thought to be ine ective at removing toxic material rom the stomach, and can increase the risk o gastric aspiration. Gastric lavage is ine ective or similar reasons. T ere is also a risk that lavage will propel toxins urther into the intestines. Gastric lavage also delays the use o activated charcoal, which has been shown to have the most e cacy in gut decontamination. Activated charcoal (AC) remains the rst-line treatment or acute poisonings. AC is indicated or GI ingestions presenting within 1 hour; however, it should not be given i the patient is obtunded and their airway is not protected. Whole bowel irrigation, or “bowel preparation” with polyethylene glycol, a non-absorbable solution that increases the osmotic gradient in the GI tract and orces water to stay in the GI lumen, causes a cathartic expulsion o ecal contents. Whole bowel irrigation may be considered to treat large ingestions o iron, lithium, and sustained release medications.

Drug Elimination T e two main therapies to enhance drug elimination include urinary alkalinization and extracorporeal techniques such as hemodialysis, plasmapheresis, and hemoper usion. Urinary alkalinization is considered the therapy o choice or severe salicylate toxicity. Additionally, it can be used in phenobarbital, chlorpropamide, and methotrexate toxicity. Factors that may aid in the decision to use extracorporeal techniques are as ollows: • •

Failure to respond to standard therapy Signs o severe toxicity 119

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• • •

PART III Organ-Based Advanced Sciences

Potential o the target drug to be removed rom the body via an extracorporeal technique Chances o increase o the total body clearance o the drug by at least 30% Impairment o the normal route o elimination

Limited data exists on drug clearance by these methods; there ore, knowledge o the pharmacokinetic properties o the drug is imperative. ypically, GI decontamination and supportive therapy are the only therapies required, but it may be necessary to include these alternate means o drug elimination in exceptional cases o severe poisoning.

Lipid Emulsion Therapy IV lipid emulsion is an e ective treatment or cardiovascular collapse due to local anesthetic toxicity. However, the mechanism behind the drug’s e cacy is not well de ned. T e lipid emulsion is thought to act as a “lipid sink,” pulling lipophilic drugs out o the target tissue and back into the serum. Based on this proposed mechanism o action, IV lipid emulsion is used or acute toxicities due to lipophilic substances such as local anesthetics. Acute pancreatitis may complicate IV lipid emulsion therapy; hence, care should be taken with administration.

SPECIFIC PHARMACOLOGIC AGENTS Amphetamines In a mild overdose, symptoms include anxiety, dry mouth, and diaphoresis, while symptoms in a severe overdose include tachycardia, hypertonia, hyperref exia, hallucinations, and hypertension. Patients may also present with supraventricular dysrhythmias leading to coma, convulsions, and hemorrhagic stroke. Additionally, electrolyte disturbances and hyperthermia may develop. Increased body temperature can lead to secondary sequelae such as rhabdomyolysis, metabolic acidosis, acute renal ailure, and disseminated intravascular coagulation (DIC), which may ultimately lead to multiple organ ailure and death. reatment or amphetamine overdose is symptomatic. AC can be considered up to 1 hour post ingestion, and benzodiazepines are generally used i the patient is agitated or psychotic. In addition to calming, benzodiazepines may centrally lower the blood pressure, heart rate, and body temperature. I the patient remains hypertensive, antihypertensive therapy should be initiated with either alpha-blockers or direct vasodilators. Beta-blockers risk unopposed alpha stimulation, which can potentiate hypertensive crisis and should there ore be avoided. Serum electrolytes should be measured and hypertonic saline can be considered or severe hyponatremia due to excessive water intake. Hyperthermia should be actively treated.

Benzodiazepines Benzodiazepine overdose is seldom severe without other CNS depressant drug ingestion or comorbidities. ypically, patients present with drowsiness, dysarthria, ataxia, and nystagmus symptoms. Hypotension and bradycardia may also be present. While paradoxical agitation and con usion can occur, this presentation is rare. A negative screening test does not rule out ingestion; consequently, history and examination ndings are vital. reatment is supportive with resuscitation as necessary. AC accomplishes GI decontamination with recent ingestion. Flumazenil, a competitive benzodiazepine receptor antagonist, reverses the e ects o benzodiazepines. Considering the relatively short hal -li e o f umazenil when compared to benzodiazepines, redosing may be necessary. Caution should be used when using f umazenil, as it has been associated with seizures in patients with chronic benzodiazepine or concomitant tricyclic antidepressant use. Slow titration o f umazenil by 0.1 mg/min to a maximum total dose o 1 mg is warranted.

Beta Blockers Clinical eatures o beta-adrenergic receptor blocker toxicity include hypotension, and atrioventricular (AV) conduction abnormalities. Lipophilic beta-blockers (propranolol, metoprolol, acebutolol, and timolol) have the potential to cause delirium, coma, and seizures as well. AV block can range rom a prolonged PR interval to complete heart block and asystole. Initial treatment should begin with GI decontamination. AC should be given with early presentation, and multiple doses may be warranted or extended release ingestions. T e primary goal is to reverse hypotension, initially with IV f uids. Caution should be used with IV f uids administration due to negative inotropic e ects o beta-blockers on myocardial contractility. Although atropine improves bradycardia and hypotension, it is generally considered ine ective in the setting o beta-blocker or calcium channel blocker toxicity. IV glucagon is considered the best next step, with 2–5 mg IV (up to 10 mg IV push is acceptable, i necessary). I the patient responds, a continuous in usion o 2–10 mg/h should be initiated to account or glucagon’s short hal -li e. Insulin and glucose should also be administered to maintain euglycemia during treatment. Calcium salts should be considered next i the patient’s hypotension is re ractory to glucagon. Calcium chloride 10% is pre erred; however, calcium gluconate 10% can also be used. Inotropes should next be considered; tachyarrhythmias may occur as large doses o inotropes may be required to overcome the beta-adrenergic blockade.

Butyrophenones (Neuroleptics) Clinical eatures associated with neuroleptic toxicity are drowsiness and extrapyramidal symptoms. Hypotension, Q prolongation, arrhythmias, and convulsions may also occur. reatment is initiated with GI decontamination i ingestion was within 1 hour. Otherwise, the patient is observed and only

CHAPTER 33

supportive treatment is necessary. Extrapyramidal symptoms can be treated with IV/IM procyclidine 5–10 mg or oral diazepam 10–20 mg.

Calcium Channel Blockers Hypotension, nausea, and varying conduction abnormalities are the predominant eatures o calcium channel blocker toxicity. First-degree, Wenckebach, and third-degree AV blocks have all been associated along with junctional rhythm and AV dissociation. Patients are at increased risk or tissue ischemia and metabolic acidosis secondary to decreased cardiac output and consequent tissue hypoper usion. CNS symptoms include lethargy, con usion, and coma. Hyperglycemia may occur due to decreased insulin secretion, and insulin resistance may be a sign o severe toxicity. Additionally, severe toxicity may still occur in those that appear well i sustained release preparations have been ingested. reatment includes AC and is otherwise supportive. T e risk that decreased cardiac output may cause mesenteric ischemia and diminished bowel motility should limit AC to one dose. IV calcium chloride, maximum 3 mmol/L serum level, is given to patients whose hypotension is re ractory to f uid resuscitation. Atropine has been used or bradycardia; however, its use is controversial and may not e ectively raise blood pressure. Hyperinsulinemic-euglycemic therapy is indicated in patients whose hypotension remains re ractory to the above therapies. An initial bolus o 1 unit/kg short-acting insulin is administered with 25–50 mL o D50 solution, which is ollowed by a 0.5–2 unit/kg/h short-acting insulin. Higher doses may be necessary, and serum glucose and potassium should be monitored and replaced as necessary.

Carbamazepine Drug metabolism o carbamazepine is slow and unpredictable. Maximum drug levels may not be seen until 72 hours a er ingestion. While drug levels o both carbamazepine and its active metabolites can be measured, these levels may not correlate well with toxicity. Clinical eatures o toxicity include nystagmus, ataxia, tremor, with intermittent coma and tachycardia or bradycardia in severe overdose. reatment relies on multiple doses o AC, which may help with elimination, even i administered up to several hours a er ingestion.

Carbon Monoxide T e diagnosis o carbon monoxide (CO) toxicity relies on a high level o suspicion, as signs and symptoms are nonspeci c. Sources o CO poisoning are exhaust umes, gasolinepowered generators, poorly unctioning heating systems, and inhaled smoke. Clinical eatures o toxicity involve headache, nausea, vomiting, hypoxia, con usion, angina, arrhythmias, syncope, and seizures. T e classic ndings o “cherry red lips” and retinal hemorrhages are uncommon, whereas hypoxia is

Central Nervous System Drug Intoxication

121

more common. Neurological sequelae also occur, and include seizures and coma. Loss o consciousness may result rom cellular hypoxia as a sign o severe toxicity. While the a nity o CO or hemoglobin is approximately 240–250 times that o oxygen, one cannot reliably use carboxyhemoglobin (COHb) as a diagnostic test. Levels may be as high as 10% in asymptomatic smokers; however, COHb levels greater than 40% are associated with signi cant toxicity. reatment involves basic resuscitation and 100% highf ow oxygen, which should be continued until the COHb level is less than 5%. It is important to note that pulse oximetry readings will overestimate the degree o hypoxia, reading 100% despite signi cant tissue hypoxia. Hyperbaric oxygen therapy can be used, and has been ound to shorten the hal li e o COHb by more than 100% oxygen. Re ractory toxicity, coma, loss o consciousness, neurologic ndings other than headache, pregnancy with COHb > 15%, signs o cardiac ischemia, and a history o cardiac disease with COHb > 20% are the suggested indications or hyperbaric oxygen therapy.

Cocaine Clinical eatures o cocaine overdose are similar to those o amphetamine overdose, including tachycardia, mydriasis, hypertension, hyperthermia, diaphoresis, euphoria, and agitation. T ere is increased risk or vasospasm-induced myocardial ischemia or cerebral in arction days a er cocaine intoxication. “Body packers” are not only prone to acute, li ethreatening systemic toxicity, but they are also at risk or small bowel obstruction i cocaine packets rupture. Metabolites are detectable in urine toxicology screening tests 24–36 hours a er use. reatment is mainly symptomatic. Benzodiazepines should be used to reduce agitation. reat myocardial ischemia with aspirin, but re rain rom using low-molecular-weightheparin or glycoprotein IIb/IIIa inhibitors due to hypertensive cerebral bleeding risk. Vasodilators such as sublingual nitrates should be administered early, which may reduce the risk o coronary vasospasm. I warranted, reper usion therapy with percutaneous coronary interventions is acceptable. Cerebral complications should be managed as indicated. For example, seizures should be managed with benzodiazepines. Lastly, any hyperthermic episodes should be managed with active cooling measures. Conservative management is suggested or symptomatic “body packers.” AC or whole bowel irrigation may be used. Surgery may be necessary or those demonstrating signs o acute toxicity, GI per oration, or bowel obstruction.

Cyanide Cyanide toxicity is rare, but rapidly atal and clinical suspicion to diagnose. Since rapid are not widely available, history is critical. sure may occur a er incomplete combustion

requires a high cyanide assays Cyanide expoo carbon- and

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nitrogen-containing compounds, and is associated with industrial manu acturing processes such as electroplating, metal re ning, photography, umigation, and precious metal extraction. Iatrogenic cyanide intoxication may occur when high doses o nitroprusside are used. Clinical symptoms o cyanide poisoning include loss o consciousness, anion gap metabolic acidosis, cardiopulmonary ailure, and CNS symptoms. CNS symptoms include headache, anxiety, agitation, seizures, con usion, and coma. Nausea and vomiting may also occur; however, the “bitter almond” odor o en described with cyanide toxicity is rarely experienced. Patients can initially present with bradycardia and hypertension progressing to hypotension with ref ex tachycardia with ultimate hypotension and bradycardia be ore asystole. reatment begins with amyl nitrate and 100% oxygen contained in “cyanide antidote kits.” A cyanide level may be obtained; however, results will o en be pending during acute management. A er initial treatment, patients with severe symptoms need dicobalt edetate 300 mg IV over 1 minute ollowed by 50 mL o D50. Another dose o 300 mg dicobalt edetate can be used i there is no response initially. I patients have mild or moderate eatures o toxicity, they should be given sodium thiosulphate 12.5 g IV over 10 minutes. An alternative or moderate toxicity is hydroxocobalamin 5 g IV, a vitamin B12 precursor, pushed over 15 minutes, which can be used i patients describe smoke inhalation where cyanide content is unknown.

Gamma Hydroxybutyric Acid (GHB) GHB is a treatment or narcolepsy. However, it is commonly used as a date rape drug, and has also been marketed as a supplement. Signs o overdose include coma, convulsions, bradycardia, hypotension, respiratory distress, and vomiting. Other symptoms include amnesia, tremors, myoclonus, hypotonia, hypothermia, decreased cardiac output, bradycardia, and coma. CNS depressants, such as alcohol, can potentiate the e ects o toxicity. GHB is not routinely collected as part o toxicology screens, but can be ordered separately as gas chromatography or mass spectroscopy. Diagnosis is typically elicited by clinical course and history elicited. Most patients who present to the hospital only require supportive care. Withdrawal symptoms ollowing requent, high doses o GHB (every 1–3 hours) consist o anxiety, insomnia, nausea, vomiting, and tremors. T ese mild symptoms may progress to delirium with mild autonomic instability within 6 hours o the last dose. Withdrawal may last as long as 2 weeks, and benzodiazepines are the initial choice in management, with propo ol and barbiturates second line.

Isoniazid Coma, respiratory depression, hypotension, and convulsions describe isoniazid toxicity. Convulsions are re ractory to standard treatments and associated with doses exceeding

80 mg/kg. AC can be used or ingestions seen within 1 hour. Benzodiazepines can be used to manage initial convulsions. I convulsions are re ractory to diazepam 10–20 mg IV or lorazepam 4 mg IV, patients should be treated with 1 g o pyridoxine per 1 g o isoniazid ingested; however, 5 g should not be exceeded.

Lithium Lithium, a treatment or bipolar and other psychiatric disorders, has a narrow therapeutic index. Patients on drugs that increase lithium reabsorption (ACE-Inhibitors, thiazides, NSAIDs) or with sodium restriction, volume depletion, and intrinsic renal ailure are at increased risk o lithium toxicity. Lithium levels do not correlate with the degree o toxicity. In mild toxicity, patients experience nausea, vomiting, ne tremor, polyuria, and weakness. In moderate toxicity, conusion, urinary and ecal incontinence, hypernatremia, and hyperref exia occur. In severe toxicity, patients present with cardiac arrhythmias, convulsions, renal ailure, and coma. In acute ingestions, GI symptoms occur rst, and CNS symptoms develop later as drug redistribution among di erent tissue layers occurs. In chronic ingestions, neurologic mani estations are typically the primary presenting symptom. With chronic lithium use, drug concentrations should be ordered immediately, and repeated every 4–6 hours. AC does not absorb lithium, and urinary alkalinization does not increase the amount o drug renally cleared. However, isotonic saline should be administered to maintain adequate kidney per usion and urinary output. Diuretics should be avoided as they can worsen lithium toxicity. With severe toxicity, hemodialysis is warranted i the patient has renal dys unction, severe CNS dys unction, a lithium level above 4 mmol/L acutely and 2.5 mmol/L in chronic overdoses, or i the patient cannot tolerate f uid replacement.

Methanol/Ethylene Glycol Ethylene glycol is ound in many anti reeze ormulations, and is metabolized to glycolic and oxalic acid by alcohol dehydrogenase. Methanol is ound in washer f uid, solvents, and homemade alcohol. Alcohol dehydrogenase metabolizes methanol into ormaldehyde, which is urther metabolized into ormic acid by aldehyde dehydrogenase. While ormic acid is responsible or the ocular impairment typically associated with toxicity, lactic acid is also produced, which is responsible or the metabolic disturbances commonly seen. In acute toxicity, both methanol and ethylene glycol cause cardiopulmonary, CNS, and electrolyte disturbances. Both substances cause an anion gap metabolic acidosis that increases and an elevated osmolar gap that resolves as the substances are metabolized. Serum levels o methanol and ethylene glycol should be ordered: levels above 50 mg/dL are signi cant, and survival correlates with the degree o disturbance o pH, anion gap, and serum bicarbonate. Symptoms o ethylene glycol toxicity include transient insobriety, acidosis, CNS depression, coma, decreased

CHAPTER 33

ref exes, intermittent seizures, tachycardia, hypertension, oliguria, f ank pain, acute tubular necrosis, and renal ailure. Methanol toxicity leads to abdominal pain, nausea, vomiting, dizziness, headache, seizures, blurred vision, photophobia, retinal edema, and blindness. AC is ine ective at absorbing either methanol or ethylene glycol. Ethanol can be used to treat toxic ingestion; however, omepizole is pre erred as it avoids CNS depression.

Opioids Opioid intoxication presents with pinpoint pupils, drowsiness, and shallow breathing ultimately leading to respiratory ailure. Additionally, hypotension, pulmonary edema, GI ileus, nausea, vomiting, and pruritus may occur. Bronchospasm is associated with heroin intoxication and methadone may cause Q prolongation and ventricular arrhythmias. While the degree o toxicity depends on agent potency, treatment is similar regardless o the opioid. Ventilatory support, correction o the patient’s hypotension, and reversal o opioid toxicity with an antagonist are immediate priorities. Naloxone is the reversal agent o choice, and can be administered intravenously, intramuscularly, sublingually, and via an endotracheal tube. T e initial dose typically ranges rom 0.02 to 0.4 mg, with the lower doses considered or chronic opioid abusers to avoid withdrawal symptoms with administration. T e e ects o naloxone are short lasting or about 60–90 minutes and patients must be redosed as necessary.

Organophosphates Organophosphates block acetylcholinesterase, which causes acetylcholine to accumulate at cholinergic receptors. T e enzyme is phosphorylated, irreversibly inhibiting acetylcholinesterase and degrading the enzyme. Organophosphates cause systemic symptoms within 5 minutes o inhalation or within 12 hours o ingestion. T e typical signs and symptoms o organophosphate poisoning can be remembered by the popular mnemonic “DUMBBELLS” which stands or diarrhea, urination, miosis, bradycardia, bronchoconstriction, (CNS) excitation, lacrimation, salivation, and sweating. A more complete listing o symptoms is shown in able 33-1. T e primary concern on presentation, however, is pulmonary toxicity rom bronchospasm, bronchorrhea, and respiratory depression. Airway management is critical or initial treatment o signi cant toxicity. Atropine is dosed at 2–4 mg IV repeated every 5 minutes, and glycopyrrolate can be used i there are no CNS symptoms present. Pralidoxime is used to regenerate acetylcholinesterase at nicotinic, muscarinic, and CNS neuromuscular junctions to improve respiratory muscle weakness. It is most e cacious i started early, and continued in conjunction with atropine. It is administered with a 1–2 gram loading dose in 500 mL normal saline over 30 minutes, and then continued as an in usion at 200–500 mg/h to maintain serum levels above 4 ug/L.

Central Nervous System Drug Intoxication

TABLE 33-1

123

Signs and Symptoms of Cholinesterase

Overdose

Muscarinic Effects

Nicotinic Effects

CNS Effects

Salivation

Muscle asciculations

Restlessness

Lacrimation

Cramping

Headache

Urination

Weakness

Drowsiness

Nausea, vomiting

Diaphragmatic atigue

Con usion, delirium

Bronchorrhea

Respiratory ailure

Slurred speech

Bronchoconstriction

Aref exia

Ataxia

Miosis

Paralysis

Seizures

Bradycardia

Tachycardia

Psychosis

Mydriasis

Respiratory depression

Phenytoin Phenytoin has slow, unpredictable absorption. Initial signs o overdose include nausea and vomiting. Neurological symptoms including drowsiness, dysarthria, ataxia, and seizures typically ollow. While cardiovascular toxicity is rare, it has been ound to be more prevalent with IV administration. reatment is primarily supportive. Multidose AC may increase elimination, but has not improved outcomes.

Selective Serotonin Reuptake Inhibitors (SSRIs) SSRIs are used primarily to treat depression. Overdose is typically mild, and clinical eatures include nausea, vomiting, diarrhea, and, rarely, CNS depression. One severe consequence o SSRI overdose is serotonin syndrome, which is caused by excess stimulation o central and peripheral serotonergic receptors. T e clinical eatures o serotonin syndrome include altered mental status that may range rom agitation to coma. Additionally, one may see autonomic dys unction, tachycardia, hyperthermia, labile blood pressures, and diarrhea. Neuromuscular symptoms may also occur and range rom tremors to myoclonus and rigidity. reatment or SSRI toxicity and serotonin syndrome primarily consists o supportive therapies and resolves in 1–3 days. AC may be used in severe settings. An EKG should assess or wide QRS complexes. For serotonin syndrome, intubation may be required i the patient’s mental status is severely altered. Benzodiazepines may be used to decrease agitation. I the neuromuscular symptoms, such as tremor and rigidity, are severe, then neuromuscular blockers may be administered.

Theophylline Acute theophylline toxicity is potentially li e-threatening. Clinical eatures include agitation, tremor, nausea, vomiting,

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and sinus tachycardia. Concentrations greater than 60 mg/L in acute overdose or over 40 mg/L in chronic use generally cause seizures, ventricular arrhythmias, hypotension, and death. A key laboratory nding is hypokalemia, which increases the patient’s risk or rhabdomyolysis. Serum theophylline levels are help ul to determine toxicity. With sustained release preparations, one may experience delayed onset and prolonged toxicity. reatment includes AC administration with serum concentrations above 40 mg/L. While hypokalemia does occur, this is generally not representative o total body potassium stores, and generally does not need repletion. Benzodiazepines can be given to treat any convulsions, and beta-blockers may be used to control any cardiac arrhythmias.

Tricyclic Antidepressants (TCAs) oxic symptoms o CAs include anticholinergic e ects such as f ushed skin, tachycardia, blurred vision, dilated pupils, and urinary retention. Respiratory depression, depressed consciousness, cardiac arrhythmias, and hypotension may occur with severe toxicity. Acidemia, hypotension, and hyperthermia have the potential to worsen the toxic e ects o CAs. reatment begins with AC and continuous cardiac monitoring. Intubation may be required or patients that are unable to protect their airway. Serum pH alkalinization to greater than or equal to 7.45 reduces the ree drug available, thereby reducing CA toxicity. Hyperventilation with administration o 50 mmol ormulations o 8.4% sodium

bicarbonate may improve outcomes by achieving this goal. Consider bicarbonate supplementation in all cases o QRS prolongation, arrhythmias with hypotension, or patients presenting with convulsions. Lidocaine may be the best antiarrhythmic to use i arrhythmias develop, and class 1a drugs should be avoided. Benzodiazepines are rst-line treatment or seizures and may prevent delirium.

Valproate While most valproic acid intoxications are benign, cerebral edema and CNS depression can occur with large ingestions. Symptoms o overdose are nausea, drowsiness, and con usion. Hypotension and respiratory depression may also occur, requiring intubation. Cerebral edema is related to an idiopathic hyperammonemia that typically occurs in the absence o hepatotoxicity. While rare, pancreatitis has been reported. Metabolic abnormalities may also occur, and include metabolic acidosis, hypernatremia, hypoglycemia, and hyperammonemia as described above. Supportive treatment is all that is necessary or valproic acid intoxication. Ammonia levels should be obtained in patients with altered mental status. AC may be used i the patient presents within the 1-hour window. Hemodialysis may be considered because valproic acid protein binding becomes saturated at high serum concentrations. While no antidote exists or valproic acid toxicity, L-carnitine may be administered in patients with signi cant toxicity and hyperammonemia.

34 C

Spinal Cord Injury Nathanael Leo and Palak Turakhia, MD

Spinal cord injury is an insult to the spinal cord, resulting in either temporary or permanent dys unction o the cord's motor, sensory, or autonomic unction. In the United States, trauma remains the number one cause o spinal cord injury. T e most common cause o traumatic spinal cord injury is motor vehicle collisions, ollowed by alls, violence (primarily gunshot wounds), and sport injuries. Direct mechanical injury rom a traumatic insult leads to hemorrhage, edema, and ischemia. Pathophysiology reveals a release o in ammatory mediators, membrane-destabilizing enzymes, disruption o electrophysiological pathways, and eventual tissue degeneration.

INITIAL MANAGEMENT Blunt trauma, especially those involving head injury, requires spinal stabilization. T e spine should be immobilized on a board and cervical collar in order to prevent urther injury. T e patient should be assessed according to Advanced rauma Li e Support (A LS) protocols. Patients who are alert with normal neurologic status and in no pain can have collars removed.

Circulation Although spinal injury may be responsible or hypotension in the setting o trauma, hypovolemia remains more common. Initial management o hypotension should be targeted at volume replacement. Management includes invasive hemodynamic monitoring (with arterial line and central venous line) and support with isotonic crystalloid and/or blood products and vasopressors, titrated to maintain an adequate hemodynamic pro le. Once hypovolemia has been ruled out through appropriate examination, imaging, and laboratory studies, neurogenic shock should be considered. Injury to the spinal cord at the level o the cervical or thoracic vertebrae causing sudden loss o underlying sympathetic stimulation o blood vessels is known as neurogenic shock. Physiologically, the body experiences decreased systemic vascular resistance and blood pressure and bradycardia due to unopposed vagal activity.

E R

T e management goal in cases o neurogenic shock is to maintain adequate per usion. Fluid resuscitation o at least 2 L o warmed crystalloid along with a vasopressor should be administered, as needed.

Airway T e need or intubation should be assessed. Rapid sequence intubation (RSI) is the most e cient way o achieving intubation in patients with respiratory compromise. For patients undergoing RSI, cricoid pressure can be maintained with an assistant utilizing one hand to support the back o the neck, and the other hand to apply rm pressure on the cricoid cartilage. Awake tracheostomy is reserved or patients with acial ractures or other, severe anomalies o airway anatomy that make sa ely securing the airway di cult and unsa e. Succinylcholine should be avoided in cases o neurogenic shock as it can increase the risk or extreme bradycardia. Atropine should be administered prior i succinylcholine must be used.

Breathing Breathing is best managed by mechanical ventilation, with ventilation or SPO2 > 95% and E CO2 = 35 mmHg. Spinal cord injuries involving C4 and cranial result in interruption o the descending bulbospinal respiratory pathways, resulting in respiratory muscle paresis and/or paralysis. General anesthesia can exacerbate abdominal and intercostal muscle weakness or paralysis, and thus increase the chances o respiratory ailure with ensuing hypoxia and hypercapnia. In such cases, long-term mechanical ventilator support is indicated. Continuous pulse oximetry and delivery o supplemental oxygen should be employed, as arterial hypoxemia is common ollowing spinal cord injury. Gastric atony and dilatation may occur and simple decompression with a nasogastric tube may acilitate ventilation.

NEUROLOGICAL ASSESSMENT Spinal Stability Evaluation o the injured spine begins with assessment o spinal stability. Spinal stability is de ned as the ability o the 125

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spine to limit displacement under physiologic loads so as not to damage or irritate the spinal cord or nerve roots. A thorough neurologic examination is warranted, including assessment o anal sphincter tone and contraction ollowing an acute injury. Whole body C scans associate patterns o injury with instability and aid in diagnosis o associated lesions. T e cervical spine is particularly vulnerable to injury due to its exposure and mobility. In contrast, the thoracic spine is less commonly injured because o its articulation with the rib cage, which makes it a relatively rigid and sti segment. T e thoracolumbar junction ( 11 to L2) is a transitional zone that is most vulnerable to injury. Although susceptible to injury, the width o the spinal canal in the thoracolumbar region is greater and most injuries do not result in neurologic de cits. In comparison to the thoracic and thoracolumbar regions, the lower lumbar spine is more mobile. Isolated ractures o the lower lumbar spine rarely injure the spinal cord or result in neurologic injury because o the relatively widened spinal canal and the termination o the spinal cord at the L2 level. Neurologic injuries rarely occur and they are usually isolated nerve root de cits or complete cauda equina lesions. Fractures o the sacral and coccyx spine and injuries to the nerve roots are very unusual. When they occur, they are requently associated with ractures o the pelvis. Pelvic ractures can be li e-threatening as many internal organs are cradled along the pelvis. Sacral ractures involving the central sacral canal can result in bowel or bladder dys unction.

MANAGEMENT OF SPINAL CORD INJURY It is important to distinguish between complete and incomplete spinal cord injury as it determines prognosis. Complete lesions have total loss o sensory and motor unction below the level o injury. Patients with incomplete lesions, where some unction remains below the primary level o injury, may have some degree o recovery.

Surgical Indications I possible, closed reduction should be attempted, as injury is irreversible af er 48 hours. In cases o incomplete injury, early surgery (< 24 hours) is requently required, especially i the spine is unstable. Other indications or early surgery include the ollowing: • • • •

Stable spine with incomplete spinal cord injury Unstable spine with progressive neurologic loss or progression rom incomplete to complete injury Unstable spine with rotational acet dislocation Unstable spine with uncooperative/agitated patient

Management o Early Complications A. Respiratory Respiratory complications are common in cervical and thoracic cord injuries in which the patient's intercostal and abdominal muscle unction has been impaired. Lesions above C6 impair the diaphragm and accessory muscles and lead to absent or insu cient ventilation. racheotomy may be required in these cases.

B. Progressive Neurologic Loss Management aims o patients with secondary spinal cord injury with worsening neurologic signs should be maintenance o MAP > 80 mmHg or at least a week. Spinal cord cooling is an option as it may limit edema and apoptosis.

C. Intraoperative Bleeding When intraoperative hemorrhage occurs, transexamnic acid (1 g IV in 10 min) may reduce blood loss.

TABLE 34-1

Early and Late Complications in Patients with Spinal Cord Injury Complication

Incidence (%)

2 years a ter injury Urinary tract in ection

Skeletal muscle spasticity

Chills and ever

Decubitus ulcer

Autonomic hyperre exia

Skeletal muscle contractures

Heterotopic ossif cation

Pneumonia

Renal dys untion

Postoperative wound in ection

30 years a ter injury Decubitus ulcers

Skeletal muscle or joint pain

Gastrointestinal dys unction

Cardiovascular dys unction

Urinary tract in ection

In ectious disease or cancer

Visual or hearing disorders

Urinary retention

Male genitourinary dys unction

Renal calculi

CHAPTER 34

CHRONIC SPINAL CORD INJURY T e sequealae o chronic spinal cord injury includes impaired alveolar ventilation, cardiovascular instability mani esting as sympathetic hyperre exia, chronic pulmonary and genitourinary tract in ections, anemia, and irregular thermoregulation. Not unlike acute spinal cord injuries, chronic cord injuries occurring more rostral along the spinal cord tend to have more signi cant systemic e ects ( able 34-1).

Autonomic Dysref exia Autonomic dysre exia is a potentially dangerous complication that occurs in patients with spinal cord injuries above the 6 level, but is possible until 12. It is due to an exaggerated autonomic response to pain below the level o spinal cord injury, resulting in hypertension. It occurs 1–6 months af er injury and may persist inde nitely. Presenting symptoms are variable with the most common being hyperhydrosis, severe headaches, and vasodilatation above the level o the neurologic loss. T e cardinal sign is paroxysmal hypertension with bradycardia. Distention or manipulation o the bladder, rectum, or abdomen are common precipitating actors that trigger massive re ex sympathetic outow, hypertension, re ex bradycardia, and vasodilatation in the part o the body above the level o the spinal cord lesion. Immediate management consists o upright positioning to reduce intracranial blood pressure and halting any stimulus below the spinal injury level (e.g., bladder decompression). In severe cases, a blood pressure lowering drug should be administered, such as phentolamine, gylceryl trinitrate, or ni edipine.

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Chronic pain is common ollowing spinal cord injury. Patients experience visceral pain produced by distention o the bladder or bowel or in some cases phantom body pain in areas o complete sensory loss. As such, consideration or potent opiates should be included when planning anesthetic management. Chronic muscle spasms are also common. About 6 months af er acute spinal cord transection, spinal cord re exes gradually return and the patient enters a chronic stage characterized by overactivity o the sympathetic nervous system and involuntary skeletal muscle spasm. A use ul modality or treating spasticity in these patients is balco en as it potentiates the inhibitory e ects o γ-aminobutyric acid.

Anesthetic Management Prevention o autonomic dysre exia during anesthetic management in patients with chronic, high-level transection o the spinal cord is key. Vasodilator drugs with short hal -li e (e.g., sodium nitroprusside) should be readily available to treat sudden-onset, systemic hypertension. When general anesthesia is selected, succinylcholine should be avoided 24 hours af er injury due to the risk o hyperkalemia. Avoidance o succinylcholine should continue until at least 6 months ollowing spinal cord transection. Nondepolarizing muscle relaxants are the primary choice during general anesthesia as they acilitate tracheal intubation and prevent re ex skeletal muscle spasms in response to surgical stimulation. emperature should be monitored closely as hypothermia or hyperthermia may occur.

Tetanus Caroll N. Vazquez-Colon, MD

etanus is an in ectious disease caused by the neurotoxin o the anaerobic, gram-negative bacillus Clostridium tetani. In developed countries it is rare due to vaccination programs. Clostridium tetani produces two exotoxins: tetanolysin and tetanospasmin. T e latter is responsible or the clinical maniestations o the tetanus disease.

PATHOPHYSIOLOGY Clostridium tetani spores enter tissues through a contaminated wound where they incubate and release tetanospasmin. T is toxin has a pre erence or inhibitory neurons and spreads by rst entering local peripheral neurons, where it is internalized. It is then transported intra-axonally and retrograde to the cell body. Once the toxin reaches the CNS, it binds to gangliosides at the presynaptic inhibitory nerves and blocks the release o inhibitory neurotransmitters. T e mechanism o action o this toxin is mostly at the presynaptic membrane where it degrades synaptobrevin, a protein involved in the usion o neurotransmitter vesicles to nerve membranes. As a result, usion is inhibited and neurotransmitters are not released into the synapse. In the spinal cord, this toxin suppresses alpha motor neurons, resulting in generalized skeletal muscle contractions or spasms. In the brain, the toxin interrupts the release o gamma-amino butyric acid (GABA) and glycinergic neurons. Autonomic dys unction with sympathetic nervous system hyperactivity occurs with disease progression.

SIGNS AND SYMPTOMS Diagnosis o tetanus is clinical and suspected a er a history o an open, contaminated wound. Dif erential diagnosis includes drug-induced dystonia, neuroleptic malignant syndrome, hypocalcemia, strychnine poisoning, sepsis, and encephalitis. T e disease commonly presents a er an incubation period during which patients complain o dysphagia, neck stif ness, and jaw stif ness. T e muscles o the head and neck are usually af ected rst with progressive spread to the rest o the body. As the disease progresses, rigidity and trismus occur. rismus

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is the presenting symptom in most patients due to masseter muscle spasms. Patients can present with ventilatory impairment that ollows a restrictive disease pattern due to intercostal and diaphragm spasms. Laryngospasm and dysphagia may occur due to laryngeal and pharyngeal muscle spasm, respectively. As disease progresses, abdominal and lumbar muscles become rigid and account or the characteristic opisthonic posture. Patients may complain o severe pain secondary to tonic-clonic skeletal muscle spasms and present with an elevated body temperature due to the increased skeletal muscle work. T e severity o the spasms can lead to rhabdomyolysis. Autonomic dys unction is a progressive mani estation that presents as tachycardia, blood pressure lability, and cardiac arrhythmias. Pro use salivation and increased bronchial secretions are among other side ef ects. Patients can also present with diaphoresis, intense peripheral vasoconstriction, and increased urinary excretion o cathecholamines (secondary to sympathetic system overactivity).

TREATMENT I the immunization status is unknown, administration o human tetanus immunoglobulin, immunization, and antibiotics are required. Intramuscular human immunoglobulin will neutralize circulating toxins and will prevent neurotoxin entry to neurons; it will not alter symptoms already present. Metronidazole IV is the antibiotic o choice against C. tetani; penicillin G is an alternative. Surgical debridement o wounds is required to eliminate the source o exotoxin. T e treatment o patients with tetanus is supportive, directed towards securing the airway, supporting ventilation, controlling skeletal muscle spasm, and preventing sympathetic system hyperactivity. Excessive spasms are treated with benzodiazepines and, i unresponsive, may require administration o neuromuscular blocking drugs and mechanical ventilation. Propo ol administration may also control spasms. Intravenous beta-blockers can manage sympathetic overactivity. Magnesium has been used to reduce the ef ects o catecholamine excess in patients with tetanus because it blocks the release o cathecholamines rom adrenergic nerve 129

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terminals and the adrenal glands. Opioids may also be helpul in reducing spasms and treating spasm-related pain.

ANESTHETIC MANAGEMENT Perioperatively, airway management can be challenging secondary to trismus, which may render oral tracheal intubation impossible. Advanced airway management techniques such as ber optic intubation may be required, and should be done in a controlled environment, avoiding stimulation to prevent skeletal muscle spasm onset. Patients with tetanus are at increased risk o aspiration due to dysphagia and increased abdominal pressures or which precautions should be taken. Autonomic instability warrants continuous pressure monitoring and adequate intravenous access. Nondepolarizing muscle

relaxants can be sa ely used but may require higher doses due to increased ef erent neural discharge. Succinylcholine use in patients with tetanus can be associated with hyperkalemic cardiac arrest and is there ore contraindicated. Pancuronium may worsen autonomic instability by inhibiting catecholamine reuptake. Volatile anesthetics are use ul agents or the maintenance o anesthesia, and patients should be deeply anesthetized and possibly paralyzed to prevent intraoperative spasms. Postoperative management should include ICU admission in cases with hemodynamic instability. T e clinical course o the disease can be prolonged as recovery requires regrowth o axon terminals and toxin destruction. Autonomic dys unction and hospital-acquired in ections are common causes o death.

36 C

Aneurysms and Arteriovenous Malformations Vanessa Gluck, MD

An aneurysm is a localized weakening o the wall o a cerebral artery causing dilation, or ballooning o a blood vessel. T e cerebral vasculature is a common site or aneurysm ormation. T e incidence o cerebral aneurysm is 1%–6% and the incidence o aneurysm rupture is 12/100,000. Aneurysm occurs at any age but peaks at ages 40–60. T e male-to- emale ratio is 2:3. T ere is a genetic component and the chromosomal loci associated with aneurysms are on chromosomes 1, 2, 7, 11, and 19. ables 36-1 and 36-2 list the inherited and noninherited risk actors or intracranial aneurysms. T e incidence o rupture depends on the size o the aneurysm according to Laplace’s Law (P = 2T/r, where P = pressure, T = tension, and r = radius), with 90% rupture o size greater than 12 mm, 5% o size greater than 12–15 mm, and 5% rupture incidence o 15 mm or less. Most aneurysms occur at the Circle o Willis: anterior communicating artery and anterior cerebral artery (30%– 35%), internal carotid artery and posterior communicating artery (25%), middle cerebral artery (20%), and the basilar artery and posterior circulation (5%–10%).

TABLE 36-1

E R

PRESENTATION Most intracranial aneurysms are asymptomatic. Symptomatic aneurysms are likely due to subarachnoid hemorrhage (SAH) rom aneurysm rupture. wenty- ve percent o SAH die be ore hospitalization. In hospital mortality approaches 50% and most survivors have permanent disability. Alternatively, aneurysms present with symptoms related to pressure on cranial nerves 3, 4, and 6. Signs and symptoms result rom aneurysm rupture with an abrupt rise in ICP that produces a severe headache with or without loss o consciousness. Described as the “worst headache o my li e,” SAH may include nausea, vomiting, and vision impairment. Blood in the CSF produces meningism, which causes photophobia, neck sti ness, and headache. T ere are several classi cation systems or SAH severity. T e Hunt and Hess classi cation is noted in able 36-3.

Diagnosis Diagnosis o SAH is made by signs and symptoms and C scan. MRI or C angiography has better detection rates and

Inherited Risk Factors for Intracranial

Aneurysms

Polycystic kidney disease

TABLE 36-2

Non inherited Risk Factors for Intracranial Aneurysms

Type IV Ehler–Danlos syndrome

Age over 50

Pseudoxanthoma elasticum

Female

Hereditary hemorrhagic telangectasia

Smoking

Neuro bromatosis type 1

Cocaine use

Coarctation o the aorta

In ection o vessel wall

Fibromuscular dysplasia

Head trauma

Pheochromocytoma

Septic emboli

Klin elter’s syndrome

Hypertension

Tuberous sclerosis

Alcohol abuse

Noonan’s syndrome

Oral contraceptive pills

Alpha glucosidase de ciency

Hypercholesterolemia

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TABLE 36-3

Hunt and Hess Classification of Subarachnoid Hemorrhage Grade*

Description

Asymptomatic, mild headache, slight nuchal rigidity

Moderate to severe headache, nuchal rigidity, no neurologic de cit other than cranial nerve palsy

Drowsiness/con usion, mild ocal neurologic de cit

Stupor, moderate to severe hemiparesis

Coma, decerebrate posturing

*Mortality is indexed with grades, least to greatest, rom grade 1 to 5.

ARTERIOVENOUS MALFORMATIONS (AVMS) AVMs are errors in vasculature development that lead to ocal arteriovenous shunts. T ey are congenital vascular mal ormations that deprive surrounding tissues o blood supply and produce venous hypertension and localized edema. AVMs most commonly present between ages o 20 and 45 with a peak in the ourth decade. AVMs present with intracranial bleed, seizure, ocal neurological de cits, hydrocephalus, or, rarely, congestive heart ailure. Cerebral damage may result rom the presence o an AVM due to a number o injuries:

cerebral angiography will ultimately determine treatment options.

• • •

MANAGEMENT

• •

Most treatments begin as soon as possible due to the risk o rebleeding and vasospasm. Major intracranial bleed with mass e ect or obstructive hydrocephalus requires urgent surgery. T e goal o treatment is to (1) prevent rebleeding, since 20% rebleed with a 60% mortality; (2) treat and prevent vasospasm; (3) detect hydrocephalus; and (4) avoid respiratory problems. Hypertension should be controlled; however, i the patient has vasospasm, it is important to raise the blood pressure. Nimodipine, a calcium channel antagonist, is used to treat SAH because it decreases the incidence o morbidity rom cerebral ischemia without causing hemodynamic disturbance.

Vasospasm Cerebral vasospasm can be diagnosed by MR angiography, C angiography, transcranial Doppler ultrasonography, or intra-arterial angiography, which is the gold standard. Incidence peaks at 7 days and clinically signi cant vasospasm occurs in 30% patients a er SAH. Vasospasm causes ischemia and subsequent cerebral edema, compromising cerebral circulation. T e exact mechanism is unclear, but vasospasm is most likely due to the presence o blood breakdown products. T e treatment or vasospasm is triple H therapy: hypervolemia, hypertension, and hemodilution. T e goal or hypervolemia is to increase CVP to at least 10 mmHg with crystalloids. Hypertension is used to increase CPP and vasopressors o choice are phenylephrine, dopamine, or dobutamine. T e goal systolic blood pressure is 160–200 mmHg in aneurysm-clipped patients and 120–150 mmHg in those without clipping. Cerebral blood f ow improves with hemodilution due to a reduction in blood viscosity. T e goal hematocrit is 33% provides optimal balance between viscosity and oxygen carrying capacity.

Steal phenomenon Ischemia rom ailure o per usion rom heart ailure Hemorrhagic in arction rom thrombosis o aneurysm o the great vein o Galen Cerebral atrophy Alterations o f ow cause by surgery

Prognosis depends on several actors, including AVM volume, the presence o deep eeding vessels and drainage, shunt f ow, AVM location, and bleeding history. Small AVMs portend greater bleeding risk due to an elevated per usion pressure. Diagnosis is by angiography and treatment is based on the patient age and comorbidities, the neurological condition, and AVM characteristics. reatment modalities are noted in able 36-4. Anesthetic goals or AVM treatment are to limit the increase in cerebral blood f ow (CBF) and ICP and decrease

TABLE 36-4

Treatment Options for AVM

Conservative management

Considered when the risk o other options is too high

Surgical removal

Indicated or noneloquent areas and surgically accessible lesions. Emergency surgery is indicated to remove an increasing intracerebral hematoma or to place a ventricular drain to treat acute hydrocephalus

Endovascular embolization

The goal is total obliteration o the lesion or to acilitate surgical resection later by decreasing the size and blood f ow through the AVM. The trans emoral arterial approach delivers N-butylcyanoacrylate, solidi ying the AVM

Stereotactic radiosurgery

Involves application o a stereotactic rame, de nition by CT scan with or without cerebral angiography, computation o dose and lesion sur ace contours, ollowed by radiosurgery and head rame removal

CHAPTER 36

in cerebral metabolic rate (CMR). All intravenous anesthetics except ketamine decrease CBF and CMR. T e blood pressure during embolization is tightly controlled to prevent blood loss during surgical resection and slow f ow through AVM eeding arteries to prevent systemic embolization o glue. Cerebral ischemia may develop during embolization, requiring protection by increasing f ow through collateral pathways with vasopressor therapy.

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Other anesthetic goals include brain protection with antiepileptic drugs, hyperventilation, urosemide, mannitol, and corticosteroids to reduce ICP as needed. Early emergence rom anesthesia is desirable or rapid assessment o neurological unction postoperatively.

Anesthesia for Interventional Neuroradiology Audrey Spelde, Binoy Bhatt, MD, Anita Cucchiaro, MD, and Jef rey S. Berger, MD, MBA

Interventional neuroradiology (INR) is rapidly supplementing and in some cases replacing traditional neurosurgery. Endovascular access is utilized to deliver therapeutic drugs and devices to the brain. Anesthetic considerations o INR procedures are similar to those or neurosurgery, such as patient selection and complications, and come with the advantages o decreased pain and aster recovery time.

PREOPERATIVE ASSESSMENT Following routine preoperative evaluation, patients require a detailed neurological assessment, Glascow Coma Scale score, and level o consciousness assessment. Signs o increased intracranial pressure should be noted. T e presence o renal insu ciency is important to determine dye load tolerance. Baseline coagulation pro les should be conducted to prepare or intraoperative anticoagulation. Allergies, including protamine, iodine, shell sh, latex, and contrast should be documented. For emale patients o childbearing age, pregnancy status should be con rmed. Arthritis o the neck and back may compromise the patient’s ability to tolerate supine positioning.

TESTING Carotid Occlusion Test T e carotid occlusion test assesses carotid artery patency and con rms adequate collateral circulation be ore elective carotid artery occlusion. ypically required or tumors involving the internal carotid artery, or or giant (> 24 mm) internal carotid and vertebrobasilar aneurysms, carotid occlusion requires consciousness or continuous neurological evaluation. Common complications include bradycardia, hypertension, and loss o consciousness.

Wada Test T e Wada test consists o behavioral testing a er an anesthetic agent, such as sodium amobarbital or sodium methohexital, injection into the internal carotid artery. T is is conducted in conscious patients to determine the dominant side or vital

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cognitive unctions, namely speech and memory, in advance o epilepsy surgery or otherwise.

Superselective Anesthesia Functional Examination (SAFE) T e SAFE is an extension o the Wada test. It is carried out be ore therapeutic embolization to exclude an inadvertent catheter tip placement proximal to the origin o normal vessels supplying important regions in the brain or spinal cord. Sodium amytal is injected into the vascular territory planned or occlusion and repeated neurological examination is conducted to exclude unctional involvement.

ANESTHETIC CONSIDERATIONS Interventional radiologists o en treat patients who cannot tolerate open surgery. However, procedures done in the IR suite are not necessarily less dangerous.

Monitored Anesthesia Care (MAC) Versus General Anesthesia (GA) GA produces optimal mapping with digital subtraction angiography by providing control o mobility, respirations, and the hemodynamic pro le. Elevated ICP and intraoperative neurological emergencies are better controlled with GA. Finally, GA provides improved airway control in patients at risk or aspiration. However, tracheal intubation during GA induction may acutely increase BP, increasing aneurysm transmural pressure, consequently risking rupture. Additionally, MAC more easily allows or intraoperative neurological assessment, and avoids the risk o intracranial hypertension with emergence by avoiding extubation. T ere is no advantage o one anesthetic agent over another; however, higher concentrations (> 1 MAC) o desurane can increase cerebral blood ow, cause higher ICP, and result in loss o autoregulation. Propo ol in particular decreases cerebral blood ow, ICP, and metabolic demands. Sedation with propo ol or dexmedetomidine can be used or INR procedures, permitting neurological testing and avoiding hemodynamic changes with GA. 135

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Opioids Opioids are not generally used in INR procedures. Respiratory depressant ef ects increase cerebral blood ow. In addition, opioids af ect consciousness and can alter the intraoperative neurologic assessment. Alternative adjunctive agents are alpha2agonists such as clonidine or dexmedetomidine that minimize respiratory depression. T ese drugs are excellent postoperative sedatives and attenuate hypertension and tachycardia.

Equipment T e anesthetic machine is best located opposite the neuroradiologist and towards the patient’s eet, permitting imaging equipment ree movement around the patient’s head. Intravenous access should be obtained at a maximal distance rom the image intensi er during uoroscopy, and there should be at least two distinct peripheral catheters. In addition, all monitoring lines should have su cient extension. Normothermia is the goal during IR procedures and active warming techniques such as orced air warming blankets should be utilized to achieve it.

Monitoring Arterial lines may acilitate pressure monitoring and blood sampling. T e trans emoral approach used by neurointerventional radiologists may permit a side port o the introducer sheath to monitor the arterial pressure i radial access is di cult. T ree arterial pressures may be monitored: (1) the emoral artery pressure; (2) the coaxial catheter in the carotid or vertebral artery; and (3) the pressure at the tip o the catheter. Bladder catheterization allows output monitoring ollowing intraoperative diuretics such as mannitol and urosemide, and radiographic contrast dye administration. Activated clotting time (AC ) is assessed at baseline, and IV heparin is given to prolong the AC by two to three times. Heparin is administered between emoral cannulation and coil insertion. AC is monitored every hour and additional heparin doses are given as indicated. Postprocedure, heparin may be continued, stopped, or reversed with protamine in consultation with the interventional neuroradiologist.

TABLE 37-1

CONSIDERATIONS FOR SPECIFIC PROCEDURES INR involves introducing catheters into the arterial circulation o the head, neck, or spine.

Cerebral Aneurysm Cerebral aneurysm is the most common INR procedure. Patients with aneurysmal subarachnoid hemorrhage (SAH) should be monitored or increased ICP, cerebral ischemia, and hydrocephalus. An IV calcium channel blocker, typically nimodipine, protects against cerebral ischemia and minimizes vasospasm. Although this increases ICP, most neuroradiologists pre er to continue nimodipine as it lessens traumatic vessel spasm during catheter passage in the neck and intracranial arteries.

Arteriovenous Malformation (AVM) GA is pre erred or AVM embolization to acilitate visualization (i.e., temporary apnea and valsalva) and prevent movement. Controlled hypotension and ow arrest reduce ow across the AVM. Arteries eeding an AVM can supply a variable amount o brain tissue; thus, a er embolization, abrupt restoration o normal systemic pressure to a chronically hypotensive vascular bed may overwhelm autoregulatory capacity and result in parenchymal hemorrhage. It is desirable to maintain an arterial pressure 15%–20% below the patient’s normal blood pressure level in the postprocedure period to avoid this complication.

COMPLICATIONS OF INR PROCEDURES Complications during INR procedures develop rapidly, resulting in signi cant morbidity and mortality ( able 37-1). Hemorrhagic and occlusive complications require dif erent approaches or management, and must be distinguished upon presentation.

Complications of INR Procedures

Complication

Examples

Treatments

Hemorrhagic

• Aneurysm perforation • Intracranial vessel injury (i.e., dissection)

• • • • •

Protamine sulfate Mannitol Packing with coils Emergency craniotomy/surgical clipping Ventricular drainage

Occlusive

• Thromboembolic complications • Displacement of coil into parent vessel, coil fracture • Vasospasm

• • • •

Mechanical lysis via guide wire or saline infusion tPA/abciximab Triple “H” therapy—hypertension, hypervolemia, and hemodilution Mechanical angioplasty*

Non-CNS complications

• Contrast reactions • Contrast nephropathy • Hemorrhage at puncture site, groin hematoma, retroperitoneal hematoma

• Pretreatment with steroids/antihistamines • N-acetylcysteine • Fluids

*If done within 2 hours of symptomatic ischemia to prevent an ischemic infarct from hemorrhaging. Reserved for patients who have not responded to triple H therapy and are at risk of developing a stroke.

CHAPTER 37

PROVIDER SAFETY Anesthesia staf should wear lead aprons at least 0.5 mm in thickness and thyroid shields. T e sources o radiation are multiple, including direct radiation rom the X-ray tube, leakage radiation through the collimators and protective shielding, and scatter radiation re ected rom the patient and surrounding area. Since digital subtraction angiography delivers more radiation than uoroscopy, the anesthesiologist should monitor the patient rom a sa e distance. T is can be done rom an adjoining console area or behind a clear lead screen at a distance o at least 4 rom the radiation source.

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SUGGESTED READINGS Hayman MW, Paleologos MS, Kam CA. Interventional neuroradiological procedures—A review or anaesthetists. Anaesth Intensive Care. 2013;41:184–201. Lee CZ, Young WL. Anesthesia or endovascular neurosurgery and interventional neuroradiology. Anesthesiol Clinics. 2012; 30(2):127–147.

38 C

Transsphenoidal Hypophysectomy Brian S. Freeman, MD

Hypophysectomy, the removal o the pituitary gland, can be per ormed through a number o surgical approaches. For large tumors that have extended beyond the pituitary ossa, a bi rontal craniotomy is o en necessary. Most pituitary tumors lie within the sella (or immediate suprasellar area) and are there ore amenable to excision via the transsphenoidal technique. ranssphenoidal hypophysectomy requires the use o a microscope or endoscope to enter the sella through the nose and sphenoid sinus. Advantages include rapid midline access to the sella with minimal risk o brain injury or bleeding. T e incision may be made in the back wall o the noise, along the ront o the nasal septum, or under the upper lip. Endoscopy enables excellent tumor visualization, opening o the diaphragmatic sellae, and decompression o the optic nerve.

PREOPERATIVE EVALUATION About 25% o pituitary tumors are considered non unctioning. Depending upon the speci c type o lesion, some tumors o the anterior pituitary have endocrine mani estations related to hormonal hypersecretion. Sometimes hyposecretion o hormones can occur due to compression o adjacent normal tissue, prior radiation therapy, hemorrhage (apoplexy), or postpartum in arction o the pituitary gland (Sheehan syndrome). In either situation, these conditions carry signi cant implications or anesthetic management: •

•

Prolactinomas—Nearly hal o all pituitary tumors are prolactinomas. T eir mass e ect on the optic chiasm is usually more clinically signi cant than the prolactin hypersecretion. Women present with secondary amenorrhea and galactorrhea, while men show signs o secondary hypogonadism, erectile dys unction, and decreased libido. T ese patients are typically on bromocriptine therapy, an agonist at dopamine D2 and various serotonin receptors. Acromegaly—T e excess o growth hormone (GH) rom a pituitary tumor leads to acromegaly. T ese patients may have problems with airway management during general anesthesia due to macroglossia, prognathism, hypertrophic oropharyngeal tissues and laryngeal structures,

• •

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and recurrent laryngeal nerve palsy. Most patients have a history suggestive o obstructive sleep apnea. Cardiac mani estations include le ventricular hypertrophy, interstitial myocardial brosis, coronary artery disease, and supraventricular dysrhythmias. Acromegalics may also have impaired glucose tolerance and diabetes mellitus. Cushing’s disease—Hypersecretion o the adrenocorticotropin (AC H) hormone rom a pituitary tumor can lead to Cushing’s disease (see Chapter 110). Hyperthyroidism— umors which release an excess o thyroid-stimulating hormone ( SH) produce symptoms o hyperthyroidism (see Chapter 105). T ese rare tumors are o en more locally invasive and carry the risk o extensive blood loss. Management o hyperthyroidism is necessary prior to hypophysectomy.

An enlarged pituitary gland may eventually produce a mass e ect on nearby structures. Usually these problems occur when the tumor is a large non unctioning macroadenoma (> 1 cm diameter) with suprasellar extension. Neurologic examination may reveal signs and symptoms o elevated intracranial pressure such as headache, nausea, and papilledema. Obstruction o cerebrospinal uid out ow can lead to hydrocephalus. In the absence o intracranial hypertension, compression o the optic chiasm can also cause visual eld de ects such as bitemporal hemianopia. Palsy o the oculomotor (third) cranial nerve can also occur.

SURGICAL CONSIDERATIONS Positioning ranssphenoidal hypophysectomy is per ormed with the patient in a supine position. T e patient’s head is usually elevated around 30° to decrease venous engorgement and bleeding during the resection. T is position increases the risk o venous air embolism (VAE). Early detection using monitors such as precordial Doppler, transesophageal echocardiography, and end-tidal nitrogen analysis should be considered. In the event o a VAE, therapeutic interventions include irrigation o the operative eld, surgical hemostasis, bilateral jugular 139

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venous compression, air aspiration through a central venous catheter, and cardiopulmonary resuscitation.

Lumbar Spinal Drain An intrathecal catheter placed through the L3 to L4 lumbar interspace can improve visualization o suprasellar adenomas during dissection. Injection o saline through the spinal catheter increases the CSF pressure, thereby displacing the suprasellar portion o the tumor down into the in rasellar surgical eld. Injection o air may assist in visualization o the tumor via intraoperative uoroscopy. I the dura has been accidentally penetrated during the excision, the lumbar drain can be used postoperatively to maintain CSF decompression. Potential complications o this procedure include in ection and development o cerebrospinal uid stulas.

ANESTHETIC CONSIDERATIONS Topicalization opical preparation o the nasal mucosa prior to surgical incision is necessary to minimize potential bleeding. Common vasoconstricting agents include oxymetazoline, cocaine, and lidocaine with epinephrine. It is important to monitor or cardiovascular side e ects such as hypertension and tachycardia.

Pharyngeal Pack During the transsphenoidal approach, blood rom the nasal tissue dissection can accumulate within the oropharynx. T is blood may enter the stomach, causing vomiting a er emergence. It may irritate the glottis, causing coughing or laryngospasm just a er extubation. Patients may also aspirate this blood during surgery as it channels past the in ated cu o the endotracheal tube. o prevent these problems, a throat pack is usually inserted a er intubation. At the end o surgery, blood and secretions should be suctioned rom the pharynx. It is imperative to con rm removal o the throat pack rom the patient’s upper airway.

Monitoring In addition to the basic standard monitors, an arterial pressure catheter is o en inserted or continuous blood pressure monitoring. Patients with acromegaly may have carpal tunnel syndrome that compromises the ulnar circulation. T e Allen test should be per ormed to determine whether a radial artery catheter is appropriate; otherwise, hand ischemia could result. In these patients, cannulation o the emoral or dorsalis pedis artery is pre erred. Because o the proximity o the pituitary to the visual pathways, the use o visual evoked potentials (VEPs) may improve visual eld de ects a er surgery. However, these potentials are highly sensitive to inhalation anesthetic agents.

Risk of Hemorrhage Blood loss during transsphenoidal hypophysectomy is typically low. However, there is the potential or catastrophic hemorrhage. A number o vascular structures lie in immediate relation to the pituitary, including the cavernous sinus and internal carotid artery. Some patients have a venous sinusoid that bridges the two cavernous sinuses but un ortunately overlies the pituitary gland. Injury to the cavernous sinus usually results in prolonged venous bleeding, while injury to the carotid artery leads to o en atal exsanguination. Cross-matched units o red blood cells should always be available, and large-bore vascular access is necessary.

Deliberate Hypotension Success ul transsphenoidal hypophysectomy depends on excellent visualization o the tumor. Continuous venous oozing in the operative ield can render surgical conditions quite challenging. he degree o bleeding depends more on the size o the mass rather than the pressures in the cavernous sinus or central venous circulation. A deliberate hypotensive technique can decrease bleeding and maintain a clear surgical ield. Drugs such as nitroglycerin, sodium nitroprusside, potent volatile anesthetics, beta-blockers, and dexmedetomidine may be help ul. he mean arterial pressure should not decrease below 65 mmHg; otherwise, cerebral per usion may become compromised in a patient in the head-up position.

Ventilation Management Hypocapnia produced by mechanical hyperventilation decreases the cerebral blood ow and intracranial volume. As a result, the arachnoid membrane is less likely to extend into the pituitary sella. T is maneuver may decrease the risk o opening the arachnoid membrane, which can lead to persistent postoperative CSF leakage and increase the risk o meningitis. Normocapnia or permissive hypercapnia (PaCO2 near 60 mmHg) may improve the excision o a large tumor that extends beyond the sella. Hypercapnia increases cerebral blood ow and intracranial pressure, thereby transiently displacing the suprasellar tumor portion into the in rasellar compartment. Hypercapnia can produce cardiovascular complications such as hypertension, tachycardia, and myocardial ischemia.

Steroid Supplementation Routine administration o supplemental steroids can prevent an adrenocortical crisis in the ace o physiologic surgical stress. Removal o the anterior pituitary corticotrophs decreases steroid release rom the adrenal gland. Patients with Cushing’s disease may need supplemental steroids because baseline steroid secretion is maximal and insuf cient or the stress o surgery and anesthesia.

CHAPTER 38

Emergence I the arachnoid membrane has been penetrated, a smooth emergence rom anesthesia is essential to prevent repeated Valsalva maneuvers. Coughing on the endotracheal tube or vomiting a er extubation can reopen a CSF leak that has been resealed with brin glue or tissue packing o the sphenoid sinus. Persistent CSF leaks increase the risk o postoperative meningitis.

POSTOPERATIVE CONCERNS (TABLE 38-1) Diabetes Insipidus T e posterior lobe o the pituitary contains the axons o neurons originating in the hypothalamus that release antidiuretic hormone (ADH). Usually this portion o the pituitary is spared during transsphenoidal hypophysectomy. In act, even

TABLE 38-1

Complications of Transsphenoidal Hypophysectomy Carotid artery injury Central nervous system injury

ranssphenoidal Hypophysectomy

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i nearly 80% o these axons are transected, enough ADH is released to maintain water homeostasis. However, transient diabetes insipidus (DI) can occur within the rst 12–24 hours postoperatively. Consequences o DI include polyuria (> 2 mL/kg/h urine output), hypovolemia, and hypernatremia. T e diagnosis is con rmed by measuring increased serum osmolality (> 295 mOsm/kg) and decreased urine osmolality (< 300 mOsm/kg). Management involves uid replacement, maintenance plus replacing urinary losses, with hypoosmolar uids such as 0.5% normal saline. Intranasal administration o ADH (desmopressin) is given or signi cant polyuria. Excessive doses o ADH can lead to an iatrogenic orm o the syndrome o inappropriate antidiuretic hormone (SIADH), which causes water intoxication and hyponatremia.

Cerebrospinal Fluid Leak Persistent leak o cerebrospinal uid rom the surgical site may occur a er surgery. o prevent this complication, a Valsalva maneuver identi es the leak and then autologous at or thigh muscle can be used to patch the leak. Symptoms o postoperative CSF leak include rhinorrhea or uid trickling in the posterior pharynx along with a headache that worsens when leaning orward.

Loss o vision Ophthalmoplegia

Steroid Supplementation

Cerebrospinal uid leak

Most patients who have undergone hypophysectomy require postoperative replacement o cortisol. T e typical regimen uses a tapering daily dose o hydrocortisone.

Meningitis Nasal septum per oration Postoperative epistaxis Postoperative sinusitis

SUGGESTED READINGS

Patients with suggestive symptoms o myocardial ischemia but without the presence o S elevations on ECG can be characterized as having NS EMI or UA, two terms that indicate a similar pathology but dif er in severity. For patients with NS EMI, ECG changes such as S depression or -wave inversion may be present and cardiac biomarkers are

O’Gara P , Kushner FG, Ascheim DD, et al. 2013 ACC/AHA Guideline or the Management o S -Elevation Myocardial In arction. Circulation. 2013;127:e362–e425. Anderson JL, Adams CD, Antman EM, et al. 2011 ACC/AHA ocused update incorporated into the ACC/AHA 2007 Guidelines or the Management o Patients With Unstable Angina/ Non-S -Elevation Myocardial In arction. Circulation. 2011;123:e426–e579.

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Perioperative Myocardial Ischemia Tom Hayes, MD

Myocardial ischemia and myocardial in arction are requent causes o death in the 30 day period ollowing noncardiac surgery. Several studies have revealed that most myocardial ischemia events occur in the rst 48 hours a er surgery, most patients are asymptomatic, and perioperative myocardial ischemia is associated with a poor prognosis. T e perioperative period is associated with a prothrombotic, in ammatory state characterized by increased levels o brinogen and C-reactive protein, increasing the risk o myocardial in arction. Although plaque rupture and subsequent coronary artery thrombus ormation is the most common overall cause o myocardial in arction in nonsurgical patients, it is not the only mechanism o myocardial ischemia in the perioperative period. T e in uences o anesthetic drugs and the physiologic stressors o surgery may cause a mismatch in myocardial oxygen supply and demand that leads to myocardial ischemia. Regardless o whether the etiology o perioperative myocardial ischemia is plaque rupture or myocardial oxygen imbalance, the management o myocardial ischemia in this population should take into consideration the physiological principles o myocardial oxygen supply and demand, as well as the limitations placed on the use o traditional antithrombotic therapy protocols in patients undergoing surgical procedures.

MYOCARDIAL OXYGEN SUPPLY T e main determinants o myocardial oxygen supply are coronary blood ow and arterial oxygen content. In contrast to peripheral tissues, the heart extracts most o the available oxygen in arterial blood. Since oxygen extraction cannot be increased, improving blood ow and oxygen content are the most important compensatory mechanisms during times o increased demand. Derived rom Ohm’s law, coronary blood ow is equal to coronary per usion pressure divided by coronary vascular resistance. Because most cardiac per usion occurs during the relatively lower pressures o diastole, coronary per usion pressure is determined by the dif erence between aortic diastolic pressure and le ventricular end diastolic pressure. Since the duration o the systolic series o

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events is relatively xed, decreasing the heart rate increases the period o time spent in diastole and there ore increases myocardial oxygen supply. Coronary artery resistance is in uenced extrinsically by compression intracardiac vessels during the cardiac cycle and intrinsically by autoregulatory mechanisms dependent on circulating catecholamines and endogenous mediators such as nitric oxide and adenosine. Finally, arterial oxygen content is described below as the product o hemoglobin concentration and oxygen saturation with a minor contribution rom dissolved oxygen: myocardial O2 supply = coronary blood ow + arterial O2 content coronary blood ow = coronary per usion pressure/resistance = (DBP – LVEDP)/resistance arterial O2 content = (1.39 × Hb × SaO2) + (PaO2 × 0.003) aking these actors together, a strategy or optimizing myocardial oxygen supply should attempt to improve coronary per usion pressure by increasing aortic diastolic pressure while decreasing ventricular end diastolic pressure, decreasing heart rate to lengthen diastolic per usion time, decreasing coronary vascular resistance, and optimizing arterial oxygen content. Depending on the likely source o myocardial ischemia, possible therapies to achieve these goals could include agents such as an alpha adrenergic agonist, beta adrenergic blockade, nitroglycerin, red blood cell trans usion (i Hb < 10), increasing FiO 2, and, i these therapies ail, an assistive device such as an intra-aortic balloon pump.

MYOCARDIAL OXYGEN DEMAND T ere are three major determinants o myocardial oxygen consumption: heart rate, contractility, and ventricular wall tension. While heart rate is relatively easy to measure and manipulate pharmacologically, contractility and ventricular wall tension are more challenging. Echocardiography can be used to qualitatively assess contractility through the observation o global/regional wall motion and quantitatively by comparing 207

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pre-ejection period and le ventricular ejection time. Ventricular wall tension can be estimated using the law o Laplace: wall tension = (pressure × radius)/(2 × wall thickness) Additionally, ventricular wall tension is in uenced by preload and a erload, as higher preload will increase le ventricular radius and higher a erload will increase the wall tension required during systole. In the setting o myocardial ischemia caused by a mismatch in myocardial oxygen balance, decreasing myocardial oxygen demand requires decreasing heart rate, contractility, and ventricular wall tension.

MONITORING AND EVALUATION OF PERIOPERATIVE MYOCARDIAL ISCHEMIA Intraoperative ECG monitoring that includes leads II and V5 has been ound to detect 80% o episodes o myocardial ischemia detectable on 12-lead ECG monitoring. In postoperative patients, a 12-lead ECG should be obtained in all patients with suspected myocardial ischemia. Continuous invasive blood pressure monitoring via an intra-arterial catheter should be considered in high risk patients. Early detection o hypotension and close management o vasoactive medication therapy are aided by the use o invasive blood pressure monitoring. Pulmonary artery catheter monitoring is not recommended or routine use in surgical patients, but may be indicated by patient actors such as ventricular ailure, pulmonary hypertension, or severe valvular disease. Intraoperative transesophageal echocardiography can detect regional wall motion abnormalities and is a sensitive monitor or myocardial ischemia in addition to providing assessment o overall ventricular unction, valvular disease, volume status, and pericardial pathology. As many as one-third o deaths a er noncardiac surgery may be attributed to myocardial ischemia, yet most patients experiencing ischemia during this period do not mani est typical symptoms including chest pain. Considering this, the

use o serial troponin measurements may aid in the detection o myocardial ischemia in high-risk patients. While some studies have advocated the routine use o postoperative troponin testing, there is no consensus on when to use routine testing in asymptomatic patients. All patients with suspected myocardial ischemia should receive at least two to three troponin measurements at 6–8 hour intervals to assess or the presence o myocardial injury. During the intraoperative period, the risk o catastrophic surgical bleeding prevents patients with signi cant S elevations rom being treated with the antiplatelet and antithrombotic therapies recommended by the ACC/AHA S EMI treatment algorithm. For patients with recognized myocardial ischemia, the treatment should ocus on optimizing myocardial oxygen supply–demand balance with the speci c goals to avoid tachycardia, hypotension, and hypertension. Pain should be treated aggressively and 100% oxygen delivered. Any identi ed pH or electrolyte abnormalities should be corrected as well as ensuring normothermia. Cardiology consultation should be obtained and postoperative medical and interventional therapies should take into consideration the potential or bleeding complications. It has been suggested that the administration o aspirin and a statin medication have a avorable risk–bene t pro le, but this area is still under investigation or patients experiencing myocardial ischemia in the perioperative period.

SUGGESTED READINGS Devereaux PJ, Xavier D, Pogue J, et al. Characteristics and shortterm prognosis o perioperative myocardial in arction in patients undergoing noncardiac surgery. Ann Intern Med. 2011;154:523–528. Botto F, Alonso-Coello P, Chan M , et al. Myocardial injury a er noncardiac surgery: a large, international, prospective cohort study establishing diagnostic criteria, characteristics, predictors, and 30-day outcomes. Anesthesiology. 2014;120:564–578. Devereaux PJ, Mrkobrada M, Sessler DI, et al. Aspirin in patients undergoing noncardiac surgery. N Engl J Med. 2014;370:1494–1503.

Coronary Artery Bypass Graf ing Lisa A. Andersen, DO, Hanwool Ryan Choi, and Tricia Desvarieux, MD

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SURGICAL CONCERNS

PREPARATION FOR CPB

Indications

Anticoagulation

Coronary artery bypass gra ing (CABG) is indicated in patients with (1) chronic stable angina and high-risk vessel disease; (2) unstable angina; (3) post-MI angina; and (4) atypical symptoms and ischemia on noninvasive testing. Anatomical indications or CABG include triple-vessel disease, le main coronary artery stenosis > 50%, severe proximal vessel stenosis > 70%, and le anterior descending or le circum ex artery stenosis in the presence o le ventricular dys unction.

For anticoagulation, heparin administered prior to cannulation prevents thrombosis in the patient and in the CPB circuit. A er 3 minutes, an activated coagulation time (AC ) measurement ensures appropriate anticoagulation has been achieved.

Contraindications CABG is not indicated or asymptomatic coronary artery disease (CAD) patients at low risk or myocardial in arction (MI) or death, or or individuals who lack viable myocardium. I the a ected coronary artery is too small or gra ing or vessel harvesting is estimated to be inadequate, CABG should not be attempted. Advanced age, due to comorbidities and increased unctional decline, may place patients at higher risk or perioperative complications.

SURGICAL TECHNIQUE CABG is per ormed through a median sternotomy incision. Following incision and cardiac exam, vessel harvesting or gra ing commences. Common vessels or gra ing include the internal thoracic (mammary) arteries, radial arteries, or saphenous veins. Once vessels have been chosen and removed, the patient undergoes preparation or cardiopulmonary bypass (CPB). CPB redirects deoxygenated venous blood away rom the right atrium (RA), removing carbon dioxide, introducing oxygen, and then returning oxygenated blood to the ascending aorta or less commonly to one o the emoral arteries. CPB permits temporary diversion o blood ow rom the heart and lungs to an extracorporeal circuit, thereby providing a unctionally similar means o ventilation and per usion while rendering the heart bloodless or vessel gra ing surgery.

Cannulation Once the patient is anticoagulated, the surgical team proceeds with vascular cannulation. Cannulation provides access or the CPB circuit to remove deoxygenated blood rom venous circulation and return oxygenated blood to arterial circulation.

Arterial Cannulation Conventionally, arterial cannulation is per ormed f rst to provide a conduit or volume resuscitation should it be required. T e ascending aorta is the pre erred site or arterial cannulation, given ease o access and minimal dissection risk, and additional incision is not required. Alternatively, a emoral, iliac, or axillary artery may be used i aortic cannulation is contraindicated due to severe atherosclerosis.

Venous Cannulation Venous cannulation is accomplished with a single atrial cannula via drainage holes in the RA only, cavoatrial cannula with drainage holes in the RA and IVC, or with bicaval cannula via drainage holes in the IVC and SVC. Single atrial cannulation is easier and aster to per orm, requiring one incision. It provides adequate right heart, IVC, SVC, and coronary sinus drainage, but quality depends on cardiac positioning and can be compromised when the heart is li ed into the circum ex position or circum ex coronary artery gra ing. A cavoatrial cannula has a similar benef t prof le with improved right heart drainage in the circum ex position, although SVC drainage may remain compromised. With the bicaval cannula approach, an 209

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additional incision into the RA is required or cannulation o both the IVC and SVC. T is technique provides better SVC drainage during circum ex positioning and better RA access; however, because drainage holes are isolated to the cavae and caval tourniquets are utilized to prevent communication with the RA (i.e., caval occlusion), blood returning to the RA via the coronary sinus cannot be drained and must be removed by opening or venting the right heart. Deciding which venous cannula is most appropriate or CPB is based on anatomy and arteries undergoing gra ing.

CARDIOPULMONARY BYPASS Once the patient is anticoagulated and cannulated, the perusionist primes the CPB machine with 1.5–2 L o uid to eliminate microemboli within the circuit and to provide hemodilution, a er which CPB is initiated. T e main components o a CPB machine include tubing to remove deoxygenated blood rom the venous cannula, a venous reservoir, a systemic ow pump (centri ugal or roller), an oxygenator (membrane or bubble), a heat exchanger, an arterial f lter, and tubing to return oxygenated blood to the arterial cannula.

Basic CPB Circuit During CPB, deoxygenated blood is drained by a gravity siphon rom the venous cannula—usually cavoatrial RA and IVC—via large bore tubing into the venous reservoir. Blood is then pumped by the systemic ow pump rom the venous reservoir through the oxygenator where CO2 is removed and O2 and volatile anesthetic are introduced, and then on to the heat exchanger or active cooling and rewarming. T e blood, now oxygenated and temperature controlled, exits the heat exchanger and passes through the arterial f lter and associated bubble trap to remove any particulate matter and gaseous microemboli that may have ormed. From there, the f ltered, oxygenated blood is returned to the arterial circulation via large bore tubing connected to the arterial cannula within the ascending aorta.

Additional CPB Components Additional accessory components include separate pumps or venting the le ventricle, aortic root suctioning, cardiotomy suctioning or blood salvage, cardiotomy reservoir with microf lter, gas blender and ow meter, anesthetic vaporizer, gas f lter, water source or the heat exchanger, a purge line or the arterial f lter, and various sensors to monitor the CPB process. In addition, a separate one-pass circuit delivers cardioplegia solutions, including a recirculation arterial line rom

the oxygenator as the cardioplegia blood source, a spur rom the arterial line to add cardioplegic solution, a separate pump and heat exchanger, as well as an antegrade or retrograde catheter to deliver cardioplegic solution to the proximal aorta or coronary sinus respectively.

Cardioplegia A er initiating CPB, the surgical team places an aortic crossclamp proximal to the arterial cannula to isolate the heart and prevent CPB circuit back ow, thereby ensuring a bloodless heart or surgery. Once clamped, cardioplegia ensures a nonbeating heart via diastolic arrest. Cardioplegia renders asystole by intermittently per using hypothermic (4°C) crystalloid solution containing high concentrations o potassium with or without blood. In addition to ensuring a nonbeating heart or surgery, hypothermic cardioplegia provides myocardial protection by lowering myocardial metabolic demand. T e lower myocardial metabolic rate prevents ischemic injury and in arction in spite o blood ow diversion rom the heart and subsequent oxygen deprivation during CPB.

ALTERNATIVES TO CPB FOR CABG Less invasive alternatives to CPB exist. O -Pump Coronary Artery Bypass (OPCAB) involves per orming CABG on a beating heart without cannulation, CPB, or cardioplegia and accounts or approximately 20% o all coronary artery bypass procedures. In general, during OPCAB a median sternotomy incision is made and special retractors (e.g., Starf sh, Octopus) are applied to the sur ace o the heart to aid in positioning and stabilization o the anastomotic site. T ese retractors use suction cups to li the anastomotic site, allowing target vessel exposure, motion reduction during bypass gra suturing, and hemodynamic stability in the reely beating heart. T ere are no clear-cut indications or the use o OPCAB as it does not provide benef t compared with CPB in terms o quality o li e or overall mortality. Other alternatives to CPB include minimally invasive direct coronary artery bypass surgery (MIDCAB), a technique in which bypass is per ormed through a 5–10 cm incision, total endoscopic coronary artery bypass with robotic technology, and transmyocardial laser revascularization, reserved or individuals unsuitable or standard CABG due to poor distal coronary anatomy. T e choice o surgical procedure depends on the patient’s a ected vessels, comorbidities and personal pre erences, and the pre erence o the surgical team per orming.

Cardiopulmonary Bypass: Overview James K. Kim, MD, and Johan Suyderhoud, MD

Cardiopulmonary bypass (CPB) is a orm o extracorporeal circulation that diverts the patient’s blood rom the heart and lungs, rerouting it, and assuming control o the normal physiological unctions o the heart and lungs, including maintaining whole body blood per usion pressure, oxygenation, and CO2 elimination during cardiovascular and thoracic surgery. CPB allows surgeons to operate on a nonbeating heart in the setting o a bloodless eld while maintaining adequate whole body tissue oxygenation and per usion.

CARDIOPULMONARY BYPASS CIRCUIT T e CPB circuit serves ve major unctions: circulation o blood, oxygenation, ventilation, systemic cooling and rewarming, and diversion o blood rom the heart to provide a bloodless surgical eld. During CPB, venous blood is drained passively rom the right atrium into a venous reservoir via a venous return cannula (Figure 56-1). T e reservoir is placed below the level o the patient to allow or gravity drainage, and serves as a large mixing chamber or all blood return (e.g., cardiotomy suction, aortic root and le atrial vents) as well as or additional uids and medications. In most cases, negative pressure is not used. T ere ore, the amount o venous drainage is accounted or by the central venous pressure (CVP), the resistance to ow in the venous circuitry, and the column height between the patient and reservoir. T e arterial pump unctions as an arti cial heart by pulling blood rom this reservoir and driving it through the oxygenator or gas exchanger (arti cial lung), a heat exchanger, and an arterial line lter. T e oxygenated, warm blood then returns to the patient’s arterial system via an arterial line typically positioned in the ascending aorta. Additional components o the circuit include pumps and tubing or cardiotomy suction, venting, and cardioplegia delivery and recirculation, along with air bubble detectors, blood sampling ports, pressure monitors, and in-line blood gas monitors (Figure 56-2). T e cannulation sites depend on the type o operation planned. Most cardiac procedures use ull CPB, which involves blood that is drained rom the right atrium and

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returned to the ascending aorta. Aorto-atriocaval cannulation is the pre erred method; however, i emergent access is needed, emoral arteriovenous cannulation may be the technique o choice. Some procedures, including surgeries involving the thoracic aorta, are per ormed using partial bypass, which is a technique that removes a portion o oxygenated blood rom the le side o the heart and returned to the emoral artery. Partial bypass allows or per usion o the head and upper extremity vessels via the beating heart, and distal perusion below the level o the aortic cross-clamp via retrograde ow by the emoral artery. Because all blood passes through the lungs, an oxygenator is not required.

PHYSIOLOGIC EFFECTS Cardiopulmonary bypass is associated with a severe in ammatory response primarily induced by contact o blood with nonendothelial extracorporeal sur aces. T is in ammatory response leads to platelet, endothelium, and leukocyte activation, initiation o the coagulation cascade, and decreases levels o coagulation actors. Various detrimental in ammatory mediators are released, resulting in tissue edema and capillary leakage. T is in ammatory process in the setting o the various comorbidities in these patients explains many o the challenges involved during the weaning process and post-bypass period, including myocardial dys unction, vasodilation, and bleeding. Other organ systems can be a ected by the perioperative stress and insults o cardiac surgery, including the central nervous system (CNS), kidneys, heart, lungs, and gastrointestinal tract.

Central Nervous System T e incidence o cerebral injury varies depending on di erent studies. CNS dys unction a er CPB can include shortterm (less than 1 month) neurocognitive de cits (25%–80%), longer term postoperative cognitive dys unction (10%–40%) to overt strokes (1%–5%). Although the mortality rate a er CABG is relatively low ( 1.2 [mg/dL]), atherosclerosis (peripheral vascular disease, cerebrovascular disease), diabetes, CHF (EF < 35%), or primary kidney disorders (polycystic kidney disease). 2. Abdominal or thoracic aortic procedures, lung transplant, and combined (CABG/valvular procedures, valvular repair/replacement) repeat cardiac surgery and emergent cardiac surgery, among other types o surgery. 3. Preoperative use o intra-aortic balloon counter pulsation and COPD, among other perioperative actors. 4. Postcardiac AKI is a consequence o many perioperative actors that contribute to injury. Various causes o renal injury during CPB include renal ischemia, reper usion injury, emboli, and the use o contrast agents.

Myocardial Function During cardiac surgery patients may su er some degree o myocardial injury, given the nature and target o the

Cardiopulmonary Bypass: Overview

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operation. Injury can be mani ested with increases in biomarkers or myocardial damage, with or without electromechanical cardiac dys unction. Risk actors or myocardial injury include acute ischemic events (acute myocardial in arction), signi icant LV dys unction, aortic crossclamping, and cardioplegia. Aortic crossclamping with cardioplegia has been associated with myocardial stunning, which typically resolves over 48–72 hours a ter an ischemic event. Cardioplegia is administered to arrest electromechanical activity in order that cardiac procedures can be per ormed in a quiescent, bloodless eld. T e main goals o cardioplegia include immediate and sustained electromechanical quiescence, maintenance o therapeutic additives in e ective concentrations, and periodic washout o metabolic inhibitors. All cardioplegic solutions contain greater than physiologic levels o potassium, but they all vary in individual chemical constituents with respect to the addition o numerous additives. For example, various substrates, such as oxygen, glucose, amino acids, and bu ers may be added, along with citrate to reduce calcium overload. Cardioplegic solutions can be either cooled or warm. Cold cardioplegia was elt early on to enhance myocardial preservation by reducing myocardial oxygen consumption, while warm cardioplegia better preserves myocardial cellular unction and reduces the incidence o both postoperative low output syndrome and cardiac enzyme release. Although there appears to be no statistical di erence in 30-day outcomes with either temperature method, there may be a slight advantage or cold cardioplegia or cases requiring prolonged aortic crossclamp times. Cardioplegia can be administered via two routes: anterograde or retrograde. Retrograde cardioplegia involves introducing the cardioplegia catheter into the coronary sinus, which allows or continuous cardioplegia administration. It is use ul in situations in which antegrade cardioplegia is dif cult to per orm, including the presence o severe aortic insuf ciency, severely diseased coronary arteries, or during aortic root/valve surgery. T e ideal per usion pressure to limit perivascular edema and hemorrhage is less than 40 mmHg. Antegrade cardioplegia delivers the solution to the heart via the coronary ostia in the normal direction o blood ow (antegrade per usion).

Pulmonary System Pulmonary complications can be one o the earliest recognized complications o cardiac surgery using CPB. CPB has negative e ects on the mechanical properties o the lungs (compliance and resistance) and the pulmonary capillary permeability. Increased permeability has been shown to cause various degrees o pulmonary edema, leading to compromised gas exchange and increased alveolar–arterial oxygen pressure gradient. Acute Respiratory Distress Syndrome (ARDS) and pulmonary dys unction a er cardiac surgery are mainly attributed to the in ammatory response and implicated in increased pulmonary endothelial permeability.

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Gastrointestinal System T e incidence o postcardiac GI complications is in requent (0.5%–5.5%). Many perioperative risk actors or GI actors have been identi ed, including the ollowing: 1. Preoperative—Age, history o CHF, renal insuf ciency, peptic ulcer disease, recent AMI, chronic lung disease, diabetes mellitus, peripheral vascular disease, use o intra-aortic balloon pump. 2. Type o cardiac surgery—Emergency surgery, cardiac transplantation, reoperations, valve or combined procedures. 3. CPB actors—Crossclamp duration, CPB duration. 4. Postoperative—Low cardiac output, vasopressor/IABP requirement, renal ailure, loss o normal sinus rhythm, reoperation or bleeding, ICU stay > 1 day, increased lactate or bilirubin, ventilation > 24 hour. Post-cardiac adverse GI outcomes include hyperbilirubinemia (3.7%), GI bleeding (1.2%), pancreatitis (0.8%), cholecystitis (0.3%), bowel per oration (0.1%), and bowel in arction (0.1%).

MANAGEMENT OF CARDIOPULMONARY BYPASS The Pre CPB Period Prior to initiating CPB, two key steps must be per ormed: anticoagulation (most commonly with heparin) and vascular cannulation. Heparin must be given prior to cannulation to decrease the risk o thrombosis in both the patient and the CPB circuit, even i it must be done emergently. A ter at least 3 minutes have gone by, an activated clotting time (AC > 450 seconds) must be checked to determine i adequate anticoagulation is achieved. A er anticoagulation, vascular cannulation is obtained with both venous and arterial cannuli in order that the CPB pump is able to divert all systemic venous blood to the pump oxygenator at the lowest possible venous pressures and deliver oxygenated blood to the arterial circulation at a pressure that is adequate or systemic per usion. Arterial cannulation is achieved rst, most commonly in the ascending aorta due to easy accessibility, a diameter that accommodates a larger cannula, and lower risk or aortic dissection (compared to emoral or iliac arteries). During aortotomy, the aortic pressure should be temporarily decreased (MAP < 70 mmHg) to decrease the risk o aortic dissection. Complications o aortic cannulation include inadvertent per oration o aortic arch vessels, aortic dissection, embolization o air or atheromatous material, and other vascular wall injury. Venous cannulation is achieved using an atrial cannula inserted through the right atrium and directing it in eriorly toward the in erior vena cava (IVC). T e drainage holes in the cannula are positioned in the IVC and the right atrium

to drain returning blood rom the lower extremities and the superior vena cava (SVC) and coronary sinus, respectively. When right atrial access is required during surgery, a bicaval cannulation technique is used, which involves cannulating the SVC and IVC. Because this technique does not provide adequate draining o the coronary sinus, an additional vent or atriotomy is mandated. In either case, care must be taken to ensure that venous ow rom the SVC is not impaired leading to SVC syndrome. During CPB, it is important to avoid le ventricular lling and distention to minimize LV wall tension, prevent myocardial rewarming, and reduce myocardial oxygen demand. Blood will naturally return to the LV rom the bronchial and thebesian veins, as well as blood that navigates through the pulmonary circulation. However, to avoid LV distention, a vent may be placed in the LV through the le superior pulmonary vein. Instilling retrograde cardioplegia will necessitate placement o an aortic root vent as well during the aortic cross clamp period.

Initiation of CPB Once cannulation is complete, CPB may be initiated, but it is wise to always complete a checklist to ensure that conditions are optimized prior to CPB ( able 56-1). When CPB is initiated, the per usionist progressively increases the delivery o oxygenated blood to the arterial system as the systemic venous blood is drained into the pump’s venous reservoir. Ideally, all systemic venous blood should be drained rom the patient to the pump reservoir once ull arterial ow is achieved. Systemic arterial hypotension is relatively common upon initiation o CPB, mainly due to the acute reduction o blood viscosity that results rom the hemodilution with nonblood priming solutions. ransitioning rom normal pulsatile blood ow to CPB-administered nonpulsatile ow will also a ect vascular resistance and MAP, though these changes are usually transient. MAP increases once hypothermia is induced due to vasoconstriction and increased systemic vascular resistance. Pump ow and pressure during CPB are titrated to careully balance surgical visualization and adequate oxygen delivery. Pump ow and pressure are determined by overall arterial impedance, which is a product o temperature, hemodilution, and arterial cross-sectional area. For example,

TABLE 56-1

Pre CPB Checklist

(1) Anticoagulation with heparin (2) Check ACT (goal > 450 s) (3) Supplemental medications (neuromuscular blockers, anesthetics, analgesics, amnestics) (4) Pulmonary artery catheter drawn back 3–5 cm to prevent pulmonary artery injury during heart manipulation by the surgeon (5) Absence o bubbles in arterial line (6) All monitoring/access catheters are unctional

CHAPTER 56

pump ows o 1.2 L/min/m² adequately per use most o the microcirculation when the hematocrit is 22% and hypothermia is induced. However, when hematocrit decreases, oxygen consumption increases, and/or temperature increases, these ows become inadequate. Nomograms are used to select the ideal pump ow based on temperature and oxygen consumption. In adults, the target ow rate during CPB is 2.2–2.4 L/ min/m² in normothermic patients. Along with nomograms, mixed venous saturation is also monitored, with a target goal o 70% or greater. However, these values do not guarantee adequate per usion because some tissue beds (muscle, subcutaneous at) may be unctionally removed rom circulation during CPB, and hypothermic venous saturation may overestimate end-organ reserves. Use o cerebral oximetry monitoring, or other physiologic measurements o brain unction, may also be used to guide optimal CPB ow rates.

Weaning from CPB Prior to discontinuing CPB, a series o steps must be taken to optimize and restore cardiac and pulmonary unction ( able 56-2). Intraoperative awareness is most common during rewarming as brain normothermia is restored in the setting o decreased anesthetic concentration. T us, additional anesthetic doses/agents may be needed in the rewarming phase (an estimated 0.01% o patients experience awareness

TABLE 56-2

Preparing to Separate from CPB

Checklist

(1) Rewarm: nasopharyngeal temperature 36–37°C, rectal/bladder temperature > 35°C, but < 37°C (2) Obtain stable cardiac rate and rhythm (using pacing i necessary) (3) All monitors and arterial line in place and unctioning (4) Ventilation reinstituted (5) Intravenous f uids restarted (6) Inotropes/vasodilators/vasopressors prepared and available (7) Metabolic parameters: arterial pH, PO2, PCO2 within normal limits, Hct: 20%–25%, potassium: 4.0–5.0 mEq/L, ionized calcium

Cardiopulmonary Bypass: Overview

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during cardiac surgery). Acid–base, calcium, and potassium abnormalities should be addressed, along with ensuring adequate hemoglobin levels. he Society or horacic Surgeons recommends that nadir hemoglobin levels or most patients undergoing CPB should be in the range o 6–7 g/dL, and in some select cases higher. Means to assist and/or maintain cardiac electrical activity should be in place as well, i so required. Be ore discontinuing CPB, the lungs must be rein ated with positive pressure, which is applied repeatedly until all areas o atelectasis are visually rein ated. Some studies show evidence o increased deadspace-to-tidal volume ratio a er CPB, which would result in increased PaCO2. Other studies illustrated modest increases in pulmonary shunt raction a er CPB, leading to suboptimal oxygenation and decreased PaO2. T e ventilatory rate should be increased by 10%–20% above pre-CPB values to compensate or increased dead space, and FiO2 should be set at 80%–100% with subsequent adjustments based on arterial blood gas analysis. Once all the steps are taken to optimize cardiopulmonary unction ( able 56-2), CPB may be discontinued. T e venous out ow line is slowly clamped, and the patient’s intravascular volume and ventricular loading conditions are restored by trans usion o per usate through the aortic in ow line. When conditions are optimal, the aortic in ow line is clamped and the patient is separated rom CPB. At this point, the patient’s oxygenation, ventilation, and per usion status must be care ully monitored, and i any o these are compromised, CPB can be restarted by unclamping the venous and arterial lines, and restoring pump ow. T is allows or systemic support while a diagnosis is made and treatment is instituted to success ully separate again rom CPB. T is may include both pharmacologic (vasopressor/inotropic/ inodilator agents in combination) and mechanical myocardial assistance measures (temporary cardiac pacing, intra-aortic balloon pump counter pulsation). Once cardiac parameters are elt to be optimized, vascular access cannuli are removed, anticoagulation is reversed with protamine sul ate, and the thoracic incisions are closed.

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Cardiopulmonary Bypass: Anticoagulation Hanwool Ryan Choi and Choy Lewis, MD

T e utilization o cardiopulmonary bypass (CPB) o ers a dichotomy in the need or complete anticoagulation in preparation or and while on CPB and or hemostasis at the end o CPB. T e surgical process itsel stimulates the release o thrombogenic substances such as tissue actor. Furthermore, blood has a natural tendency to clot when it encounters oreign sur aces and in addition, the presence o a oreign substance incites an in ammatory response that urther increases the propensity o the blood to clot. Because o this, the blood circulating through the cardiopulmonary bypass circuit is at high risk or clotting i special anticoagulation strategies are not employed. Such strategies include but are not limited to anticoagulation o the patient’s blood and the bypass circuit priming solution prior to placement o cannulas in the patient, as well as the use o heparin bonded bypass circuits. Patients are generally kept anticoagulated or the duration o the bypass period. At the completion o the bypass period, the heparin e ect is reversed, usually with protamine. T is is done to achieve hemostasis in an e ort to stave o or limit postoperative bleeding. In this chapter, we will review anticoagulation in preparation or and during CPB and strategies to achieve hemostasis a er the bypass period.

HEPARIN Anticoagulation is necessary in order to avoid the ormation o thrombus in the CPB circuit and prevent acute disseminated intravascular coagulation while on bypass. Un ractionated heparin is most commonly used or anticoagulation in preparation or CPB and while on CPB. Heparin is a large sul ated glycosaminoglycan polymer, which is negatively charged at physiologic pH. Because o its polarity and size, it stays primarily in the intravascular space. Peak onset o action is approximately 1–3 minutes a er administration invtravascularly and its elimination hal -li e is 1–1.5 hour. Heparin is excreted via the kidneys and is also metabolized by the reticuloendothelial system. Its anticoagulation e ect is via a special pentasaccharide sequence on the molecule that binds to antithrombin III and potentiates its inhibitor e ect primarily on thrombin and actor Xa and to a lesser extent on IXa, XIa, and XIIa as

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well. T e end result is a disruption o both the intrinsic and common pathways o plasma coagulation. Dosing or heparin is generally by weight or by dose– response titration. As or the weight-based method, most places use 300–400 U/kg in preparation or going on bypass. Keep in mind that or morbidly obese patients it may be better to dose to ideal body weight initially and give additional heparin i needed. T e dose response curve is generated by measuring the activated clotting time (AC ) be ore and a er a speci c dose o heparin (e.g., 200 U/kg). A line is drawn between the two results and via extrapolation; the dose o heparin needed to achieve the desired AC is acquired. With this strategy, the CPB priming solution also needs to have a heparin concentration (3–4 units/mL) similar to that o the patient’s bloodstream in order to prevent dilution. In order to achieve this, 5000–10,000 units o heparin is added to 1500 mL o the CPB priming solution.

ACTIVATED CLOTTING TIME T e degree o anticoagulation can be assessed by measuring the AC or the whole body heparin concentration. T e AC is the most requently used. For this test an activator, kaolin or celite, is added to activate clotting and then the time to clotting in a test tube is measured. T is can be done manually but is done via a machine in most places. Normal AC is 110–140 seconds. arget AC or cannulation and the initiation o CPB varies amongst institutions. In most places cannulation can begin with AC > 300 seconds. CPB initiation can generally occur with AC 400–480 seconds. AC is measured every 30 minutes to an hour while on CPB and additional heparin given i needed to maintain the desired level o AC . It is important to note that the AC may be independently prolonged by hypothermia and hemodilution and may lead to an overestimation o the degree o anticoagulation rom heparin. At temperatures less than 25°C, the degree o prolongation rom hypothermia may be so severe that you cannot reliably assess the level o anticoagulation rom heparin. Whole body heparin concentration (heparin concentration assays) may be used as an alternative to AC while 217

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on CPB. T e idea here is to keep the heparin concentration the same as be ore going on CPB to achieve the desired AC . T is approach may help with eliminating the CPB-induced distortion o the AC -heparin dose–response relationship. Drawbacks to this approach include the possibility o not anticoagulating enough as patients have varying sensitivity to heparin. In addition, the blood volume must be calculated when using this approach to determine the dose o protamine that is needed or heparin reversal. T is can be challenging while on CPB.

anticoagulants such as direct thrombin inhibitors (lepirudin, bivalirudin, danaparoid, and argatroban) should be considered. An alternative but less popular strategy is the use o heparin in conjunction with a platelet inhibitor such as epoprostenol or tiro ban. For patients with a history o HI but no detectable antibodies, a standard anticoagulation protocol with heparin can be used. I an acute occurrence o HI is suspected, heparin should be discontinued and plasmapheresis immediately instituted to remove heparin/PF4 antibody complexes. An alternative anticoagulant should then be administered until the normal platelet count is recovered.

HEPARIN RESISTANCE Some patients may require a much larger dose o heparin than anticipated to achieve a target AC . T is is called heparin resistance. Potential causes include antithrombin III de ciency (acquired or amilial), sepsis, pregnancy, drugs (heparin, nitroglycerin), and patients at the extremes o age. Antithrombin III de ciency is o en suspected as the most common cause. In patients with either acquired or congenital antithrombin III de ciency, a standard dosing o heparin alone achieves inadequate anticoagulation. For most cases o antithrombin III de ciency with milder resistance to heparin, additional doses o heparin can compensate. When the resistance cannot be overcome with more heparin (e.g., >600 units/kg total, >100 units/kg per 30 min, or minimal increase in AC a er 300 units/kg), an in usion o 2–4 units o resh rozen plasma or 500–1000 units o antithrombin III concentrate (human or recombinant) may be administered in order to acquire adequate anticoagulation.

HEPARIN-INDUCED THROMBOCYTOPENIA Heparin induced thrombocytopenia (HI ) describes an entity where the use o heparin induces platelet aggregation, thereby causing a drop in platelet count. In some sources this is reported to occur in up to 30% o patients who use heparin. HI type I is more acute and has more subtle clinical mani estations. T is orm o HI usually occurs within 2–5 days o heparin use and is characterized by a mild decrease in platelet count without any noticeable thrombosis or immune response. HI ype II is more severe and can be atal with some sources reporting a mortality rate o 7%–8%. It is suggested when the platelet count decreases by 50% or more without any other reasonable explanation or with thrombosis ormation 5–14 days a er heparin exposure or cardiac surgery. HI ype II is immune-mediated. Heparin orms a complex with platelet actor 4 (PF4) and antibodies orm to this complex. T is leads to platelet, endothelial cell, and complement activation. T e end result is thrombocytopenia and up to 20% o patients will also have thrombosis. For patients presenting to cardiac surgery with a history o HI and signi cant antibody titers, alternative

PROTAMINE When there is no longer a need or CPB, protamine is administered to reverse the heparin-induced anticoagulation. T is occurs via a neutralization reaction where positively charged protamine molecules bind to negatively charged heparin molecules to orm a large complex that is eliminated by the reticuloendothelial system. T e e ect is noticed within 2–5 minutes o the administration o protamine. Strategies or dosing protamine post bypass vary amongst providers. In the empiric approach, protamine is dosed based on the amount o heparin initially given. Protamine 0.6–1.3 mg per 100 units o heparin is generally given. Another approach uses a heparin dose–response curve, calculated be ore bypass. Here the heparin blood concentration is estimated immediately prior to neutralization and a dose o protamine deemed to be appropriate is administered. Another method involves administering a de ned dose and then checking or adequacy o reversal. Lastly, automated in-vitro heparin–protamine titration assays can help determine the optimal dose o protamine that is needed or reversal. When administering protamine, an initial test dose o protamine (10–20 mg) should be given over 60 seconds ollowed by a slow administration o the ull neutralizing dose over 10 minutes. Adequacy o reversal should be assessed by checking the AC 3–5 minutes a er the administration o protamine. Additional protamine may be required. Heparin may be released rom plasma proteins or endothelial cells and cause a subsequent rise in AC a er the initial neutralization. T is is sometimes called heparin rebound. In this situation, an additional dose o protamine (30–50 mg) may be suf cient to bring AC back to baseline. Similarly, when heparinized blood is given a er protamine has been administered, one may see a rise in AC because protamine does not remain in the blood stream or very long. A small bolus o 1–2 mg or protamine per 20 mL o heparinized blood given should provide neutralization. Protamine may cause adverse e ects (hypotension, pulmonary hypertension, cardiac depression) in some patients, especially when administered too quickly. T is is sometimes called a “protamine reaction.” Such reactions may be anaphylactoid or anaphylactic in nature. Hypotension is the most common adverse e ect and can be caused by vasodilation, pulmonary hypertension, or myocardial depression.

CHAPTER 57

T e vasodilatory e ect may be countered with a vasoconstrictor. In addition, volume loading may help to curb the e ect o vasodilation on blood pressure. Where an anaphylactoid or anaphylactic reaction is suspected, small boluses o epinephrine may prove bene cial, especially when there is recalcitrant hypertension. Marked pulmonary hypertension via pulmonary vasoconstriction is another serious adverse reaction o protamine. T is is believed to be caused by protamine-induced release o thromboxane rom pulmonary macrophages and may lead to right and le heart ailure. Inodilators in conjunction with vasoconstrictors may be help ul in this situation where there is combined severe pulmonary hypertension and hypotension. Mild cases o protamine reactions are usually sel -limiting. More severe cases may require a return to CPB and in that case a ull anticoagulating dose o heparin should be administered. rue anaphylactic reaction to protamine is rare but special precaution must be taken or patients with a history o prior reaction to protamine. Such patients should be given a very dilute test dose o protamine (1 mg in 100 mL over 10 minutes) and i no reaction occurs, the ull dose o protamine should be given slowly. Currently, there are no recommended alternatives to protamine that can e ectively restore AC . T is creates a problem or patients who cannot receive protamine because heparin, when not reversed post CPB, leads to persistent hemorrhage, trans usion requirement, hypovolemia, and consumptive coagulopathy. T ere was hope or platelet concentrates, synthetic polycators such as hexadimethrine, methylene blue, and heparinase I, but none has proven e ective in suf ciently and sa ely reversing protamine post CPB.

POST-BYPASS HEMOSTATIC DISORDERS CPB may incite various abnormalities that, i not tempered or treated, will lead to persistent bleeding and even hemorrhage postoperatively despite appropriate surgical hemostasis. Such abnormalities include thrombocytopenia, platelet dys unction, coagulopathy, brinolysis, and endothelial cell dys unction. able 57-1 lists these abnormalities, their causes, and strategies employed during CPB in an e ort to prevent them. Management o post bypass hemostatic disorders should be individualized to the patient and cause(s) or lack o hemostasis. Strategies include, but are not limited to, maintaining

Cardiopulmonary Bypass: Anticoagulation

TABLE 57-1

219

Abnormalities as a Result of CPB Protective Strategy

Abnormality

Cause

Thrombocytopenia

(1) Hemodilution (2) Sequestration (3) Consumption

(1) Priming bypass circuit with blood (2) Heparinbonded circuits (3) Minimized bypass circuit

Platelet dys unction

(1) Contact with bypass circuit (2) Hypothermia (3) Drugs (antiplatelet therapy preoperatively, heparin, protamine (4) Fibrin degradation products

(1) Heparinbonded circuits (2) Adequate rewarming post CPB (3) Appropriate heparin and protamine dosing (4) Anit brinolytics (5) Minimized bypass circuit

Coagulopathy

(1) Hemodilution (2) Consumption o coagulation actors

(1) Retrograde prime o CPB circuit (2) Heparinbonded circuits (3) Conservative administration o intravenous f uids

Fibrinolysis

(1) Release o endothelial plasminogen activators (2) Activation o plasmin rom in response to brin ormation

(1) Anti brinolytics

Endothelial cell dys unction

(1) Contact o blood with extracorporeal sur aces

(1) Heparinbonded circuits (2) Minimized CPB circuits

normothermia, continuation o anti brinolytic therapy, and trans usion o blood products (platelets, plasma, cryoprecipitate, recombinant Factor VIIa [rFVIIa]). Algorithms or trans usion may be bene cial in limiting the amount o blood products needed to gain hemostasis.

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Cardiopulmonary Bypass: Antif brinolysis Adam J. Rubinstein, MD

Physiologic hemostasis is a complex interplay between procoagulant and anticoagulant orces combining cellular and humoral actors so that neither excess hemorrhage nor clotting occurs. Surgery, cardiopulmonary bypass (CPB), trauma, and the associated resuscitation requently alter this nely tuned equilibrium, resulting in pathological hypercoagulable or hemorrhagic states. One o the critical components o physiologic coagulation is the generation o brin. Normally, very little circulating brin exists as it is produced de novo at the site o injury rom its widely distributed precursor, brinogen. As the nal product o the common coagulation pathway, the insoluble orm o brin serves as the structural ramework on which a dynamic hemostatic plug is created. In addition to its role as a template or coagulation, a highly concentrated brin network acts as a governor to limit the spread o thrombin and the proli eration o abnormal systemic coagulation. Fibrin production is tightly conserved and dependent not only on brinogen levels, but requires the presence o active thrombin, platelets, and Factor XIII (FXIII). In the uid phase o coagulation, brinogen is cleaved at N-terminal peptides by thrombin. T is leads to the ormation o soluble brin monomers, which rapidly polymerize with neighboring molecules into an insoluble brin matrix. T e presence o thrombin indirectly contributes to the stability o the resultant brin network through tissue expression o the anti brinolytic protease, plasmin activator inhibitor 1 (PAI-1). T rombin is also required to activate FXIII, which is integral to the constitution o stable, crosslinked brin and in the incorporation o endogenous anti brinolytics alpha2-antiplasmin (α2-AP) and activated thrombin-activatable brinolysis inhibitor ( AFIa) into the matrix. Additionally, the brin complex acilitates platelet aggregation and activation via glycoprotein IIa/IIIb receptors, thereby augmenting and urther stabilizing the hemostatic plug in the cellular phase o coagulation. T e role o the brin complex transcends that o primary hemostasis in that it is also involved in complex immunologic and in ammatory interactions enabling broblast proli eration, endothelial cell spreading, angiogenesis, and leukocyte signaling. While brin generation is essential to enabling physiologic hemostasis, equally important is its modulation by a

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complementary series o lytic proteases (Figure 58-1). In its circulating orm, plasminogen is unctionally inert and demonstrates little intrinsic brinolytic activity. However, when combined with brin and tissue plasminogen activator (tPA), active plasmin is produced. In vivo, tPA binds to αC domains on the brin matrix along with plasminogen to orm a ternary complex. T is con ormation causes plasminogen to convert into the active protease, plasmin. Subsequently, active plasmin cleaves the brin and exposes additional sites or plasminogen binding, thereby driving urther brinolysis. Highly crosslinked brin, which is typically encountered proximate to sites o vascular injury, is resistant to plasmin-mediated brinolysis due to the presence o the antibrinolytics α2-AP and AFIa. Moreover, plasmin production is inhibited in these areas by PAI-1 suppression o tPA release. Consequently, physiologic brinolysis is maintained towards the periphery o the hemostatic plug, away rom the site o injury, and is usually limited by available substrate. During CPB a variety o hemostatic trans ormations occur which a ect physiologic brin regulation. Shortly af er the initiation o CPB, the body is subjected to hemodilution and activation o circulating coagulation actors and cellular elements including red blood cells and platelets. Systemic thrombin generation increases dramatically, although most o it is inactivated by the administration o exogenous heparin and the ormation o the anti-thrombin III–heparin complex. Nonetheless, some o the excess circulating thrombin binds to protease activated receptors (PAR) in the vascular endothelium, leading to the release o endogenous tPA and contributing to abnormal brinolysis. With systemic heparinization and the associated inactivation o thrombin, total brin levels decline although CPB is characterized by the appearance o increasing amounts o systemic, soluble brin monomers. T ese aberrantly high levels o soluble brin along with brin deposition on the CPB circuit provide strong stimuli or plasminogen activation and the propagation o brinolysis. T e urther initiation and stimulation o the brinolytic system ensues via alternative pathways. Circulating actor XII (FXII) actuates upon contact with CPB sur aces into the active orm, FXIIa. T is leads to the creation o kallikrein, which not only activates additional FXIIa, but in turn yields bradykinin and triggers the release o tPA. Moreover, FXIIa 221

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Bra dykinin

Ka llikre in P la s minoge n

tP A

FXIIa P la s min

PAR

α 2-AP TAFIa

PAI-1

Fibrin

FDP

FIGURE 58-1

Fibrinolysis pathway. Schematic diagram o the f brinolysis mechanism. Green arrows indicate acilitation, while red arrows indicate inhibition. See text or abbreviations.

has been implicated in the direct conversion o plasminogen to plasmin and it may be involved with the recruitment o the complement system. Currently available anti brinolytic medications are synthetic analogs o the amino acid lysine and include the drugs epsilon-aminocaproic acid (EACA) and tranexamic acid ( XA). A third anti brinolytic, aprotinin, a bovine-derived nonspeci c serine esterase inhibitor which a ects plasmin, thrombin, kallikrein, and protein C, was removed rom the market in 2007 af er concerns o renal toxicity and increased mortality as compared to existing drugs. T e lysine analogs are thought to unction by competitive inhibition at lysine

binding sites on plasminogen, thus preventing the conversion to the active plasmin protease. Additionally, at higher doses these drugs may inhibit plasmin directly. O the two medications, XA is more potent and has a longer hal -li e than EACA, although it has been associated with an increased risk o seizures af er CPB. Side e ects and allergic reactions are rare, although caution should be used in patients with a history o thrombosis, and XA should be avoided in patients with acquired disturbances o color vision. Numerous clinical studies and meta-analyses o the current literature suggest that at clinical doses, both agents reduce the risk o bleeding without increasing the risks o MI, stroke, DV , PE, or mortality.

SUGGESTED READINGS Mosesson MW. Fibrinogen and brin structure and unctions. J T romb Haemost. 2005 August;3(8):1894–1904. Muszbek L, Bereczky Z, Bagoly Z, Komaromi I, Katona E. Factor XIII: a coagulation actor with multiple plasmatic and cellular unctions. Physiol Rev. 2011 July;91(3):931–972. Bolliger D, Gorlinger K, anaka KA. Pathophysiology and treatment o coagulopathy in massive hemorrhage and hemodilution. Anesthesiology. 2010 November;113(5):1205–1219. Sniecinski RM, Chandler WL. Activation o the hemostatic system during cardiopulmonary bypass. Anesth Analg. 2011 December;113(6):1319–1333. Ortmann E, Besser MW, Klein AA. Anti brinolytic agents in current anaesthetic practice. Br J Anaesth. 2013 October;111(4):549–563.

Cardiopulmonary Bypass: Anesthetic Considerations John A. Hodgson, MD

PREBYPASS PERIOD Prior to placing a patient on CPB, the bypass machine must be linked to the patient via arterial and venous cannulas. Placement o these cannulas is acilitated by skilled management o the patient’s blood pressure. T e arterial cannula is placed in the ascending aorta and in some cases, the emoral artery or axillary artery. T e venous cannula(s) are placed in the right atrium and IVC/SVC. During aortic cannulation it is the responsibility o the anesthesiologist to limit the systolic blood pressure to 100 mmHg to minimize the risk o aortic dissection during aortotomy. T is can be achieved by either increasing the inhaled anesthetic concentration or using vasodilators such as nitroglycerin. Once the aortic cannula is placed, the pressure is allowed to rise as the risk o complications during venous cannulation with respect to systolic blood pressure is minimal. In addition, at this point, in many centers, the institution o retrograde autologous priming will commence. In an e ort to decrease the hemodilution that occurs during CPB, a retrograde autologous prime can be per ormed in which the crystalloid prime o the CPB machine circuit is displaced by a retrograde ow o blood through the aortic cannula and into the CBP circuit. Roughly 1000 mL o blood is used to accomplish this prime. During this period, which usually lasts a ew minutes, the patient will o en require vasopressor support to maintain an adequate blood pressure. T is is also con ounded by the very recent need to lower SBP to acilitate aortic cannulation; thus, vasodilators may still be having an e ect. Once the prime is complete and the venous cannula is placed, the patient is ready or the institution o cardiopulmonary bypass (CPB). In some cases, the cardioplegia cannulas are placed be ore the start o CPB and in others this will occur a er.

BYPASS PERIOD Once CPB is initiated, during ull support, the arterial pressure tracing will lose its characteristic pulsatile wave orm, and, once the heart is arrested, will be completely devoid o any pulsatile activity, although a mean arterial pressure will be visible

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on the at pressure tracing. As long as the heart is arrested, the patient is cooled, and the per usionist is dosing cardioplegia at regular intervals, the main concern or the anesthesiologist is cerebral per usion and by de ault systemic per usion. It is generally accepted that as long as the MAP is maintained at 50–100 mmHg, the cerebral blood ow is preserved in otherwise normal patients. T is MAP target should be adjusted to 60 mmHg in patients with preexisting hypertension. T e physiologic response to CPB is complex and mimics the Systemic In ammatory Response Syndrome, causing decreased insulin release, increased insulin resistance, and hyperglycemia. Hyperglycemia has been shown to be detrimental to neurologic recovery in areas o the brain subjected to ischemia and these outcomes are worse in patients with blood glucose levels exceeding 180 mg/dL. T ere ore, the administration o insulin during CPB is an important step in minimizing adverse neurologic outcomes. It is not uncommon to administer 10 units/h while on CPB, keeping close attention to the blood glucose levels, and quickly titrating the in usion once CPB is completed. Since the lungs are bypassed, the delivery o “inhaled” anesthetic alls on the per usionist. A vaporizer with a volatile agent, usually iso urane, is an integral part o every CPB machine and upon institution o CPB, the anesthesiologist should pay attention that the iso urane vaporizer is turned to 1% and titrated as needed. Should there be problems with the vaporizer, the anesthesiologist can administer anesthetic agents via a total IV route. In addition, the anesthesiologist can administer neuromuscular blockers, but only a er ensuring the patient is receiving an adequate dose o anesthetic and analgesic agent. T e dosage requirements or anesthetic agents are reduced during hypothermia, but the anesthesiologist should always consider that during rewarming, the anesthetic requirements increase, and the administration o IV agents such as midazolam should be strongly considered. Although the control o temperature is by and large out o the hands o the anesthesiologist and related to the heat exchanger on the CPB machine and direct application o ice, the anesthesiologist should monitor temperature in order to approximate core and cerebral temperatures. Bladder, rectal, and esophageal temperatures approximate the core or body 223

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temperatures and the nasopharynx and tympanic membranes will most closely approximate brain temperatures. Keep in mind that the CMRO2 decreases by 7% or each drop in temperature by 1°C. Blood gas measurements are requent during CPB. In normal practice these blood samples are heated to 37°C be ore being analyzed. T e use o these blood gas measurements during CPB is re erred to as alpha-stat management. T is is the most common method in cardiac surgery. T e premise with alpha-stat management is to maintain electrical neutrality between H and OH ions which both decrease in concentration with decreasing temperature and the decreased concentration o H ions is re ected in an alkalosis at this lower temperature, which disappears once the blood sample is warmed in an analyzer. pH-stat management is used primarily in children on circulatory arrest. T is method involves temperature correcting the blood gas analysis to report the pH at the actual hypothermic temperature and attempting to maintain a pH o 7.4 and CO2 tension o 40 by adding CO2 to the oxygenator gas in ow to the patient. T e physiologic result o this practice is dilation o the cerebral vasculature, resulting in increased cerebral blood ow. T is results in greater brain cooling prior to deep hypothermic circulatory arrest but can lead to a greater risk o emboli in patients with atheromatous disease, thus the popularity in children but not in adults. T ere is little evidence o one technique over the other in terms o outcomes except or pH-stat management o children undergoing circulatory arrest.

SEPARATING FROM BYPASS When the time to separate rom bypass is imminent, a help ul pneumonic to remember is “ HIEVES”: • • • •

Temperature—T e patient should be normothermic to maximize cardiac contractility, and decrease the incidence o arrhythmias. Hemoglobin—It should be at least 7 g/dL. Infusions—I the patient will require inotropic support, these should be started a er removal o the aortic cross clamp. Electrolytes—Potassium should be approaching the normal range o 4–5 mEq/L.

• •

•

Ventilation—T e lungs should be ully expanded, ventilated, and a volatile agent being delivered i the patient can tolerate. ECG—T e heart should be paced at 90 bpm, the optimal rate or balancing oxygen demand with rate, f lling, and cardiac output in a heart with decreased compliance ollowing CPB. Special Considerations—Did the patient have an intraaortic balloon pump, or ventricular assist device and does this mechanical support need to be used again? I a EE is in place, the adequacy o deairing maneuvers can be assessed, and i valve repair or replacement perormed, the e ectiveness o the new or repaired valve can be determined.

T e time period o separating rom cardiopulmonary bypass requires close communication between the per usionist, surgeon, and anesthesiologist. During the weaning period, the per usionist decreases systemic output through the aortic cannula while the surgeon applies a clamp to the venous drainage to f ll the heart and allow the heart to take over the work o per using the body. T e anesthesiologist should be monitoring the systemic blood pressure, assessing cardiac contractility, and titrating vasoactive in usions to either increase contractility, increase systemic vascular resistance, or both as needed. Once the CPB machine has stopped pumping through the aorta and the venous return to the pump has been clamped, the patient is o CPB. At this point, blood pressure, contractility, and cardiac output are the responsibility o the anesthesiologist, although the per usionist can o en continue to trans use through the aortic cannula as needed until the blood in the reservoir has been utilized.

SUGGESTED READINGS Stein EJ, Glick DB, Minhaj MM, Drum M, ung A. Relationship between anesthetic depth and venous oxygen saturation during cardiopulmonary bypass. Anesthesiology. 2010;3(1):35–40. Heijmans J, Fransen E, Buurman W, Maessen J, Roekaerts P. Comparison o the modulatory e ects o our di erent asttrack anesthetic techniques on the in ammatory response to cardiac surgery with cardiopulmonary bypass. J Cardiothorac Vasc Anesth. 2007;21(4):512–518. Chakravarthy M, et al. Conscious cardiac surgery with cardiopulmonary bypass using thoracic epidural anesthesia without endotracheal general anesthesia. J Cardiothorac Vasc Anesth. 2005;19(3):300–305.

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Cardiopulmonary Bypass: Myocardial Preservation John A. Hodgson, MD

T e primary method o myocardial protection during cardiopulmonary bypass (CPB) remains the administration o cardioplegia and the institution o hypothermia.

CARDIOPLEGIA Cardioplegia solution composition varies between institutions but is generally composed o a combination o the ollowing: 1. Potassium (10–40 mEq/L) or arresting the heart in diastole, which is an easily reversible state; 2. Blood and/or crystalloid as the carrier; 3. Bicarbonate and/or HAM solution or bu ering the excessive acid metabolites on bypass; 4. Mannitol to help reduce edema; 5. Magnesium to reduce calcium overload; and 6. Citrate-phosphate-dextrose and amino acids such as glutamate and aspartate, or supplying any remaining metabolic demand o the heart which may only be present in the nal “hot shot” which warms the heart and removes any remaining metabolites and cardioplegia. T is cardioplegia solution is administered in an either antegrade or retrograde ashion. With antegrade administration, cardioplegia is injected in the aortic root space between the aortic valve and the aortic cross clamp. As the pressure in the aortic root builds, cardioplegia is orced down the le main and right coronary arteries and is delivered to the myocardium. In some patients, such as those with high-grade coronary blockages or aortic insu ciency, retrograde cardioplegia is given by placing a cannula in the coronary sinus which can be palpated by the surgeon and placement conrmed with EE. T rough this cannula, cardioplegia can be given in the reversed direction o normal blood f ow, beginning with the venous system and then being delivered to the myocardium. T is method avoids the need or a competent aortic valve and theoretically will deliver cardioplegia to those areas that are not per used well with the antegrade approach due to highgrade coronary blockages, while avoiding LV distension

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and incomplete protection that would occur with aortic insu ciency during antegrade administration. T e reason retrograde administration is not the only delivery method is that this route generally does not cover the le ventricle completely. Compared to antegrade administration, which is delivered through the arterial system and able to tolerate high f ow pressures, the retrograde route must be monitored and the recommended high pressure limit is 40 mmHg in order to avoid hemorrhage rom damage to the coronary sinus and venous systems which are di cult to repair. In most cases, a combination o antegrade and retrograde is used or the most complete coverage and protection o the myocardium. Other modi cations to this approach include the injection o cardioplegia directly into the coronary ostia a er aortotomy using small hand-held cannulas and the injection o cardioplegia into the bypass gra s a er the distal anastomoses are completed. Dosing intervals are usually every 20 minutes or when cardiac activity is observed, whichever comes rst. T is is due to gradual washout and rewarming and the need to remove the metabolites that inhibit anaerobic metabolism.

HYPOTHERMIA T e secondary method o myocardial protection is controlled hypothermia. T is is achieved by actively cooling the patient using the heat exchanger on the cardiopulmonary bypass machine and by directly applying ice slush to the heart. T is hypothermic state reduces metabolic rate, reduces oxygen consumption, preserves high-energy phosphate, and reduces excitatory neurotransmitter release. For each degree o temperature drop there is a 7% reduction in metabolic rate, meaning that at 28°C, the metabolic rate is cut by 50% and or systemic hypothermia the e ects are both neurological and myocardial. Myocardial temperatures can reach as low as 10°C with the direct application o ice and cold cardioplegia. Disadvantages o hypothermia include an increase in blood viscosity and the promotion o myocardial edema. Overall, however, the bene ts o hypothermia ar outweigh these risks. 225

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SUGGESTED READINGS Suleiman MS, Hancock M, Shukla R, Rajakaruna C, Angelini GD. Cardioplegic strategies to protect the hypertrophic heart during cardiac surgery. Perfusion. 2011;26:48–56.

Zeng J, He W, Qu Z, ang Y, Zhou Q, Zhang B. Cold blood versus crystalloid cardioplegia or myocardial protection in adult cardiac surgery: a meta-analysis o randomized controlled studies. J Cardiothorac Vasc Anesth. 2014;28(3):671–684.

Extracorporeal Membrane Oxygenation Bryan Laliberte, MD

Extracorporeal membrane oxygenation (ECMO) is an adaptation o the conventional cardiopulmonary bypass system or use as prolonged pulmonary and cardiopulmonary support. ECMO is generally instituted at specialized centers as a last resort or patients with respiratory or cardiac ailure unresponsive to conventional therapies. T e term ECMO is considered a broad ranging term or the range o methods or extracorporeal blood oxygenation and carbon dioxide removal. Other similar terms in current use include those listed in able 61-1. T is is considered a closed circuit system, which di erentiates it rom cardiopulmonary bypass (CPB) circuits, in that there is no blood reservoir and no arterial lter. T e early 1970s brought the introduction o ECMO as a treatment modality or acute respiratory distress syndrome (ARDS). Early advances in the design included improvements in the membrane lung, the access catheters, and bladder systems. Additionally, the concept o anticoagulation titration o the system with heparin reduced bleeding complications. T e year 1976 brought the rst neonatal survivor o ECMO by Dr Robert H. Bartlett or the treatment o a chemical pneumonitis secondary to meconium aspiration. Further research and monitoring o the state o ECMO was advanced in the 1980s by the introduction o multiple registries and nally by the charter o the Extracorporeal Li e Support Organization (ELSO), which houses the largest registered case series and promotes multi-institutional research. ECMO use is generally limited to those neonatal, pediatric, and adult patients with ailing respiratory and/or cardiac

TABLE 61-1

Artificial Cardiac or Pulmonary Support Acronyms ECMO

Extracorporeal membrane oxygenation

ECLS

Extracorporeal li e support

ECCOR/ECCO2R

Extracorporeal carbon dioxide removal

PECCO2

Partial extracorporeal carbon dioxide removal

AVCOR

Arteriovenous carbon dioxide removal

ECLA

Extracorporeal lung assist

IVOX

Intravascular oxygenator

E R

TABLE 61-2

ECMO Indication Indices for > 80% Predicted Mortality ○ Oxygenation Index (OI) > 40 or > 35 or 4 h ■ OI = (MAP × FiO2 × 100) / PaO2 ○ Ventilation Index (VI) > 90 or 4 h ■ VI = RR × PIP – PEEP/1000 ○ Alveolar–arterial oxygen dif erence (A – a)DO2 > 600–624 mmHg (at sea level) despite 4–12 h o medical management ■ (A – a)DO2 = (atmospheric pressure – 47) – (PaCO2 + PaO2)/FiO2 ■ 47 being vapor pressure at sea level ○ PaO2 < 50 mmHg or 2–12 h (FiO2 o 100%) ○ Acute deterioration PaO2 < 30–40 mmHg (FiO2 o 100%) ○ pH < 7.25 or 2 h ○ Intractable hypotension MAP = mean airway pressure, FiO2 = ractional inspired oxygen concentration, Pa O2 = oxygen tension (partial pressure) o arterial blood, Pa CO2 = carbon dioxide tension (partial pressure) o arterial blood, RR = respiratory rate, PIP = peak inspiratory pressure, PEEP = peak end expiratory pressure.

systems who do not respond to maximal medical therapy or those patients with inability to wean rom cardiopulmonary bypass. T e institution o ECMO is o en considered a last resort and is predicated on the act that there is no underlying lung damage caused by mechanical ventilation or that the cardiac insult is reversible. Mortality is increased with increasing lung injury patterns whether related to volutrauma, barotrauma, or oxygen toxicity. Several indices o re ractory hypoxemia are used to quali y patients or ECMO, all o these estimating a predicted mortality o > 80% without the treatment. T ese indices are listed in able 61-2 and are generally gained rom looking at retrospective data, and thus should be assessed in concert with other patient actors. T e primary goals gained rom an ECMO run are to remove CO2 and oxygenate the lung; improve oxygen delivery to tissues; provide lung rest and/or cardiac o oading; and to allow the normal physiologic metabolic environment to unction at tissue levels.

ECMO CIRCUIT T e ECMO circuit is composed o several di erent parts, all o which have variations with their own bene ts and risk. 227

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Inflow lume n

Right a trium

Dra ina ge lume n

Inflow lume n

5 cm Dra ina ge lume n Fluids a nd drugs

He pa rin Blood re turn Blood dra ina ge Bridge

He a t excha nge r Me mbra ne oxyge na tor

S e rvore gula te d pump

FIGURE 61-1

VV ECMO circuit. (Reproduced with permission rom Barrington KJ, Finer NN. Recent advances. Care o near term in ants with respiratory ailure. BMJ. 1997 Nov 8;315(7117):1215-1218.)

Figure 61-1 shows an example o a VA ECMO circuit. First is the blood pump, o which there are two main types, the roller pump and the centri ugal pump. T e roller pump needs to be routinely repositioned so as to avoid undue wearing o the tubing walls. An advantage o the roller pump is a decreased incidence o clinical hemolysis in in ants and neonates as compared to centri ugal pumps. Centri ugal pumps have the advantage o not being able to be blown out at normal pressures even with the arterial line occluded in VA ECMO. T e disadvantage o the centri ugal systems is that they do not have back ow valves and thus i the pump stops during VA ECMO, the patient can bleed out backwards. T e oxygenator or membrane lung is the second important component o the ECMO system. T e two primary variations o oxygenators are hollow ber and spiral wound silicone membrane. T e hollow bers showed good gas exchange and low circuit resistance; however, they were prone to early ailure as seen by decreased gas exchange. New developments in the coating o the bers have continued their use to this day. T e size o the membrane is dictated by the body sur ace area o the patient, the type o oxygenator, and the speci cations o the manu acturer. Frequently, the oxygenators have built-in heat exchangers, negating the need or a separate system and minimizing the circuit priming volume. Regardless o which oxygenator is used, there is a common issue o loss o insensible uids across the membrane, o en quoted as 5–10 mL/m 2/h at 37°C.

Heat exchangers employ a countercurrent mechanism to achieve optimal heating. T e water bath is kept at a low pressure (3–4 psi) to ensure that i a leak occurs the water does not leak into the circuit causing potentially disastrous results. Monitoring o the ECMO circuit consists o the measurement o in ow and out ow pressures, temperature, blood gases, mixed venous oxygen saturation (SmvO2, on VA ECMO), and a ow control meter. ubing length can be short or long depending upon the needs o the patient and the predicted need or road trips to the radiology scanners and/or the operative suite. ubing diameter varies rom ¼″ to ½″ depending upon the patient size. Heparin-coated circuit tubing is a mainstay to improve thromboresistance and to decrease the amount o systemic anticoagulation necessary or ECMO. Unlike CPB, the ECMO circuit contains a bridge between the patient drainage tubing and the out ow tubing. T is allows or isolation o the patient rom the circuit without decannulation, o en or routine tubing or oxygenator changes, but also or eventual decannulation planning. While usually clamped during the ECMO run, it is regularly unclamped to ensure patency. Due to the lack o a reservoir in the ECMO circuit, the patient’s body is the most compliant part o the system. T is can lead to third space edema and intravascular volume expansion when the circuit is overloaded. A bladder, the lowest point on the venous drainage side o the circuit, introduces a small variable volume component (~35 mL); however,

CHAPTER 61

this volume is not transportable to other parts o the circuit like a reservoir would do. T e primary unction o the bladder is to help monitor or hypovolemia or impaired venous drainage. T e sensing o a collapsed bladder by the monitors would shut o the blood pump so as not to entrain air into the system. A newer variation o the ECMO circuit is an integrated circuit, meaning an ECMO circuit is recon gured into a CPB circuit to allow switching between the two with eventual plans to separate completely and become an ECMO circuit independent o the CPB. T is con guration is being used or speci c pediatric congenital lesions that o en require urther support post repair. T is includes the arterial switch operation (ASO) or transposition o the great arteries, total anomalous pulmonary venous connection ( APVC), and anomalous le coronary artery rom pulmonary artery (ALPACA). T e noncollapsible reservoir and the collapsible bladder are connected in parallel and can be isolated depending upon whether CPB or ECMO is being used.

TYPES OF ECMO ECMO is generally divided into veno-venous (VV) and venoarterial (VA) ECMO. VV is primarily used to provide respiratory support, where the addition o cardiovascular support necessitates VA ECMO or even veno-arterial-venous (VAV) ECMO. T e right side o the heart is o oaded in VA ECMO and is used or rest. Because the ow is nearly nonpulsatile, a narrow pulse pressure is used to assess per usion, generally acceptable at 10–15 mmHg. T e preoxygenator O2 saturation is used as a measure o adequate oxygenation in this circuit. VA ECMO is maintained at 80% o calculated total ow because at 100%, T ebesian return to the le ventricle can result in distension and lead to subendocardial hypoperusion. With partial VA ECMO support, a major concern is that coronary blood ow rom the LV can be desaturated due to T ebesian return to the le side o the heart, resulting in hypoxic coronary per usion. A cannula in the right brachiocephalic artery can direct ow down the aortic root causing increased LV a erload and thus increased workload on the possibly distended le heart. As noted above, VV ECMO does not support the circulation and thus usually does not a ect the patient’s hemodynamics. Since blood is removed essentially removed rom the right atrium and returned there, oxygenation is blood ow dependent and aided by maintaining a higher hematocrit. Measurement and monitoring o oxygenation is done via arterial oxygen saturation (SaO2), mixed venous oxygen saturation (SmvO2, which is o en high), and preoxygenator saturation. An SaO2 o less than 70% is indicative o inef cient O2 delivery. VV ECMO can be accomplished via two single or one double lumen cannula. Recirculation o already oxygenated blood can be a major problem with single cannula ECMO circuits. T is can be minimized by optimizing pump ow, positioning o the catheter lower in the superior

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vena cava and by enhancing cardiac output so as to promote orward ow. Lower ows can be used with VV ECMO when used primarily or CO2 removal, since it is such an easily di usible gas. Conversion rom VV ECMO to VAV ECMO is done when previously cardiac stable patients become unstable and require urther support.

INDICATIONS/CLINICAL CRITERIA While indications or ECMO support also include the mortality-based indications discussed previously, patient clinical actors also play an important role. Most centers have varying criteria or their speci c ECMO program based on ast and slow entry criteria rom earlier studies on ECMO, so there is no one absolute set o guidelines. T ese criteria include oxygenation assessed on speci c settings during a speci c time course o the acute disease process, in addition to other actors. able 61-3 is an ever-growing, but not completely encompassing, list o indications or ECMO. Criteria or ECMO support is broadly broken down into respiratory and cardiac parameters, as listed in able 61-4.

INITIATION OF ECMO VV ECMO access can be accomplished via a singly cannulated vessel with a double lumen cannula, o en in the internal jugular or to the right atrium, otherwise double cannulation is used. Access or VA ECMO is generally extrathoracic but can be intrathoracic in postcardiac surgery patients. Positioning o the patient is done in the reverse- rendelenburg position with the head turned to the contralateral side o the cannula site. Most patients will be previously intubated and will simply need recon rmation o tube placement and securing. Anesthesia is otherwise accomplished with narcotics and paralytics. Blood and other resuscitative uids should be available at bedside in the event o massive blood loss during cannulation. Cannula size is determined by the surgeon and usually the largest size possible is chosen to optimize venous drainage and ECMO ow. Speci c to in ants, pressure is applied to the liver during cannulation to avoid air embolism. With carotid artery cannulation in VA ECMO, risks include hypotension and bradycardia related to the nearby lying vagus nerve. Further arrhythmias may occur due to cannula irritation o myocardial sur aces. Anticoagulation o the patient and the circuit is accomplished with heparin. T is must generally be done several minutes prior to cannulation. Heparin is redosed as necessary during the cannulation procedure according to activated clotting time levels. Heparinized cannulas and circuit tubing have also been used to help decrease the amount o systemic heparinization needed, thus decreasing bleeding complications. T e ECMO circuit or neonates and small in ants is primed with blood to a hematocrit o 40%, crystalloids, colloids, and bu ers to normalize pH. Potassium and

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TABLE 61-3

Indications for ECMO

TABLE 61-4

Criteria for ECMO Support

Neonatal indications

Respiratory

Congenital diaphragmatic hernia

Persistent pulmonary hypertension o the newborn

Asphyxia

Fast inclusion criteria • PaO2 < 50 mmHg or > 2 h at FiO2 100% plus maximal medical therapy or 24–120 h OR • PaO2/FiO2 < 50 mmHg at PEEP > 10 cmH2O OR • PaO2/FiO2 < 70 mmHg at PEEP > 10 cmH2O or 96 h

Respiratory distress syndrome

Meconium aspiration syndrome

Pneumonia

Sepsis

Slow inclusion criteria

Pro ound cyanosis due to intracardiac shunting (congenital heart disease)

Low cardiac output syndrome

Failure to wean rom cardiopulmonary bypass

Re ractory arrhythmias

• PaO2 < 50 mmHg or > 12 h at FiO2 > 60% and PEEP > 5 cmH2O plus maximal medical therapy or > 48 h; intrapulmonary shunt > 30%; thoracopulmonary compliance < 30 mL/cmH2O • Maximal medical therapy for 24–120 h. PaO2/FiO2 < 50 mmHg at PEEP > 10 cmH2O; intrapulmonary shunt > 30% at FiO2 100%; extravascular lung water > 15 mL/kg; thoracopulmonary compliance < 30 mL/cmH2O; recurrent barotrauma • 48–96 h after standard therapy plus three of four criteria: • PaO2/FiO2 < 150 mmHg at PEEP > 5 cmH2O or > 2 h • PaCO2 > 60 mmHg at minute ventilation > 200 mL/kg • Peak inspiratory pressure > 40 cmH2O • Thoracopulmonary compliance 30%

Pulmonary hypertension with circulatory ailure

Cardiac

Bridge to transplantation

Respiratory ailure

Re ractory metabolic acidosis Supramaximal inotropic support Inadequate tissue per usion Mixed venous PA saturations < 50% Cardiac index < 2 L/min/m 2 Impending multiorgan ailure/dys unction Peripartum cardiomyopathy Myocarditis Decompensated re ractory myocardial ailure

Pediatric indications

Cardiac surgery indications 15

Cardiogenic shock not responding to maximal therapy

Global myocardial ailure

Failure to wean rom cardiopulmonary bypass

Bridge to cardiac rest and recovery

Other indications 19

Acute respiratory distress syndrome (ARDS)

Acute severe asthma/status asthmaticus

Chronic obstructive airway disease

Massive pulmonary embolism

Bridge to lung transplantation

Postcardiac arrest support

Support o the tracheobronchial tree ollowing surgical repair

Mediastinal masses (airway compression)

Organ donor support

calcium levels are checked and adjusted accordingly. T e circuit may be primed without blood products in patients over 35 kg. T e initiation o ECMO is a controlled process o rst unclamping the oxygenated/arterial line, then the bridge and nally the venous/drainage line. Flow is increased slowly rom 20 mL/kg/min to 100–150 mL/kg/min. T is is done to allow slow mixing o the prime solution with the patient’s blood. Final ow rate is determined by assessing

Exclusion criteria for extracorporeal membrane oxygenation includes • Terminal disease • Chronic myocardial dysfunction, but not a candidate for transplant • Irreversible CNS injury • Recent neurosurgical procedure • Grade II or greater intracranial hemorrhage • Uncontrolled metabolic acidosis • Multiorgan dysfunction system • Prolonged cardiopulmonary resuscitation • Immunode ciency • Age > 60 • Prolonged ventilation > 5–7 d • PaO2/FiO2 < 100 or > 5–10 d

oxygenation and per usion parameters, using a minimum RPM and by minimizing cardiovascular changes; a per usion pressure o 40–50 mmHg is targeted in neonates. Inotropes are weaned to minimal values while on ECMO. Once the patient is stable, ows are optimized to maintain PaO 2 at 85–100 mmHg.

PATIENT MANAGEMENT ON ECMO During the initiation o ECMO, patients can experience signi cant blood pressure abnormalities, with hypertension being more common than hypotension. A decrease in aortic pulse

CHAPTER 61

pressure is seen ollowing decreases in systolic and diastolic pressures. Mean and peak blood ow velocities decrease initially but are returned to normal within 48–72 hours. Arrhythmias can occur during cannulation and should be treated appropriately, o en with cannula repositioning. Bradyarrhythmias are most common, but atrial or ventricular ectopy, atrial brillation, or supraventricular tachycardia can also be seen. Echocardiography may show increased ventricular size during systole along with decreased ractional shortening. Right and le stroke volumes are nearly equal and vary with pump ow rate. As noted previously, during VV ECMO, there are very minimal hemodynamic changes seen i any. Despite this, changes can be seen in the pulmonary vasculature during VV ECMO. Because o increased blood ow to the pulmonary artery (PA), increases in pulmonary vascular resistance and RV a erload are seen, untreated this can lead to pulmonary hypertension and eventually right heart strain and ailure. T e increased oxygen delivered to the PA by VV ECMO partially helps to o set these increases along with treatment aimed at decreasing RV a erload and avoiding increases in LV a erload. Oxygen delivery and exchange is an important part o ECMO and is monitored via several variables described above. T e delivery o oxygen is determined by several actors: ow in the circuit, oxygenation in the membrane lung, oxygen uptake through the native lung, and native cardiac output. T e most important actor is the blood/membrane lung inter ace. Factors that improve ef ciency include larger membrane sur ace area, longer time or the blood to be in contact with the membrane, and disruption o laminar ow (creation o turbulent ow). Oxygen consumption must also be assessed in the patient and be minimized by appropriately managing temperature, sedation, paralysis, nutrition and underlying illnesses to include sepsis. While the body usually can compensate or increased consumption by increasing the extraction rate, this hits a critical point when oxygen delivery is only twice consumption, resulting in SmvO2 < 50%. CO2 transport during ECMO is much more ef cient than oxygen exchange. CO2 trans er can occur up to six times aster than O2 or similar membrane lungs. T is can become problematic when ECMO is used or total gas exchange and hypocapnia develops. T is leads to respiratory alkalosis and its resultant complications. T e problem can be mitigated by adding CO2 gas to the ventilator gases. T ere is very little research on drug disposition during ECMO runs; most data is extracted rom that done on cardiopulmonary bypass. Factors that in uence this include protein-binding, physicochemical properties, injection site, volume o distribution, circuit ow rates, and other physiological changes. T e hemodilution that occurs upon initiation o ECMO can unpredictably alter drug levels. Multiple drugs have been shown to have signi cant uptake into circuit components, to include opioids, benzodiazepines, heparin, and phenobarbital, all requiring increased dosing. Hemo ltration can also have e ects on the pharmacokinetics o many drugs. ECMO is generally aimed at allowing lung rest so ventilator settings are usually minimized as there will always be

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blood owing in the lungs. Goals include low tidal volumes o 6–8 mL/kg, plateau pressures less than 25 cmH 2O, peak pressures under 35 cmH 2O, oxygen ows o around 40%, and minimal positive end-expiratory pressure o 5–10 cmH 2O. Normocarbia is maintained to avoid organ damage. Highrequency oscillatory ventilation can be used to help with recruitment. Other recruitment measures in use include nitric oxide, sur actant administration, prone positioning, and percussive ventilation. racheostomies are o en completed early in the course o cases where long ECMO runs are anticipated. As discussed above, the actual circuit monitors include the in ow and out ow pressures, temperature, gas line pressures, and a ow control meter. Patients themselves monitored by many parameters to include temperature, standard ASA monitors, arterial blood gases, mixed venous oxygen saturation (SmvO2, on VA ECMO), activated clotting time, ventilator settings, cardiac and abdominal ultrasounds, among several others. Vital signs and AC are measured hourly, blood count, electrolyte, and coagulation labs are measured at least daily, with chest X-rays and ultrasounds being done as required. Up to 50 mL o blood can be used daily or these tests in a newborn. Several other organ systems are important to the management o patients and must be ocused on as well. Risks o cerebral thrombosis and bleeding are major determinants o morbidity and mortality and can be increased by venous cannulation o neck vessels that impair cerebral drainage. Renal dys unction is usually much worsened on ECMO and should be monitored by the measurement o urine output, and serum and urine electrolytes. Hemo ltration has been shown to be very bene cial or management o this problem and can even improve outcomes. Indications or hemoltration include management o luid overload resistant to diuretic therapy, electrolyte balance, and avoidance o luid retention in blood product and ull-volume nutrition administration. Skin breakdown around invasive line sites and pressure points are important considerations to these patients as well. Antibiotic and gastrointestinal prophylaxis is usually by institution protocol. Parenteral or enteric nutrition is a vital component o the healing process but must be adjusted and monitored closely to avoid large luid shi ts. Weaning rom ECMO is process done over several hours and only indicated in patients who have showed signs demonstrating that lung and/or cardiac unction are improving. Requirements generally include reasonable ventilator settings, adequate gas exchange and low pump ows. Pump ows are generally weaned slowly every 20–30 minutes down to ows o 100 mL/min. SmvO2, arterial pressures, CVP, and blood gases are monitored during this time period to ensure a stable patient. Decannulation is completed a ew hours a er clamping the circuits and isolating the patient. Anesthesia is required or this procedure and additionally blood products, uids and vasoactive medications should be available as or cannulation.

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COMPLICATIONS One o the most important jobs o the anesthesiologist is in management o the ECMO team during transport or radiologic procedures, and transport to catheterization and operative suites or elective and emergent procedures. Common ECMO-speci c complications during these transport maneuvers include power ailure, oxygenator ailure, tubing/circuit disruption, breakage or leakage, and pump ailure. Speci c complications during the cannula insertion procedure include vascular damage and bleeding. Other patient speci c complications include neurological complications, barotrauma, renal ailure, cardiovascular ailure, metabolic disorders, and most importantly bleeding. Once patients come o o ECMO they are met with a host o morbidities that can a ect the remainder o their hospitalization. Neonates o en su er rom eeding dif culties in up to one-third o cases; they also have increased rates o rehospitalization. Increased rates o sensorineural disabilities, developmental delays to include academic dif culties and attention de cit disorders, epilepsy, neuromotor de cits, and sensorineural hearing loss are seen. Adults develop a state o severe chronic obstructive lung disease ollowing prolonged ECMO; this includes poor CO2 clearance and chest X-ray changes. Adult patients are also at increased risk o deep vein thrombosis and should be monitored or such. A syndrome o uid overload, anemia, hypoproteinemia, and malnutrition can occur ollowing ECMO weaning and should be monitored or and steps taken to avoid it to improve success to discharge. A meta-analysis o 12 studies and over 1700 patients on mostly VA ECMO had an overall mortality o 54% at 30 days postsupport. T e most common complications associated with ECMO were renal ailure, bacterial pneumonia,

bleeding, sepsis, and oxygenator mal unction. Other less common complications included liver dys unction, venous thrombosis, CNS complications, GI bleeding, and disseminated intravascular coagulation. T ere are several predictors o mortality that are monitored during and a er ECMO support. Increased mortality and death are seen in patients with long ECMO runs, low pH, renal ailure, high blood trans usion amounts, and sepsis. Lactate is o en used as a vital measure during ECMO support and has been ound to be use ul in predicting outcomes. T e Extracorporeal Li e Support Organization (ELSO) is the largest international registry o ECMO cases. Since 1989 they have documented almost 59,000 cases o ECMO and extracorporeal cardiopulmonary resuscitation (ECPR), this rom over two hundred centers. T e January 2014 summary report shows an overall survival on extracorporeal li e support as 72% and a 60% survival to discharge. Neonatal patients with respiratory support enjoy the greatest success with 84% survival on support and 74% survival to discharge. Further data and in ormation can be ound at ELSOnet.org.

SUGGESTED READINGS Chauhan S, Subin S. Extracorporeal membrane oxygenation, an anesthesiologist’s perspective: physiology and principles. Part 1. Ann Card Anaesth. 2011;14(3):218–229. Chauhan S, Subin S. Extracorporeal membrane oxygenation–an anaesthesiologist’s perspective–Part II: clinical and technical consideration. Ann Card Anaesth. 2012;15:69–82. Zangrillo A, Landoni G, Biondi-Zoccai G, et al. A meta-analysis o complications and mortality o extracorporeal membrane oxygenation. Crit Care Resusc. 2013;15(3):172–178.

62 C

Deep Hypothermic Circulatory Arrest Brian S. Freeman, MD

Deep hypothermic circulatory arrest (DHCA) is an established technique used during certain types o surgery in which blood ow ceases in all blood vessels while the patient’s core body temperature is lowered dramatically. Its use was rst reported in 1959 in children undergoing repair o etralogy o Fallot. DHCA is necessary or cardiac surgery in which standard cannulation o the proximal aorta will not achieve cerebral per usion. Circulatory arrest enables the surgeon to operate in a bloodless eld with improved exposure since no cannulae or clamps are necessary. At the same time, deep hypothermia decreases cerebral metabolism and oxygen consumption, enabling a longer period to operate during interrupted cerebral per usion. Since the brain is the organ most susceptible to ischemia, adequate cerebral protection implies that other vital organ systems should be protected as well.

INDICATIONS

• • • • • • • •

1. Cardiac surgery: • • • •

Aortic arch reconstruction (aneurysm, rupture, dissection) Pulmonary thromboendarterectomy Repair o complex congenital heart de ects (transposition o the great arteries, total anomalous pulmonary venous return, hypoplastic le heart syndrome) Vascular reconstruction during cardiac transplant

2. Non-cardiac surgery: • • • • •

Surgery on the thoracoabdominal aorta Repair o giant cerebral aneurysms Resection o cerebral arteriovenous mal ormations Resection o renal cell carcinoma with caval invasion Resection o other tumors with caval invasion

DHCA TECHNIQUE AND ANESTHETIC CONCERNS T e basic components o achieving deep hypothermic circulatory arrest are as ollows:

• •

E R

Ensure adequate anticoagulation prior to commencement o DHCA Eliminate glucose rom all intravenous solutions to reduce the risk o hyperglycemia Administer anesthetics and neuromuscular blocking drugs to decrease oxygen consumption and ensure paralysis Deep levels o anesthesia may decrease the harm ul physiologic stress responses to DHCA Reduce temperature to 15–22°C. T e cooling should occur slowly (over 30–60 minutes) to ensure homogenous hypothermia. Maintain ull ow CPB or at least 30 minutes to ensure adequate cerebral cooling Veri y cerebral electrical silence on electroencephalography or bispectral index Establish circulatory arrest by discontinuing CPB ow. At normothermia, brain injury occurs a er around our minutes o circulatory arrest. But the duration o DHCA that is considered sa e is controversial. A er 40 minutes o circulatory arrest, the stroke rate increases. A er 65 minutes, overall mortality increases. When easible, maintaining a low level o pulsatile CPB ow (“trickle”) improves microcirculatory ow and the balance between myocardial oxygen supply and demand. T e optimal hematocrit during DHCA is unknown. Hemodilution improves the microcirculation but may lead to cerebral hypoxia.

Rewarming the patient rom DHCA is not without risk. Initial reper usion with cold blood or at least 10 minutes prior to rewarming enables removal o metabolic waste and ree radicals. By increasing cerebral blood ow, excessively rapid rewarming increases the risk o cerebral edema, embolization, and hyperthermic cerebral injury. Rewarming should be gradual and cease at 37°C (nasopharyngeal), 36°C (esophageal), or 34°C (bladder). T e gradient between core and peripheral temperature should be 5–8°C. Extracranial sites o temperature monitoring underestimate brain temperature by about 5°C during rewarming. Signs o electrical hyperactivity on the EEG may require additional anesthetic agents or lowering body temperature. 233

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It is important to note that cerebral ischemia can still occur in the postoperative period. A er rewarming, cerebral blood ow and cerebral vascular resistance are still altered or several hours.

CEREBRAL PROTECTION DURING DHCA 1. Hypothermia—Hypothermia is the most important component o DHCA to protect the brain. It is de ned as core body temperature below 35°C (32–35°C: mild; 26–31°C: moderate; 20–25°C: deep; 100 ms are incomplete RBBBs, >120 ms are complete RBBBs). Right bundle branch blocks are usually o no clinical signi cance but can be associated with structural heart disease.

2. Premature ventricular contractions—Premature ventricular contractions (PVCs) occur due to an ectopic site in the ventricle (Figure 68-13). T e stimulus spreads through the ventricular conducting system, orming a wide QRS complex (>120 ms). Unlike premature atrial beats, PVCs block the next signal rom the SA node. New onset premature ventricular contractions could possibly lead to more deleterious conditions such as ventricular tachycardia or brillation due to the R-on- phenomenon. I the patient is hemodynamically stable, a beta-blocker can be considered. I unstable, lidocaine or amiodarone should be considered. 3. Ventricular tachycardia—Ventricular tachycardia is de ned as three consecutive PVCs. Sustained ventricular tachycardia lasts greater than 30 seconds while nonsustained ventricular tachycardia terminates in less than 30 seconds. Ventricular tachycardia can be monomorphic (exhibiting a similar pattern o QRS complexes; V6

V1 Norma l

R′ r RBBB T S

q S

Norma l

LBBB

Firs t-de gre e AV block T S e cond-de gre e AV block (2:1)

Third-de gre e AV block

FIGURE 68-11

Atrioventricular blocks.

FIGURE 68-12

Characteristic bundle branch block ndings. (Reproduced with permission rom Kasper DK, Fauci A, Hauser S, Longo D, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York, NY: McGraw-Hill Education, Inc.; 2015: Fig. 268-10.)

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FIGURE 68-13

Premature ventricular contractions. (Reproduced with permission rom Gomella LG, Haist SA, eds. Clinician’s Pocket Reference: The Scut Monkey. 11th ed. New York, NY: McGraw-Hill Education, Inc.; 2007: Fig. 19-14.)

Figure 68-14) or polymorphic (exhibiting di erent patterns o QRS complexes. orsades de pointes is a type o polymorphic V with a long Q c interval (Figure 68-15). T e causes o prolonged Q c interval include myocardia ischemia, hypertrophic obstructive cardiomyopathy, electrolyte disturbances, and medications. Beta-blockers can be used to prevent torsades in patients with a prolonged Q interval. Internal cardioverter-de brillator placement is a de nitive therapy. In patients with ventricular tachycardia who are hemodynamically stable, the underlying cause should be treated. T e patient should also receive amiodarone. Other potential treatments include lidocaine, sotalol, procainamide, or electrical cardioversion. I the patient is

hemodynamically unstable but has a palpable pulse, synchronized DC cardioversion should be per ormed. I the patient is hemodynamically unstable with a nonpalpable pulse, cardiopulmonary resuscitation with Advanced Cardiac Li e Support should be per ormed. orsades de pointes is treated with intravenous magnesium. 4. Ventricular brillation—Ventricular brillation is a rapid and irregular rhythm that occurs when many irritable ventricular pacemakers rapidly re (Figure 68-16). T e causes o ventricular brillation include myocardial ischemia, hypoxia, hypothermia, electrolyte imbalance, and medications. T e treatment is cardiopulmonary resuscitation as speci ed by the Advanced Cardiac Li e Support algorithm.

FIGURE 68-14

Monomorphic ventricular tachycardia. (Reproduced with permission rom Gomella LG, Haist SA, eds. Clinician’s Pocket Reference: The Scut Monkey. 11th ed. New York, NY: McGraw-Hill Education, Inc.; 2007: Fig. 19-17.)

FIGURE 68-15

Torsades de pointes. (Reproduced with permission rom Knoop KJ, Stack LB, Storrow AB, Thurman RJ, eds. The Atlas of Emergency Medicine. 3rd ed. New York, NY: McGraw-Hill Education, Inc.; 2010: Fig. 23-34B.)

FIGURE 68-16

Ventricular brillation. (Reproduced with permission rom McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS, eds. Principles and Practice of Hospital Medicine. New York, NY: McGraw-Hill Education, Inc.; 2012: Fig. 121-1.)

69 C

Management of Pacemakers and AICDs Nilda E. Salaman, MD

E R

T e perioperative period poses a unique challenge in providing care or patients with cardiovascular implantable electronic devices (CIEDs). CIED is a term that encompasses pacemakers or bradyarrhythmia treatment, implantable cardioverter de brillators (ICDs) or tachyarrhythmia management, and cardiac resynchronization therapy (CR ) devices or systolic dys unction with conduction delays. Perioperative management should be multidisciplinary and individualized to the patient, the type o CIED and the procedure being per ormed.

5. Ideally, determining the CIED unction by having the device interrogated is pre erred. I this is not possible then, determine whether the device will capture when it paces (i.e., produce a mechanical systole with a pacemaker impulse). 6. Contacting the manu acturer or perioperative recommendations may be a consideration.

PREOPERATIVE EVALUATION

Preparation and intraoperative management or patient sa ety during the perioperative period includes the ollowing:

A ocused evaluation should establish whether a patient has a CIED, de ne the type o device, determine whether a patient is pacemaker-dependent, determine the CIED unction, and determine the magnet behavior. T is can be accomplished through the ollowing: 1. A ocused history including patient interview, review o medical records, available chest X-rays (CXR), electrocardiograms, or available monitor or rhythm strip. Examination o the CXR can immediately provide in ormation about lead con guration, and whether the device is a single- or dual-chamber pacemaker, a biventricular device, or an ICD. Device manu acturer markings may be visible on CXR. 2. A ocused physical examination, which includes checking or scars and palpating or a device. 3. De ning the type o device by obtaining manu acturer’s identi cation card rom patient or other source. Re er to supplemental resources (i.e., manu acturer’s databases, cardiologist consultation). 4. Determining the dependence on pacing unction o the CIED through verbal history or medical record documentation o the ollowing: a. Symptomatic bradyarrhythmia resulting in CIED implantation. b. Success ul atrioventricular nodal ablation resulting in CIED implantation. c. CIED evaluation showing clinically evident hemodynamic compromise when the pacing unction is programmed to VVI mode at the lowest programmable rate.

Preparation and Intraope rative Manag ement

1. Determining whether electromagnetic inter erence (EMI) is likely to occur during the planned procedure. 2. Determining i reprogramming pacing unction to asynchronous mode or disabling rate responsive unction is advantageous. 3. Suspending antitachyarrhythmia unctions i present. 4. Evaluating the possible e ects o anesthetic techniques and o the procedure on CIED unction and patient– CIED interactions. Anesthetic technique should be dictated by the underlying physiologic disorder and patient comorbidities. 5. Intraoperative monitoring which includes both continuous ECG and continuous peripheral pulse monitoring as per the American Society o Anesthesiologists (ASA) standard. Peripheral pulse can be monitored by palpation o the pulse, auscultation o heart sounds, pulse plethysmography or oximetry, a tracing o arterial wave orm, or ultrasound peripheral pulse monitoring.

Management of Potential CIED Dysfunction as a Result of EMI Management o potential CIED dys unction as a result o EMI includes the ollowing: 1. Advise the individual per orming the procedure to consider use o a bipolar electrocautery system or ultrasonic (harmonic) scalpel or to minimize prolonged bursts o 263

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monopolar cautery at the lowest easible energy levels, i this is the only option or the stated procedure. 2. Properly position the electrocautery grounding pad so the current pathway does not pass through or near the CIED system.

Management of Other Sources of EMI Management o other sources o EMI includes the ollowing: 1. Radiofrequency (RF) ablation—Advise the individual per orming the procedure to avoid direct contact between the ablation catheter and the pulse generator and leads. T e RF’s current path should be as ar away rom the pulse generator and lead system as possible. 2. Extracorporeal shock wave lithotripsy (ESWL)—It is no longer contraindicated or patients with CIEDs—advise the individual per orming the procedure to avoid ocusing the lithotripsy beam near the pulse generator. I the lithotripsy system triggers on the R wave, consider preoperative disabling o atrial pacing. 3. Magnetic resonance imaging (MRI)—It is generally contraindicated in patients with CIEDs. I an MRI must be per ormed, consult with the ordering physician, the patient’s cardiologist, the diagnostic radiologist, and the CIED manu acturer. 4. Radiation therapy—It can be sa ely per ormed in patients who have CIEDs. Surgical relocation o the CIED is recommended i the device will be in the eld o radiation. Radiation therapy is not associated with EMI; however, ionizing radiation can cause cumulative damage to the insulation o the leads and the semiconductor circuitry within the pulse generator. 5. Electroconvulsive therapy (ECT)—EC appears sa e or patients with pacemakers or ICDs because little current f ows within the heart due to the high impedance o body tissues. Nevertheless, consultation with the ordering physician, the patient’s cardiologist, a CIED service, or the CIED manu acturer is recommended. T e presence o a CIED should not deter standard resuscitation e orts with the ollowing measures taken: 1. A complete array o drugs and equipment must be immediately available or cardio-pulmonary resuscitation. 2. Immediate availability o temporary pacing and de brillation equipment should be ensured. a. ranscutaneous electrodes pads can be placed be ore the start o the operative procedure. T ey should be placed as ar (more than 6 in. or 15 cm) rom a CIED as possible. b. T e three recommended electrode placements are as ollows: (1) anteroposterior placement; (2) apex-anterior placement; and (3) apex-posterior placement. c. I it is technically impossible to place the pads or paddles in locations that help to protect the CIED, then

de brillate/cardiovert the patient in the astest possible way. Be prepared to provide pacing through other routes. Use a clinically appropriate energy.

POSTOPERATIVE MANAGEMENT Maintain vigilance and monitoring in accordance with ASA standards. Continuously monitor cardiac rate and rhythm and have back-up pacing and de brillation equipment immediately available throughout the immediate postoperative period. 1. Interrogate and restore CIED unction in the immediate postoperative period. 2. Restore all antitachyarrhythmic therapies in ICDs. 3. Assure that all other settings o the CIED are appropriate. Device should also be interrogated in the ollowing ways: 1. Patients who underwent hemodynamically embarrassing surgeries such as cardiac surgery or signi cant vascular surgery. 2. Patients who experienced signi cant intraoperative events, including cardiac arrest, requiring temporary pacing or cardiopulmonary resuscitation and/or tachyarrhythmias requiring external electrical cardioversion during surgery.

EMERGENCY DEFIBRILLATION OR CARDIOVERSION 1. For the patient with an ICD and magnet-disabled therapies or ICD and programming-disabled therapies, advise the operator per orming the procedure to terminate all sources o EMI while the magnet is removed. 2. Remove the magnet to re-enable antitachycardiac therapies/re-enable therapies through programming i the programmer is immediately available and ready to be used. 3. Observe the patient and the monitors or appropriate CIED therapy. I the above activities ail to restore ICD unction, proceed with emergency external de brillation or cardioversion.

USE OF MAGNETS T e e ect o placing a magnet over a pacemaker or ICD can vary quite considerably depending on the device manuacturer, model, and individual programmed modes. T is in ormation may be obtained by consulting the device manu acturer. I a magnet is to be used during a procedure, the e ects o the magnet should be tested be ore the start o the procedure to ensure that the desired e ects will occur. T e

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magnet-activated switches in the pacemaker generator was incorporated to produce pacing behavior that demonstrates remaining battery li e and sometimes pacing threshold sa ety actors. Not all pacemakers revert to an asynchronous mode with the application o a magnet. Not all models rom a particular company behave the same way. For all generators, contacting the manu acturer remains the most reliable method or determining magnet response. 1. Most pacemakers will switch to a xed-rate pacing mode when a magnet is placed. However, the response o a pacemaker to a magnet placement may also include the ollowing: a. Asynchronous pacing without rate responsiveness b. No response c. Brie (10–100 beats) asynchronous pacing d. Continuous or transient loss o pacing 2. T e response o an ICD to magnet placement is di erent rom that o a pacemaker. a. Magnets will disable tachyarrhythmia detection and therapy, except in some early generation devices, where the latter unctions are re-enabled when the magnet is removed.

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b. Magnets will not af ect the pacing mode or rate o ICDs. T ere ore, the pacemaker in an ICD can be inappropriately inhibited by electrocautery even when a magnet is placed. c. It is important to remember that some early generation ICDs are permanently disabled when a magnet is placed or more than 30 seconds. T e ICD will not be reactivated when the magnet is removed. o reactivate the ICDs, the magnet has to be reapplied over the ICD or more than 30 seconds and then removed generally with a ew exceptions.

SUGGESTED READINGS Practice advisory or the perioperative management o patients with cardiac implantable electronic devices: pacemakers and implantable cardioverter-de brillators: an update report by the American Society o Anesthesiologists task orce on perioperative management o patients with cardiac implantable electronic devices. Anesthesiology. 2011;114:247–261. Stone M, Salter B, Fischer A. Perioperative management o patients with cardiac implantable devices. Br J Anaesth. 2011;107(S1):116–126.

70 C

Cardiomyopathies Adrian M. Ionescu, MD, and Brian S. Freeman, MD

Cardiomyopathies re er to a heterogeneous group o myocardial pathology that impairs normal cardiac unction in the absence o acute coronary ischemia or chronic valvular dysunction. T e group can be classi ed into primary cardiomyopathies, which predominantly a ect the myocardium and secondary cardiomyopathies, capable o impairing normal myocyte unction, while producing widespread systemic dysregulation and multiorgan dys unction. Primary cardiomyopathies can be urther subdivided according to the etiology producing the cardiac pathology: (1) genetic; (2) mixed; and (3) acquired.

HYPERTROPHIC CARDIOMYOPATHY Hypertrophic cardiomyopathy (HCM) is the most common primary cardiomyopathy with a genetic origin. It re ers to a heterogeneous group o autosomal dominant disease with variable genetic penetrance and expressivity that produces diastolic dys unction as well as asymmetric hypertrophy o the upper interventricular septum with subsequent dynamic obstruction o the le ventricular out ow tract (LVO ). T e ow acceleration produced in the LVO during cardiac systole generates a Venturi e ect on the anterior mitral lea et, which distorts the mechanical geometry o the mitral valve and the mitral subvalvular apparatus. T e coaptation point o the anterior and posterior mitral lea ets moves anteriorly into the LVO , producing systolic anterior motion (SAM), incomplete closure o the mitral valve lea ets, and mitral regurgitation, which signi cantly diminishes the e ective antegrade cardiac output, leading to systemic hypotension (Figure 70-1). Clinical parameters that exacerbate SAM o the anterior mitral valve lea let include positive inotropic support (i.e., increased myocardial contractility), decreased preload (i.e., hypovolemia, venodilation), and decreased a terload (i.e., decreased systemic vascular resistance [SVR] and arterial vasodilators). Factors that help to alleviate SAM o the anterior mitral valve lea et include negative inotropy (i.e., decreased myocardial contractility), increased preload (i.e., intravenous administration o crystalloid, colloid, or blood products), and increased a erload (i.e., increased SVR and arterial hypertension).

E R

Le ft a trium

Mitra l va lve

Le ft ve ntricle *LVOT o bs truc tio n

FIGURE 70 -1

SAM o the anterior mitral valve lea et due to the Venturi ef ect. (Reproduced with permission rom Wasnick JD, Hillel Z, Kramer D, Littwin S, Nicoara A, eds. Cardiac Anesthesia and Transesophageal Echocardiography. New York, NY: McGraw-Hill Education, Inc.; 2011: Fig. 10-1.)

All patients presenting with HCM should be considered at high risk o developing dysrhythmias as well as myocardial ischemia, primarily as a result o (1) the mismatch between the increased oxygen demand o the thickened myocardium and the decreased supply provided by the coronary arteries; (2) the diastolic dys unction contributing to a decreased le ventricular lling time; and (3) the decreased coronary per usion gradient caused by the increase in le ventricular enddiastolic pressure (LVEDP). On physical examination, patients with HCM o en have an audible murmur as a result o the turbulent, accelerated blood ow in the LVO . An ECG can help support the diagnosis o HCM as it typically displays evidence o le 267

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ventricular hypertrophy (i.e., increased QRS voltage). T e ECG may also occasionally reveal the presence o Q waves as well as the presence o S segment abnormalities during the ventricular repolarization period. T e diagnosis o HCM can also be supported echocardiographically, by the presence o ventricular hypertrophy (especially upper ventricular septal hypertrophy), a high ejection raction (greater than 80%) o en accompanied by SAM o the anterior mitral valve lea let, and mitral regurgitation. I de nitive diagnosis o HCM is necessary or desired, then myocardial biopsy with subsequent DNA analysis can be per ormed in order to genetically con rm the diagnosis. Medical therapy or HCM is primarily aimed at reducing the risk o sudden death by decreasing the incidence o myocardial ischemia, increasing the myocardial diastolic (ventricular lling) time, and reducing the incidence o LVO obstruction in order to improve cardiac output. In asymptomatic patients, or patients presenting with mild symptoms, the initiation o a beta-adrenergic blocker or calcium channel blocker is an appropriate pharmacologic means o symptomatic treatment, which also reduces the incidence o sudden death. Both vasoactive agents increase the diastolic, le ventricular lling time, decrease the myocardial oxygen demand, and alleviate the dynamic LVO obstruction by attenuating the sympathetic response during periods o increased catecholamine production (e.g., exercise, surgical stimulus and pain). In patients with severe symptoms re ractory to pharmacologic medical therapy, de nitive surgical intervention (upper septal myomectomy) can produce relie o symptoms by reducing the thickness o upper interventricular septum, as well as by reducing the incidence o LVO obstruction. Occasionally, patients may also require antidysrhythmic therapy with amiodarone and, in re ractory cases, the placement o an ICD. T e anesthetic management o patients presenting with hypertrophic obstructive cardiomyopathy should aim to reduce the propensity o LVO obstruction by means o the ollowing: • • • • •

Avoiding positive inotropic support (e.g., epinephrine, milrinone, dobutamine) Maintaining adequate venous return and avoiding hypovolemia (maintenance o preload) Maintaining normal SVR and avoiding hypotension (maintenance o a erload) Avoiding tachycardia Ensuring that the positive pressure ventilation does not adversely a ect intrathoracic pressure and subsequently venous return

In addition to the standard ASA monitors, an invasive arterial blood pressure monitor as well as transesophageal echocardiography (to monitor or LVO obstruction) should be utilized. In general, any parameter that stimulates catecholamine release (i.e., pain, hypoxia, hypercarbia, shivering

or anxiety) should be minimized in order to avoid LVO obstruction with subsequent hypotension.

DILATED CARDIOMYOPATHY Dilated cardiomyopathy is best classi ed as a primary cardiomyopathy with a mixed, multi actorial etiology. T e most prominent echocardiographic eature o dilated cardiomyopathy includes systolic dys unction accompanied by bilateral ventricular dilatation. T e etiology o dilated cardiomyopathy is likely multi actorial: (1) in ectious (i.e., Coxsackie B virus, HIV); (2) genetic; (3) ischemic pathology (i.e., coronary artery disease, uncontrolled hyperthyroidism, uncontrolled hypertension, and tachycardia); (4) substance abuse (i.e., alcohol, cocaine); and (5) cardiotoxic drugs (i.e., doxorubicin). Overall, dilated cardiomyopathy remains the most prevalent cardiomyopathy as well as the most common indication or a heart transplant. Patients af icted by dilated cardiomyopathy present with signs o congestive heart ailure such as dyspnea, angina, atigability, and ailure to thrive. Physical examination may reveal murmurs (consistent with aortic and mitral insu ciency), jugular venous distention, hepatomegaly, and pitting edema in the extremities. T e ECG o en supports the diagnosis o dilated cardiomyopathy as it typically displays evidence o S segment abnormalities, le bundle branch block (LBBB), and, in severe cases, atrial brillation. Echocardiographic evaluation typically reveals marked dilation o all cardiac chambers, especially the le ventricle, which may contain mural thrombi adherent to hypokinetic regions. he treatment o dilated cardiomyopathy is based upon the underlying etiology and generally includes luid restriction and a low-sodium diet, weight monitoring and control, avoiding alcohol and illicit drugs (i.e., cocaine), and cardiac rehabilitation. In patients with severe le ventricular hypokinesis or atrial brillation, anticoagulation must be strongly considered in order to decrease the propensity or thrombus ormation and systemic embolization to end organs. In selected patients, the le ventricular systolic dysunction may be supported by the implantation o a le ventricular assist device (LVAD) as a destination therapy or as a bridge to heart transplantation. Currently, the only de nitive treatment or dilated cardiomyopathy remains cardiac transplantation.

RESTRICTIVE CARDIOMYOPATHY T e heterogeneous group o restrictive cardiomyopathies generally mani est with severe diastolic dys unction as the result o an underlying in ammatory or in ltrative process, which ultimately decreases myocardial compliance. T e most common etiologies producing a restrictive physiology include (1) amyloidosis (most common); (2) hemochromatosis; (3) carcinoid syndrome; and (4) systemic sarcoidosis.

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Patients with restrictive cardiomyopathy typically present with the typical symptoms o congestive heart ailure (i.e., dyspnea, angina, atigability and ailure to thrive) in the absence o cardiomegaly. In advanced or severe cases, patients may also develop conduction abnormalities (i.e., heart blocks or ventricular dysrhythmias) as a result o the in ltrative processes a ecting the underlying myocardial conduction pathways. Echocardiographic evaluation generally reveals impaired ventricular relaxation and diastolic dys unction with preserved biventricular systolic unction. ypically, there is no evidence o cardiomegaly since both ventricles remain normal in size. De nitive diagnosis o the underlying etiology o the restrictive cardiomyopathy can be made with a biopsy o the endomyocardial sur ace. T e treatment strategy o patients with a restrictive cardiomyopathy is primarily ocused on relieving the symptoms o diastolic heart ailure. Generally, diuretics are use ul in managing the symptoms o pulmonary congestion caused by volume overload. In patients with more advanced disease or atrial enlargement su ering rom atrial brillation, the treatment is primarily aimed at maintaining normal sinus rhythm as the lling o sti er, less compliant ventricles is augmented by the normal contribution o both atria. Avoiding bradycardia is equally important to maintaining normal sinus rhythm in patients with diastolic dys unction since the stroke volume is xed, and thus the cardiac output is primarily dependent on the heart rate. T e placement o an AICD with pacemaker capability is o paramount importance in patients with restrictive cardiomyopathy who develop either bradycardia or aberrant atrioventricular conduction.

PERIPARTUM CARDIOMYOPATHY Peripartum cardiomyopathy is a rare orm o dilated cardiomyopathy, which typically originates in the third trimester o pregnancy and extends up to 6 months postpartum. T e risk actors associated with the development o peripartum cardiomyopathy include (1) advanced maternal age; (2) obesity; (3) multiparity or multi etal gestation; and (4) the development o pre-eclampsia or eclampsia during the gestation. Patients af icted by peripartum cardiomyopathy present with signs o heart ailure, which include dyspnea, angina, atigability, and ailure to thrive. T e diagnosis o peripartum cardiomyopathy is typically supported an echocardiographic evaluation, which reveals marked dilation o all our cardiac chambers and especially le ventricular systolic dys unction. T e treatment o peripartum cardiomyopathy aims to reduce the symptoms o heart ailure and typically includes a combination o diuretics, vasodilators (i.e., hydralazine), as well as digoxin. In this patient population, the mortality rate may approach as high as 50% in the rst 3 months postpartum and is usually the result o rapid progression o congestive heart ailure. LVAD

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implantation or cardiac transplantation remains an option or re ractory patients who ail to improve over time.

COR PULMONALE Cor pulmonale speci cally re ers to right ventricular hypertrophy or dilation, usually as a result o pulmonary hypertension secondary to a congenital or chronic pulmonary pathology (i.e., chronic obstructive pulmonary disease, idiopathic pulmonary brosis, or thrombo-embolic pulmonary hypertension). I untreated, cor pulmonale will gradually progress to right heart ailure. In patients with cor pulmonale, the right ventricle generally remodels in response to the increased pulmonary vascular resistance and a erload. Initially, the right ventricle hypertrophies in order to compensate or the pulmonary hypertension—chronically, the increased metabolic demands o the hypertrophied right ventricle exceed the supply provided by the coronary circulation and the right ventricle gradually begins to dilate with increasingly compromised systolic unction. Patients su ering rom right heart ailure generally present with dyspnea, peripheral edema, severe tricuspid regurgitation, jugular venous distention, and hepatomegaly. T e ECG examination o patients with cor pulmonale o en reveals evidence o right ventricular hypertrophy with right axis deviation (RAD), right bundle branch block (RBBB) o en prominent in lead V1, as well as evidence o right atrial enlargement with peaked P waves in the in erior leads (II, III, aVF). Echocardiographic examination o en supports the diagnosis o cor pulmonale with evidence o pulmonary hypertension, main pulmonary artery dilation, right ventricular hypertrophy, and severe tricuspid regurgitation. T e treatment o cor pulmonale is primarily aimed at reducing the degree o pulmonary hypertension and subsequently the wall-tension generated by the right ventricle. Supportive strategies include the administration o supplemental oxygen to maintain an arterial oxygen pressure (PaO 2) o at least 60 mmHg, avoiding hypercarbia by maintaining an arterial carbon dioxide pressure (PaCO 2) less than 40 mmHg, as well as maintaining a normal, physiologic pH and body temperature. T e treatment o pulmonary hypertension with phosphodiesterase inhibitors (e.g., sildena l) or with potent pulmonary vasodilators (i.e., inhaled nitric oxide or inhaled epoprostenol) can also improve symptoms, while reducing the rate o right ventricular remodeling. In patients re ractory to pharmacologic therapy, de nitive treatments with bilateral lung transplantation or with combined heart–lung transplantation remain as viable alternatives.

SUGGESTED READING Maron BJ. T e 2006 American Heart Association classi cation o cardiomyopathies is the gold standard. Circ Heart Fail. 2008;1:72–76.

Cardiac Transplantation Massimiliano Meineri, MD

Heart transplantation remains the ultimate treatment or congestive heart ailure (CHF), a disease which carries a 50% veyear mortality and a nine old increase in the risk o sudden death. Cardiomyopathy (54%) and coronary artery disease (37%) are the two main underlying causes o CHF in transplant recipients. Other causes include congenital heart disease (2.9%), valvular disease (2.8%), and retransplantation (2.5%). Since the rst success ul transplant in 1963, suboptimal modulation o the immune response to control rejection prevented initial success o this procedure until the introduction o cyclosporin A in the 1970s. For all adult and pediatric heart transplants between 1982 and 2011, survival rates were 81% at 1 year and 69% at 5 years with a median survival time o 11 and 13 years or those surviving the rst year. Outcomes have not signi cantly changed but likely re ect a widening o indications and higher risk recipients. Young age remains the sole most important determinant o survival.

PREOPERATIVE ASSESSMENT Indications or cardiac transplantation include the ollowing: 1. 2. 3. 4. 5.

Hemodynamically unstable CHF Re ractory cardiogenic shock Dependence on intravenous inotrope therapy Recurrent untreatable angina Recurrent symptomatic ventricular arrhythmias unresponsive to therapy

Absolute contraindications or cardiac transplantation include the ollowing: 1. 2. 3. 4.

Systemic illness with li e expectancy less than 2 years Malignancy within the previous 5 years AIDS or other opportunistic diseases Systemic lupus erythematosis, sarcoidosis, or amyloidosis with multisystem involvement 5. Irreversible hepatic or renal ailure in patients considered or heart transplant alone 6. Severe obstructive pulmonary disease 7. Fixed pulmonary hypertension

E R

A multidisciplinary assessment o heart transplant recipients ocuses on the ollowing: • • • •

Likelihood o surviving the surgery Compliance with postoperative medical treatment and ollow up Identi cation o potentially reversible medical conditions Optimization o HF therapy

Once listed, the heart transplant recipient is given a code status based on the short-term prognosis. Status IA (highest priority) includes one o the ollowing actors: dependency on intravenous inotropes, mechanical ventilation, mechanical circulatory support, or device-related complications. Patients with status IB are stable on mechanical circulatory support. All other patients are status II (lowest priority). Heart ailure commonly mani ests with decreased stroke volume. T is decline in cardiac output is initially compensated by ventricular dilatation and increased sympathetic drive. Progressive chamber dilatation will result in unctional valvular abnormalities, alteration o myocardial mechanics, and pump ailure. Chronic sympathetic activation will be counteracted by downregulation o the beta-adrenergic receptors. T e management o patients with end-stage CHF who are candidates or cardiac transplantation consists o the ollowing: • • •

•

Angiotensin converting enzyme (ACE) inhibitors reduce le ventricular hypertrophy, provide relie o symptoms, and improve overall mortality. Beta-adrenergic receptor blockers counteract the elevated sympathetic tone, promote ventricular remodeling, and improve overall mortality. Loop diuretics are the irst choice or mild heart ailure. Spironolactone, a potassium-sparing aldosteroneantagonist, is the only diuretic associated with signi cant outcome bene t or patients with advanced heart ailure. Resynchronization therapy with a dual-chamber pacemaker is e ective or patients with depressed ejection raction and widened QRS complexes. 271

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Automated implanted cardiac de brillators are placed or those CHF patients with a high risk or developing li e-threatening ventricular arrhythmias. T e AICD may incorporate biventricular pacing unction. An intra-aortic balloon pump can provide short-term solution to increase coronary per usion and decrease le ventricular a erload. Since the REMA CH trial in 2001, le mechanical assist devices (LVADs) have taken a leading role in the management o end-stage CHF management. LVADs allow patients awaiting heart transplant to preserve end-organ unction and may potentially improve the post-transplant outcome. LVADs are also used as a bridge to candidacy since they allow assessment o pulmonary vascular resistance (PVR) in patients with pulmonary hypertension a er relie o upstream pulmonary venous congestion. T e FDA has approved two implantable continuous ow pumps, both o which require systemic anticoagulation and allow patients to be discharged home ully mobile. A total arti cial heart and combined right and le ventricular support (BiVAD) are o ered to patients with biventricular CHF that does not respond to medical therapy.

Cardiac transplantation usually takes place on an emergency basis. Preoperative anesthetic evaluation time is o en limited and should ocus on the ollowing: •

•

Airway assessment—Dif cult airways should be identied promptly in order to gather adequate equipment and avoid delays. Patients presenting or transplant are not properly asted given the short notice so aspiration precautions should be taken. Vascular access assessment—Most patients have had multiple venous cannulations and may present to the operating room with di erent lines in place. It is important to assess scars, collect a history o previous cannulations, and identi y permanent catheters and devices. Preemptive ultrasound evaluation may be help ul to plan best vascular access. Inotropic and mechanical support— ype and doses o inotropic support must be assessed in order to plan optimal anesthetic induction. Concentration o inotropes may vary among units and hospitals and should be identi ed. ype o mechanical support should be checked to provide correct external controller and monitor. Pulmonary, hepatic and renal complications associate with end-stage CHF—Hepatic insuf ciency a ects drug metabolism and hemostasis. Renal unction should be monitored during the case with a lower threshold or instituting hemodialysis during cardiopulmonary bypass. Pacemakers and AICD—T e de brillatory unction o the AICD should be deactivated. Permanent pacemakers require reprogramming to a mode that is not a ected by electrocautery.

•

Medications—Patients taking ACE inhibitors are at increased risk o re ractory intraoperative hypotension due to baseline low systemic vascular resistance. Vasopressin may be required to treat this problem. Many heart transplant recipients take oral anticoagulation to prevent intracardiac thrombus ormation as a result o the underlying disease o a mechanical assist device. Reversal o anticoagulation is usually only obtained a er weaning rom cardiopulmonary bypass using resh rozen plasma or actor concentrates.

THE DONOR HEART T e donor heart is harvested rom suitable brain-dead donor patients. T e most common causes o brain death in heart donors are head trauma and stroke. Donor suitability is assessed based on medical history, electrocardiography, chest radiography, and the need or inotropic support. Coronary angiography is only mandatory or males over age 45 and emales over age 50. T ere is a 10% incidence o signi cant coronary disease in the donor heart. Valvular abnormalities should be excluded by echocardiography. Le ventricular hypertrophy usually leads to organ re usal i the le ventricular thickness is more than 1.4 cm, which has been associated with decreased survival. A er brain death, systemic vascular resistance suddenly increases due to the release o endogenous catecholamines. T is physiologic change is ollowed by several hours later by hypotension due to hypovolemia and polyuria secondary to diabetes insipidus. Electrolyte disturbances are common in this phase and can trigger dangerous ventricular arrhythmias. Clinical management should be directed to protect the donor heart by providing best coronary per usion and avoid arrhythmias. T e use o vasopressors is commonly accepted but intermediate doses o inotropes may prevent nal harvesting. Harvesting o the donor heart is carried out through a midline sternotomy and ull laparotomy. A er pericardiectomy, assessment o external anatomy and palpation o coronary arteries precedes nal organ acceptance. When all main organ vessels are isolated, the ascending aorta is clamped and cold crystalloid cardioplegia is injected into the aortic root under pressure. A er achieving asystole, the heart is harvested by transecting the superior and in erior vena cava, the aortic arch, and the main pulmonary artery. T e le atrium is transected as a cu , leaving the pulmonary veins in the donor. Cold cardioplegia and ice remain the only means o minimizing ischemic damage. Sophisticated “exvivo” per usion systems allow ongoing per usion o the donor heart while per orming angiographic and echocardiographic assessment prior to implantation. Donor–recipient matching is based on the donor heart size and recipient body sur ace area and blood type. As a general rule, the donor’s body weight should not be less than 30% o the recipient body weight. Patients with pulmonary

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hypertension should receive a heart rom a larger donor. Female heart transplanted in a male recipient results in a slightly worsened outcome.

escalating doses. Although mechanical assist devices prevent hemodynamic collapse at induction, special attention should be paid to RV unction in patients with an LVAD.

PERIOPERATIVE MANAGEMENT

Surgical Technique

Monitoring Standard intraoperative monitors or cardiac transplantation include ve-lead electrocardiography, pulse oximetry, core temperature, capnography, spirometry, and invasive and noninvasive blood pressure. Preinduction arterial cannulation is essential and may be challenging in patients on continuous LVAD ow pumps. Ultrasound-guided cannulation may be the only option in this group o patients. T e brachial artery is pre erred in some centers as it may be more reliable. Femoral arteries are also used due to the pressure gradients between radial and emoral lines during the procedure. A er induction, a pulmonary artery catheter is used to calculate the transpulmonary gradient ( PG, mean pulmonary artery pressure–pulmonary capillary wedge pressure) and PVR. Patients with a PG greater than 15 mmHg and PVR o more than 200 dyn s/cm 5 are at high risk o postoperative right ventricular (RV) ailure. A comprehensive transesophageal echocardiographic examination is per ormed a er induction. T is monitor is used to assess ventricular unction, intracardiac thombi, and aortic disease. In the presence o an intracardiac thombus, the heart should be manipulated with extreme caution. Patients undergoing a redo sternotomy should have de brillator pads applied be ore induction o anesthesia.

Vascular Access For central venous access, the le internal jugular vein is the pre erred route due to the need or requent postoperative intracardiac biopsies though the right internal jugular vein. An additional central venous catheter is o en inserted at this time or at the end o the case. Maximal sterile technique should be used or central lines, given the need or postoperative immunosuppression. Removal o old lines, especially i placed urgently, should be considered whenever possible be ore or immediately a er surgery.

Induction Prior to initiating cardiopulmonary bypass, maintenance o end-organ per usion is the primary hemodynamic goal. Induction o anesthesia should commence only when the donor heart has been nally accepted. Anesthetic agents should be care ully titrated to provide a smooth induction with minimal hemodynamic compromise. Prophylactic increases o inotropes and vasopressors may be necessary due to a slow circulation time rom low cardiac output. Downregulation o beta-adrenergic receptors in patients with end-stage CHF o en results in a blunted response to inotropes requiring

A er a median sternotomy, the surgeon exposes the heart and dissects major vessels. T e native heart dissection should be completed with the patient ready to be placed on cardiopulmonary bypass when the heart is delivered. T e superior and in erior vena cava are cannulated as ar as possible rom the right atrium and snared with tourniquets. T e distal ascending aorta is cannulated to allow room or crossclamp and aortotomy. T e heart is excised without injecting any cardioplegia. T e pulmonary artery catheter is withdrawn a er initiation o cardiopulmonary bypass. Orthotopic heart transplantation has been per ormed using two techniques. T e Shamway technique has our anastomoses: two atrial cu s, aorta, and pulmonary artery. T e Sievers technique consists o ve anastomoses: superior and in erior vena cava, le atrial cu , aorta, and pulmonary artery. T e latter approach is pre erred due to better short-term results that include preservation o tricuspid valve unction, sinus rhythm, and lower atrial pressures. Minimizing donor heart ischemic time is essential. Cold ischemic time is calculated rom aortic clamping in the donor to removal o the aortic clamp in the recipient. Ischemic time longer than 210 minutes is associated with signi cant 1- and 5-year acute gra ailure.

Separation from Cardiopulmonary Bypass Using transesophageal echocardiographic guidance, the donor heart is care ully deaired. Achieving and maintaining a stable cardiac rhythm is essential or separation rom bypass. Ischemic injury and sympathetic denervation o en results in bradycardia and junctional rhythm. emporary pacing wires are usually placed to provide pacing at 90–100 beats per minute. Re-establishment o mechanical ventilation requires care ul attention to minimize hypercapnia, hypoxia, and acidosis in order to maintain low PVR. A er decreasing cardiopulmonary bypass ow by hal , RV unction is assessed. Inotropic support may be necessary to maintain adequate mean arterial pressure or coronary per usion. T e superior vena cava cannula is removed immediately a er cessation o bypass. Coagulopathy is common especially a er repeat sternotomy and in patients with hepatic insuf ciency or taking oral anticoagulation. T e use o cell salvage and tranexamic acid is the standard o care. T omboelastography is used to guide optimal hemostasis management.

COMPLICATIONS RV ailure is most eared intraoperative complication and accounts or 20% o deaths. Cardiopulmonary bypass, trans usion o blood products, and hypoxemia can increase the PVR.

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T e newly transplanted and stunned right ventricle may not be able to generate enough orward ejection pressures, leading to ailure. T e management o RV ailure requires inotropic and chronotopic support to decrease PVR and increase coronary per usion. Phosphodiesterase III inhibitors (e.g., milrinone) are the inotropic agents o choice or RV ailure. T ese drugs decrease PVR and act synergistically with catecholamines such as epinephrine. High rate pacing will increase cardiac output and may override arrhythmias. Nitric oxide and inhaled prostaglandin are success ully used to improve oxygenation and decrease PVR. High doses o pressors such as vasopressin and nor-pinephrine are commonly used to maintain a normal mean arterial pressure and assure optimal coronary per usion. RV assist devices and ECMOs have been o ered to patients with RV ailure re ractory to optimal medical therapy. Primary gra dys unction occurs in 2.5% o cases and results in irreversible biventricular ailure and death. T e primary risk actors or gra ailure are prolonged ischemic time and donor recipient mismatch. Gra rejection is rare due to current immunosuppressive regimens. However, it can still occur within the rst year a er transplant. Rejection usually presents with new onset CHF and requires treatment with an acute course o corticosteroids. HF may be controlled by acute course o steroids.

Systemic hypertension, in ection, and malignancy may also develop in transplant recipients, o en related to immunosuppressant and steroid therapy.

NONCARDIAC SURGERY AFTER CARDIAC TRANSPLANTATION Patients who have received a transplanted heart o en require noncardiac surgery. T ere are several key physiologic and anesthetic concerns or these patients: • • • • • •

Denervation o the vagus nerve results in a high resting heart rate. Denervation o the sympathetic nervous system results in a blunted response to hypotension and hypovolemia. T e transplanted heart is preload-dependent (normal Starling relationship). Preoperative evaluation should assess the degree o accelerated coronary artery disease in the transplanted heart and the potential or silent ischemia and in arction. Electrocardiography may show two P waves (residual native and donor). Indirect-acting drugs (e.g., ephedrine, atropine) have little e ect compared to direct-acting agents (e.g., epinephrine, isoproterenol).

Cardiac Tamponade Andrew Winn, MD, and Brian S. Freeman, MD

Cardiac tamponade is a clinical syndrome in which uid accumulates within the pericardial sac, leading to increased pericardial pressures that compress the chambers o the heart and restrict cardiac lling. Cardiac tamponade can be caused by myocardial in arction, myocarditis, cardiac surgery, Dressler’s syndrome, dissecting aortic aneurysms, and iatrogenic trauma that may occur during percutaneous coronary intervention, electrophysiology studies, and cardiopulmonary resuscitation. Blunt and penetrating trauma may rapidly lead to hemopericardium and subsequently acute tamponade. Pericardial e usions, which can lead to tamponade physiology, also have a variety o etiologies: in ection, malignancy, autoimmune, uremia, and collagen vascular disease, among others. T ere are several subtypes o cardiac tamponade: • •

•

Acute cardiac tamponade, of en resulting rom trauma or medical procedures, can rapidly progress to cardiogenic shock in minutes to hours. Subacute cardiac tamponade is usually caused by chronic pericardial e usions, such as those seen in patients with malignancy or renal ailure, though most e usions are deemed idiopathic. T ey develop over days to weeks, allowing or gradual expansion o the pericardial sac. Patients may initially be asymptomatic. However, once the pericardial pressure reaches a critical threshold, patients experience dyspnea, chest ullness, peripheral edema, and atigue. Regional cardiac tamponade occurs when there is compression o a portion o the heart, of en caused by a localized hematoma or loculated e usion af er pericardiotomy or myocardial in arction. Because only certain regions o the heart are compressed, the typical signs o cardiac tamponade may be absent. Low-pressure cardiac tamponade is uncommon. It occurs in severely hypovolemic patients due to hemorrhage, hemodialysis, or overdiuresis and is characterized by low lling pressures (intracardiac and pericardial diastolic pressures o approximately 6–12 mmHg). Clinical ndings commonly associated with cardiac tamponade, such as elevated heart rate, jugular venous distention, and

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pulsus paradoxus, are rarely seen. Although some patients are critically ill, most present in a stable condition.

PATHOPHYSIOLOGY In cardiac tamponade, the rapid accumulation o uid in the pericardial sac transmits intrathoracic pressure to the cardiac muscle that decreases cardiac lling. amponade is a spectrum o hemodynamic abnormalities o varying severity. It is not all-or-nothing obstructive shock. Pathophysiologic changes include the ollowing: • • • • •

Increased intrapericardial pressure →compression o all heart chambers Decreased ventricular compliance →decreased lef ventricular lling Decreased systemic venous return →decreased right ventricular lling Decreased stroke volume →low cardiac output Equalization o all cardiac lling pressures with the intrapericardial pressure

Compensatory e orts o the sympathetic nervous system and circulatory systems to maintain cardiac output include tachycardia and peripheral vasoconstriction (increased systemic vascular resistance). Ventricular interdependence re ers to the interaction between the right and lef ventricles that occurs throughout the cardiac cycle. When a healthy individual inspires, thoracic pressure decreases, causing two major e ects on blood ow to the heart. First, there is increased venous return to the right heart. Second, as a result o decreased pulmonary vascular pressure, there is a decrease in venous return to the lef heart. As cardiac tamponade develops, right-sided venous return decreases because expansion o the ree wall o the right ventricle is limited by external pressure ( uid in the pericardial sac). When coupled with the decreased venous return to the lef heart that occurs naturally with inspiration, the right ventricle accommodates incoming blood by expanding the interventricular septum towards the lef ventricle. T is shif 275

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causes a urther decrease in venous return to the lef ventricle with ensuing cardiac cycles, and ultimately decreases cardiac output.

PRESENTATION AND DIAGNOSIS Physical Examination Cardiac tamponade typically produces dyspnea and tachypnea in the conscious patient. Low stroke volume leads to hypotension, narrow pulse pressure, and compensatory tachycardia. Oliguria is a common nding due to peripheral hypoper usion. Ventricular interdependence results in pulsus paradoxus, a drop in systolic blood pressure greater than 10 mmHg during inspiration. Hypotension, decreased heart sounds, and elevated jugular venous pressure are the three components o “Beck’s triad.” When tamponade is caused by in ammatory pericarditis, a riction rub may be heard on exam. Kussmaul’s sign, where the jugular venous pressure does not decrease during inspiration, is a rare nding in cardiac tamponade.

Electrocardiogram T e electrocardiogram of en shows sinus tachycardia and lowvoltage QRS complexes. Low voltage is present when the maximum QRS amplitude is less than 5 mm (0.5 mV) in leads I, II, and III. Electrical alternans, in which the voltage o the QRS complex varies with each beat, is a speci c but insensitive nding or cardiac tamponade. I tamponade results rom pericarditis, the ECG may demonstrate di use concave S elevation and PR depression, including reciprocal S depression and PR elevation (usually in lead aVR).

Chest Radiography I tamponade is slow to develop, cardiomegaly on the chest radiograph appears as an enlarged cardiac silhouette (“water bottle-shaped heart”) with clear lung elds. In acute cardiac tamponade, cardiomegaly is a rare nding. Enlargement o the cardiac silhouette requires at least 200 mL o uid present in the pericardial sac.

Right Heart Catheterization Pulmonary artery catheterization reveals low cardiac output and elevated central venous pressure. T e central venous pressure wave orm shows a decrease in the y descent because o impaired cardiac lling in late diastole. Eventually all diastolic lling pressures increase to equilibrate with the elevated intrapericardial pressure (usually 10–30 mmHg). Catheterization demonstrates equalization o right atrial pressure, right ventricular end-diastolic pressure, pulmonary artery diastolic pressure, and pulmonary capillary wedge pressure. Lef -sided pressures simultaneously decrease during inspiration.

Echocardiography I tamponade is moderate to severe, echocardiography shows the heart swinging inside the pericardial sac. Be ore patients become hemodynamically unstable, chamber collapse, especially in the low-compliant right heart, is of en detected. Late diastolic collapse o the right atrium is highly speci c and sensitive or cardiac tamponade. Early diastolic collapse o the right ventricular ree wall, while less sensitive or tamponade than right atrial collapse, is also highly speci c. T ese changes lead to interventricular septal attening. Regional tamponade may show collapse o certain sections o the myocardium, including hypertrophic ventricular chambers. T e echocardiogram is also particularly e ective in demonstrating changes in cardiac volume and ow that occur with respiration. Such changes are exaggerated in cardiac tamponade due to ventricular interdependence. With normal physiology, ow across the mitral and tricuspid valves changes no more than approximately 25% during respiration. During cardiac tamponade, pulsed wave Doppler shows decreased (30%) peak mitral and increased (60%) tricuspid in ow velocities during inspiration. Because o increased central venous pressure, the in erior vena cava may appear dilated and ail to reduce its diameter o at least 50% during inspiration.

TREATMENT T e de nitive treatment or cardiac tamponade is drainage o uid. T e acuity with which pericardial uid is removed depends on the hemodynamic stability o the patient. In early tamponade, patients are generally stable and can be monitored with serial physical exams and echocardiograms while exploring the cause o the e usion. emporizing measures include maintenance o stroke volume by in using crystalloid or colloid solutions. Catecholamines (e.g., isoproterenol, dobutamine, atropine, dopamine) should be administered to maintain cardiac output. Metabolic acidosis resulting rom low cardiac output should be corrected to improve myocardial depression and the inotropic e ects o exogenous catecholamines. I instability becomes evident, intervention is required. Catheter pericardiocentesis involves gaining access to the pericardial space by skin puncture under echocardiographic guidance, with subsequent drainage o uid rom the pericardial space through the catheter. It is less expensive than surgery and is the pre erred modality in unstable patients because it can be per ormed rapidly. It is generally sa e, but rarely may be complicated by acute lef ventricular ailure with pulmonary edema or acute dilation o the right ventricle. In patients with liver disease and coagulopathy, the subcostal approach is avoided because severe bleeding can occur. In patients with aortic dissection or ruptured myocardium, pericardiocentesis should be avoided because removal o the pericardial uid may lead to severe, continuous bleeding. Finally, with small, loculated e usions, needle aspiration should be avoided unless the operator is highly skilled and experienced. When pericardiocentesis is not considered optimal, surgery is recommended.

CHAPTER 72

Surgical options or uid removal include subxiphoid pericardiostomy, thoracoscopic pericardiostomy, or thoracotomy with pericardiostomy. T ere are several advantages to surgical removal o pericardial uid. T ese include retrieval o tissue or biopsy, direct visualization, pericardiectomy, and pericardial window ormation. Furthermore, surgery is of en pre erred or cases due to trauma, purulent pericarditis, and recurrent malignant e usions. With surgical access to the pericardial space, washout can be per ormed, and any trauma to the pericardial sac can be repaired. For recurrent e usions, a pericardial window can be per ormed to prevent reaccumulation. A disadvantage to surgical drainage is that general anesthesia is required, which may worsen hypotension in the setting o tamponade. T ere is a relative contraindication to pericardial drainage during cardiac tamponade or patients with severe pulmonary hypertension. In such cases, the e usion may be preventing critical dilatation o the right ventricle. Removal o the uid may lead to loss o this mechanical support o the right ventricle, causing worsening o right ventricular unction and more severe tricuspid regurgitation. However, when a patient has symptomatic cardiac tamponade, the bene ts o uid removal outweigh the risks. Once drained, pericardial uid should be tested to determine the etiology o the e usion, and then treated i possible. T e patient should be monitored with telemetry and requent vital signs or approximately two days. An echocardiogram be ore discharge is advised to con rm removal o the uid and assess or reaccumulation. It can be repeated at ollow-up, depending on the cause o the e usion and the likelihood o reoccurrence.

ANESTHETIC MANAGEMENT Patients requiring a pericardial window are susceptible to hypotension and cardiac arrest due to the induction o

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277

general anesthesia. Intravenous and inhalation anesthetics promote peripheral vasodilation and direct myocardial depression. In addition, positive-pressure ventilation will increase intrathoracic pressure thereby decreasing venous return. Both interventions lead to urther impairment in cardiac output. Ideally, unstable patients with acute cardiac tamponade are treated with percutaneous pericardiocentesis under local anesthesia. I surgical drainage under general anesthesia is required, an intra-arterial catheter should be placed prior to induction so that acute changes in hemodynamics can be detected and corrected. For severe cardiac tamponade, the patient should undergo surgical preparation and draping with the surgeon scrubbed at the operating room table ready or incision prior to induction. T e physiologic goals are to maintain tachycardia, optimize preload to maximize lef ventricular lling, and maintain an elevated systemic vascular resistance (“ ast, ull, and tight”). Vasodilation and hypotension should be avoided. T ese three parameters work together to ensure adequate cardiac output. Medications used during general anesthesia should be consistent with these goals. Catecholamine in usions (e.g., norepinephrine, dopamine, epinephrine) should commence prior to induction. Small boluses o epinephrine may be help ul or temporary inotropy and chronotropy. Ketamine is the pre erred intravenous anesthetic due to its promotion o sympathetic output. Suitable options or maintenance include midazolam, entanyl, nitrous oxide, and pancuronium (which also induces tachycardia). I possible, maintenance o spontaneous respiration can avoid positive intrathoracic pressure which decreases venous return. Positive pressure ventilation may be delayed until drainage o the pericardial space is imminent. Once the pericardium is drained, venous return can enter the heart and hemodynamics will rapidly normalize (or swing to hypertension).

Pulmonary Embolism Raj N. Parekh, MD, and Hiep Dao, MD

Pulmonary embolism (PE) is a process where a clot, usually blood, orms within the body and eventually travels to the pulmonary vasculature. T e clinical presentation o PE ranges rom lack o symptoms to acute hemodynamic compromise and death. Operations that demonstrate a higher incidence o pulmonary embolism include acute spinal cord injury, trauma, neurosurgery, hip racture repair, total knee arthroplasty, and total hip arthroplasty. Because o its sometimes vague symptomatology, clinicians should maintain a high level o clinical suspicion or a possible intraoperative PE.

CAUSES T e etiology or the vast majority o pulmonary emboli stem rom thromboembolic events, usually a deep vein thrombosis. T e basis or all thromboses in the body is described via “Virchow’s triad”: hypercoagulability, hemodynamic changes (e.g., venous stasis), and endothelial dys unction. Once a deep vein thrombus begins to orm in the lower extremity, parts o the newly ormed thrombus can break o and travel in the venous system to the heart. Once at the heart, the clot can pass through to the lungs and become lodged within the pulmonary artery or one o its branches, ultimately leading to ischemia within the lungs. Risk actors or developing DV s include malignancy, surgery, traveling or long distance, and inherited hypercoagulable disorders. Because the venous system depends on muscular contraction to move blood orwardly, prolonged immobilization can lead to blood stasis and clot ormation. Pulmonary at emboli usually occur a er traumatic injury to the musculoskeletal system or a er a surgical procedure. Fractures o the pelvis and long bones are especially susceptible to producing at embolus, o en leading to fat embolism syndrome (FES). Fat emboli are usually small and multiple, leading to damage to multiple unctional systems including pulmonary, dermatological, and neurological. Diagnosis is di cult, but petechiae are a common eature since the small atty emboli lead to microhemorrhages in the skin. I atty emboli reach the pulmonary vasculature,

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catastrophic consequences may ensue including cor pulmonale and sudden death. T e exact pathophysiology o at emboli origin is still not ully elucidated; however, the general principle includes the idea that a er a skeletal injury, intramedullary pressure rises, orcing at globules into the venous system. Once in the venous system, the at globules have the potential to advance into pulmonary vasculature, leading to symptoms o pulmonary embolism. Pulmonary air embolism occurs when air becomes entrapped in the venous or arterial circulation. T is occurs most o en in the surgical setting when air is introduced into an intra-arterial or intravenous line, or when air gets entrapped directly into the surgical eld. Air emboli are not very common due to the high pressure gradient in the venous and arterial system compared to atmospheric pressure. Veins within the head and neck are the exceptions. T ese veins typically have pressures lower than atmospheric pressure, allowing a avorable gradient or air to enter the circulatory system. In the surgical setting, especially in laparoscopic procedures, the high circulatory pressures can be overcome when positive pressure insu ated air is introduced into the abdominal or pelvic cavity. Entrapped air in the venous system usually ends in the lung, rarely causing symptoms; however, i air embolism is not dissolved, then pulmonary pressures can increase leading to right-heart strain and thus symptoms consistent with PE. Entrapped air in the arterial system is ar more dangerous as this can lead to end-organ ischemia in the brain or kidneys.

PATHOPHYSIOLOGIC CHANGES Pulmonary • • • •

Increased alveolar dead space, right-to-le shunting, and ventilation/per usion mismatch Pulmonary edema, sur actant loss, and alveolar hemorrhage Atelectasis Regional bronchospasm

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Cardiovascular • • • • • • • • •

Increased pulmonary vascular resistance Increased right ventricular a erload Decreased right ventricular stroke volume Compensatory tachycardia and vasoconstriction Increased right atrial pressures Right ventricular dilatation Interventricular septal shi into le ventricle Decreased le ventricular preload Decreased cardiac output

DIAGNOSIS History and Physical Findings T e signs and symptoms o a pulmonary embolus span a wide range. Common signs and symptoms in a conscious patient include pleuritic chest pain, dyspnea, tachycardia, hemoptysis, and tachypnea. Auscultation o the heart and lungs may reveal an S4 gallop, accentuated S2 heart sound, and pulmonary crackles or wheezing. Platelet activation and the release o serotonin and thromboxane A2 predisposes the patient to developing bronchospasm. Jugular venous distension may be present. Since these ndings are sensitive but nonspeci c or PE, clinicians must maintain a low threshold to pursue diagnostic testing. Originally developed in 1995, Wells’ Criteria have been used by clinicians to ascertain the likelihood o PE being present in patients ( able 73-1). T e more criteria that the patient meets, the more likely a pulmonary embolus has occurred. A score o 12.5 correlates to a 41% risk o PE.

Diagnostic Testing 1. Electrocardiography—Common ECG ndings include a large S wave in lead V1, S depression in lead II, and -wave inversion with a Q wave in lead III. Right bundle branch block, right ventricular hypertrophy, and right axis deviation can also be evident. 2. Arterial blood gas—Blood gas testing in the patient with PE will usually show arterial hypoxemia, which is the most sensitive nding. I the patient is spontaneously breathing, the ABG may also demonstrate respiratory alkalosis and hypocapnia.

TABLE 73-1

Wells’ Criteria for Pulmonary

Embolism

(1) Symptoms concerning for DVT/PE: 3 points (2) PE is currently most likely diagnosis: 3 points (3) Heart Rate > 100 bmp: 1.5 points (4) Previous diagnosis of PE or DVT: 1.5 points (5) Surgery in the past 4 weeks or immobilization for at least 3 days: 1.5 points (6) Presence of hemoptysis: 1 point (7) Presence of malignancy: 1 point

3. Capnography—T e lack o per usion to a ventilated portion o the lung causes an acute increase in alveolar dead space. I the patient cannot compensate appropriately by raising minute ventilation, then arterial PaCO2 increases. Expired gas rom normal alveoli now mixes with gas that does not contain any expired CO2 since it comes rom alveoli no longer receiving per usion. Consequently, endtidal carbon dioxide (PE CO2) measurements acutely decrease and the PaCO2–PE CO2 gradient increases. 4. Laboratory studies—Other tests that may be per ormed include measurements o D-dimer, roponin I, and roponin . D-dimer is a brinogen degradation product. Increased levels o this can be a marker or PE. T e sensitivity o a D-dimer assay ranges rom 80%–100%, while the speci city o this study ranges rom 10%–64%. Due to its high sensitivity, i the clinician believes there is a low pretest probability or a PE, then a negative D-dimer study is very highly sensitive or ruling out PE as the diagnosis. However, i the D-dimer assay is negative and the clinician still has a high suspicion or PE, then urther diagnostic studies must be pursued. 5. Radiologic studies—Findings which may support the diagnosis o PE on chest radiographs include atelectasis, pleural e usion, pleural opacities, elevated diaphragm, and decreased pulmonary vascularity. Ventilation/perusion (V/Q) scans were once a widely popular de nitive study or diagnosing PE. V/Q scans use medical isotopes and scintigraphy to measure ventilation and per usion within the lung. When a V/Q scan reads the lung as having multiple areas o poor per usion with adequate ventilation, there is a high probability o PE. T is imaging study has since been supplanted by C angiography as the gold standard to con rm or exclude PE due to its high speci city (81%–100%). Venous contrast is necessary to per orm the test; there ore, it is relatively contraindicated in patients with renal ailure or patients with severe allergies to contrast media.

ECHOCARDIOGRAPHY A presumptive diagnosis o pulmonary embolus can be made in the operating room without interrupting the surgery using transesophageal echocardiography ( EE). Echocardiography has much better accuracy or diagnosing a massive pulmonary embolus rather than small emboli. EE ndings consistent with pulmonary embolism include EE ndings include right ventricular dilation with hypokinesis, a f attened or D-shaped interventricular septum, and the inability to compress the in erior vena cava during inspiration. “McConnell’s sign,” a distinct pattern o RV dys unction with akinesia o the ree wall but normal contraction at the apex, is suggestive o PE. T e sensitivity and speci city o McConnell’s sign or PE versus other etiologies that cause RV dysunction such as primary pulmonary hypertension are 77% and 94%, respectively.

CHAPTER 73

A common hemodynamic mani estation o PE is pulmonary hypertension. Clues or pulmonary hypertension on EE are visible f attening o the interventricular septum during diastole and tricuspid regurgitation. T e degree o pulmonary hypertension is positively correlated with the size o the pulmonary embolus as well as the patient’s preexisting cardiopulmonary disposition. Certain EE ndings can help clinicians identi y patients at greater risk o death or poor prognosis. T ese ndings include right ventricular hypokinesis, patent oramen ovale, persistent pulmonary hypertension, and direct visualization o a ree f oating thromboemboli in the right heart. Patent oramen ovale is a common cause o stroke in patients with PE. T is occurs as the right atrial pressures exceeds pressures in the le atrium allowing or re-opening o the oramen ovale; thus, allowing the thrombus to travel to the brain.

TREATMENT reatment or PE is patient-tailored depending on the severity o the PE and i hemodynamic compromise is evident. I the patient is stable, then treatment is usually similar to the treatment or deep vein thrombosis. T e mainstay o treatment or hemodynamically stable PE is chemical anticoagulation. Common anticoagulant medications include war arin, un ractionated heparin, low molecular weight heparin, and ondaparinux. In a typical treatment regimen, heparin (un ractionated or low molecular weight heparin) is started. P is usually titrated to 1.5–2 times normal. A er 3–4 days and once P is at goal, heparin is still continued and war arin is commenced. arget INR or treating PE is usually 2–3. However, i this is recurrent PE and the patient is not at increased risk or bleeding, target INR rise to 2.5–3.5. Once the target INR is reached, heparin can be discontinued and the patient continues taking war arin or 3–6 months. Frequent monitoring o INR is crucial or monitoring the resolution o the PE as well as or titrating the dosage o war arin. T e idea behind bridging to war arin is that i war arin is commenced be ore another orm o anticoagulation is started, then the patient may actually be at risk o being in a procoagulation state instead o an anticoagulation state as war arin may pre erentially block Protein C and S (natural anticoagulants) over Factors II, VII, IX, and X. T rombolytic therapy is reserved or massive pulmonary emboli that cause hemodynamic instability. Hypotension results rom the acutely elevated pressures within the pulmonary arterial system leading to acute right-heart strain and ischemia. I uncorrected, immediate and irreversible cardiac dys unction will ensue. I possible, an echocardiogram should be done to evaluate or right ventricular strain as well

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as to evaluate i there are any visible clot ormations within the clot. Clot lysis is necessary to restore hemodynamic stability; however, bleeding, including cerebral hemorrhage, is a major adverse event when administering thrombolytics. T e most common thrombolytic currently used is tissue plasminogen activator (tPA). Several studies have supported the use o thrombolytic therapy in massive PE, but little support exists or its utility in submassive PE. Pulmonary thrombectomy is another therapeutic option or hemodynamically comprised patients with severe massive PE. T is is in requently used due to reports o poor outcomes. A similar procedure called pulmonary thromboendarterectomy (P E) is used to treat chronic PE that has led to pulmonary hypertension. P E carries a high mortality risk (5%) due to the use o cardiopulmonary bypass, circulatory arrest, and deep hypothermia.

PREVENTION In erior vena cava (IVC) lters are used when medical treatment has ailed or there is a contraindication to anti-coagulation, usually high risk or serious bleeding. T e IVC lter is designed to be able to prevent massive emboli, usually rom DV , rom traveling to the pulmonary artery. IVC lters are not e cient in preventing smaller sized emboli rom reaching the lungs, however. In the hospital setting, several orms o prophylaxis exist or preventing PE. Heparin and LMWH are common chemical prophylactics used. Even though guidelines are not speci cally clear on which patients should receive prophylaxis, several demographics have been shown to bene t rom chemical prophylaxis. Factors that avor the need or prophylaxis in the hospital-setting include cancer, obesity, longterm immobilization, previous history o V E, and trauma/ surgery in past months. Sequential compressive devices (SCDs) are also used in bed-bound patients in the hospital setting. T ey are usually bilateral and extended rom the ankle to below the knee. When connected, the SCD sleeves are lled with air leading to a pressurized state within the lower limbs, orcing the movement o blood and lymph out o the lower extremities. T is promotes circulation o blood and prevents blood stasis, thus preventing DV and ultimately PE.

SUGGESTED READING Desciak M, Martin D. Perioperative pulmonary embolism: diagnosis and anesthetic management. J Clin Anesth. 2011;23:153–165.

Hypertension: Preoperative Evaluation Hannah Schobel, DO

DEFINING HYPERTENSION Hypertension is de ned as elevated arterial blood pressure. T e Joint National Committee on Evaluation, Detection, and Prevention o High Blood Pressure de nes the optimal blood pressure or adults less than 120/80. Prehypertension

>120/80–139/89

Hypertension

>140/90

Stage I

>140/90–179/109

Stage II

>180/110

Stage II hypertension is classi ed as urgent or emergent hypertension. Stage II becomes emergent with signs o end organ damage including headache, blurred vision, stroke, congestive heart ailure, myocardial ischemia, and acute kidney injury. T e normal blood pressure measurements or children increase with age: Infants

70/45

Children

85/55

Adolescents

100/75

PATHOPHYSIOLOGY T e pathophysiology o hypertension can best be explained by separating systolic, diastolic, and pulse pressure hypertension.

Systolic Hypertension Systolic hypertension is a macrovascular disease. It is caused by atherosclerosis o the aorta and large arteries. T e aorta becomes less compliant and less distensible in response to ventricular and aortic out ow rom the heart. Decreased compliance o the arterial tree increases blood pressure and a erload. Risk actors or systolic hypertension include age > 60, diabetes mellitus, hyperlipidemia, and smoking.

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Diastolic Hypertension Diastolic hypertension is a microvascular disease. It is caused by atherosclerosis o the small vessels 75% stenosis. Gadolinium-enhanced magnetic resonance angiography (MRA) is a nonionizing imaging modality that can be perormed rapidly and has excellent image quality. In act, it has virtually replaced traditional catheter-based angiography— the gold standard diagnostic tool. It has both high sensitivity (90%) and speci city (97%) in the detection o stenotic vessels in the lower extremities. Its main disadvantage is that it cannot be used in patients with metallic implants (e.g., pacemakers, coils, clips) and patients with compromised renal unction (GFR < 30 mL/min).

MEDICAL MANAGEMENT VERSUS INTERVENTIONAL THERAPY T erapy or PVD is centered on two main goals: decreasing cardiovascular events and improving symptoms and quality o li e. Li estyle modi cation is at the heart o both and

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includes smoking cessation, lipid lowering therapy, tight glycemic control, and a supervised exercise program. In higher risk patients, antithrombotic therapy with aspirin or clopidogrel may be used or secondary prevention. Cilostazol, a phosphodiesterase type 3 inhibitor, has been used to improve claudication due to its vasodilatory and antiplatelet activities. It should be used with caution due to a contraindication in patients with congestive heart ailure or patients with an ejection raction o 5 cm) or symptomatic (chest or back pain, cough, hoarseness). For asymptomatic abdominal aortic aneurysms, an elective repair is recommended when greater than 5.5 cm in diameter because o a 10% per year risk o rupture. I the rate o growth is more than 0.5 cm in a 6 month period or the patient is symptomatic, elective repair may also be recommended. T oracic aneurysms involving the ascending aorta or aortic arch usually require open surgery. Descending aortic aneurysms are routinely treated with endovascular gra ing. T oracoabdominal aortic aneurysms can be repaired open, endovascular, or with a hybrid technique. T e patient’s comorbidities, physiologic reserve, anatomy, and experience o the treating team determine which approach should be pursued. Open repair o an aortic aneurysm is the traditional approach that is durable but carries higher risk. T e risk o operative mortality with open repair is 3%–5%. More commonly, aortic aneurysms are repaired using minimally invasive techniques: endovascular aneurysm repair (EVAR). Speci c anatomic criteria must be met or a patient to undergo EVAR. An increasing number o patients are candidates or EVAR as technology and gra s evolve. T e technique involves emoral artery access and gra deployment in the aorta to exclude the aneurysm sac rom circulation. EVAR is associated with lower perioperative morbidity and mortality but may have higher long term morbidity and mortality. T e risk o operative mortality with EVAR is 0.5%–2%. Regardless o technique, all patients undergoing aortic aneurysm repair should be evaluated and prepared as i undergoing an open repair given the risk o conversion to an open repair during EVAR.

TABLE 78-1

Preoperative Comorbidities and Work Up for Patients with Aortic Disease System

Evaluation

Cardiovascular

Hypertension Coronary artery disease Peripheral vascular disease Congestive heart ailure

ECG Stress testing Echocardiography Radionuclide imaging Coronary angiography

Pulmonary

COPD

Chest radiography Pulmonary unction testing

Renal

Chronic renal ailure

Creatinine BUN Electrolytes

Metabolic

Diabetes

Hemoglobin A1C

back pain, hypotension, and a pulsatile abdominal mass. Approximately hal o the patients with a ruptured AAA present with this triad o symptoms. Fortunately many o the ruptures are into the le retroperitoneal space which may tamponade the bleeding preventing exsanguination. Although the patient may be in hypovolemic shock, it is not recommended to aggressively hydrate prior to surgical repair as this can lead to increase in blood pressure and loss o tamponade, resulting in exsanguination and death.

TABLE 78-2

Anesthetic Considerations and Monitoring for Thoracic Aorta Repair System

Monitoring/Considerations

Cardiovascular

• TEE • PA catheter • Right radial + right emoral arterial lines º Cross clamp proximal to subclavian artery = no le t radial pressure º Loss o right radial tracing = innomate artery occlusion º Cerebral per usion + distal organ per usion º Goal during cross clamp: upper extremity MAP ≥ 100 mmHg º Lower extremity MAP ≥ 50 mmHg

Neurologic

• SSEPs not help ul • MEPs to monitor anterior spinal cord (not use ul i muscle relaxants used) • Lumbar drain (goal pressure < 10 cmH2O)

Pulmonary

• One-lung anesthesia (double lumen tube or endobronchial blocker)

Hematologic

• Potential or massive blood loss • Potential or coagulopathy • Consider acute normovolemic hemodilution

Renal

• • • •

ANESTHETIC MANAGEMENT (TABLE 78-2) Preoperative Assessment Many patients presenting or aortic aneurysm repair have multiple comorbidities, including heart disease, diabetes mellitus, hypertension, lung disease, and renal dys unction. Preoperative identi cation and optimization o these conditions is imperative as it minimizes complications. T ere are several common coexisting diseases associated with aortic aneurysms ( able 78-1). It is recommended that all patients have a preoperative EKG, given the high prevalence o cardiovascular disease in the patient population. Basic labs including coagulation studies, complete blood count, and chemistry panel are also recommended. T e other preoperative studies listed in able 78-1 should be done only i indicated based on the patient’s comorbidities and symptoms. Rupture o an abdominal aortic aneurysm is the eared complication and an emergency that requires immediate surgical repair. T e classic triad o symptoms includes severe

Associated Diseases

Maintain urine output Cold per usion Low-dose dopamine, mannitol, urosemide N-acetylcysteine

CHAPTER 78

Choice of Anesthesia Open aortic aneurysm repair is done under general anesthesia with or without supplemental epidural anesthesia. EVAR can be per ormed under regional anesthesia, total intravenous anesthesia, local anesthesia with conscious sedation, or the more common approach is general anesthesia. A general anesthetic plan is outlined below.

Induction Intravenous induction agent should be chosen based on cardiovascular unction. Etomidate should be considered i the patient has depressed cardiac unction. In patients with renal ailure, cisatracurium is an optimal muscle relaxant. Pancuronium should be avoided as it can cause tachycardia. It is important to maintain normal blood pressure and heart rate. Prior to gentle direct laryngoscopy, ensure the patient is under deep anesthesia. opical lidocaine is help ul or blunting these hemodynamic changes.

Maintenance Most o en a balanced anesthetic technique with oxygen, air, volatile anesthetic and opioids is used. Blood pressure and heart rate control are imperative to avoid myocardial ischemia. For open repair, consider epidural anesthesia along with the balanced technique. T e epidural should be placed be ore systemic anticoagulation. Phenylephrine may be needed to maintain normotension in patients with an epidural catheter to compensate or sympathetic blockade. Nitrous oxide can be used but may cause bowel distention inter ering with the surgical eld. Full muscle relaxation is needed throughout procedure.

Blood and Fluid Requirements Large-bore peripheral intravenous access is imperative. Packed red blood cells should be available. Acute normovolemic hemodilution is an acceptable technique or this operation. Urine output is maintained at 0.5–1 mL/kg/h. With EVAR, blood loss is usually minimal but can be massive i complications occur. Major blood loss is expected with the open approach. A blood-salvaging device may be help ul.

Monitoring In addition to standard basic monitors, an arterial catheter should be placed in the right radial artery or EVAR. T e le upper extremity must remain available or the surgeon to access the le brachial artery. A central venous catheter is help ul or monitoring central venous pressure and administering vasoactive drugs. A pulmonary artery catheter (PAC) is used or thoracic aortic surgery but rarely used or abdominal aortic aneurysm resection. T e PAC is indicated in patients with an abdominal aortic aneurysm i there is a history o recent myocardial in arction, congestive heart ailure, unstable angina, or i the resection is an emergency. ransesophageal echocardiography is extremely valuable to monitor anatomical

Aortic Aneurysms

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changes during cross-clamping and unclamping. A urinary catheter should be placed to monitor urine output.

AORTIC CROSSCLAMP: PATHOPHYSIOLOGY Preclamp Management Renal protection is necessary as injury can result rom hypoper usion o the kidneys or embolism o debris into the renal arteries. Prior to aortic crossclamping, it is important to maintain adequate intravascular volume, cardiac output, and urine output. Use o mannitol, loop diuretics, and enoldopam is controversial as literature does not show bene t. Despite lack o evidence, it is generally accepted to give mannitol 0.25–0.5 g/kg IV immediately be ore clamping to maintain urine output and preserve renal unction. Five minutes prior to crossclamp, heparin may be given. A baseline AC should be checked prior to heparin administration, 3 minutes a er administration, and then every 30 minutes while the clamp is in place.

Crossclamping During the repair o an abdominal aortic aneurysm, the main derangements that occur with the placement o a clamp across the aorta include (Figure 78-2) the ollowing: • • • • •

Sudden increased a erload Decreased preload Increased lling pressure Decreased renal per usion Decreased per usion to viscera below clamp

T e placement o the clamp determines the degree o derangement. An in rarenal clamp avoids ischemia to most P a s s ive ve nous re coil dis ta l to cla mp

AoX

↑ Ca te chola mine s (a nd othe r ve nocons trictors )

Active ve nocons triction proxima l a nd dis ta l to cla mp ↓ Venous ca pa city

↑ Blood volume a nd flow in mus cle s proxima l to cla mp

S hift of blood volume proxima lly to cla mp

↑ Lung blood volume

↑ Intra cra nia l blood volume

S upra ce lia c AoX

↑ Ve nous re turn, pre loa d

S hift of blood volume into s pla nchnic va s cula ture

↑ Ve nous re turn, pre loa d (If s pla nchnic ve nous tone is high)

↓ Ve nous re turn, pre loa d (If s pla nchnic ve nous tone is low)

Infra ce lia c AoX

FIGURE 78-2

Pathophysiology o aortic crossclamping. (Reproduced with permission rom Gelman S. The pathophysiology o aortic crossclamping and unclamping. Anesthesiology. 1995;82:1026.)

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major organs and has the least hemodynamic ef ects and complications. Renal ailure remains a consideration even with an in rarenal clamp as renal blood ow is decreased by up to 60%. A suprarenal clamp af ects the kidneys, spine, and lower extremity blood supply and ischemia o these organs is possible. Supraceliac clamp produces the most drastic hemodynamic changes and postclamp complications. T e more proximal the clamp, the greater amount o stress on the heart due to increased a erload. Kidneys, intestines, and liver are all ischemic with supraceliac clamp; there ore, coagulopathy, acidosis, and renal injury are likely. Vasodilators helps to maintain normotension during crossclamping. Nitroglycerin in usions (0.25 mcg/kg/min) decrease systemic vascular resistance and preload while increasing coronary blood ow by relaxing vascular smooth muscle. Sodium nitroprusside is also requently used to decrease blood pressure because o its aster onset.

Unclamping Response to unclamping depends on the length o time the aorta is clamped and location o the clamp. Hypotension during aortic clamp release can occur as blood ow is reestablished (Figure 78-3). T ere are two main mechanisms by which hypotension occurs: relative hypovolemia and myocardial depression as a result o washout o acid, metabolites, and

AoX

Dis ta l tis s ue is che mia

“Me dia tors ” re le a s e

↑ Pe rme a bility (by e nd of cla mping pe riod)

Dis ta l va s odila tion ↓ R a rt Uncla mping

↓ Myoca rdia l contra ctility

“Me dia tors ” production a nd wa s hout

P ulmona ry e de ma

↑ Rpv Dis ta l s hift of blood volume

Ce ntra l hypovole mia

Los s of intrava s cula r fluid

↓ Ve nous re turn

↓ Ca rdia c output

Hypote ns ion

FIGURE 78-3

Pathophysiology o aortic unclamping. (Reproduced with permission rom Gelman S. The pathophysiology o aortic crossclamping and unclamping. Anesthesiology. 1995;82:1026.)

vasoactive substances rom the ischemic tissue when ow is restored. For hypotension that persists longer than our minutes despite adequate uid resuscitation, alternative etiologies include allergic reaction to gra material or myocardial dysunction. I there is pro ound hypotension a er unclamping, consider reclamping as this is the most important temporizing measure.

Anterior Spinal Cord Ischemia Spinal cord ischemia is attributed to intraoperative hypotension, the location and length o crossclamp, decreased arterial per usion and increased spinal canal pressure, and decreased arterial per usion o important eeding arteries such as the great vertebral radicular artery (Artery o Adamkiewicz). Because this artery originates rom variable levels o the aorta (typically 8–L1), cord ischemia is usually associated with thoracic aortic repair, but is also possible with high crossclamp or AAA repair. Spinal cord protective strategies include the placement o a lumbar drain or cerebrospinal uid drainage, intraoperative monitoring o motor evoked potentials, regional or systemic cooling, use o distal aortic per usion, and arterial blood pressure augmentation.

POSTOPERATIVE MANAGEMENT Patients undergoing EVAR are usually extubated postoperatively. Pain management may include local anesthetic in ltration at the groin site in the OR ollowed by minimal intravenous analgesics in the recovery room. For open repair, preexisting lung disease, length o operation, amount o uids administered, age o patient, and temperature o patient at the end o surgery all contribute to the decision o whether immediate postoperative extubation is warranted. Given the extent o the incision, use o moderate to large doses o narcotics, and large uid shi s, it is sa est to extubate a er several hours o weaning in the intensive care unit. Post-operative pain control can be accomplished with an epidural or intermittent IV narcotic. T romboembolic events are a major concern a er vascular operations. Dextran is commonly used a er open repair. Dextran is an antithrombotic, antiplatelet drug that decreases viscosity o blood, dilutes clotting actors, and impedes platelet adhesion. Un ortunately, a small minority o patients, 0.03%–5%, can have an anaphylactic allergic reaction to dextran. Symptoms range rom ushing to cardiovascular collapse. Promit is an intravenous medication containing dextran-1 and sodium chloride that can be administered prior to dextran to mitigate the severity o an allergic reaction to dextran. Patients with sensitivity to dextran have antibodies that bind to dextran and orm allergic complexes. Promit can greatly reduce the incidence and severity o anaphylactic reactions by binding the antibodies to orm inactive complexes. I dextran is administered a er promit, there are ewer antibodies to react with dextran.

Cardiopulmonary Resuscitation Kasra Razmjou, MD, and Brian S. Freeman, MD

T e American Heart Association (AHA) estimates 295,000 out-o -hospital cardiac arrests each year. About 3%–8% o these patients will survive to discharge. T e most in uential variable or survival is the time interval rom cardiovascular collapse until de brillation. T e chance o survival rom a witnessed ventricular brillation event declines by 7%–10% or every minute that CPR is not provided. T us, adequate training in Advanced Cardiac Li e Support (ACLS) is imperative. T is may be more important in the out-o -hospital setting where only one provider may be present as opposed to the hospital setting where a team o providers can simultaneously per orm chest compressions, de brillation, and airway management.

BASIC LIFE SUPPORT Initial Evaluation Once the patient is ound unresponsive, the patient’s chest should be scanned or 5–10 seconds to evaluate or breathing. I the patient is not breathing, an automatic external de brillator (AED) should be made available. T e carotid pulse should be checked or 5–10 seconds. I no pulse is detected, chest compressions should be initiated. raditionally, ACLS providers were guided by the sequence o A–B–C (Airway, Breath, Circulation). However, as noted above, the most important barrier to survival is the time to onset o chest compressions. I the A–B–C sequence is ollowed, valuable time can be lost in order to achieve adequate ventilation. T us, the 2010 AHA guidelines recommended changing the sequence to C–A–B or both adult and pediatric basic li e support.

Chest Compressions A er it is determined that a pulse is not palpable, chest compressions should be per ormed or 2 minutes. Proper quality o chest compressions is vital to proper circulation during a cardiac arrest. Chest compressions are inadequate i end-tidal CO2 is less 10 mmHg or diastolic blood pressure is less than 20 mmHg. Prior guidelines recommended a compression depth o 1.5–2 inches at a rate o approximately 100 times per

E R

minute. T e 2010 AHA guidelines now recommend a depth o at least 2 inches at the same requency (a pattern associated with higher survival rates). In addition, there should be complete recoil o the chest between compressions. A er 2 minutes o chest compressions, a pulse check should be per ormed or a maximum o 10 seconds. I a de brillator is present and a shockable rhythm is identi ed, de brillation should occur. I a nonshockable rhythm is identi ed at any point, CPR should be continued. According to the AHA, 383,000 out-o -hospital cardiac arrests occur annually and 88% occur at home. Un ortunately, 70% o Americans are not com ortable administering CPR. In the past, it was recommended that bystanders per orm chest compressions and ventilation. However, since most adults do not receive bystander CPR due to lack o bystander com ort, the recommendations have been simplied. T e 2010 AHA guidelines recommend that untrained bystanders per orm only compressions until other responders arrive at the scene. Once a trained responder arrives, ventilation should be initiated. T e reason or this new recommendation is two old. First, compression-only CPR is easier or bystanders to per orm. Second, survival rates were similar in patients who received compressions and ventilation versus just compressions.

Ventilation For every 30 compressions, two breaths should be provided to the patient. I an advanced airway is placed, chest compressions do not have to be interrupted to give rescue breaths. Instead, one breath can be given every 6–8 seconds (8–10 breaths per minute). Continuous capnography is recommended or intubated patients in order to monitor CPR quality and determine the return o spontaneous circulation (ROSC). In the past, cricoid pressure was used to prevent gastric in ation and aspiration during bag-mask ventilation. However, several studies have showed that aspiration can still occur with cricoid pressure and that cricoid pressure can even impede ventilation. For this reason, routine use o cricoid pressure is no longer recommended. 299

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ADVANCED CARDIAC LIFE SUPPORT Def brillation Once a de brillator is available, it should be powered on. T e electrode pads should be placed in one o our acceptable positions: anterolateral, anteroposterior, anterior-le in rascapular, or anterior-right in rascapular. At this point, it is important to distinguish between the our possibilities underlying cardiac arrest. T e management o each rhythm ollows a dif erent algorithm (Figure 79-1). Ventricular brillation (VF) and pulseless ventricular tachycardia (V ) are the two dysrhythmias which can be success ully de brillated. Asystole is a state o no cardiac electrical activity and is identi ed by a at-line tracing on the ECG. Pulseless electrical activity (PEA) is identi ed by organized electrical activity on the ECG but no evidence o a pulse. Both asystole and PEA cannot be terminated by de brillation. I a shockable rhythm like VF or V is present, the patient should be de brillated. I a monophonic de brillator is used, a single 360 J shock is recommended. For biphasic de brillators, the usual energy depends on the manu acturer, but it typically alls in the range o 120–150 J. De brillation

brie y terminates all electrical activity in the heart. I the myocardium is still viable, the intrinsic pacemaker cells will initiate. During the initial period a er a pulse returns, the rhythm is too slow to provide adequate per usion. For this reason, CPR is typically continued immediately a er a shock until ROSC)occurs.

Medications Ideally, central venous access is available. However, peripheral access is easier to establish during CPR. T e caveat is that medications require 1–2 minutes to reach central circulation, which can be acilitated by raising the extremity or about 10–20 seconds a er medication delivery. Medications can also be given via the endotracheal route i intravenous or intraosseous access cannot be achieved. ypically, the medication is given through the endotracheal tube at a dose o 2–2.5 times the intravenous dosage. Once access has been established, vasopressors should be given. Epinephrine 1 mg can be given every 3–5 minutes. Since it is a vasoconstrictor, it increases blood pressure. However, high doses o epinephrine have not been ound to

VENTRICULAR FIBRILLATION OR P ULS ELES S VENTRICULAR TACHYCARDIA Imme dia te de fibrilla tion within 5 minute s of ons e t; 60 – 90 s e conds of CP R be fore de fibrilla tion for de lay ≥ 5 minute s If re turn o f c irc ulatio n fails Bradyarrhythmia /As ys to le

2 minute s of che s t compre s s ions a t >100/min followe d by re pe a t s hock; re pe a t s e que nce twice if ne e de d If re turn o f c irc ulatio n fails

Puls e le s s Ele c tric al Ac tivity

CP R, intuba te , IV a cce s s

Continue che s t compre s s ions , intuba te , IV a cce s s [Confirm a s ys tole] Epine phrine , 1 mg IV - or - va s opre s s in, 40 units IV; follow with re pe a t de fibrilla tion a t ma ximum e ne rgy within 30 – 60 s e conds a s re quire d; re pe a t e pine phrine

Ide ntify a nd tre a t ca us e s

If re turn o f c irc ulatio n fails Epine phrine , ↑ Dos e

Antia rrhythmics

Amioda rone: 150 mg ove r 10 min, 1 mg/min Lidoca ine: 1.5 mg/kg; re pe a t in 3 – 5 min

• Hypoxia • Hype r-/hypoka le mia • S e ve re a cidos is • Drug ove rdos e • Hypothe rmia

Na HCO 3 , 1 me q/kg (↑ K+) (no longe r for routine us e; ma y be us e d for pe rs is te nt a cidos is - s e e te xt)

Ma gne s ium s ulfa te: 1– 2 gm IV (polymorphic VT) P roca ina mide: 30 mg/min, to 17 mg/kg [monomorphic VT]

Epine phrine 1 mg IV (re pe a t)

—

• Hypovole mia • Hypoxia • Ta mpona de • P ne umothora x • Hypothe rmia

Atropine — 1 mg IV (only for bra dyc a rdia)

If re turn o f c irc ulatio n fails De fibrilla te , CP R: Drug – S hock – Drug – S hock

FIGURE 79-1A&B

[As s e s s blood flow]

• P ulmona ry e mbolus • Drug ove rdos e • Hype rka le mia • S e ve re a cidos is • Ma s s ive a cute MI

S odium bica rbona te 1 me q/kg IV (no longe r for routine us e; ma y be us e d for pe rs is te nt a cidos is s e e te xt)

P a cing —Exte rna l or pa cing wire

Management o cardiac arrest. (Reproduced with permission rom Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J (eds). Harrison’s Principles of Internal Medicine, 19th ed. McGraw-Hill Education, Inc., 2015. Fig. 327-3A&B.)

CHAPTER 79

improve survival. Forty units o vasopressin can be used as a substitute or the rst or second dosage o epinephrine. An antiadysrhythmic agent such as amiodarone can also be used or re ractory ventricular brillation or tachycardia (initial dose 300 mg ollowed by subsequent doses o 150 mg). T e 2010 AHA guidelines no longer recommend atropine or PEA/asystole. Adenosine is used in the treatment o stable, wide-complex tachycardia. However, it cannot be used

TABLE 79-1

Cardiopulmonary Resuscitation

301

or irregular wide-complex tachycardias because it can convert into ventricular brillation.

Causes During the resuscitation period, the providers should evaluate and treat the reversible causes o the cardiac arrest ( able 79-1).

Reversible Causes o Cardiac Arrest (“Hs and Ts”)

Causes

Clues

Treatment

Hypovolemia

History o dehydration, blood loss, and vasodilation. Flat neck veins

Volume in usion

Hypoxia

History o hypoventilation, low inspired oxygen, shunt, V/Q mismatch, and di usion impairment

Place an advanced airway, oxygenate, and ventilate

Hydrogen ion (acidosis)

Metabolic: • Anion Gap (MUDPILES) º Methanol º Uremia º Diabetic ketoacidosis º Propylene glycol º Iron/Isoniazid º Lactic acidosis º Ethylene glycol/Ethanol º Salicylates • Non-Anion Gap º Diarrhea º Renal tubular acidosis º Medications Respiratory: • Central respiratory depression by central disease or medications • Neuromuscular disease • Airway obstruction • Primary lung diseases

Treat the underlying cause and give sodium bicarbonate. Ventilate the patient in order to decrease carbon dioxide and hydrogen levels

Hyperkalemia

ECG ndings: Peaked T waves, widened QRS, and decreased P waves History o renal ailure, mineralocorticoid de ciency, medications, rhabdomyolysis, tumor lysis syndrome, hemolysis, massive blood trans usion

Treat with calcium, sodium bicarbonate, glucose and insulin, and albuterol

Hypokalemia

ECG ndings: at T waves, presence o U waves, widened QRS, prolonged QT interval, and wide-complex tachycardias History o alkalosis, urinary or gastrointestinal loss, medication use

Treat with potassium and magnesium

Hypothermia

ECG ndings: J or Osborne waves History o exposure to cold

Rewarm the patient

Tension pneumothorax

Dif cult to ventilate, unequal breath sounds, jugular venous distension, tracheal deviation History o trauma or primary lung pathology

Needle decompression and chest tube placement

Tamponade

Jugular venous distension History o pericardial e usion secondary to cancer, uremia, cardiac surgery, myocardial rupture, trauma

Pericardiocentesis

Toxins

Bradycardia, neurologic exam, history o medication intake

Intubate and treatment with speci c antidotes

Thrombosis (pulmonary embolism)

History o deep vein thrombosis or pulmonary embolism, jugular venous distension

Surgical embolectomy or brinolytic therapy

Thrombosis (myocardial in arction)

ECG ndings: Q waves, ST-segment changes, T-wave inversions Cardiac risk actors, cardiac markers

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Return o Spontaneous Circulation Once ROSC has been achieved, the patient should be transported to a critical care unit. Oxygenation and ventilation should be optimized. T e FiO2 should be titrated to an SpO2 > 94%. T e purpose o this is to avoid the oxidative injury that occurs with an elevated oxygen content. T e patient should be ventilated with 10–12 breaths per minute and the rate can then be titrated to an end-tidal CO2 o 35–40 mmHg. A systolic blood pressure o >90 mmHg should be achieved using intravenous uids and vasopressor in usions. In order to decrease the oxygen requirements o the organs, therapeutic hypothermia can be initiated in adult patients who remain comatose. T e goal temperature is 32–34°C or a period o 12–24 hours. T is can be achieved with cold intravenous uids, ice bags, or sur ace cooling devices.

PEDIATRIC CARDIOPULMONARY RESUSCITATION Pediatric resuscitation is similar to the adult version with a ew important dif erences. T e depth o chest compressions should measure approximately at least one-third o the child’s anteroposterior diameter. T e compression-to-ventilation ratio in adults is 30:2, regardless o the number o rescuers. In pediatric patients, this ratio is 30:2 i only a single rescuer is present and 15:1 i two rescuers are present. When de brillation is used, 2–4 J/kg should be use. Subsequent shocks should be at least 4 J/kg but should not exceed 10 J/kg.

MANAGEMENT SUMMARY 1. Scan patient’s chest or 5–10 seconds to evaluate or breathing. 2. I the patient is not breathing, activate the emergency response system and request an AED. 3. T e carotid pulse should be checked or 5–10 seconds. I no pulse is detected, chest compressions and ventilation should be initiated in a 30:2 ratio. An advanced airway should be considered. 4. A er 2 minutes o chest compressions, a pulse check should be per ormed or a maximum o 10 seconds. I a de brillator is present and a shockable rhythm such as ventricular tachycardia or ventricular brillation is identi ed, de brillation should occur and chest compressions should be restarted immediately. I a nonshockable rhythm such as pulseless electrical activity or asystole is identi ed, chest compressions should be continued or another two minutes. 5. Epinephrine 1 mg can be given every 3–5 minutes during the resuscitation period. T is can be substituted with vasopressin or amiodarone. 6. Reversible causes o the cardiac arrest should be identi ed and treated during the resuscitate period. 7. I an organized rhythm is present and a pulse is palpable a er a 2-minute cycle o chest compressions, ROSC has occurred. T e patient should be transported to a critical care unit, where oxygenation, ventilation, and hemodynamics should be optimized. T erapeutic hypothermia should be considered in comatose patients.

80 C

Nutrition Matthew de Jesus, MD

T e body requires the intake o water, energy, and nutrients in order to unction properly and maintain body mass. Energy substrates are derived rom ingested carbohydrates, proteins, and ats or mobilized rom stored sources. A nal source o nutrients may be the catabolism o muscle. A large amount o nutrients required or bodily unction can be synthesized, but essential nutrients must be ingested, which include various amino acids, ats, vitamins, and minerals. Metabolic rates can be calculated via indirect calorimetry, in which oxygen consumption and carbon dioxide production are measured using equipment known as a metabolic cart, and then used to determine the respiratory quotient (RQ) and resting energy expenditure (REE): RQ = carbon dioxide production/oxygen consumption REE (via abbreviated Weir Equation) = (3.94 × VO2) + (1.1 × VCO2) T e Harris–Benedict equation was derived rom indirect calorimetry studies. T e Harris–Benedict equation described in 1919 was revised by Roza and Shizgal in 1984, as shown below. First, the basal metabolic rate is calculated based on gender, body weight, height, and age: BMR male = 88.362 + (13.397 × kg weight) + (4.799 × cm height) – (5.677 × age) BMR emale = 447.593 + (9.247 × kg weight) + (3.098 × cm height) – (4.33 × age) Once the basal metabolic rate is calculated, a multiplier based on activity level is applied to estimate the subject’s daily kilocalorie requirement: Little to no exercise

BMR × 1.2

Light exercise (one to three times per week)

BMR × 1.375

Moderate exercise (3–5 d per week)

BMR × 1.55

Heavy exercise (6–7 d per week)

BMR × 1.725

Very heavy exercise (two times per day)

BMR × 1.9

E R

A simpli ed ormula or energy requirements o a healthy adult recommended by T e American College o Chest Physicians is 25 kcal/kg/d, with 15%–20% composed o protein, based on the patient’s ideal body weight. Under the stress ul conditions o critical illness, metabolic requirements increase. Septic patients may have an increased nutritional requirement o 30% and severe burn patients may increase requirements by 100% o their basal needs. Severe malnutrition can lead to morbidity and mortality in the critically ill, whereas nutritional repletion may improve healing, and immune unction. Studies have shown that enteral nutrition (EN) has bene ts over parenteral nutrition (PN), including reduced in ection, reduced organ ailure, and reduced hospital stay. Peripheral nutrition should be reserved only or situations where enteral eeding is not an option such as bowel obstruction and short gut syndrome, or when nutritional requirement are not met by enteral means. Optimal start time or EN is unknown, but some evidence points towards reduced in ectious complications o critically-ill patients when initiation is within 24–48 hours o injury or ICU admission. Diarrhea is a complication associated with enteral eeding which may be related to hyperosmolarity o the solution or to lactose intolerance. Gastric distention due to decreased gut motility can lead to increased aspiration risk, and may be decreased with prokinetic agents, elevation o the head o the bed to 30°–45°, and postpyloric eeding tube placement. Un ortunately, there is no evidence o reduced ventilator requirements, duration o ICU stay, or mortality with postpyloric eeding. Gastric residual volumes have been used as a marker to guide enteral eedings, but there is no study to validate its sole use. Studies show that gastric residual volumes do not accurately ref ect gastric emptying or eeding complications. Gastric residual volumes greater than 500 mL have been correlated with vomiting. Holding eedings or GRVs less than 500 mL can lead to an undernourished patient. T e use o residual volumes in combination with other clinical signs and symptoms such as pain, distention, cramping, or emesis may be a more appropriate guide or eeding therapy. 303

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T e predominant morbidities associated with PN are complications rom central line insertion (such as vascular injury or pneumothorax) and line in ection. Excess carbohydrate in PN can lead to an increased respiratory quotient, leading to hypercarbia, as well as hyperglycemia. Hyperglycemia can delay wound healing, inhibit the immune response, cause dieresis leading to hypovolemia and electrolyte abnormalities, and increase morbidity. Acute discontinuation o PN can result in hypoglycemia, thus changes to PN administration should be ollowed with close blood glucose monitoring and insulin regiment adjustment.

SUGGESTED READINGS Alhazzani W, Almasoud A, Jaeschke R, et al. Small bowel eeding and risk o pneumonia in adult critically ill patients: a systematic review and meta-analysis o randomized trials. Crit Care. 2013;17(4):R127. Doig GS, Heighes P , Simpson F, Sweetman EA, Davies AR. Early enteral nutrition, provided within 24 h o injury or intensive care unit admission, signi cantly reduces mortality in critically ill patients: a meta-analysis o randomised controlled trials. Intensive Care Med. 2009;35(12):2018– 2027. McClave SA, Lukan JK, Ste ater JA, et al. Poor validity o residual volumes as a marker or risk o aspiration in critically ill patients. Crit Care Med. 2005;33(2):324–330.

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Morbid Obesity M. Alexander Pitts-Kiefer, MD, and Medhat Hannallah, MD

T e presence o obesity is determined by the Body Mass Index (BMI), which can be calculated as ollows:

Body Mass Index =

weight (kg) (height [m])2

A patient who weighs 75 kg and is 1.8 meters tall would have a BMI o 23.1 kg/m 2. Based on BMI, the patient can be classi ed as normal, overweight, obese, or extremely obese ( able 81-1). It should be noted that the term “morbid obesity” has been replaced by “extreme obesity”. Obese patients are at increased risk or a variety o intraoperative and postoperative complications. In addition to BMI, waist circum erence can be used as a predictor o increased risk. A waist circum erence o 35 inches or greater in women or 40 inches or greater in men is associated with increased cardiovascular risk. Because obese patients present many challenges to anesthesiologists, an understanding o the pathophysiologic e ects o obesity on anesthesia practice is imperative or sa e practice.

AIRWAY CHANGES Obese patients have an increased risk or di cult mask ventilation, direct laryngoscopy, and intubation due to increased tongue size, redundant oropharyngeal tissue, and a limited range o motion at the atlantoaxial joint due to accumulation o cervical adipose tissue. Presternal at pads can also inter ere with direct laryngoscopy, complicating airway management.

TABLE 81-1

Classification of Obesity Based on

the BMI

BMI (kg/m2 )

Classification

Extreme obesity

E R

Preoperative airway assessment should be conducted with special attention paid to the Mallampati classi cation, neck circum erence, thyromental distance, mouth opening, prognathism, and cervical range o motion. I the anesthesiologist is concerned that the patient will not be able to be sa ely intubated using direct or indirect laryngoscopy, the patient should be prepared or an awake ber-optic intubation. T e likelihood o a success ul direct laryngoscopy and intubation can be improved by ensuring the patient is in a head-elevated laryngoscopy position (HELP). o achieve this position, a ramp is ormed under the patient’s upper back and cervical spine using blankets, pillows, or a commercially available device. T e head is elevated above the hips with the neck extended. T is ensures alignment o the external auditory meatus with the sternal notch, which compensates or the limited exion caused by cervical adipose tissue. Following induction o anesthesia, the pharyngeal muscles and tongue relax resulting in airway obstruction. A two-handed mask ventilation technique with a jaw thrust maneuver and the placement o an oral or nasal airway may be required to success ully mask ventilate the patient. At the end o the surgery, care should be taken to not extubate the patient prematurely. Many obese patients demonstrate signs and symptoms o obstructive sleep apnea (OSA) even i no ormal diagnosis has been recorded. It is a serious but underappreciated comorbidity that is associated with di cult mask ventilation, hypoxemic events, coronary artery disease, arrhythmias, and sudden death. T e induction o general anesthesia urther increases these risks. T ere are several screening tools including the American Society o Anesthesiologists (ASA) Checklist or the “S OP-BANG” questionnaire to identi y patients with undiagnosed OSA. Anesthetic management o an obese patient with OSA does not di er rom other patients with OSA and is discussed in detail elsewhere. Brie y, anesthetic management ocuses on minimizing the use o opiates, benzodiazepines, and other drugs that suppress respiratory drive. T e use o regional anesthesia and nonopioid adjuvants is appropriate. T e postoperative, postextubation time period is the most common time period or complications rom OSA. Patients should be encouraged to bring their CPAPs, i available, or use in the 305

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postoperative period. Otherwise, a CPAP should be available or on stand-by or use in the PACU. For outpatients with suspected OSA, the ASA practice guidelines recommend an additional 3-hour observation period prior to discharge. I an obstructive or hypoxemic event occurred, the guidelines suggest a 7-hour observation period af er the last event.

RESPIRATORY CHANGES T e total compliance o the pulmonary system is reduced in morbidly obese patients. Chest wall compliance is decreased due to signi cant deposits o adipose tissue on the chest and abdomen, and lung compliance is decreased secondary to increased pulmonary blood ow and blood viscosity. It should be noted that in early disease, lung compliance may be normal be ore compensatory changes occur. T e e ect o decreased total pulmonary compliance is a restrictive pattern o lung disease. T e decreased pulmonary compliance also leads to a reduction o unctional residual capacity (FRC). Because FRC provides or continued oxygenation o pulmonary capillary blood during exhalation and apnea, the reduced FRC in obese patients causes a rapid arterial oxygen desaturation upon induction o anesthesia. In addition, closing capacity, which is the capacity at which small airways begin to close, may approach FRC in obese patients. T is can result in small airway collapse at normal tidal volumes leading to right to lef shunting, ventilation–per usion (V/Q) mismatch, atelectasis, and arterial hypoxemia. Shunting is exacerbated by the supine position. T e restrictive pattern o lung disease, V/Q mismatch, and increased metabolic demands rom increased total and lean body mass contribute to chronic systemic hypoxemia. Patients will also have a decrease in vital capacity, FEV1, and expiratory reserve volume. Residual volume generally remains normal ( able 81-2). Work o breathing is increased due to hyperventilation to compensate or small tidal volumes and hypoxia, which will result in hypocapnea. Obese

patients can su er rom obesity hypoventilation syndrome, which results in the suppression o the central respiratory drive. Complete preoxygenation, or denitrogenation, prior to induction can prevent rapid arterial oxygen saturation and should be routine practice in obese patients. T e proper technique is to have the patient breathe 100% inspired oxygen via a snug- tting acemask in the head-up position until the endtidal oxygen concentration is greater than 90%. Patients are at increased risk or deep venous thrombosis and pulmonary embolus ollowing the procedure.

CARDIOVASCULAR CHANGES Obese patients have both an increase in total body weight and lean body mass that increases metabolic demands and systemic vascular resistance. T is leads to a larger total blood volume and increased cardiac output. In chronically obese patients, hypertension and lef ventricular hypertrophy (LVH) are common. Coronary artery disease is a signi cant risk in these patients, which can be exacerbated by LVH. Cor pulmonale is the ultimate process that develops in patients with chronic lung hypoxia and the subsequently increased pulmonary vascular resistance and pulmonary hypertension.

GASTROINTESTINAL CHANGES T ere is an increased risk o aspiration o gastric contents during induction o anesthesia in obese patients. T is is secondary to increased gastric volume, increased abdominal pressure, increased incidence o hiatal hernias, and concurrent gastroesophageal re ux disease. T e pH o the gastric uid can also be decreased, which may worsen e ects o aspiration events. Aspiration precautions are appropriate. Many anesthesiologists will premedicate patients with H 2-blockers, prokinetic agents, or proton pump inhibitors.

PHARMACOKINETIC CHANGES TABLE 81-2

Pulmonary Function Tests in a Morbidly Obese Patient Lung Volume/Capacity

Change

FRC

Decreased

ERV

Decreased

TLC

Decreased

FEV1

Decreased

Normal

Obese patients have an increased sensitivity to the respiratory depressant activities o opioids, benzodiazepines, and other drugs. Lipophilic drugs will have an increased volume o distribution, increased distribution to adipose tissue, and longer elimination hal -li e in obese patients. Drug dosing based on ideal body weight (IBW) will lead to underdosing. Dosing based on total body weight ( BW) will lead to overdosing. Dosing based on lean body mass (LBM) is the most appropriate to produce the anticipated therapeutic e ect. LBM is total body mass minus at mass. It can be approximated by adding 20%–40% to IBW or calculated using online calculators. Some inhalational agents can accumulate in adipose tissue and take longer to clear, resulting in delayed emergence.

82 C

Anesthesia for Bariatric Surgery Janelle D. Vaughns, MD

Bariatric surgery is an option to acilitate weight loss or select patients with obesity. Current guidelines or patient selection include BMI > 40 kg/m 2 or ≥ 35 kg/m 2 with comorbid disease states (e.g., hypertension and obstructive sleep apnea). Although bariatric procedures have plateaued in the United States, morbid obesity (>40–44.9 kg/m 2) rates continue to increase. Important clinical advances in bariatric surgery include the expansion o operative techniques (laparoscopy), improved sa ety outcomes, and reversal o comorbidities. Many academic centers also o er bariatric procedures in the obese adolescent population ( 15, acute liver ailure, acute alcoholic hepatitis, or high serum bilirubin (>11 m/dL).

PREOPERATIVE EVALUATION T e goal o preoperative screening is to detect undiagnosed liver disease in the least invasive manner.

Child–Turcotte –Pugh Scoring System for Liver Disease

Clinical Trait

1 Point

2 Points

3 Points

Ascites

None

Present

Moderate/severe

Encephalopathy

None

Grade 1–2

Grade 3–4

Bilirubin (mg/dL)

Albumin (g/dL)

>3.5

2.8–3.5

A thorough history and physical examination is required, with particular attention to history o hepatitis or jaundice, prior blood trans usions, tattoos, recreational drug use, alcohol use, sexual history, and amily history o liver disease. Prior halothane-induced hepatitis should be identi ed in the preoperative assessment due to potential sensitization to other volatile anesthetics. Medications should be thoroughly reviewed, including nonprescription medications and herbs/supplements. Review o systems should include questions about excessive atigue, weight loss, dark urine, pale stools, right upper quadrant (RUQ) pain, bloating, pruritus, and easy bruising. During the physical exam, special attention should be placed on signs o chronic liver disease, including jaundice, palmar erythema, spider telangiectasia, hepatosplenomegaly, dilated abdominal veins, ascites, oxygen saturation, lower extremity edema, gynecomastia, testicular atrophy, temporal wasting, loss o muscle mass, in ection, and altered mental status. Routine preoperative liver laboratory workup is not recommended or otherwise healthy patients due to the low prevalence o liver disease in the general population. I liver unction test results are obtained, asymptomatic patients with mild elevation o liver enzymes (within 3× normal limits) and normal bilirubin levels may proceed with surgery. Signi cant elevation o liver enzymes (above 3× normal limits) or abnormalities o bilirubin or coagulation actors should prompt de erment o elective surgery until liver workup is completed. Acute hepatitis is a contraindication or elective surgery due to increased morbidity and mortality, and may even be cause or delaying urgent surgery in severe cases. A complete evaluation or hepatic disease should include the ollowing: • • •

Imaging—RUQ Doppler ultrasound/C /ERCP or choledocholithiasis, C /MRI or evidence o cirrhosis or portal hypertension

Mortality (%)

A B C

•

Viral etiologies—Hepatitis A IgM, hepatitis B sur ace and core antigens, hepatitis C antibody Metabolic etiologies—Wilson’s disease (ceruloplasmin), hemochromatosis (iron studies), α1-antitrypsin level Autoimmune liver disease serum markers—Primary biliary cirrhosis (antimitochondrial antibodies), primary sclerosing cholangitis

PREOPERATIVE CONSIDERATIONS Nutrition Alcoholic patients should be assessed or nutritional de ciencies. T iamine, olate, and vitamin B12 may require supplementation prior to providing enteral/parenteral nutrition or glucose to prevent inducing Wernicke–Korsako syndrome. Patients should also be monitored or alcohol withdrawal symptoms, including tachycardia, diaphoresis, anxiety, and hallucinations in order to prevent progression to delirium tremens (tactile/visual hallucinations, con usion, diaphoresis, hypertension). Benzodiazepines should be administered as appropriate. Patients with end-stage liver disease may also need nutritional supplementation due to increased energy expenditure postoperatively and risk o hypoglycemia rom impaired gluconeogenesis and decreased glycogen stores. Autoimmune hepatitis may be treated with daily steroids. T ese patients may need stress-dosed steroids intraoperatively. Patients with Wilson disease may be taking D-penicillamine which can impair wound healing. T e dosage may need to be decreased 1–2 weeks pre- and postoperatively. Patients with hemochromatosis should be assessed or complications including diabetes and cardiomyopathy.

Coagulopathy Liver disease can result in coagulopathy rom several di erent mechanisms: • • •

Vitamin K de ciency due to cholestasis Factor de ciency due to hepatocellular damage T rombocytopenia due to splenomegaly and portal hypertension

T ese underlying causes should be addressed appropriately, with vitamin K (1–5 mg PO or SC daily), resh rozen plasma (target INR < 1.5), or platelets.

Ascites Ascites increases the risk o wound dehiscence and abdominal wall herniation. It may also a ect respiratory dynamics such as decreasing unctional residual capacity (FRC). Reduced FRC can lead to quicker desaturations upon induction do to less oxygen reserve. Management includes sodium restriction (diet, IV uids), diuretics (spironolactone), and paracentesis. Aspirated luid should be checked or signs o in ection. Paracentesis prior to surgery is controversial, with supporters proposing lower airway pressures and improve cardiopulmonary unction, which is desirable prior to anesthesia and surgery.

CHAPTER 83

Encephalopathy Encephalopathy may be precipitated by an acute insult such as in ection, GI bleed, hypovolemia, or sedatives. During the preoperative evaluation, check or signs o altered mental status. Ammonia levels may be help ul in making the diagnosis. Lactulose, which inhibits intestinal ammonia production, is the recommended therapy or encephalopathy.

Hepatorenal Syndrome (HRS) Hepatorenal syndrome is the most drastic renal mani estation o cirrhosis, marked by retention o salt and water as well as renal hypoper usion and decreased glomerular unction. HRS starts with portal hypertension. Local production o vasodilators (particularly nitric oxide) leads to splanchnic vasodilation and subsequent decrease in e ective circulating blood volume and decrease in mean arterial pressure. T is then results in activation o the sympathetic nervous system, the renin– angiotensin–aldosterone axis, and the vasopressin system. T e outcome is a severe drop in renal per usion and glomerular ltration with impaired excretion o ree water. T ere are two types o HRS. ype I is associated with rapidly progressive renal ailure. ype II is more gradual and characterized by re ractory ascites. Management o HRS involves targeting the underlying portal hypertension and/or splanchnic vasodilation. Vasoconstrictors (AVP, somatostatin, and their analogs) and α-agonists (norepinephrine, midodrine) together with volume expansion are use ul or managing ype I HRS. AVP and analogs are particularly use ul due to the abundance o their V1 receptors in the splanchnic circulation. Placement o a transjugular intrahepatic portal shunt ( IPS) may be use ul in both ype I and ype II HRS by lowering portal pressure and decompressing the splanchnic circulation. T e de nitive treatment o HRS is liver transplantation. Outside o the USA, terlipressin (a vasopressor) with albumin volume expansion is also an e ective option.

Hepatopulmonary Syndrome (HPS) Hepatopulmonary syndrome is characterized by the triad o liver dys unction, otherwise unexplained hypoxemia, and intrapulmonary vascular dilatation (IPVD). HPS causes an increased A–a gradient, a right-to-le shunt leading to hypoxemia, decreased pulmonary vascular resistance (PVR), and decreased mean pulmonary artery pressure (mPAP) with no change in pulmonary artery occlusion pressure (PAOP). T e etiology is poorly understood, though nitric oxide, splanchnic endotoxemia, decreased clearance o in ammatory mediators, and/or angiogenesis are believed to be involved. T ere are two types o IPVDs. ype I IPVDs result in unctional shunts due to a massive increase in pulmonary capillary diameter (8–15 µm to 50–500 µm). As patients with cirrhosis tend to have hyperdynamic circulation, the end result is insuf cient time or oxygen di usion through the

Hepatic Disease: Preoperative Evaluation

313

entire stream o capillary blood and thus a ow o poorly oxygenated blood. Administration o oxygen should correct the hypoxemia by increasing oxygen di usion through the dilated capillary. In contrast, ype II IPVDs are not correct by 100% oxygen as these behave as true anatomic shunts. HPS is also characterized by orthodeoxia. Since IPVDs tend to occur at the base o the lungs, standing worsens hypoxemia whereas supine position redistributes blood to the apices and results in improved oxygenation o blood. Diagnosis o HPS requires to ul ll three criteria: chronic liver disease, A–aDO2 ≥ 15 mmHg, or ≥20 mmHg, or ≥to the age-adjusted value, and intrapulmonary vascular dilatation con rmed by contrast echocardiography with injection o agitated saline or less commonly, radiolabeled albumin lung per usion scan. HPS severity is categorized based on PaO2: mild (≥80 mmHg), moderate (≥60 and 4 mg/dL.

Prehepatic Dysfunction A. Hemolysis Jaundice secondary to hemolysis is characterized by anemia and indirect (unconjugated) hyperbilirubinemia with preservation o normal serum alkaline phosphatase and alanine transaminase (AL ). Potential causes include breakdown o trans used erythrocytes rom multiple blood trans usions, reabsorption o extravasated blood (e.g., retroperitoneal or intra-abdominal hematomas rom trauma or ruptured aortic aneurysms), ABO incompatibility, hemolytic anemia, glucose-6-phosphate dehydrogenase de ciency, malaria, sickle cell anemia, and kidney diseases leading to hemolytic uremic syndrome.

B. Ischemic Hepatitis Decreased hepatic clearance secondary to hepatic hypoper usion can also cause hepatic dys unction. Cardiogenic shock due to congestive heart ailure can lead to ischemic hepatitis. T is condition is characterized by rapid elevations in serum levels o AS , AL , and LDH, o en 10- old above normal limits and potentially associated with jaundice and prolongation o prothrombin time. T ese elevations may last 3–11 days and rapidly return to normal therea er. Noncardiogenic shock, such as septic shock, can also lead to hepatic dys unction. Accidental ligation o the hepatic artery or its branches can occur during cholecystectomy, resulting in hepatic ischemia and necrosis with elevations in AS and AL . Endotoxemia is another potential culprit o ischemic hepatitis.

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PART III Organ-Based Advanced Sciences

Intrahepatic Dysfunction

D. Total Parenteral Nutrition

A. Drug Induced Hepatotoxicity

Patients receiving PN requently have abnormal liver tests results. Characteristics include atty liver with mild elevations o AS , AL , and alkaline phosphatase. Less common but more serious is the development o jaundice with abnormal liver test results developing days to weeks ollowing institution o PN, seen mostly in children. Biopsy ndings are nonspeci c and diagnosis is one o exclusion.

Many dif erent drugs may cause liver injury resembling acute hepatitis. Patients who develop elevated AS /AL levels postoperatively should be checked or acetaminophen dosage. Acetaminophen causes liver injury via a toxic metabolite ormed by P450 2E1. T is enzyme may be induced by alcohol as well as a number o drugs. Acetaminophen is typically toxic above 7.5 g as a single dose; due to enzyme induction, care must be taken with alcoholic patients as even therapeutic levels o acetaminophen (3–4 g/d) may cause hepatotoxicity in these patients. Most drug-induced hepatotoxicity occurs at least 2 weeks a er surgery—thus, abnormal liver test results within 2 weeks o surgery are unlikely to be due to drugs that were started postoperatively. Furthermore, drugs taken or over 12 months preceding the surgery are also unlikely to be the culprit. Other hepatotoxic drugs include tetracyclin, ri ampin, cephalasporins, penicillin, NSAIDS, steroids, oral contraceptives, and IV contrast.

B. Viral Hepatitis Acute viral hepatitis is rare postoperatively among patients with normal preoperative liver test results. It is characterized by gradual rise in AS and AL with or without systemic symptoms. Serum LDH is only slightly elevated in comparison to the aminotrans erases and is thus use ul or distinguishing viral hepatitis rom ischemic and drug-induced hepatotoxicity. Patients who receive a blood trans usion and develop elevated AS or AL over 3 weeks ollowing blood product exposure should be checked or serum hepatitis C RNA via polymerase chain reaction—a very rare possibility unless the donor was incubating the virus at time o donation. Note that serum antibodies to HCV may be negative during acute in ection, hence the importance o checking serum HCV RNA. Hepatitis A or B tests typically are not necessary in this case as these rarely cause posttrans usion hepatitis.

C. Anesthetic Induced Hepatotoxicity Halothane is well known to cause hepatotoxicity via a toxic metabolite; modern inhalation agents are less extensively metabolized by the liver and thus less likely to cause liver injury. First exposure incidence is around 1 per 10,000, and a er multiple exposures around 10–15 per 10,000. Halothane hepatotoxicity is characterized by ever or jaundice, typically 7–14 days a er a single exposure or 5–7 days a er multiple exposures. AS and AL levels rise beyond 10- old above normal limits. Severe injury may result in elevated serum bilirubin and prolongation o prothrombin time. Eosinophilia and renal insu ciency may also occur. Risk actors include emales, age greater than 40 years, repeat exposures, obesity, and amily predisposition.

E. Other Causes Additional contributors to hepatic dys unction include direct hepatocellular injury, severe hypotension, perioperative hypoxemia, hepatic allogra rejection, hepatic artery thrombosis, primary biliary cirrhosis, Gilbert’s syndrome, and Crigler–Najjar syndrome.

Posthepatic Dysfunction Postoperative hepatic dys unction may present with obstructive jaundice or cholestatic jaundice, pale stools, dark urine, and severe pruritus, caused by interruption to the drainage o the bile in the biliary system. T e most common lab nding is elevated direct and indirect bilirubin and alkaline phosphatase.

A. Benign Postoperative Cholestasis Benign postoperative cholestasis typically occurs within 10 days o surgery. Risk actors include sepsis, cardiovascular surgery, and multiple trans usions. Serum bilirubin may be elevated in some cases, potentially as high as 40 mg/dL. Alkaline phosphatase is requently elevated, with normal or mildly elevated AS and AL (under ve old). Albumin may be normal or slightly reduced. Prothrombin time is usually normal. Liver biopsy may show cholestasis and variable degrees o at. Patients who recover rom surgery and the complications typically have resolution o the cholestasis, hence the term “benign.” However, patients with serum bilirubin above 6 mg/dL have a high risk o mortality i the underlying etiology was intra-abdominal trauma or sepsis. Such complications include renal ailure, acute respiratory distress syndrome, and multiple organ system ailure.

B. Bile Duct Obstruction Obstructive jaundice results in direct (conjugated) hyperbilirubinemia. Bile duct injury a er biliary tract or gastric surgery is most common. Postoperative choledocholithiasis is rare. Patients will develop clinical jaundice without cholangitis days to weeks a er the surgery. Diagnosis involves endoscopic retrograde cholangiopancreatography or transhepatic cholangiography. Postoperative pancreatitis can also cause bile duct obstruction via edema o the head o the pancreas. Diagnosis involves elevated serum amylase and C abdomen showing edema o the pancreas and bile duct dilation. T is jaundice typically resolves ollowing resolution o the pancreatitis.

CHAPTER 84

Patients who have not had biliary tract or gastric surgery and do not have evidence o pancreatitis may have another cause o jaundice. Acute calculous or acalculous cholecystitis may present with abnormal liver test results and jaundice. T ese patients will have right upper quadrant pain and ever. Ultrasound may show pericholecystic uid, thickening o the gallbladder wall, and stones. Several actors indicate a poor prognosis rom postoperative obstructive jaundice, including malignancy, malnutrition, hypoalbuminemia, hematocrit < 30%, azotemia, and the level and duration o hyperbilirubinemia. Acute renal ailure in conjunction with obstructive jaundice is a very poor prognostic indicator.

EVALUATION AND MANAGEMENT Liver dys unction occurring within two weeks o surgery should raise concern or ischemic, anesthetic-related, or drugrelated hepatitis. Evaluation should include complete liver unction tests in addition to history and physical examination ( able 84-1). Cholestasis ollowing biliary tract or gastric surgery suggests injury to the bile duct. Major cardiac or abdominal surgery, in ection, or multiple blood trans usions raise concern or benign postoperative cholestasis. Abnormal liver test results over 2 weeks a er surgery suggest drug or PNassociated liver injury, or bile duct injury i gallbladder surgery was per ormed. Abdominal pain and ever should be managed

TABLE 84-1

Postoperative Hepatic Dys unction

317

with ultrasound or potential cholecystitis. Elevations o AS or AL more than 3 weeks a er blood trans usion should be checked with a serum HCV RNA level. Liver ailure is the most common cause o postoperative mortality in patients with cirrhosis. Injury to hepatocytes may result rom anesthesia, intraoperative hypotension, sepsis, or viral hepatitis. Potential sequelae o liver ailure include severe sepsis and disseminated intravascular coagulation; patients should be closely monitored or worsening jaundice, encephalopathy and ascites, with a low threshold or intensive care. Furthermore, patients must be monitored or deep vein thromboses and pulmonary embolism, as an elevated INR due to advanced cirrhosis is not protective or these conditions. Surgical sites should be monitored or in ections, bleeding, and dehiscence. Patients with encephalopathy may need special attention with respect to sedatives (particularly benzodiazepines) and pain medications due to the increased hal -li e o drugs metabolized by the liver. Encephalopathy may also be worsened by poor stooling rom postoperative ileus or constipation (narcotic or immobility related). Patients who remain obtunded or comatose ollowing an operation should be treated to decrease production o ammonia. Lactulose can be administered via nasogastric tube or enema to lower intestinal pH and decrease survival o ammonia-producing bacteria. Flumazenil may improve level o consciousness in certain cirrhotic patients with severe hepatic encephalopathy.

Preoperative and Postoperative Hepatic Dysfunction

Disorder

Type of Surgery

Fever

Onset Postoperatively

Halothane hepatitis

No relationship

Common

2–15 d

>500

Slight ↑

Viral hepatitis

No relationship

Uncommon

>3 weeks

>500

Slight ↑

Benign postoperative jaundice

Major surgery with sepsis

Common

500

Slight ↑ (LDH)

Bile duct injury

Biliary tract and stomach

Common

Days to weeks

200–300

↑↑

ALT: alanine aminotransferase; AP: alkaline phosphatase.

ALT (U/L)

85 C

Liver Transplantation Jef rey Plotkin, MD

Liver transplantation is an extremely complex surgical procedure that requires expertise and experience rom both the surgeon and the anesthesiologist to ensure a success ul outcome or the patient as it is the second largest organ and is intimately associated with major blood vessels such as the in erior vena cava, portal vein, and hepatic artery. T ere are currently over 6000 transplants per ormed annually in the United States and over 16,000 people actively listed or a liver transplant.

PREOPERATIVE EVALUATION Cardiovascular Patients with end-stage liver disease demonstrate the presence o a hyperdynamic circulation: high cardiac output with low systemic vascular resistance. T e le ventricular ejection raction should be greater than 60% (probably closer to 75%–80%), with the exception o ulminant hepatic ailure (FHF). Cardiovascular changes have not had su cient time to develop in patients with FHF, so the ejection raction should be evaluated as the normal population. All patients should be evaluated with a 12-lead electrocardiogram and an echocardiogram. T e Revised Cardiac Risk Index (RCRI) has been validated in several studies to predict risk or perioperative cardiac events in patients undergoing noncardiac surgery. Dobutamine echocardiography is the stress test o choice or coronary artery disease and should be per ormed in patients with long standing diabetes mellitus and/or two or more o the ollowing RCRI risk actors: • • • • • • •

Age greater than 50 High-risk surgery (major vascular) Ischemia heart disease (prior MI, angina, Q waves, S changes) History o congestive heart ailure History o stroke Diabetes Renal dys unction (creatinine > 2, creatinine clearance < 60)

E R

Causes o end-stage liver disease that may have direct myocardial involvement include alcoholic cirrhosis, Wilson’s disease, hemochromatosis, amyloidosis, and autoimmune hepatitis.

Pulmonary Hepatopulmonary syndrome is mani ested by orthodeoxia (hypoxia worsened when standing) and platypnea (dyspnea worsened when standing). T is condition is present in approximately 25% o patients with end-stage liver disease; however, ew patients actually develop hypoxemia requiring supplemental oxygen. I suspected, obtain arterial blood gases on both room air and 100% oxygen. ransthoracic echocardiography will reveal intrapulmonary shunting upon the rapid injection o agitated saline (bubbles appear in the le atrium a er 3–4 heart beats via the pulmonary veins, not a PFO). Portopulmonary hypertension (PPH N) is present in 2%–10% o patients presenting or liver transplantation. Mild PPH N exists i the mean pulmonary arter pressure is greater than 25 mmHg, moderate i greater than 35–40 mmHg, and severe i greater 50 mmHg (assuming that the pulmonary capillary wedge pressure is less than 15 mmHg). I PPH N exists, right heart unction must be care ully evaluated by echocardiography and/or right heart catheterization. Right ventricular dys unction in the ace o PPH N is a relative contraindication to orthotropic liver transplantation. Epoprostenol (prostacyclin or PGI2) may be used to manage PPH N preoperatively and intra-operatively to manage acute pulmonary vasoconstriction. Although mild to moderate PPH N can be managed during liver transplant with these techniques, severe PPH N is a contraindication to transplant. Ventilation–per usion (V/Q) mismatching may occur due to the above concerns in addition to portopulmonary shunting, intrapulmonary shunting, pleural e usions, decreased muscle mass, and decreased unctional residual capacity rom signi cant ascites. Suspected pulmonary dysunction should be evaluated with an arterial blood gas, chest radiograph, and pulmonary unction tests to evaluate or obstructive and/or restrictive disease. 319

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PART III Organ-Based Advanced Sciences

TABLE 85-1

Grades of Hepatic Encephalopathy According to Symptoms Grade I

Trivial lack of awareness Euphoria or anxiety Shortened attention span Impaired performance of addition

Grade II

Lethargy or apathy Minimal disorientation (time or place) Subtle personality changes Inappropriate behavior Impaired performance of subtraction

Grade III

Somnolence to semistupor, but responsive to verbal Confusion Gross disorientation

Grade IV

Coma

Neurologic Patients with end-stage liver disease o en develop hepatic encephalopathy ( able 85-1). In patients with coma grade III–IV, intracranial pressure (ICP) may be elevated due to signi cantly increased cerebral blood f ow (hyperemia). Full ICP monitoring guidelines and precautions must be ollowed.

Renal Preoperative renal unction testing is required. Normal serum levels o blood urea nitrogen and creatinine may not rule out renal dys unction as these patients may be on low protein diets and have decreased muscle mass. T e di erential diagnosis o azotemia in these patients includes acute tubular necrosis, chronic renal insu ciency, and the hepatorenal Syndrome. It is absolutely imperative to know whether or not the patient makes urine preoperatively. Some immunosuppressant medications decrease creatinine clearance by an average o 30%. In addition, patients with renal ailure (especially those with FHF) may be on some orm o renal replacement therapy (e.g., CVVH) at the time o surgery, which should be continued intra-operatively.

Hematologic T e degree o preoperative coagulopathy secondary to liver ailure must be appreciated (laboratory assessment o hematocrit, platelets, prothrombin time, and preoperative thromboelastogram). T e ideal hematocrit is 28%, as this represents a balance between oxygen carrying capacity and viscosity. I the patient’s white blood cell count is elevated, the cause must be determined as an active in ection may preclude transplantation.

INTRAOPERATIVE MANAGEMENT Liver transplantation requires invasive monitoring including intra-arterial blood pressure monitoring, invasive volume

measurement (central venous and/or pulmonary artery catheters), and large-bore intravenous access or volume. Some centers routinely use transesophageal echocardiographic monitoring as well. Additional specialized equipment unique to liver transplantation may include rapid in user technology (capable o delivering up to 1500 mL/min o warmed blood/ blood products/f uids), thromboelastography to monitor coagulation status, and venovenous bypass.

Pre anhepatic Phase T is phase proceeds rom induction o anesthesia through clamping o the hepatic vessels and vena cava. Rapid sequence induction required rom the high aspiration risk secondary to liver disease and ascites. Furthermore, not all patients will truly have asted. During the pre-anhepatic phase, most o the surgical dissection takes place, which increases the risk or major blood loss. As the ascites is initially drained upon entering the abdomen, additional ascites continues to orm which is added to the overall f uid loss. It is extremely important to keep up with lost volume as well as maintaining the body’s biochemical and coagulation balance. During the pre-anhepatic phase, all major laboratory values are checked hourly, including ionized calcium, serum glucose levels, pH, clotting actors, hematocrit, and thromboelastography. As the surgeons get closer to clamping the major vessels, volume loading to a central venous pressure o 12–15 mmHg must occur to be able to tolerate cross clamping o the vena cava, whether or not venovenous bypass is used. Some centers may pre er the “piggyback technique” whereby the liver is dissected o the vena without complete crossclamping. T is approach also requires volume loading as the “side biter” clamps still a ect vena cava blood f ow and hence preload.

Anhepatic Phase T is phase proceeds rom clamping o the major vessels (in rahepatic IVC, suprahepatic IVC, portal vein, and hepatic artery) until reper usion is complete. Since the liver is now removed rom the circulation, the biochemical unctions o the liver are gone in addition to the loss o preload. T ere ore, increasing lactic acidosis, worsening coagulopathy and ongoing blood loss can occur. Continuing volume replacement (typically with blood and blood products) and more requent laboratory monitoring is essential. Laboratory values should be checked every 15–30 minutes during the anhepatic phase with aggressive correction o all abnormalities be ore reper usion. It is also critical to prevent hyperkalemia prior to reper usion as potassium levels can elevate signi cantly upon release o the clamps. Upon reper usion, abrupt hemodynamic changes may occur due to an acute inf ux o blood that is hyperkalemic, acidemic, and cold rom preservation solution. T is blood also contains vasoactive substances released rom the gra ed liver and ischemic splanchnic bed. Initially, blood pressure may rise as a result o increased venous return. However,

CHAPTER 85

hypothermia, bradyarrhythmias, decreased systemic vascular resistance, hyperkalemia, and impaired myocardial contractility may occur and present as hypotension and high cardiac lling pressures. Epinephrine is the agent o choice or resuscitation. Full-scale cardiopulmonary resuscitation may be necessary. Additionally, brinolysis can occur due to tissue plasminogen activator release rom the newly per used and gra ed liver. T is problem should be treated with aminocaproic acid based on the thromboelastrogram.

Neohepatic Phase T is phase proceeds rom reper usion to closure and transport to the intensive care unit. T e hepatic artery and bile duct anastamoses will commence as well as surgical hemostasis. Assuming the liver is unctioning, the patient should stabilize.

Liver ransplantation

321

Hepatic lactate metabolism, protein synthesis, and glucose homeostasis occur during the neohepatic phase. I these processes ail, the surgeons may need to evaluate the anastamoses. T e postreper usion syndrome is de ned as a decrease in systemic mean blood pressure more than 30% below baseline or at least one minute during the rst ve minutes a er liver reper usion. It has an estimated incidence o 10%–60%. T is syndrome may last a ew hours and require vasopressor support. Assuming the liver is unctioning, postreper usion syndrome should improve over the next ew hours with decreasing vasopressor requirement. I improvement does not occur and the vasopressor requirement increases, this may be a sign that the liver is not working as well, and must be communicated to the surgeon. ypically, patients will remain intubated and transported to the intensive care unit or a slow emergence over the next 12–24 hours.

86 C

Intestinal Obstruction Daniel Bassiri, MD, and Alessia Pedoto, MD

Intestinal obstruction accounts or 20% o surgical admissions. Conditions leading to intestinal obstruction are classi ed according to the relationship between the obstructing agent and the intestinal wall ( able 86-1). T e obstruction can be extraluminal (surgical adhesions rom prior surgery and neoplastic disease), intraluminal (strictures and abdominal ileus), intramural (in ammatory bowel disease, e.g., Crohn’s), complex (vascular causes, e.g., strangulation), or closed loop obstruction (e.g., volvulus, where both proximal and distal obstruction o the loop o bowel is present). In most cases, the obstruction is localized in the small intestine and results rom adhesions. Less common causes include hernias with strangulation, malignancy (cholangiocarcinoma and pancreatic cancer), in ammation, endometriosis, volvulus, oreign body, and the use o nonsteroidal anti-in ammatory drugs. Large bowel obstruction is less common and result rom tumor involvement (colon and ovarian cancer), diverticulitis, or volvulus. Mortality rates range rom

TABLE 86-1

Common Causes of Intestinal

Obstruction

Adhesions Neoplasms Metastatic small bowel cancer Local tumor invasion Carcinomatosis Hernias External causes (inguinal/femoral) Internal (past roux-en-y bypass) Chron’s disease Volvulus Intussusception Radiation induced strictures Post ischemic strictures Foreign body Galls stones Diverticulitis Meckel’s diverticulum Hematoma Congenital abnormalities (webs, duplications, malrotations) (Reproduced with permission from Brunicardi FC, Andersen DK, Billiar TR, et al. Schwa rtz’s Principles of Surgery, 10th ed . McGraw-Hill Education, Inc., 2015. Tab le 28-3, p. 1146.)

E R

5% to 10% when the obstruction is caused by adhesions and 15%–20% when due to cancer, gangrene, or when localized in the large bowel. Mortality also increases in the presence o malnutrition and hypoalbuminemia. Perioperative risks increase in cases o delayed treatment, high obstruction, strangulation with tissue necrosis, sepsis, cardiovascular instability, extreme o age, multiple comorbidities, and poor nutritional status.

PHYSIOLOGIC DERANGEMENTS Hemodynamic instability is the result o both hypovolemia, due to uid sequestration, pro use vomiting (or stomach suction), and decreased venous return. T e intestine reabsorbs 6–9 L o uids on a daily basis, secreting only 400 mL. In the case o obstruction, uids accumulate in the bowel and lead to intravascular volume depletion. Vomiting usually begins when 3 L is sequestered, while hypotension, tachycardia, and oliguria occur with ≥6 L. Distention o the intestine compresses the in erior vena cava and upwardly displaces the diaphragm. T e resulting increase in intrathoracic pressure is associated with a decrease in venous return which may aggravate the hypotension and tachycardia. Gastric decompression or pro use vomiting can contribute to urther uid loss. Renal injury, shock, and death can result. Proximal obstruction is characterized by hypokalemic hypochloremic acidosis, with a gradual decrease in sodium and chloride. Hyponatremia aggravates hypotension and causes mental status changes. Hypokalemia will cause ECG changes including alterations in the S segment as well as dysrhythmias. Metabolic acidosis results rom dehydration, starvation, ketoacidosis and loss o alkali, as well as severe tissue hypoper usion or hypovolemia. Metabolic alkalosis is rare and results rom marked gastric uid loss. Hyperventilation results in respiratory alkalosis to compensate or the loss o alkali and the increase in serum lactate. Respiratory compromise can be secondary to signi cant abdominal distention, especially in the case o large bowel obstruction. A decrease in unctional residual capacity, an increase in intrapulmonary shunt and hypoxemia may be present. Diaphragmatic motion is limited causing hypoventilation and increased work o breathing, especially in the supine position. Hypoventilation will lead to hypercapnia 323

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and respiratory acidosis. Decompression o the stomach prior to surgery may help improve the respiratory symptoms and decrease the risk o aspiration. Bacteremia and sepsis may also occur secondary to bowel ischemia and translocation o exotoxins, endotoxins, and heme breakdown products into the peritoneal cavity and circulation. T e changes in the intraluminal ora cause an increase in gram negative bacteria. T e earliest signs o sepsis will be ever, chills, lactic metabolic acidosis, hyperventilation, and altered mental status. reatment o gram-negative sepsis includes timely administration o antibiotics and de nitive surgical management to remove the source o in ection.

PRESENTATION AND DIAGNOSIS T e location o the obstruction determines the symptoms. When in the small bowel, uids and gas accumulation cause distention. T is may lead to mucosal ischemia and strangulation with subsequent tissue necrosis, especially i prolonged. In the early stages, peristalsis is increased as an attempt to overcome the obstruction, causing high pitched abdominal sounds on auscultation. With the progression o the disease, bowel sounds decrease until they disappear. Patients may complain o cramping abdominal pain and distention, as well as chronic nausea and vomiting leading to dehydration and electrolyte abnormalities. T e risk o aspiration is increased. Large bowel obstruction may present with more insidious symptoms related to distention and rupture, most commonly localized in the cecum. Patients complain o over ow diarrhea rather than nausea and emesis. Symptoms are milder when the obstruction is partial. In the late stages o the obstruction, ever, tachycardia, and rebound tenderness are more pronounced. Rotation o the bowel loops can cause a decrease in blood supply, which can lead to ischemia and necrosis. Adhesions are the most common cause o this “strangulation.” Intestinal volvulus is due to a “closed loop obstruction” where both proximal and distal obstructions are present, decreasing the in- and out ow. Progression to ischemia is very rapid, and surgical decompression is usually necessary. “Pseudo-obstruction” is a rare condition characterized by marked intestinal distention without a mechanical cause. It is usually secondary to a localized decrease in peristalsis. It can be acute (postoperative abdominal ileus, retroperitoneal hemorrhage, spinal or pelvic trauma, myocardial ischemia, hypokalemia, medications) or chronic (rare and related to neuropathy or idiopathic). First-line treatment is usually medical, ollowed by surgery in re ractory cases.

DIAGNOSIS Radiographic examination usually con rms the diagnosis o bowel obstruction. Abdominal and chest radiographs in the supine and sitting position show dilated small bowel loops,

air uid levels in the sitting lms, and paucity o air in the colon. A “transition point” is evident on contrast C scans, which is characterized by bowel distention above the lesion and the absence o gas distal to the obstruction. A gap is also noted in the contrast imaging at the level o the obstruction, with little gas in the colon. T is sign is absent in the case o pseudo-obstruction. Manometric studies o the small and large intestine demonstrate low amplitude contractions. T is test is used in the case o pseudo-obstruction related to diabetic and postvagotomy gastroparesis, or abnormalities o the intestinal muscles and the nervous system as seen in endocrine disorders, chronic in ections, autoimmune diseases, neurological disorders, and paraneoplastic syndromes. Pseudo-obstruction may show prolonged transit time rom the stomach to the colon on barium study. A barium enema can also be used to rule out colonic obstruction. However, the use o this test is limited by the patient’s ability to swallow. Due to large volumes o liquid in the gastrointestinal tract, the risk o worsened nausea, vomiting, and possible aspiration increases. T ere are no speci c laboratory studies pathognomonic or the diagnosis o intestinal obstruction or ischemia. Elevated blood urea nitrogen, hemoconcentration, hyponatremia, hypokalemia, hypomagnesemia, and high urinary speci c gravity are all secondary to dehydration and loss o electrolytes. Leukocytosis may be a sign o bowel ischemia with bacterial translocation.

MANAGEMENT Medical Ileus prevention should be the rst step in medical management. T is can be accomplished by identi ying and avoiding common causes such as electrolyte abnormalities (hypokalemia, hypomagnesemia), hypoalbuminemia, and certain medications ( able 86-2). Bowel rest and gastric decompression should be initiated simultaneously to prevent aggravation o abdominal distension. A radial artery catheter and central

TABLE 86-2

Common Electrolyte Abnormalities and Medications Associated with Ileus Electrolytes Abnormalities

Medications

Hypokalemia

Anticholinergic

Hypomagnesemia

Opiates

Hypermagnesemia

Phenothiazines

Hyponatremia

Calcium channel blockers Tricyclic antidepressants

(Reproduced with permission from Brunicardi FC, Andersen DK, Billiar TR, et al. Schwa rtz’s Principles of Surgery, 10th ed. McGraw-Hill Education, Inc., 2015. Tab le 28-4, p. 992.)

CHAPTER 86

venous monitoring may be needed or this purpose, especially when bowel ischemia is present. Goal-directed therapy, the means to increase oxygen delivery by balancing intravenous uids and vasopressors, is gaining more popularity in the postoperative period. Studies in both elective and emergency bowel operations have shown a decrease in postoperative respiratory and renal complications as well as shorter hospital length o stay. Evaluation o serial hematocrit and urinary output are more common ways to monitor uid status despite lack o in ormation about oxygen delivery. I not an emergency, surgery should be postponed or 18–24 hours rom the presenting symptoms, to replace uid loss, hypoalbuminemia and electrolytes, and to rest the bowel. Balanced salt solutions such as Lactated Ringer’s are recommended since the composition o the uid lost is similar to plasma. Hypokalemia should be corrected with potassium supplementation only a er adequate urine output is established. Antibiotics are indicated when there is bacterial spread. In the absence o strangulation or bowel ischemia, the majority o intestinal obstructions will resolve with conservative management. Surgery is indicated in the presence o vascular compromise, an unstable patient, or when there is no resolution o symptoms a er 3 days o conservative management.

Surgical Surgical procedures utilized to relieve the obstruction include endoscopic stent placement, lysis o adhesions, reduction o intussusception or incarcerated hernia, and resection o an obstructive lesion or strangulated bowel. In some cases an enterotomy is required, with the placement o an ostomy to be reversed at a later time. Surgery allows to relieve the obstruction and to per orm a thorough intraoperative exam o the intestinal loops to assess per usion and peristalsis, palpate mesenteric pulses, as well as evaluate blood ow using uorescein staining or Doppler measurements.

ANESTHETIC MANAGEMENT In the case o bowel obstruction, the main goal o general anesthesia is to avoid aspiration o stomach content or ecal material. Lung injury is related to the volume o uid aspirated (>25 cc), the pH ( 400 mL/d). Azotemia, a hallmark o AKI, is a condition marked by abnormally high concentrations o nitrogen-containing compounds such as BUN and creatinine. T e causes o AKI are divided into prerenal, intrinsic renal, and postrenal etiologies ( able 87-2).

DIAGNOSIS OF AKI Consensus criteria or classi cation o AKI by the Acute Kidney Injury Network (AKIN) require a rapid time course (less than 48 hours) and either an absolute increase in serum creatinine concentration o more than 0.3 mg/dL compared to baseline, a percentage increase in serum creatinine o 50% or a reduction in urine output to less than 0.5 mL/kg/min or more than 6 hours. T e RIFLE criteria assess degree o elevation o serum creatinine or change in GFR, severity and duration o oliguria, and the requirement or renal replacement therapy (RR ). T e acronym RIFLE strati es ndings by severity ranging rom risk o injury (R) to end-stage renal disease (E) ( able 87-1).

TABLE 87-1

Risk, Injury, Failure, Loss and End Stage Kidney (RIFLE) Classi ication Class

Serum creatinine increase

GFR decrease

Oliguria (urine output < 0.5mL/kg/h)

Risk

×1.5

>25%

>6 h

Injury

×2

>50%

>12 h

Failure

×3 (or>4 mg/dL, with an acute increase >0.5 mg/dL)

>75%

>24 h

TABLE 87-2

Causes o Acute Kidney Injury Postrenal Azotemia

Prerenal Azotemia

Renal Azotemia

Hemorrhage

Acute glomerulonephritis

Nephrolithiasis

Gastrointestinal uid loss

Vasculitis

Benign prostatic hyperplasia

Trauma

Interstitial nephritis (drug allergy, inf ltrative disease)

Clot retention

Surgery

Acute tubular necrosis

Bladder carcinoma

Burns

Ischemia

Cardiogenic shock

Nephrotoxic drugs (aminoglycosides, NSAIDs)

Sepsis

Solvents (carbon tetrachloride, ethylene glycol)

Hepatic ailure

Heavy metals (mercury, cisplatin)

Aortic clamping

Radiographic contrast dyes Myoglobinuria

Loss

ARF > 4 weeks

Renal artery camping

ESRD

ARF > 3 months

Thromboembolism

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PRERENAL Prerenal azotemia accounts or nearly hal o all hospitalacquired cases o AKI and is rapidly reversible i the underlying cause is corrected. I sustained, prerenal azotemia is the most common actor leading to ischemia-induced acute tubular necrosis. Elderly patients are particularly susceptible due to hypovolemia resulting rom poor f uid intake and renovascular disease. Prerenal azotemia may also result in the setting o congestive heart ailure, liver dys unction or septic shock, or may be a result o anesthetic induced decreases in renal blood f ow, particularly in the setting o surgical blood loss. Evaluation o acute oliguria should include assessment o volume status and drug therapy to identi y potential causes. Invasive monitoring may be required to assess intravascular volume status. Urinary indices may be use ul in distinguishing prerenal causes rom intrinsic renal causes based on the assumption that sodium and water absorption is maintained in pre-renal causes o AKI, but is lost or impaired in tubulointerstitial disease or acute tubular necrosis (A N) ( able 87-3).

Intrarenal

constriction ultimately decreases RBF and GFR, leading to irreversible cortical necrosis. Vascular reper usion may also cause injury due to inf ux o inf ammatory mediators, cytokines and ree radical species. Ischemia and toxins requently work together to cause AKI in severely ill patients (i.e., sepsis). Allergic reactions to drugs may cause acute interstitial nephritis, which may also lead to AKI. Other causes o renal azotemia include glomerulonephritis, pyelonephritis, renal artery emboli, renal vein thrombosis, and vasculitis.

Postrenal Postrenal AKI is usually due to an obstruction distal to the renal collecting system. T is may occur as a result o a blood clot in the ureter, bladder or urethra, or kinking o a Foley catheter. It may also be caused by benign prostatic hyperplasia or cancer o the prostate or cervix. I obstruction is not relieved, postrenal azotemia leading to AKI ensues. Prompt diagnosis o postrenal etiologies is important because the potential or recovery is inversely related to the duration o obstruction. Renal ultrasonography aids diagnosis and percutaneous nephrostomy can improve outcomes.

Intrinsic renal disease may involve the glomerulus, renal tubules, interstitium, or renal vasculature. Renal tubules most o en su er injury rom ischemia or nephrotoxins (i.e., aminoglycosides or radiocontrast agents). Prerenal azotemia and ischemic tubular necrosis are a spectrum o the same pathophysiologic process, whereby decrease in renal per usion initially triggers normal compensatory responses rom the kidney, aimed at conservation o sodium and water and restoration o intravascular volume. T is mani ests acutely as oliguria. I hypoper usion is prolonged, a erent arteriolar

AKI is a result o complex interactions o multiple actors ( able 87-4). Certain surgical procedures, such as vascular surgery involving aortic manipulation, have a particularly high incidence o AKI. Patient actors that have been associated with an increased risk o development o AKI include advanced age, hypertension, diabetes mellitus, ventricular dys unction, sepsis, hepatic ailure, and chronic kidney disease

TABLE 87-3

TABLE 87-4

Urinary Indices in Patients with Acute Oliguria rom Prerenal or Renal Causes Index

Prerenal Causes

Renal Causes

Urinary sodium concentration

40 mEq/L

Urine osmolality

>500 mOsm/L

1.5

150 µM have a high incidence o polyuric renal ailure. Isof urane produces peak f uoride levels less than 4 µM. Compound A, a vinyl ether ormed by degradation o sevof urane at low f ow through carbon dioxide absorbents, induces renal injury in rats. Clinically signi cant renal injury with the use o low-f ow sevof urane anesthesia has not been reported in patients, even with moderate preexisting renal dys unction. FDA guidelines recommend maintaining resh gas f ow o at least 2 L/ min to inhibit compound A ormation and its rebreathing during sevof urane anesthetics.

•

acidosis and rapid azotemia, with rapid increase in serum creatinine and BUN. Serial serum total creatinine phosphokinase (CPK) levels determine the severity, with renal damage likely when total CPK exceeds 10,000 units/L. Prevention o tubular necrosis depends on maintenance o high RBF and tubular f ow. Urine f ow o 100–150 mL/h should be maintained with intravenous mannitol, with or without addition o urosemide. Urine pH should be kept above 5.6 with intravenous sodium bicarbonate or acetozalomide. However, the urine pH should not be increased at the expense o signi cant acid–base disturbance. Calcium should be given to treat hyperkalemia. Hemolysis and hemoglobinemia—Acute intravascular hemolysis due to mismatched blood trans usion (ABO incompatibility) presents a devastating renal insult. Renal damage is secondary to red blood cell stroma rather than to ree hemoglobin; nevertheless, management remains the same as or rhabdomyolysis. Jaundice and bilirubinemia—T ere is a direct correlation between the degree o preoperative obstructive jaundice and postoperative renal dys unction. When conjugated bilirubin increases to above 8 mg/dL, bile salt excretion ceases, resulting in portal septicemia and renal damage. Circulating endotoxins induce renal vasoconstriction and vasomotor nephropathy.

HEPATORENAL SYNDROME (HRS) HRS re ers to impairment o renal unction, or its complete ailure, in spite o morphologically intact kidneys ( able 87-5). T e syndrome occurs almost exclusively in patients with ascites and categorized into HRS types 1 and 2. ype 1 is rapidly progressive and is thought to be secondary to signi cant reduction in e ective circulating volume secondary to splanchnic vasodilation and inadequate cardiac output to compensate or the decrease in renal per usion pressure. ype 2 progresses more slowly. Overall, HRS is a orm o prerenal AKI, which results rom imbalance o vasodilating and vasoconstricting processes. Decreased systemic vascular resistance is thought to be due to splanchnic vasodilation caused by nitric oxide, prostaglandins and other vasoactive

PIGMENT NEPHROPATHY AKI can occur due to the nephrotoxic e ect o the heme pigments myoglobin, hemoglobin and bilirubin. •

Rhabdomyolysis—It describes a condition whereby myoglobin, the oxygen carrying pigment in muscle, is released into the blood stream and excreted by the glomerulus. At a urine pH o less than 5.6, myoglobin is trans ormed to errihematin, which precipitates in the proximal tubule. Nephrotoxic damage is exacerbated by hypovolemia and acidic urine. Because o associated hypercatabolic state, oliguria is associated with acute hyperkalemia, hypocalcemia, anion-gap metabolic

TABLE 87-5

Criteria or Diagnosis o Hepatorenal

Syndrome

Cirrhosis with ascites Serum creatinine > 1.5 mg/dL No sustained improvement o serum creatinine a ter at least 2 d o diuretic withdrawal and volume expansion with albumin; recommended dose 1 g/kg/d o body weight up to max o 100 g/d Absence o shock No current or recent treatment with nephrotoxic drugs Absence o parenchymal disease as indicated by absence o proteinuria > 500 mg/d, microhematuria > 50 RBC per HPF and/or abnormal renal ultrasonography

CHAPTER 87

TABLE 87-6

Pathophysiology o Renal Disease

Complications o AKI

System

Symptoms

Causes/Treatment

Neurologic

Con usion, ataxia, somnolence, seizures, polyneuropathy

Related to the build-up o protein and amino acids in the blood, may be improved by dialysis

Cardiovascular

Systemic hypertension, congestive heart ailure, pulmonary edema EKG changes: peaked T waves, widened QRS Uremic pericarditis

Due to sodium and water retention

Hematologic

331

Due to hyperkalemia Due to elevated BUN

Anemia Hct 20%–30% Abnormal bleeding

Due to hemodilution and decreased erythropoietin production Due to uremia induced platelet dys unction. May require preoperative dialysis or DDAVP to increase vWF and FxVIII

Gastrointestinal

Anorexia, nausea, vomiting and ileus Gastrointestinal bleeding

Uremia induced gastroparesis H2 blockers and PPI to decrease the risk o bleeding

Immunologic

Impaired immune responses leading to requent in ections which are a leading cause o morbidity and mortality; respiratory and urinary tracts commonly involved, especially where breaks in normal anatomic barriers occur due to indwelling catheters

Due to uremia-induced impaired immunity

Metabolic

Metabolic acidosis and hyperkalemia

Due to impaired tubular processing o metabolic wastes and electrolytes; may require dialysis

substances released in patients with cirrhosis and portal hypertension. Initially, increased circulating plasma volume, and the hyperdynamic circulation with increased heart rate and cardiac output are able to maintain renal per usion and GFR. When a trigger actor, such as spontaneous bacterial peritonitis, presents itsel , activation o sympathetic nervous system, renin–angiotensin–aldosterone system and release o ADH occurs and oliguria ensues.

COMPLICATIONS OF AKI T e complications o AKI are listed in able 87-6.

TREATMENT OF AKI Management o AKI depends on identi ying and treating the underlying cause, supporting renal unction by maintaining RBF and oxygen delivery, and avoiding nephrotoxic agents.

T ere is little evidence supporting the use o colloids over crystalloids. raditionally, normal saline has been a pre erred crystalloid or patients in AKI because it lacks potassium. However, hyperchloremic metabolic acidosis that it produces can secondarily lead to hyperkalemia. T ere has been a concern with regard to vasopressor therapy and its renal vasoconstrictive e ects in patients with AKI associated with sepsis. In the setting o AKI, the direct α1-agonist mediated renal vasoconstriction plays only a minor role, and the overall e ect o vasopressors in septic patients is to increase the GFR and urinary output. Low-dose dopamine (1–3 mcg/kg/min), historically used in septic patients, does not con er clinical bene t.

88 C

Renal Failure: Anesthetic Considerations Mofya S. Diallo, MD, MPH

Renal ailure a ects multiple organ systems and increases the risk o perioperative morbidity and mortality. T ere are multiple etiologies o renal ailure ( able 88-1).

TABLE 88-2

E R

Complications of Chronic Renal Disease

Cardiovascular

Hypertension, accelerated CAD, LVH dys unction, cardiomyopathy, congestive heart ailure, uremic pericarditis, hemodynamic instability due to neuropathy

Neurologic

Uremic encephalopathy, uremic neuropathy

Cardiopulmonary

Hematologic

Anemia, platelet dys unction, uremic prothrombin consumption, thrombosis

Hypertension is both a common complication and a cause o chronic renal disease. In patients with limited urine production, volume overload can lead to signi cant hypertension and/or pulmonary edema, particularly without the aid o dialysis. T ere ore, the rst line o therapy is either hemodialysis or diuretic therapy. Chronic renal ailure (CRF) and end-stage renal disease (ESRD) also have direct e ects on the heart. With long-standing hypertension, le ventricular hypertrophy and dys unction occur. Coronary artery disease develops in an accelerated manner as well. Uremic pericarditis can occur in patients who are treated with dialysis. I pericarditis develops, tamponade should be ruled out. Finally, low-pressure pulmonary edema may occur in patients without volume overload. Physical examination, ECG, chest X-ray, and cardiac stress testing assist in evaluation.

Immune system

In ection

Gastrointestinal

Malnutrition, delayed gastric emptying

Fluid and electrolytes

Hypervolemia, hyperkalemia, hypocalcaemia, metabolic acidosis

Endocrine

Hyperparathyroidism, vitamin D def ciency

Musculoskeletal

Renal osteodystrophy

SYSTEMIC MANIFESTATIONS (TABLE 88-2)

Hematologic Anemia commonly ensues with CRF secondary to decreased erythropoietin production. Iron replacement and human recombinant erythropoietin prescriptions attempt to normalize hematocrit levels. T is regimen limits blood trans usions

TABLE 88-1

Common Causes of Renal Failure

Diabetes mellitus Hypertension Polycystic kidney Pyelonephritis Renovascular disease Glomerulonephritis

and consequently limits trans usion-related cardiovascular complications. Hemoglobin and hematocrit should be checked prior to surgery. Platelet dys unction associated with abnormal platelet actor III and increased prothrombin consumption lead to prolonged bleeding time in renal ailure patients. Hemodialysis decreases these e ects but not completely.

Neurologic Neurologic changes with CRF worsen as the kidney disease progresses. Initially, mild symptoms such as irritability and cognitive impairment may occur, but progression to seizures, uremic encephalopathy, and coma occurs i le untreated. Peripheral neuropathy with paresthesias and weakness is another common mani estation o CRF. Dialysis may reverse or slow down some o these neurologic e ects.

Gastrointestinal Renal ailure patients tend to have malnutrition, nausea and vomiting related due uremia. T e malnutrition causes decreased plasma albumin levels and reduced protein binding. 333

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PART III Organ-Based Advanced Sciences

Elevated levels o ree (unbound) drugs increase the risk o toxic drug levels in CKD patients. Delayed gastric-emptying is a common nding in the setting o chronic renal ailure. Special precautions may be necessary to avoid aspiration, such as antiemetic medications, nonparticulate antacids, and rapid sequence intubation.

Electrolyte Abnormalities Hyperkalemia is common in renal ailure as potassium excretion is largely dependent on renal unction. A potassium level less than 5.5 mEq/L is recommended. Patients should undergo hemodialysis 24 hours prior to elective surgery to minimize the risk o hyperkalemia and uremia. ECG evaluation rules out cardiac e ects o elevated serum potassium, such as peaked waves, shorted Q interval, and S segment depression. Metabolic acidosis is a common nding in patients with renal ailure secondary to the inability to excrete hydrogen ions. Acidosis results in the release o intracellular potassium, which can worsen hyperkalemia. Symptomatic hyperkalemia should be treated with potassium elimination via dialysis or loop diuretic therapy. emporary treatment includes 10 units o intravenous insulin with an in usion o 50 mL o 50% dextrose, or inhaled beta-2 agonist such as albuterol to avor potassium di usion into cells. Additionally, calcium administration decreases myocardial excitability to temporize cardiac e ects.

Infection Renal ailure predisposes patients to in ection and is a leading cause o morbidity and mortality in CRF. Chemotaxis and macrophage phagocytosis are impaired in renal ailure. Aseptic techniques should be employed to prevent nosocomial in ections. Impaired immunity also risks opportunistic in ections. Hemodialysis urther increases the incidence o exposure to blood-borne in ections such as hepatitis and HIV in these patients.

PREOPERATIVE CONSIDERATIONS Surgical intervention or patients with AKI is reserved or emergencies. T e perioperative risk or morbidity and mortality in patients with AKI exposed to surgical trespass and anesthetic is approximately 20%–50%. Anesthetic management aims to avoid urther renal injury by maintaining renal per usion with adequate blood pressure and intravascular volume. Vasopressors may be necessary to achieve this goal and invasive blood pressure monitoring is recommended to assess blood gases values, including pH, electrolytes, hemoglobin levels, and hemodynamic perturbations. Nephrotoxic medications should be avoided. Fluid overload can be treated with diuretic therapy or i necessary, postoperative dialysis when easible.

PHARMACOLOGIC EFFECTS Opioids Fentanyl undergoes hepatic metabolism and has no active metabolites; accordingly, it behaves unaltered in renal ailure patients, but can theoretically accumulate due to 7% urinary excretion. In contrast, morphine is metabolized into morphine-3 glucuronide and morphine-6 glucuronide, which build up in the presence o renal ailure. Morphine-6 glucuronide causes respiratory depression. Hydromorphone is metabolized to hydromorphone-3-glucuronide, and accumulates in renal ailure but may be cleared with dialysis. Without dialysis, high levels o hydrmorphone-3-glucuronide produce deleterious side e ects. Meperidine is metabolized to normeperidine, a potent analgesic and neuroexitatory toxin that causes seizures. Consequently, meperidine should be avoided in renal ailure patients. Al entanil and remi entanil both require reduced dosing due to increased potency, but recovery rom both is not signi cantly prolonged.

Neuromuscular Blockers Administration o succinylcholine results in release o potassium, increasing serum potassium by 0.5 mEq/L. Without dialysis, symptomatic hyperkalemic may occur within 24 hours. It is recommended that succinylcholine be avoided in renal patients who potentially have hyperkalemia. Nondepolarizing neuromuscular blocker drug elimination is prolonged in renal ailure. Pancuronium elimination is substantially prolonged, as 40%–50% is excreted by the kidneys. Vecuronium and rocuronium predominantly undergo biliary excretion; however, prolonged neuromuscular blockade can occur with repeated dosing. Atracurium is metabolized by ester hydrolysis and Ho man degradation with no active metabolites. Cis-atracurium also undergoes Ho man degradation. T e hal -li e o atracurium and cis-atracurium is independent o renal unction and consequently remains unchanged with renal ailure. Laudanosine, a metabolite o cis-atracurium and atracurium, is a mild CNS stimulant that leads to seizures in supraclinical doses. T e risk o “recurarization,” or delayed weakness a er neuromuscular blockade reversal, is low in renal ailure patients secondary to reduced cholinesterase-inhibitor clearance.

Inhalational Agents Inhalational agents have minimal e ects on renal unction as elimination is primarily via pulmonary exhalation. Fluoride levels that accumulate a er exposure to inhaled anesthetics do not a ect renal unction. Prolonged exposure to sevof urane can theoretically lead to accumulation o f uoride to nephrotoxic levels.

CHAPTER 88

Vasoactive Drugs Vasoactive medications pose a risk o toxicity in renal ailure. Nitroprusside is broken down to cyanide and thiocyanate. T ese byproducts accumulate to toxic levels in a renal ailure patient. Nitroglycerine is rapidly hepatically metabolized and may alternatively be used. T e e ects o antihypertensives, such as labetalol and hydralazine, are prolonged and can lead to unwanted side e ects. Esmolol, a short-acting antihypertensive metabolized by red cell esterases, is a better option in renal ailure.

INTRAOPERATIVE CONSIDERATIONS Intravenous f uids should be administered with caution in renal ailure patients. Potassium-containing f uids such as lactated ringers have the potential to produce hyperkalemia i not administered judiciously. Normal saline lacks potassium and has typically been used; however, hyperchloremic metabolic acidosis may result rom this approach. In addition, volume replacement should be cautious to avoid hypervolemia, particularly in patients requiring dialysis. Positioning is important to avoid injury to arteriovenous stulas. Intermittent intraoperative checks or a “thrill” are recommended to ensure adequate stula per usion. Blood pressure monitoring is also avoided in the extremity with the stula. Venipuncture in proximity to arteriovenous stulae

Renal Failure: Anesthetic Considerations

335

and gra s should be avoided to decrease the risk o in ection, stenosis, and thrombosis. Regional anesthesia is an appropriate choice in patients with renal ailure. Brachial plexus nerve blocks are o en used in arteriovenous stula surgery with sa e outcomes. Neuraxial blocks should be per ormed with extra caution in patients receiving hemodialysis. Heparin is o en used during hemodialysis, which can contribute to platelet dys unction associated with chronic renal ailure. T ese actors may increase the risk or epidural hematoma.

POSTOPERATIVE CARE Evaluation o f uid status or renal ailure patients is important during the postoperative period. A chest radiograph rules out pulmonary edema, particularly a er a lengthy procedure. Continuous ECG monitoring is recommended due to the increased risk o electrolyte abnormalities and potential cardiac complications. I a patient appears f uid overloaded, dialysis or diuretic therapy should be considered.

SUGGESTED READING Craig RG, Hunter JM. Recent developments in perioperative management o adult patients with chronic kidney disease. Br J Anaesth. 2008;101:269–310.

89 C

Renal Transplantation Patrick Laughlin, MD, and Jef rey Plotkin, MD

T ere are more than 10,000 deceased donor and 6000 live donor kidney transplants per ormed annually in the United States. According to the National Kidney Foundation, there are currently 123,175 people waiting or organ transplants in the United States, 82% o which are awaiting kidney transplants. T at list continues to grow as nearly 3000 new patients are added to the kidney waiting list each month, and un ortunately, approximately 12 people die each day o end-stage renal disease. Kidney donors can be classi ed as living and deceased, with living donors having a higher success rate long term than those rom deceased donors. Since the rise in the use o laparoscopic surgery, the number o live donors has increased as well, mostly due to a decrease in pain and scarring, as well as a swi er recovery. About 98% o people who receive a living-donor kidney transplant live or at least 1 year a er their transplant, and about 90% live or at least 5 years, whereas 94% o people who receive a deceased-donor kidney transplant live or at least 1 year a er their transplant, and about 82% live or at least 5 years.

PREOPERATIVE EVALUATION T e average wait time or kidney recipients is 3 years, which makes it di cult to maintain up-to-date assessments on these patients. However, these patients require accurate preoperative optimization o multiple organ systems.

• •

• • •

K+ 4–5.5 mEq/L BUN < 60 mg% Creatinine < 10mg%

Laboratory Status •

Metabolic acidosis, hypocalcemia, and hyperkalemia may require preoperative correction with dialysis.

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Coagulation status requires assessment o P , INR, P , brinogen, and platelet count due to the concern or potential uremic platelet dys unction. Evaluation o hemoglobin levels is necessary because most patients will be anemic prior to their transplant. Because the ailing kidneys do not synthesize su cient erythropoietin, the bone marrow produces ewer red blood cells. Other contributors to anemia in ESRD include blood loss rom dialysis and low levels o iron, vitamin B12, and olic acid.

Cardiovascular Status Preoperative evaluation o cardiac unction by electrocardiography and echocardiography is the minimal required workup or every patient preparing to undergo kidney transplant. Follow-up studies should be repeated on an annual basis. T e optimization o cardiac comorbidities such as hypertension, coronary artery disease (CAD), uremic cardiomyopathy, dysrhythmias, and pericardial e usion is o crucial importance. Each o these cardiovascular implications are quite common in the undialyzed patient. Dobutamine stress echocardiography (DSE) should replace a regular echocardiogram and be repeated every year or all o the ollowing: • •

Volume Status Hemodialysis patients will usually know their “dry weight,” which can be used preoperatively to estimate volume status. It is important to remember that patients may be hypovolemic ollowing dialysis. Postdialysis goals include the ollowing:

•

Diabetic mellitus (DM) Any two risk actors or coronary artery disease (H N, obesity, amily history o coronary artery disease (CAD), hyperlipidemia, and smoking history) Any previous CAD and/or symptoms

INTRAOPERATIVE MANAGEMENT Monitors Standard basic monitors as de ned by the American Society o Anesthesiologists and a radial arterial line or beat-to-beat pressure monitoring are essential. Central venous pressure (CVP) monitoring is another option, but is le to the discretion o the attending anesthesiologist, but is necessary i the immunologic suppressant thymoglobulin is going to be used, since that drug requires central administration. I used, CVP 337

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goals should be 10–15 mmHg to optimize cardiac output and ensure renal blood f ow.

Induction Standard induction techniques are acceptable in kidney transplant, although many attending anesthesiologists will opt or a rapid sequence induction (RSI) during intubation i there is concern or a ull stomach secondary to gastroparesis (as mentioned above).

Fluid Management During renal transplantation, patients typically receive 0.9% sodium chloride (“normal” saline) in usions as the crystalloid o choice to avoid adding potassium to a patient who may already be hyperkalemic. During the early portion o the case, moderate hydration should be maintained, but during the vascular anastomoses, hydration should be aggressive with either crystalloid or colloid (speci cally during the unclamping portion). I necessary, the colloid o choice is 5% albumin. Blood products (red blood cells, plasma, and platelets) can be assessed on a need basis since renal transplantation is no longer an overly “bloody” procedure during which major blood loss is an issue. I bleeding occurs due to uremic platelet dys unction, the treatment is desmopressin (DDAVP, 0.3 mcg/kg over 30 minutes). A Foley should be placed, which will be le unclamped during the initial portion o the case, and lastly, an OG tube should be placed to be removed at the end o surgery. During maintenance, baseline ABG, electrolytes, and Hgb/Hct should all be obtained with repeat draws every 1–2 hours as needed.

Maintenance A balanced maintenance approach to muscle relaxation and analgesia can be accomplished with entanyl and either cisatracurium (drug o choice) or rocuronium. Succinylcholine is not contraindicated, but special attention is required in regards to the patient’s potassium level prior to its use, as many o the ESRD patients are hyperkalemic at baseline.

Reperfusion T e external iliac vein is clamped rst and the renal vein-toiliac vein anastomosis is per ormed. T e external iliac artery– renal–artery anastomosis is then per ormed and the clamps

are released. Five minutes be ore the renal vasculature clamp is released, it is customary to administer urosemide and mannitol to achieve diuresis. During unclamping, an expected drop in blood pressure should prompt aggressive administration o f uids and/or decrease in volatile anesthetic concentration ensures adequate renal per usion. A set o laboratory data should be drawn 5 minutes be ore unclamping with corrections o any signi cant abnormalities accomplished be ore the clamps are released. Reper usion syndrome hyperkalemia is a concern a er perusion is reestablished. Depending on the surgeon’s pre erence, he or she may directly inject verapamil i there is a suspicion o renal artery vasospasm. Systemic hypotension due to verapamil may be reversed with administration o calcium chloride. At the direction o the surgeon, the anesthesiologist will clamp the Foley catheter and open the clamp on the antibiotic irrigation solution used to ll the bladder. Once the ureter has been reimplanted, the urinary catheter is unclamped. Urine output should be brisk. I the urine output is not greater than 1 mL/kg/h a er unclamping, low-dose dopamine in usions and additional urosemide and mannitol may help augment the urine output.

POSTOPERATIVE CARE Following the procedure, patients can be extubated and taken to the recovery room i all extubation criteria are met. Once trans er criteria rom the post-anesthesia recovery unit are met, patients can go directly to a surgical f oor with transplant experience and do not necessarily warrant intensive care unit (ICU) admission. Generally speaking, renal transplant patients have a low incidence o postoperative ICU requirement (~1%), and i they do, it is usually or respiratory ailure, but sepsis or f uid overload are also causes. Urine output should be closely monitored and any signi cant decline should raise suspicion o a possibly correctable mechanical problem. I there is concern or inadequate per usion, a renal ultrasound study should be obtained immediately, and re-exploration o the wound should not be delayed i kinking o the vasculature or obstruction o the ureter is suspected. Some patients will continue to require dialysis immediately ollowing kidney transplant due to delayed gra unction.

90 C

Perioperative Oliguria and Anuria Mariam Salisu and Jef rey S. Berger, MD, MBA

Oliguria and anuria are de ned as urine output less than 0.5 mL/kg/h and less than 50 mL/d, respectively. Frequently observed in the postoperative period, oliguria and anuria may be the initial presenting sign o acute kidney injury (AKI), a condition associated with signi cant perioperative morbidity. Acute renal ailure (ARF) in the perioperative setting is a serious surgical complication as over 50% o acute hemodialysis patients have perioperative ARF. T e mortality rate or perioperative ARF remains in the range o 20%–80% depending upon patient comorbidities. More than 90% o perioperative ARFs result rom relative hypovolemia with inadequate renal per usion. T e Kidney Disease Improving Global Outcomes (KDIGO) criteria or AKI are de ned in able 90-1.

• • •

ETIOLOGY In the situation o severe renal hypoper usion, there is a narrow window o only 30–60 minutes between the onset o oliguria and the initiation o ischemic acute tubular necrosis (A N). T e causes o oliguria can be classi ed as prerenal, intrarenal, or postrenal. T is classi cation provides a use ul structure or the systematic approach to therapy and is summarized in able 90-2.

Prerenal AKI is caused by decreased renal per usion due to decreased intravascular blood volume or impaired renal hemodynamics. T e causes include the ollowing: •

Hypovolemia—Hypovolemia is the most common cause o perioperative oliguria. Intravascular volume depletion

TABLE 90 -1

Kidney Disease Improving Global Outcomes (KDIGO) Criteria for Acute Kidney Injury 1. An increase in serum creatinine o ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours 2. An increase in serum creatinine o ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days 3. Urine volume 5.5 mEq/L or rapidly increasing K+

Uremia

Pericarditis or altered mental status

Metabolic acidosis

pH < 7.1

91 C

Dialysis and Hemof ltration Jessica Reidy, MD, and Brian S. Freeman, MD

In the United States, there are now approximately 530,000 patients with ESRD. T e incidence rate is 350 cases per million per year; however, it is disproportionately higher in A rican Americans, 1000 per million per year. Diabetes mellitus is the leading cause o ESRD, accounting or 55% o newly diagnosed cases each year. In addition, hypertension causes about 33% o newly diagnosed cases; other causes include glomerulonephritis, polycystic kidney disease, and obstructive uropathy. In the United States, the mortality rate o patients on dialysis is 18%–20% per year with a 5-year survival rate o approximately 30%–35%. T ese deaths are mainly due to cardiovascular disease (50%) or in ection (15%). Older age, male sex, nonblack race, diabetes mellitus, malnutrition, and underlying heart disease are all predictors o mortality in these patients.

DIALYSIS Dialysis is the main treatment modality o end stage renal disease (ESRD) patients. ESRD may be managed with hemodialysis, peritoneal dialysis—either continuous ambulatory peritoneal dialysis (CAPD) or continuous cyclical peritoneal dialysis (CCPD), or transplantation. Although there are multiple options, greater than 90% o ESRD patients in the United States are treated with hemodialysis. Hemodialysis can be broken down in to three essential components: the dialyzer, the dialysate, and the blood delivery system (Figure 91-1). In addition, there must be a way to access this blood—the dialysis access.

Indications Indications or dialysis can be broken in to two categories: acute dialysis or chronic (maintenance) dialysis. Acute dialysis is indicated in severe hyperkalemia, unrelenting metabolic acidosis, uid overload, symptomatic uremia, metabolic encephalopathy, pericarditis, coagulopathy, re ractory gastrointestinal symptoms, and drug toxicity. Uremia is usually only seen i the GFR is below 25 mL/min. Neurological, metabolic, hematological, cardiovascular, pulmonary, gastrointestinal, endocrine, skeletal, and skin mani estations ( able 88-2) can all be seen

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as symptoms o “uremia.” Indications or starting maintenance dialysis include uremic symptoms, hyperkalemia unresponsive to conservative measures, persistent extracellular volume expansion despite diuretic therapy, acidosis re ractory to medical therapy, a bleeding diathesis, and a creatinine clearance or estimated glomerular ltration rate below 10 mL/min.

Dialysis Access Dialysis access is obtained through a stula, gra , or catheter. Fistulas are created by the anastomosis o an artery to a vein; the most common being the Brescia–Cimino stula. In a Brescia–Cimino stula the cephalic vein is anastomosed endto-side to the radial artery. Fistulas have the highest long-term patency rate o all access options however they are only created in a minority o patients. An arteriovenous gra is the option o choice or many dialysis patients. In placement o the gra there is an interposition o prosthetic material (polytetra uoroethylene) between an artery and a vein. T e last option is a tunneled dialysis catheter, which is used in patients who have AV stulas and gra s that have ailed or cannot have a stula or gra due to anatomic reasons.

The Dialyzer T e dialyzer is the plastic chamber through which blood and dialysate ow at very high rates. T e most common dialyzer used in the United States is the hollow- ber dialyzer. It is composed o bundles o capillary tubes. Blood circulates within the capillary tubes with the dialysate owing outside o the ber bundle. T ese capillary tube membranes can consist o cellulose, substituted cellulose, cellulosynthetic, and synthetic. In recent years advances have been made to move rom cellulose to synthetic membranes. Cellulose is the most bioincompatible, meaning it activates the complement system. T ere are ree hydroxyl groups on the membrane sur ace that are key in activating the complement system. In substituted cellulose and cellulosynthetic membranes, these hydroxyl groups are chemically bound making them less bioincompatible. T e most biocompatible, or the membrane that causes the least activation o the complement system, is the synthetic 341

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Ve nous Arte ria l Dia lys a te

Wa te r tre a tme nt (de ioniza tion a nd reve rs e os mos is )

Ac id c o nc e ntrate Na + Cl– K+ Ace ta te – Ca 2 + Mg 2 +

Na Bica rb Na Cl

V Arte riove nous fis tula Dia lys a te A

Ve nous line

Arte ria l line

Hollow fibe r dia lyze r Arte ria l pre s s ure Ve nous pre s s ure Blood flow ra te Air (le a k) de te ction Dia lys a te dra in

Dia lys a te flow ra te Dia lys a te pre s s ure Dia lys a te conductivity Blood (le a k) de te ction

“De live ry” sys te m

FIGURE 91-1

The dialysis unit. (Reproduced with permission rom Kasper DK, Fauci A, Hauser S, Longo D, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York, NY: McGraw-Hill Education, Inc.; 2015: Fig. 336-1.)

membrane. T ese are generally composed o polysul one, polymethylmethacrylate, or polyacrylonitrile. T e majority o dialyzers in the United States now use synthetic membranes.

The Dialysate T e composition o the dialysate determines how much uid and cations are pulled o during a dialysis treatment. T e potassium concentration o dialysate can vary rom 0 to 4 mmol/L depending on the predialysis serum potassium concentration. T e calcium concentration is usually 1.25 mmol/L (2.5 mEq/L); this can be modi ed in certain settings. For example, a higher calcium concentration in the dialysate would be used in patients with hypocalcemia due to secondary hyperparathyroidism or parathyroidectomy. T e sodium concentration o the dialysate is normally 140 mmol/L, which is generally isotonic with the blood. A lower dialysate sodium concentration would lead to more sodium, and there ore more water, being taken o the patient. T is requently leads to hypotension, cramping, nausea, vomiting, atigue, and dizziness. In patients who o en develop hypotension during dialysis, “sodium modeling” can be used to counterbalance urea-related osmolar gradients. In sodium modeling the dialysate sodium concentration begins around 145–155 mmol/L and is lowered near the end o dialysis treatment o 140 mmol/L. T is increases the chances o patients having a positive sodium balance, though, so it should not be

used in hypertensive patients or in patients with large weight gains between dialysis treatments.

The Blood Delivery System T e nal component o the dialysis unit is the blood delivery system. It is composed o the extracorporeal circuit (dialysis machine) and the dialysis access. T e dialysis machine consists o a blood pump, dialysis solution delivery system, and sa ety monitors. T e blood pump moves blood rom the dialysis access, through the dialyzer, and back to the patient. Blood ow ranges rom 250 to 500 mL/min, usually depending on the type and integrity o the dialysis access. T e dialysis solution delivery system dilutes the dialysate with water and monitors the temperature, conductivity, and ow o the dialysate. T e hydrostatic pressure o the dialysate can be modi ed to a ect uid removal—negative hydrostatic pressure on the dialysate side can achieve higher uid removal, which is called ultra ltration. In addition, dialysis membranes have di erent ultra ltration coef cients so that uid removal may be varied.

Complications During Dialysis T e most common acute complication o hemodialysis is hypotension, especially in the diabetic patient population. T ere are many risk actors increasing the risk o hypotension including: excessive ultra ltration, impaired autonomic

CHAPTER 91

responses, overuse o antihypertensive agents, and reduced cardiac reserve. A less common cause o hypotension in dialysis patients is the development o high output heart ailure due to shunting o blood through AV stulas or gra s. T e incidence o hypotension can be decreased with the use o sodium modeling described above under the section “T e Dialysate.” Muscle cramping is another common complication o hemodialysis though the etiology o these cramps is not well de ned. It has been suggested that changes in muscle per usion due to aggressive volume removal and the use o lowsodium-containing dialysate may precipitate cramping. Anaphylactic type reactions to the dialyzer are a serious but rare complication o dialysis. T ese reactions most o en occur on the rst use o the dialyzer and with bioincompatible membranes. With the recent shi towards the synthetic, or biocompatible, membranes the incidence o anaphylactoid reactions has decreased. reatment with steroids or epinephrine may be necessary i symptoms are severe. Although not necessarily a complication o hemodialysis, cardiovascular events and mortality rates are extremely high in this patient population. Amongst hemodialysis dependent ESRD patient deaths, 50% are due to cardiovascular disease. Cardiovascular events and mortality rates are higher in the dialysis patient population than in patients post kidney transplant. T is may be due to shared risk actors or ESRD and cardiovascular disease, that is, diabetes mellitus, hypertension, and atherosclerotic and arteriosclerotic disease. Other risk actors or cardiovascular events in the ESRD population include inadequate treatment o hypertension, dyslipidemia, anemia, dystrophic vascular calci cation, hyperhomocystenemia, and alterations in hemodynamics during dialysis treatment. T ere ore, blood pressure control and lipid-lowering agents based on the individual patients’ cardiovascular risk are bene cial.

•

While intermittent hemodialysis is the treatment o choice or most patients, patients in the ICU o en require continuous renal replacement therapy (CRR ). Most patients who receive CRR have acute oliguric renal ailure along with hypotension, uid overload, and organ ailure. Compared to conventional hemodialysis, CRR has lower ow rates and there ore patients are less prone to develop hemodynamic instability. Critical-care patients are o en already hemodynamically unstable. T ere ore, in order to avoid urther hypotension and possible organ ischemia, CRR may be avorable. T ere are several advantages o CRR compared to intermittent hemodialysis: • •

Better clearance o small solutes over time Ability to manage intravascular uid intake on an hourly basis in critically patients who may require large volumes o uid

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Increased hemodynamic stability with ewer episodes o hypotension Possible removal o in ammatory cytokines in patients with systemic in ammatory response syndrome or sepsis

•

T e disadvantages o CRR include: •

Anticoagulation to prevent premature clotting within the lter o the extracorporeal circuit Intensive nursing care Restricted patient mobility Higher equipment and laboratory costs

• • •

CRR comes in di erent modalities: continuous venovenous hemo ltration (CVVH), continuous venovenous hemodialysis (CVVHD), slow continuous ultra ltration (SCUF), and continuous arteriovenous hemo ltration (CAVH). T ese di erent modalities are de ned by their vascular access and mechanism o solute and water removal (Figure 91-2). CAVH, continuous arteriovenous hemo ltration, requires cannulation o both an artery and a vein. Cannulation o the artery carries risk o thrombosis, limb ischemia, and hemorrhage. Due to the high risks associated with CAVH, it is not o en used. More commonly, continuous venovenous modalities are used: CVVHD, CVVH, or SCUF. T e distinction lies between

VV S CUF

CVVH Rpre

Rpos t

Qb = 100–250 mL/min Quf = 5–15 mL/min

HEMOFILTRATION Continuous Renal Replacement Therapy

Dialysis and Hemo ltration

Qb = 100–250 mL/min Qf = 15–60 mL/min

CVVHD

CVVHDF Rpre

V Do

Di Qb = 100–250 mL/min Qd = 15–60 mL/min

FIGURE 91-2

Rpos t

Di Do Qb = 50–200 mL/min Qf = 10–30 mL/min Qf = 15–30 mL/min

Schematic representation o the most common continuous renal replacement therapy (CRRT) set-ups. Black triangles represent the blood ow direction; gray triangles indicate dialysatereplacement solutions ows. CVVH, continuous venovenous hemof ltration; CVVHD, continuous venovenous hemodialysis; CVVHDF, continuous venovenous hemodiaf ltration; Di, dialysate in; Do, dialysate out; Qb, blood ow; Qd, dialysate solution ow; Q , replacement solution ow; Qu , ultraf ltration ow; Rpost, replacement solution postf lter; Rpre, replacement solution pref lter; SCUF, slow continuous ultraf ltration; U , ultraf ltration; V, vein; VV, venovenous. (Reproduced with permission rom Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia, 8th ed. Philadelphia: Elsevier; 2015. Fig. 107-8.)

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hemodialysis and hemo ltration. In hemodialysis (CVVHD), the patient’s blood and dialysate are separated by a semipermeable membrane, which allows di usive solute transport. CVVHD generally allows or clearance o small molecules, less than 300 Da. T e rate o water removal in CVVHD is low and there ore patients are less likely to become hypovolemic. In contrast, hemo ltration solute transport is convective. It can also clear larger molecules, up to 20 kDa in size. T ere are higher rates o uid removal in CVVH and there ore the circuit is in used with physiologic replacement uids to counteract the tendency towards hypovolemia. T e rate and composition o replacement uid in usion can be altered depending on the electrolyte and uid management goals or the patient.

Slow continuous ultra ltration (SCUF) is similar to CVVH in that it has a high amount o uid removal. T e di erence is the hourly rate o SCUF is much lower; there ore, these patients do not require uid replacement and have less risk o hypovolemia. SCUF is mainly used when the goal is uid management and not solute clearance. T ere are several pharmacokinetic considerations while receiving CRR : • • • •

CRR membranes are permeable to most drugs in their ree raction orm Larger molecules (>500 Da) are less e ective cleared Highly protein bound drugs undergo minimal clearance Slower ow rates will decrease drug clearance

92 C

Lithotripsy Alan Kim, MD

Nephrolithiasis a ects nearly 1.2 million people each year and can progress to a debilitating renal colic requiring inpatient care. reatment depends on the type and size o the stone. Patients with underlying renal disease are at higher risk or acute injury when a complete obstruction occurs. Given that the management o stones varies with their etiology, even rst time kidney stones should be identi ed and their source addressed. Recurrent obstructions can stimulate the brogenic cascade, leading to renal parenchymal injury. Recurrence rates or stone ormation increase with each passing year. Reports have calculated this risk o recurrence to over 50% at a 10 year period. T is recurrence rate has been reported to decrease with some simple preventative measures. T ese measures are usually dietary modi cations and increased uid intake.

NEPHROLITHIASIS

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radiates to the ipsilateral groin and can be associated with severe nausea. It initiates in the deep ank on the same side as the obstruction, without radiation to the groin. At the ureterovescial junction, the symptoms consist more o voiding dif culties; including increased requency and pain ul urination. Furthermore, this location is associated with a suprapubic location o pain. Unique to this location are associated gastrointestinal symptoms such as diarrhea and tenesmus. Other potential symptoms include those associated with nausea and vomiting, a urinary tract in ection, or hematuria. When the stones are too large to pass through the system, such as the case with staghorn calculi, they o en do not present with pain. Instead, they present as in ection or hematuria. Untreated stones may develop into perinephric hematomas, kidney in ections, urinary obstruction rom stone impactions, stomach or intestinal ulcerations, and post procedural kidney impairment.

Pathophysiology and Presentation

Treatment

T e term nephrolithiasis speci cally re ers to renal calculi, but is o en used to also describe both ureteral and renal calculi. For stones to orm, the components must be present in the urine at a high enough concentration to precipitate out o solution. o be o clinical consequence, these initial clots must grow. T ere are several types o stones that may develop calcium, struvite, uric acid, and cysteine. Calcium stones are the most common. Knowledge o the stone composition helps identi y the appropriate dietary modi cation. Its location will dictate the potential therapeutic interventions. O en times, renal colic is the presenting symptom o nephrolithiasis. Renal colic is an acute, incapacitating pain due to the dilation, stretch and spasm caused by a complete ureteral obstruction. T e pain is o en described as the worst pain the patient has ever elt. T is pain presents di erently at di erent locations. At the ureteropelvic junction, neophrolithiasis can present as an ipsilateral deep ank pain without radiation. In the ureter, it can present as a severe colicky pain in the ank and lower abdomen. Unlike the ureteropelvic location, this pain

1. Expectant management—About 80%–85% o stones will pass spontaneously. I the stone is 4 mm or less in size, conservative management o hydration and pain medications is employed. Stones this size have an 80% chance o spontaneous clearance. When stones are greater than 8 mm in size, they only have a 20% chance o clearing on their own. Urine alkalinization can urther help break down noncalcium stones. 2. Percutaneous stone removal—Percutaneous stone removal is employed or stones are too large or in too di cult a location to undergo either shock wave or laser lithotripsy. T is removal consists o a surgical excision into the ank, with scope placement through incision into the a ected kidney. T e stone is then removed directly rom the kidney. 3. Aggressive urgent management—It is required when obstruction presents concurrently with an upper urinary tract in ection. T is combination can lead to a perinephric abscess, urosepsis, and death. T e proximity o the highly vascularized kidney to the nidus o in ection causes this propensity towards systemic in ection. 345

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EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY Extracorporeal shock wave lithotripsy was rst used in Germany in 1980. T e rst generation o this machine suspended a patient in a bathtub with sca olding. T ere are three components to every lithotripter. T e energy source generates an explosive shock wave. A focusing element directs the wave into a narrow e ective target range. T is wave propagates until it reaches an inter ace where the acoustic impedance changes and allows it to release its energy. Water and human tissue have very similar acoustic impedances, so the wave travels unmolested through both. However, at the body–stone and stone–body inter aces, there are marked changes, allowing the release o several G orces. An imaging component con rms stone location and redirect shock waves. High- requency repetitions o these shock waves break down the stone. T is process was initially per ormed in a patient who was completely submerged in a bathtub to reduce unintentional energy loss. More recent lithotripters do not require this immersion. Instead, the patient lies on a water- lled cushion. T e presence o any other inter aces may impede the ull energy trans er to the stone. For an e ective lithotripsy session, all devices in the wave blast path should be removed. I the patient is placed under epidural anesthesia, the catheter and all associated tape should be secured to the nonprocedural side. Furthermore, the use o the loss o resistance to air method o epidural placement should be limited.

Pathophysiology of Water Immersion Submerging a patient into water has many physiologic e ects. Immersion increases central blood volume with concurrent increases in central venous and pulmonary arterial pressures. T ese increases are o set by the peripheral pooling and decreased venous return caused by the sitting position. T e degree o the net increase in ow depends on the depth o immersion. A person submerged to their clavicles has a reduction in their unctional residual capacity by about 20%–30%. T is e ect is due to the combination o the hydrostatic pressure imparted on the thorax and the restricting straps used to the secure the patient to the seating sca old. Decreased unctional residual capacity coupled with an increased pulmonary blood ow due to the increased venous return exacerbates the underlying ventilation-per usion mismatch, leading to hypoxemia. Immersion promotes diuresis, natriuresis, and kaliuresis. It is thought that an inhibition o ADH and renal prostaglandins is the cause.

Equipment Shockwave lithotripters have evolved over the years. First generation lithotripters required a patient to be completely

submerged. T ey used water as a medium or the waves. Second- and third-generation models do not require this ull immersion. T ese newer devices have a more ocused area o e ect, by narrowing the ocus range and there ore causing less pain rom collateral wave damage. However, these models do require the patient in the prone or lateral decubitus position.

Procedure Requirements o maximize the success o the procedure, the urologist requires a stationary target with a clear line o sight to the stone. T e target stone must be stationary to bear the ull brunt o the shockwaves. I the target moves in and out o the ocus range, the shock waves are only a ecting the stone when it is in range. Muscle relaxation with controlled ventilation is ideal or this goal. Inter aces where the acoustic impedance changes are potential sites o energy loss. o minimize energy losses rom the ocusing element to the target, all obstacles that are o a di erent inter ace rom the body should be removed. Even the oam padding used in covering epidurals can reduce the energy output by a signi cant percentage. T is is less o a concern with the newer lithotripters as they are.

Contraindications T ere are several contraindications to shock wave lithotripsy. Absolute contraindications include pregnancy, untreated bleeding disorders, and abdominally placed pacemakers. Relative contraindications include pectorally placed pacemakers, internal de brillators, abdominal aortic aneurysm, and orthopedic prostheses. Patients with pectorally placed pacemakers should have the usual preoperative work up or any other procedure. T e make and model o the pacemaker should be identi ed, as well as recent interrogations noted. T e pacemaker programmer should be available to evaluate and reprogram the pacemaker as needed a er the procedure. T e shock wave should be gradually increased, with close monitoring. Automated implantable cardioverter-de brillators and lithotripter manu acturers consider these devices incompatible. However, ESWL has been used or patients with AICDs success ully. De brillators should be shut o prior to and reactivated a er the procedure. Most de brillators can be deactivated with the use o a magnet. However, this should be con rmed prior to any procedures. Shock waves can precipitate arrhythmias in 10%–14% o patients. T e mechanical stress o the pulse wave rather than the electrical stimulus is the cause o these arrhythmias. Pulses should be synchronized with the patient to be delivered in the re ractory part o the cardiac cycle. Patients with aortic aneurysms and orthopedic implants can have the procedure, as long as the aneurysm or implant are out o the way o the blast path. Patients with morbid obesity have an innately higher risk rom the compromised respiratory mechanics involved

CHAPTER 92

in immersion. However, this is coupled with a decreased e icacy. he narrow ocus range limits the range o movement that can be tolerated be ore the treatment is rendered ine ective. Heavier patients have a larger degree o diaphragmatic excursion (the distance their torso moves due to respiratory cycles). In these patients, the urologist should attempt to ocus on the stone with the lithotripter targeting tools prior to the administration o anesthetic agents.

ANESTHESIA FOR LITHOTRIPSY Local Anesthesia/Sedation T is procedure can be per ormed with local/sedation. However there are some drawbacks. First, diaphragmatic excursion can be signi cant in even patients with a normal body weight. Although narcotics can be given to reduce this excursion, there is an upper limit to this e ect as set by the patient’s depressed respiration. Second, the patients have an increased incidence o recall with a concurrent increase in dissatis action.

Deep Sedation Under deep sedation, the patient may be breathing at a slow steady rate with high tidal volumes. T is large shi in movement can take the operative view out o ocus and is called the diaphragmatic excursion. Further, the deep breathing can also move the stone spontaneously distal or proximal to the starting location. T is can make retrieval or lithotripsy more dif cult.

Regional Anesthesia A neuraxial technique can be employed with several concerns. When placing an epidural catheter, the loss o resistance to air technique should be minimized. T e change in acoustic impedance due to an air bubble can cause the harm ul redirection o energy to the spinal column rom the kidney stone. Local tissue injury can occur in these inter aces. Furthermore, o lesser importance, is the slow onset o an adequate epidural level which may reduce the overall turnover times. A spinal anesthetic provides a quick, dense block but can be af liated with signi cant hypotension that is urther exaggerated in an immersed state.

General Anesthesia Depending on the position o the patient and the lithotripter setup, general anesthesia with an appropriate airway device (laryngeal mask or endotracheal tube) can be used. Adequate pain control may be challenging in these patients. T ose who are actively nauseous and vomiting should undergo rapid sequence induction with an endotracheal tube.

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347

For patients undergoing a general or neuraxial technique, hypothermia is a concern. Both techniques cause peripheral vasodilation. Coupled with immersion in water, heat loss can occur. Depending on how the water temperature is monitored and corrected, reports o both hypothermia and hyperthermia have been noted.

OTHER TYPES OF LITHOTRIPSY Laser Lithotripsy Laser lithotripsy is a newer technique with which stones are broken under direct visualization. A laser is transmitted through a iber optic wire and exits at its tip. Energy is only released over a short distance at the tip o the wire. Laser lithotripsy is limited to stones that can be directly visualized. When choosing between ESWL and laser lithotripsy, size is the main distinguishing actor. ESWL are e ective against stones that are 2 cm wide. T e procedure is per ormed in the lithotomy position. Preprocedural X-rays should in orm the general location. T e urologist will insert a scope to con rm the stone’s location. I the stone cannot be visualized, additional radiographic imaging is per ormed to localize the stone. As with any cystoscopy, irrigation uid is needed to provide an exposure site. I the procedure is prolonged, the high volume o irrigation uid can contribute to volume overload. o minimize this potential, the uid is isotonic and the procedures kept to a shorter duration. T ere are several types o lasers. Pulsed dye lasers are used or biliary and urinary stones. Holmium: YAG lasers employ in rared wavelengths (2150 nm). T ese lasers have both coagulative and ablative e ects and the standard o care. T e type o laser does not have a signi cant impact on the type o anesthesia that is applied.

A. Anesthetic Technique T ese procedures are per ormed under general anesthesia in the supine position. Muscle relaxation is employed to minimize diaphragmatic excursion or the same reasons as seen in ESWL or diaphragmatic excursion. Even so, some outpatient centers o er spinals as the primary technique.

B. Precautions Given the use o a high energy laser, special goggles should be used by both sta and patients. As mentioned be ore, uid overload can also be an issue i the procedure takes an unexpectedly long time. T ere are physiological changes associated with being in the lithotomy position that may be exacerbated in patients who are larger. O these, adequate ventilation is the most common concern. T e use o a larger endotracheal

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tube and pressure control ventilation mode help ameliorate that risk.

Ultrasonic Lithotripsy Ultrasonic lithotripsy generates ultrasonic waves to break up the stone directly. T e ultrasound probe is deployed in the urinary system, and placed right next to the stone. Its main limitation is that given its size and rigidity, it cannot reach stones past the lower ureters. T is modality sometimes used in conjunction with ESWL.

Electrohydraulic Lithotripsy Electrohydraulic lithotripsy was the rst version o shock wave therapy. It generated a charge between two electrodes. T is spark created a cavitation bubble in the irrigation uid, which in turn generated a shock wave. T e shock wave was used to break up the stone. Its main limitation is that it can cause signi cant tissue damage. It has allen out o avor given its poor sa ety margin and the advent o sa er modalities.

93 C

Transurethral Resection of Prostate Brian S. Freeman, MD

ransurethral resection o the prostate ( URP) is a common urologic procedure that is used to treat patients with symptomatic benign prostatic hypertrophy (BPH). It is a less invasive approach than traditional suprapubic or retropubic open prostatectomy.

SURGICAL AND ANESTHETIC TECHNIQUE A resectoscope is inserted through the urethra into the prostate to excise layers o prostatic tissue while preserving the prostatic capsule. Resection is achieved with a diathermy loop via traditional electrocautery or laser vaporization. T e conventional approach (M- URP) uses a monopolar electrode that transmits a high energy electrocautery current rom a single-limb electrode through the body to the patient’s grounding pad. Newer B- URP resectoscopes now utilize bipolar electrodes in which the continuous bidirectional ow o current does not leave the con nes o the resectoscope. Several studies have shown lower rates o complications, trans usion, and URP syndrome with bipolar URP procedures compared to monopolar currents. In contrast to both these approaches, laser vaporization resectoscopes (L- URP) enable the actual coagulation and sealing o open prostatic veins during the resection. T e laser can vaporize prostate tissue in millimeter layers. Compared to monopolar URP, using a laser signi cantly reduces surgical time, blood loss, uid absorption, and hospital length o stay. URP requires the use o a continuous solution or distension, visualization, and irrigation o the bladder and prostate. T e ideal solution should be transparent, isotonic, and have nontoxic solutes. Crystalloids such as lactated Ringer’s and normal saline are highly ionized. Since electrolytes can disperse the electric current to surrounding tissues causing burns, the solution should be electrically inert. Plain distilled water, which is very clear and has no electrolytes, can lead to signi cant intravascular hemolysis when absorbed due to its very low osmolality. Distilled water has been replaced by solutions which are moderately hypotonic, maintain transparency, and cause no signi cant hemolysis. T e most common solutions used today are glycine 1.5% (230 mOsm/L) and

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sorbitol 2.7%–mannitol 0.54% combination (195 mOsm/L). However, the newer techniques o URP—bipolar and laser—prevent electrical dispersion and minimize irrigant absorption. T ere ore, an electrolyte-containing solution such as normal saline may now be used, which has reduced the morbidity associated with hypo-osmolar solutions. Anesthesia or URP may be achieved through either general or neuraxial anesthesia. Studies have not demonstrated any di erence in the incidence o postoperative complications (e.g., myocardial in arction, stroke, pulmonary embolus), postoperative cognitive dys unction, and mortality in patients who received general versus regional anesthesia. General anesthesia has become more acceptable due to the decreased risk o irrigant absorption and URP syndrome when using the newer bipolar and laser URP techniques. Spinal anesthesia to 10 provides satis actory com ort, pelvic relaxation, and the ability to monitor or early symptoms o excessive uid absorption and bladder or prostate capsule per oration in a conscious patient. Compared to epidural anesthesia, the subarachnoid approach usually ensures block o the sacral (S2–S4) parasympathetic bers carrying a erent visceral pain sensation rom the prostate and bladder.

COMPLICATIONS RELATED TO ABSORPTION OF IRRIGATING SOLUTION When the prostatic venous sinuses are opened during URP, direct intravascular absorption o the irrigating solution usually occurs. T e hydrostatic driving pressure o the irrigating uid (especially i the container is suspended higher than 70 cm) urther compounds the problem. T e average amount o uid absorbed during URP is approximately 20 mL/min o resection time. Longer resections, especially lasting more than one hour, lead to greater uid absorption. I the resectoscope violates the prostate capsule, even greater volumes o solution may now enter the circulation through the peritoneal or retroperitoneal spaces. Complications rom irrigant absorption depend upon the type and volume o uid as well as the duration o surgery. 349

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PART III Organ-Based Advanced Sciences

TABLE 93-1

Signs and Symptoms of TURP Syndrome

Cardiovascular and Respiratory

Central Nervous System

Metabolic

Other

Hypertension

Agitation/confusion

Hyponatremia

Hypo-osmolality

Bradyarrhythmias, tachyarrhythmias

Seizures

Hyperglycinemia

Hemolysis

Congestive heart failure

Coma

Hyperammonemia

Pulmonary edema and hypoxemia

Visual disturbances (blindness)

Myocardial infarction Hypertension Reproduced with permission from Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia, 8th ed. Philadelphia: Elsevier; 2015. Table 72-13.

Excessive Circulatory Volume T e absorption o large volumes o irrigant solution can lead to circulatory overload. Symptoms o circulatory overload depend upon the volume and speed o uid absorption and the patient’s underlying cardiac status. Mannitol irrigating solutions are iso-osmolar but can acutely expand the intravascular volume be ore causing an osmotic dieresis. Circulatory overload can also occur upon resolution o spinal anesthesia when venous capacitance decreases. Movement o the excess uid into the interstitial space can lead to pulmonary edema.

TURP Syndrome T e “ URP syndrome” is a clinical diagnosis o the serious neurologic and cardiovascular sequelae resulting rom signi cant absorption o hypo-osmolar electrolyte- ree irrigation uids ( able 93-1). T e syndrome shortly a er resection begins up until the rst postoperative day. Excessive water intoxication leads to hyponatremia, serum hypo-osmolarity, and metabolic acidosis. Neurologic symptoms range rom dizziness, nausea, and restlessness to mental status changes, seizures, and coma. T ese mani estations occur because the acute decrease in serum osmolarity causes cerebral edema—not because o hyponatremia. Consequently, patients may develop increase intracranial pressure, bradycardia, and hypertension (Cushing re ex). Early cardiopulmonary complications rom the rapid intravascular expansion include systemic hypertension (with increased pulse pressures), re ex bradycardia, elevated central venous pressure, pulmonary edema, and circulatory collapse. Late cardiovascular e ects o severe hyponatremia (18.5 g/dL in men; >16.5 g/dL in women) and either the presence o a JAK2 mutation or two o the ollowing: hypercellularity o the bone marrow, a subnormal serum erythropoietin (EPO) level, or endogenous erythroid

Vis cos ity

2 0

100

He ma tocrit (%)

FIGURE 95-1

Viscosity of heparinized normal human blood as a function of hematocrit. (Reproduced with p ermission from Lichtman MA, Kipps TJ, Seligsohn U, et al. Willia m’s Hematology, 9th ed. McGraw-Hill Education, Inc., 2016.)

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PART III Organ-Based Advanced Sciences

RBC mass is an isolated nding. Examples o secondary polycythemia due to hypoxia include the ollowing: • • • • •

Acute and chronic mountain sickness Signi cant cardiopulmonary disease, that is, congenital heart diseases with lef to right shunting leading to cyanosis Chronic pulmonary disease, or example, Pickwickian syndrome (extreme obesity) leading to the development o hypoventilation Inherited de ects in hemoglobin Disorders or drugs producing methemoglobinemia

Secondary polycythemia due to increased EPO production is of en ound in patients with EPO-secreting tumors including renal cell carcinoma, uterine myomas, hepatomoas, and cerebellar hemangiomas. Benign renal conditions, that is, hydronephrosis, polycystic kidney disease, and renal cysts, are also capable o secreting EPO. Finally, the surreptitious use o recombinant EPO by high-per ormance athletes also results in secondary polycythemia.

Relative Polycythemia Relative polycythemia, which results rom a reduction o plasma volume, is typically due to dehydration. Diuretic use precipitates the dehydration with excessive sweating, or inadequate oral intake.

CLINICAL MANIFESTATIONS T e clinical signs and symptoms o polycythemia largely depend on the underlying disease process and the rate o disease progression. issue oxygen delivery is optimal at when hematocrit concentrations all in the range o 33%–36%. Above this level, an increase in viscosity tends to slow blood ow and decrease oxygen delivery. T is e ect is relatively minor until hematocrit becomes greater than 55% (a li e-threatening value), as blood ow to vital organs signi cantly decreases and the risk o venous and arterial thrombosis rises. Forty percent o polycythemia patients with hematocrit greater than 55% experience at least one thrombotic event during their illness, most prominently coronary and cerebral events. Patients with chronic polycythemia, such as seen in chronic lung disease, complain o relatively ew symptoms until hematocrit exceeds 55%–60%; at that point, headaches and constitutional symptoms (i.e., easy atigability) are the most common complaints. Other presenting eatures include splenic pain, pruritus, gout, and hemorrhage (especially o the skin or GI tract).

COMPLICATIONS Although the incidence o complications associated with polycythemia is low, the perioperative morbidity and mortality are

substantial. Approximately 30% o patients will die o thrombotic complications and another 30% will succumb to cancer (i.e., myelo brosis and acute leukemia). T rombosis, the most common complication, risks pulmonary emboli, renal ailure secondary to renal vein or artery thrombosis and intestinal ischemia rom mesenteric vascular thrombosis. Hemorrhages, acute leukemia and myelodysplasic syndrome are other worrisome, but less common complications. Myelo brosis and pancytopenia, which may arise later, in what is considered the “spent phase” o polycythemia, carry a threat o in ections and bleeding. rans usions are commonly required in this subset o patients.

TREATMENT While there is no single treatment available or polycythemia, the current recommendation is to risk-strati y patients with the major aim o preventing thrombotic events. T e mainstay o therapy is phlebotomy, which is aimed at reducing hyperviscosity by decreasing the venous Hct level to less than 45% in white men and 42% in blacks and women. While eatures o using phlebotomy alone are attractive—given that it is a simple procedure without many risks and carries a low rate o malignancy, these patients tend to experience more thrombosis events during the rst ew years o treatment and are at risk or the eventual development o iron-de ciency anemia. argeting platelet unction with aspirin therapy remains another possibility as long as there are no contraindications. Patients treated with myelosuppressive agents and supplemental phlebotomies avoid this early thrombotic risk, but in turn have signi cant malignant trans ormation af er about six years o therapy. T ere ore, strati ying patients by age and thrombotic risk is use ul.

PERIOPERATIVE MANAGEMENT Polycythemia is a risk actor or thromboembolic and hemorrhagic events that requires meticulous attention and perioperative assessment o a patient’s blood pro le along with vigilance to avoid hypoxia. Phlebotomy, adequate hydration, and recognition o thrombotic and bleeding problems are the pillars to success ul anesthetic management o such patients.

Preoperative Preparation Laboratory evaluation o RBC mass and determination o treatment history are critical. T rombophilia screening or high-risk individuals is an important part o the preoperative anesthetic assessment. Any medical history o hypertension, hyperlipidemia, diabetes mellitus, and a present or past history o smoking, or history o prior thrombotic events quali es these patients as at higher risk or thrombus ormation. Hemorrhagic diathesis, while rarer and less ominous, normally a ects patients with very high platelet counts. In

CHAPTER 95

the majority o patients, the risk o hemorrhage is due to an acquired von Willebrand disease caused by abnormally low amounts o von Willebrand Factor (vWF) multimers, essential to platelet adhesion. Both phlebotomy and the avoidance o dehydration lower the risk o thrombosis and hemorrhage during the perioperative period. It is advisable to maintain blood values at re erence range levels by regular examination and treatment. Fasting or periods beyond 4–6 hours should be accompanied by ample preoperative hydration as prolonged asting leads to dangerously high Hct levels in patients already predisposed to hypercoagulability. For high-risk individuals, coagulation pro les, including INR, ought to be considered.

Intraoperative Considerations Both regional and general anesthetic techniques have been used success ully in patients with polycythemia. During surgery, baseline hypercoagulability increases by a 100- old; aggressive hydration along with strict monitoring or adequate urine output during the intraoperative period is thus o utmost importance. Adequate intravenous access is needed. It is important to be aware that emergency surgeries, where preoperative preparation may be hastened, may require intraoperative phlebotomy. T is, however, must be done with extreme caution, taking care to replace lost volume and avoid vasoconstriction rom volume depletion. Vitals monitoring

Polycythemia

359

and clinical evaluation or the possibility o stroke or hemorrhage should continue throughout the perioperative period. Patients with polycythemia vera are at risk or perioperative hypercoagulability and hemorrhage. In order to reduce the risk o thrombohemorrhagic complications, Hct reduction to 45% be ore surgery is recommended. Additionally, thrombocytosis should be decreased to less than 400,000 platelets/mm 3 prior to surgical intervention to prevent complications. In the case that bleeding occurs, both cryoprecipitate and desmopressin improve vWF levels. Nonetheless, patients should be advised to withhold rom aspirin use or at least 7 days prior to surgery. For patients with secondary polycythemia, anesthetic management varies depending on the speci c cause. While patients with mild hypoxic polycythemia may require no speci c treatment, those with very high hematocrit of en require phlebotomy to reduce the thrombotic and hemorrhage complications o the disorder.

Postoperative Considerations Early ambulation is the paramount postoperative consideration given that these patients are predisposed to the ormation o deep vein thromboses. Additionally, compression stockings help to prevent clot ormation while peripheral local anesthetic block relieves postoperative pain and enables early ambulation.

96 C

T rombocytopenia and T rombocytopathy Jeremy Epstein, MD, and Vinh Nguyen, DO

Formation o a hemostatic plug can be broken down into primary hemostasis and secondary hemostasis. Primary hemostasis involves platelet adhesion, change in platelet shape, platelet aggregation, and secretion o platelet actors. Secondary hemostasis involves the activation o the coagulation cascade. Platelets play a vital role in the ormation o a hemostatic plug. Platelets are originally produced in the bone marrow as ragments o the cytoplasm rom megakaryocytes, which circulate in the blood or 7–10 days. T e normal circulating platelet count is 150,000–450,000/µL and approximately 15,000–45,000/µL platelets are made per day to maintain a steady state. At any given time, up to one-third o all platelets are transiently sequestered in the spleen. T e likelihood o bleeding is inversely proportional to platelet unction and count. I the endothelial cell continuity is disrupted, and the underlying matrix is exposed, a series o events are coordinated to seal the injured area. Platelets play a primary role in this process by interacting with subendothelial von Williebrand actor (vWF) via a membrane glycoprotein (1b) complex. Platelets adhere to each other via GP IIb/IIIa—platelet aggregation. Platelets also contain alpha and dense granules, which contain hemostatic proteins and proaggregatory actors, respectively. Furthermore, once platelets are activated to orm a hemostatic plug, they recruit additional platelets through the release o proaggregatory materials and synthesis o thromboxane A2 and arachidonic acid. It is imperative to take a detailed amily history, and history and physical or these patients to determine i the disease is caused by an inherited, acquired, or primary and secondary hemostatic disorder. Primary disorders will commonly have epistaxis, bleeding gums, and metromenorrhagia. Physical exam may show areas o easy bruising, purpuric spots, petechiae, ecchymosis, hemarthrosis, and enlarged spleen due to sequestering o platelets. Additionally, a peripheral smear, coagulation studies, bleeding time, and CBC can aid in the diagnosis o the type o platelet dys unction. It is important to remember spurious thrombocytopenia may occur due to clumping o platelets in the specimen, or dilutional thrombocytopenia due to replacement o uid or blood without concomitant platelet replacement.

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THROMBOCYTOPENIA T rombocytopenia can be urther subdivided into increased destruction, decreased production, and distribution in circulation. Due to the plethora o platelet disorders, only the most commonly encountered types will be discussed below.

Reduced Platelet Production Aplastic anemia is a ailure o total cell line production that o en occurs within the bone marrow. Several disease states can cause decreased production including tuberculosis, leukemia, and granulomatous disorders that result in bone marrow ailure. Additionally aplastic anemia can occur due to radiation or chemotherapy in cancer patients. oxic chemicals may also lead to platelet production ailure. Furthermore, several common drugs such as alcohol, estrogens, diuretics, and various antibiotics cause reduced cell lines. In ltration o the bone marrow by hematopoietic malignancies, such as leukemias, lymphomas, or myeloproli erative disorders can reduce bone marrow volume, and space that would normally be utilized or platelet production. Inef ective thrombopoiesis is seen with patients with vitamin B12 or olate de ciency, commonly seen in alcoholics and those with de ective metabolism o olate. reatment includes replacement o olate, or vitamin B12, which should elevate platelet count to a normal level within several days. Li e-threatening surgeries can be treated with platelet trans usions.

Increased Platelet Destruction Increased destruction is due to an autoimmune mechanism or increased utilization o platelets. Disseminated intravascular coagulation (DIC) is caused by an increased intravascular consumption via excessive activation o the entire coagulation process. DIC can result in a severe coagulopathy, with marked reduction in platelet count, and prolonged coagulation actors mani esting in signi cant bleeding. It can be a chronic condition in cancer patients, but usually presents acutely, such as a patient with an amniotic uid embolism. Laboratory data show a 361

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reduction o platelets, prolonged prothrombin and partial thromboplastin times, and elevated D-dimer levels. T e only de nitive treatment or DIC involves treating the underlying cause. Plasma exchange and platelet trans usion constitute supportive care. T rombotic thrombocytopenic purpura is rare but is classically described as a pentad o mani estations: thrombocytopenia with purpura, RBC ragmentation, renal ailure, neurologic dys unction, and ever. raditionally patients report a u-like illness 2–3 weeks prior. A DIC screen would be negative in these patients, but they may have elevated LDH, thrombocytopenia, and schistocytosis. Hemolytic-uremic syndrome is seen in children with bloody diarrhea secondary to E. Coli 0157:H7 or Shiga-like toxin. T ey present with renal ailure, decreased platelets, and anemia. Most children recover with hemodialysis spontaneously. HUS and P should receive platelet trans usions or li e-threatening bleeding, as trans usions may result in greater harm. HELLP syndrome is requently encountered as a complication o pregnancy. T rombocytopenia, elevated liver enzymes, and red blood cell hemolysis are noted. reatment involves controlling hypertension with subsequent delivery, usually results in cessation o this process.

Autoimmune Thrombocytopenia Heparin-induced thrombocytopenia (HI ) involves two main types. HI type 1 (nonimmune) occurs within the rst day o initiation o un ractionated heparin therapy, and is transient. HI II is immune-mediated and occurs >5 days a er heparin introduction, where heparin-platelet actor 4 complexes orm with platelets. A greater than 50% reductions in platelet count can signal the appearance o HI II, and heparin should be immediately stopped and a direct thrombin inhibitor should be started. Idiopathic thrombocytopenic purpura (I P) is a diagnosis o exclusion in adults. Acute I P usually occurs in children aged 3–5 years old, and have a history o a previous acute viral syndrome. Chronic I P is usually seen in adults 20–40 years old. rans usion o platelets results in platelets with a shortened li e span, which are also rapidly destroyed. T e chronically low platelet count is balanced by an increased platelet production inside the bone marrow. I severe I P mani ests, it is a medical emergency requiring high-dose corticosteroids, and i emergent surgery is necessary, IVIG and platelet transusions are continued regardless o platelet count.

THROMBOCYTOPATHIES Acquired Abnormalities of Platelet Function Patients with severe uremia may show platelet dys unction, with prolonged bleeding times. Correction involves hemodialysis, acutely DDAVP, or in usion o conjugated estrogen will shorten bleeding time. Cirrhosis patients may mani est with generalized bleeding, and should be considered a er a bleeding varices or ulcer is ruled out. Reduced production in actor VII prolongs P , in addition to chronic low-grade DIC.

Qualitative Platelet Disorders Patients with von Willebrand’s Disease (vWD) lack normal amounts o von Willebrand actors. Platelet unction can be restored i given drugs that increase plasma vWF levels. Since vWF serves as a carrier or actor VIII, a prolonged P may be seen, in addition to reduced vWF activity and numbers. reatment includes vWF replacement, and/or DDAVP.

Drug-Induced Platelet Dysfunction Aspirin irreversibly binds to platelets, thus making them ine ective. Nonsteroidal anti-in ammatory agents, clopidogrel, ticlopidine, and abciximab strongly inhibit platelet unction. Normal platelet numbers are expected, but poor cessation o bleeding may be present due to platelet dys unction, that may require additional platelet trans usion.

ANESTHETIC CONSIDERATIONS Platelet trans usions may be appropriate in the setting o li e-threatening hemorrhage, bleeding into a closed vault, or imminent li e-saving surgery. Varying procedures require di erent platelet minima, which is largely in contention. A general guideline is as ollows: minor procedures including biopsy, catheter insertions platelets should be >20,000– 30,000/µL. Major surgeries may require platelet counts >50,000–100,000/µL to limit major bleeding. Generally, one unit o apheresis platelets should increase the platelet count by approximately 50,000/µL or a 70 kg adult patient assuming no increased destruction or alloimmunization. It is important to note that spontaneous bleeding may occur at less than 10,000–15,000/µL.

97 C

Congenital and Acquired Factor Def ciencies Vinh Nguyen, DO

Hemostasis relies on an intact coagulation cascade or adequate clotting. Any disruption or de ciencies in the cascade can lead to severe and devastating clinical complications. T e classic plasma-mediated hemostasis has been depicted as two independent pathways—the intrinsic and extrinsic pathways. ogether, they will lead into a common pathway to generate thrombin and ultimately brin monomers or clotting. issue actor-initiated coagulation has three phases: initiation phase, ampli cation phase, and a propagation phase. T e extrinsic pathway is recognized as the initiating phase to generate small amount o thrombin through the release o tissue actor. T e ampli cation and propagation phase is due to the small amount o generated thrombin rom the extrinsic pathway to activate important actors o the intrinsic pathway to increase thrombin production. Ultimately, the byproduct o these two pathways leads to the activation o brinogen to produce hemostasis.

CONGENITAL FACTOR DEFICIENCIES Factor VIII Def ciency T e most common hereditary de ciency is hemophilia A ( actor VIII de ciency) with a requency o 1:10,000 births. T e occurrence is higher or this particular blood disorder because o the X-linked recessive inheritance nature. Males are generally more a ected than emales. Most commonly, patient may present with hematuria, hemarthroses, or spontaneous hemorrhage. T e severity o hemophilia A depends on the level o actor VIII represented by the type o mutation. Levels as low as 1%–5% o normal are adequate to reduce the severity o spontaneous bleeding in joints, muscles and vital organs. In the case o a major surgical procedure, actor VIII levels must be elevated to near normal level o 100%. Since the hal -li e o actor VIII is 8–12 hours, replacement is needed twice daily in the perioperative period. T is requires the use o a actor VIII concentrate in usion and the use o monitors to measure the peak and trough levels repeatedly or the desired level. Alternatively, actor VIII replacement can be given in the orm o plasma or cryoprecipitate. Plasma contains 1 unit

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o procoagulant per milliliter, cryoprecipitate contains 5–10 U/mL, while recombinant concentrates contain up to 40 U/mL. T e exposure to plasma derivatives should be minimized and recombinant concentrates are pre erable because they do not carry in ectious risk. Postoperatively, therapy should be continued or up to 2 weeks to avoid any postoperative bleeding. For minor procedure, DDAVP may be e ective to release endogenous stores in mild hemophiliac patient. Overtime, repeated actor VIII recombinant concentrates in usion can lead to the production o actor VIII circulating inhibitors. T is occurs in 30%–40% o severe hemophiliac patients. T ere are two types o actor VIII inhibitors, low or high responders. Low responders has low titers o inhibitors thus they can be managed with higher than usual concentrates o actor VIII dosages. High responders have high titers activity and cannot be treated with actor VIII concentrates. Recombinant actor VIIa (rFVIIa) or partially activated prothrombin complex concentrates, such as actor VIII inhibitor bypass activity (FEIBA), are the most e ective therapy or these patients. Some perioperative considerations to manage hemophiliac can been seen in able 97-1.

Factor IX Def ciency Hemophilia B ( actor IX de ciency), or Christmas disease, is the second most common hemophiliac disorder with a requency o 1:30,000 male births. T e gene is associated with the X-linked sex chromosome a ecting males more than emales. Hemophilia B has a similar clinical disease spectrum resembling hemophilia A. Severe bleeding is associated with actor IX levels o less than 1% normal, whereas moderate disease is seen with 1%–5% o actor IX and mild disease is greater than 5%. Perioperative management is no di erent than hemophilia A. Hematologist consultation is needed to replace actor IX to near 100% activity level using actor IX recombinant concentrates. T e concentrates need to be continued postoperative or up to 2 weeks. Since its hal -li e is longer than actor VIII, 18–24 hours, longer therapy interval compared to hemophilia A is su cient to keep actor IX plasma level above 50%. 363

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TABLE 97-1

coagulation testing (prothrombin or partial thromboplastin time) can help detect abnormal bleeding disorders. T ese coagulation tests are nonspeci c and a more con rmatory laboratory test using a modi ed P assay or that speci c actor de cient plasma is warranted. T e best overall treatment or these disorders is to give speci c manu actural actor concentrates. Although resh rozen plasma (FFP) can be given to all actor de ciencies patients, it is considered a second-line therapy due to the potential in ectious transmission risk. Since actor V concentrate is not commercially available, FFP is recommended as the rst line treatment or actor V-de cient patients. Other plasma derivatives such as cryoprecipitate concentrates can be speci cally used or brinogen and actor XIII de ciency, while platelets concentrates can be used as an alternative or Factor V de ciency. For minor procedures, certain actor de ciencies will bene t rom anti brinoytic or DDAVP administration.

Perioperative Concerns or Patients with Hemophilia Preoperative considerations • Consultation with hematologist to establish the correct diagnosis • Check actors levels and determine treatment plan, including use o desmopressin or concentrates actor • Consider staging procedure to reduce actor exposure • Eliminate any use o platelet-inhibiting medications (ASA, clopiderol) Intraoperative considerations • Judicious use o regional anesthesia, intramuscular medications, NGT, nasal intubation, and other procedure that may increase bleeding • Limit medications that can increase bleeding (i.e., ketorolac) • Follow coagulation prof les, especially actor-def cient proteins • May need additional actor concentrates to treat bleeding • Alternatively, may need blood products to treat bleeding in severe cases • Consider recombinant activated actor VII or uncontrolled bleeding Postoperative considerations • Continue actor concentrates or specif c time as recommended by the hematologist • Ensure availability o blood products and actors rom the blood bank • Anticipate and treat bleeding episodes

ACQUIRED FACTOR DEFICIENCIES Acquired coagulation disorders are seen more of en than inherited disorders in clinical practice ( able 97-3). Most common bleeding problems can stem rom vitamin K de ciency, liver disease, disseminated intravascular coagulation (DIC), and overdosing o anticoagulants. Other less common acquired bleeding diathesis disorders include malignancy, drug-induced, or autoimmune disease. Patients with end-stage liver disease lack the necessary production o procoagulants or hemostasis. Vitamin K-dependent actors

Other Congenital Def ciencies Beside the X-linked de ciencies, other rare congenital actor de ciencies have been identi ed ( able 97-2). T ese disorders have an autosomal inheritance pattern and may clinically present with severe or asymptomatic bleeding. Routine

TABLE 97-2

Rare Coagulation De iciency Characteristics and Treatment Considerations

Autosomal Inheritance Pattern

Coagulation Factors

De iciency State Name

Fibrinogen

Af brino-genemia

Recessive or dominant

Prothrombin

Hypoprothrominemia

Factor V

Bleeding Diathesis in Severe De iciency

Screening Tests in De iciency

Blood Product Treatment

Recombinant Concentrate

Min Plasma Level Required or Hemostasis

Min Plasma Level Required or Surgery

PTT

Severe

éçè

CRYO or FFP

RiaSTAP (CSL Behring)

50 mg/dL

100 mg/dL

Recessive

Severe

FFP

PCC

~5%

30%

Parahemophilia

Recessive

Moderate to severe

FFP or PLATELETS

None

~10%

25%

Factor VII

Serum prothrombin conversion accelerator def ciency

Recessive

Moderate to severe

çè

FFP

NovoSeven PCC

5%–10%

15%–25%

Factor X

Stuart–Prower actor def ciency

Recessive

Severe

éçè

FFP

PCC actor X concentrate

~10%

25%–40%

Factor XI

Hemophilia C

Recessive or dominant

Asymptomatic to moderate

çè

FFP

HEMOLEVEN actor XI concentrate

15%

30%–40%

Factor XIII

Fibrin stabilizing actor def ciency

Recessive

Severe

çè

CRYO or FFP

Cori act recombinant actor XIII

1%–2%

20%–50%

CHAPTER 97

TABLE 97-3

Acquired Factor De iciencies

Disseminated intravascular coagulation (DIC) Dilution o procoagulants Massive blood trans usions Liver disease Vitamin K def ciency (a) Malabsorption (sprue, celiac disease) (b) Vitamin antagonist therapy (war arin) (c) Biliary obstruction Newborn Malignancy Drug-induced therapy (Penicillin) Pregnancy Inhibition o coagulation (a) Specif c inhibitors, or example, antibodies against actor VIII (b) Non-specif c inhibitors, or example, antibodies ound in some autoimmune (systemic lupus erythematosis, rheumatoid arthritis)

Congenital and Acquired Factor De ciencies

365

(II, VII, IX, X) can be eliminated through malabsorption, biliary obstruction, or oral anticoagulants. DIC causes a consumption o coagulation actors and platelets alongside intravascular deposits o brin. T ese changes will result in abnormal bleeding and widespread thrombosis. Some patients may develop bleeding syndrome associated with circulating antibodies against actor VIII or other clotting actors. T is can occur in systemic lupus erythematosus (SLE), postpartum or malignancy patients.

98 C

Disseminated Intravascular Coagulation Christopher Potestio, MD, and Vinh Nguyen, DO

Disseminated intravascular coagulation (DIC) is a disease process in which the entire coagulation pathway undergoes activation. All critically ill patients undergo some degree o coagulation activation due to in ammation and hemodynamic changes. In some cases, the balance o anticoagulations and procoagulants is tipped in avor o procoagulants, leading to DIC. No single laboratory test de nes DIC, and there is no gold standard or diagnosis. Laboratory assays allow practitioners to de ne the state o the disease and assess the risk o bleeding and thrombosis. able 98-1 lists laboratory values that assist in the diagnosis and management o DIC. T e International Society o T rombosis and Haemostasis has devised a diagnostic algorithm or DIC (Figure 98-1). A score o 5 or more carries a 93% sensitivity and 98% speci icity or development o acute DIC. he scoring system also correlates with severity and can predict mortality in patients with sepsis. It is important to recognize, diagnose, trend, and treat DIC because clinical studies suggest an increased risk o morbidity and mortality associated

TABLE 98-1

E R

with its diagnosis—this is how DIC has earned the alias “Death is Coming.”

LABORATORY STUDIES DIC is a microangiopathic hemolytic anemia, so one may also nd the classic schistocytes on peripheral smear. T romboelastogram ( EG) analysis is a use ul tool or assessing the progress o acute DIC. T ere are two classic EG results or a patient with DIC. “Early” DIC will yield a shortened reaction plus clotting time (R + K time) and shortened lysis time (L time) due to the hypercoaguable state. “Late” DIC occurs a er consumption o coagulation actors and yields a long R + K time and decreased maximum amplitude (mA) due to a decrease in platelets (Figure 98-2). rending laboratory values (e.g., every 2 hours) allows the practitioner to estimate the trajectory o the disease and predict impending complications. In acute DIC, repeated measures o coagulation show progression o thrombocytopenia and hypo brinogenemia with

Laboratory Test in the Diagnosis and Management of DIC Confounding Physiologic State

Laboratory Test

System Tested

Acute DIC

Chronic DIC

Activated partial thromboplastin time (aPTT)

Coagulation (intrinsic pathway)

Increased

Normal

Liver disease, anticoagulant therapy

Prothrombin time

Coagulation (extrinsic pathway)

Increased

Normal

Liver disease, anticoagulant therapy

Speci c coagulation actors

Coagulation (intrinsic/extrinsic pathway)

Decreased

Normal

Hemophilia

Platelet count

platelet number (not unction)

Decreased

Increased/decreased

Splenomegaly, sepsis

Fibrin split products

Fibrin Degradation

Increased

Pulmonary embolism

D-dimer

Fibrin Degradation

Increased

Pulmonary embolism

Antithrombin III

Intrinsic anticoagulation

Decreased

Increased/decreased

Protein C

Intrinsic anticoagulation

Decreased

Increased/decreased

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Ris k a s s e s s me nt: Doe s the pa tie nt have a unde rlying dis orde r known to be a s s ocia te d with ove rt DIC? If ye s : p roc e e d ; if no: d o not us e this a lg orithm;

2. Orde r globa l coa gula tion te s ts (pla te le t count, prothrombin time [P T], fibrinoge n, s oluble fibrin monome rs or fibrin de gra da tion products )

3. S core globa l coa gula tion te s t re s ults •

pla te le t count (>100 = 0; 6 s e c = 2)

•

Fibrinoge n leve l (< 1.0 g /L = 0; < 1.0 g /L = 1)

4. Ca lcula te s core

5. If ≥ 5: compa tible with ove rt DIC; re pe a t s coring da ily If < 5: s ugge s tive (not a ffirma tive ) for non-ove rt DIC; re pe a t next 1–2 days ;

FIGURE 98-1

Algorithm or the diagnosis o DIC. (Reproduced with permission rom Taylor FB Jr, Toh CH, Hoots WK, et al. Towards de nition, clinical and laboratory criteria, and a scoring system or disseminated intravascular coagulation. Thromb Haemost. 2001 Nov;86(5):1327-1330.)

increasing prolongation o P and increased levels o split products.

brin

PATHOPHYSIOLOGY Exact pathophysiology o DIC depends on the causative condition, but it can be boiled down to activation o thrombin generation and inhibition o brinolysis—an imbalance o the coagulation system. T is imbalance is the result o a three-part mechanism, described below: 1. Exposure o tissue actor leads to activation o coagulation cascade—Initiation o coagulation and thrombin generation is mediated through exposure o tissue

“Ea rly” DIC

“La te” DIC

FIGURE 98-2

Characteristic thromboelastogram analysis or “early” and “late” DIC.

actor ( F) and activated actor 7a (aVII). F and aVII are exposed due to vascular injury, expression on neoplastic cells, or release o proin ammatory cytokines such as IL-6. Cytokines, themselves, cause vascular microinjury, which leads to additional exposure o F and propagates a cycle o coagulation and vascular injury. Cytokines that most readily activate the coagulation system in DIC are NFalpha, IL1, and IL6. 2. Prolonged activation o coagulation cascade leads to loss o anticoagulants—T e longer this unchecked coagulation lasts, the more it depletes endogenous anticoagulants like anti-thrombin III (A 3), protein C, and tissue actor pathway inhibito ( FPI). In DIC, all natural anticoagulant pathways appear to be impaired due to a combination o consumption, degradation by elastase or activated neutrophils, and decreased synthesis. 3. Prolonged activation o coagulation leads to inappropriate release o plasminogen activator inhibitor-1, which inhibits the f brinolytic system—T is prolonged cycle o tissue injury and coagulation leads to inappropriate sustained release o plasminogen activator inhibitor-1 (PAI-1), leading to increase in circulating levels. PAI-1 is the main inhibitor o the brinolytic system. Its release leads to the progression o vascular microthrombi. issue actor leads to excess coagulation which causes a decrease in anticoagulation (A 3) and decrease in brinolysis (PAI-1).

CHAP ER 98

1. Acute orm—DIC occurs acutely ollowing any one o the causes listed above. T ree major mechanisms trigger DIC: the release o tissue actor/ actor VIIa to the extrinsic pathway o coagulation, widespread injury to the endothelium, and phospholipid exposure. 2. Chronic orm—Other than the typical DIC picture, DIC can be observed in association with chronic progressive diseases such as certain types o malignancies (especially mucin-producing adenocarcinomas and acute promyelocytic leukemias) where it is merely a laboratory phenomenon. In these chronic disease states, DIC will only lead to signi cant bleeding in exceptional cases such as acute promyelocytic leukemia and acute myeloblastic leukemia (M3 subtype). Chronic DIC states are identi ed by relatively normal coagulation studies and elevated concentration o brin and brinogen degradation products.

PREVALENCE AND ASSOCIATIONS DIC is estimated to be present in 1.72% o hospitalized patients. It is always associated with in ection, in ammation, or malignancy. A number o other conditions can increase the risk o DIC ( able 98-2). It is estimated that 1%–5% o all chronic disease states such as solid tumors and aortic aneurysms are complicated by DIC. Any in ammatory state can precipitate either acute or chronic DIC, but malignancy is particularly associated with the chronic orm o the disease. Some o the commonly associated diseases are as ollows: •

Sepsis—DIC occurs in 30%–50% o patients with sepsis regardless o underlying bacteremia, viremia, ungemia, and protozoemia. During sepsis, hemorrhagic necrosis to the skin over extremities and buttocks is known as purpura fulminans, and is a poor prognostic indicator.

TABLE 98-2

Clinical Conditions Commonly Complicated by DIC Obstetric

ICU Setting

Miscellaneous

Amniotic f uid embolism

Sepsis/severe in ection

Malignancy (usually chronic DIC)

Abrupto placentae

Trauma/burns/ heatstroke

Aortic aneurysms

HELLP syndrome

Severe allergic reactions/ trans usion reactions

Other vascular mal ormations

Preeclampsia, eclampsia

Hypovolemic shock

Retained products o conception, molar pregnancy

TTP, intravascular hemolysis

•

Disseminated Intravascular Coagulation

369

rauma/burns—Extensive exposure to damaged tissue leads to large amount o F introduced to circulation. As described above, F exposure leads to imbalance o the coagulation cascade and DIC. Placental abruption—Large amounts o F introduced into circulation rom damaged placenta and uterus. Amniotic uid has been shown to activate coagulation in vitro, and the degree o placental separation correlates with the extent o DIC, suggesting that leakage o thromboplastin-like material rom the placental system is responsible. en percent o placental abruption are associated with DIC (Levi). Malignancy—Solid tumor cells express dif erent procoagulant molecules including F and cancer procoagulant (a cysteine protease with actor X activating properties).

CLINICAL MANIFESTATIONS T e clinical mani estation o DIC is varied but can be grouped into two major categories: bleeding and thromboembolism. Bleeding is much more common and can lead to hypovolemic shock (14%). T romboembolism is less common but carries the risk o multiorgan dys unction. •

•

Bleeding—DIC most o en leads to bleeding by consumption o clotting actors, platelets. DIC with severe thrombocytopenia or low A 3 levels is a poor diagnostic indicator or hospital mortality. T rombocytopenia is also an independent risk o morbidity/mortality in ICU. Hypovolemic shock and massive bleeding typically occurs only when platelet counts are less than 50,000. T romboembolism—Arterial and venous thromboembolisms are concerning in patients with overt DIC, as it leads to multi-organ dys unction syndrome (MODS). Multiple organ dys unction seems to be associated with obstruction o the microcirculation by brin and the agglutination o platelets and neutrophils. Complex pathophysiology that connects DIC and MODS remains unclear.

Kidneys and lungs are particularly vulnerable to ischemia rom microthrombi, which is why acute renal ailure (25%) and respiratory dys unction (16%) are among the most common clinical mani estations o DIC.

TREATMENT T e rst and most important step in treatment o DIC is ef ective treatment o underlying disorder. Establishment o hemodynamic stability (especially or patients with MODS) allows or a ocus on the management o coagulopathy. Supporting coagulation by administration o resh rozen plasma (FFP) or platelets may be bene cial, although there is concern or worsening the DIC process. T e current recommendations are as ollows:

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•

• • •

•

PAR III Organ-Based Advanced Sciences

Administer platelets i º platelet count is less than 50,000 and active bleeding or invasive procedure º platelet count is less than 20,000 and high risk o bleeding Administer FFP i º INR > 1.5 brinogen < 1.5 and active bleeding º Administer cryoprecipitate i º active bleeding despite FFP with persistent hypo brinogenemia Prothrombin complex concentrate (PCC) may inhibit urther bleeding i none o the above measures are success ul

•

Special considerations:

•

Prophylaxis or patients with abnormal laboratory ndings is not necessary. (discuss trans usion threshold, active bleeding, procedure, etc.) FFP is mainstay, but large volumes are needed to correct coagulopathy (10–15 mL/kg). rFVIIa and prothrombin complex concentrate can be used i volume is a concern, but can lead to progressive thrombosis in patients with severe DIC. Speci c actors are recommended or actor de ciency.

•

Cryoprecipitate contains use ul actors VIII, XIII, vW , brinogen, and rbrinonectin. In addition, a low volume o cryoprecipitate may be bene cial in the setting o respiratory dys unction in an otherwise hemodynamically stable patient. Antithrombin-3 (A 3) and activated protein C (APC) have shown improvement in animal models o DIC. However, replacement is a controversial topic at this time and shows mixed results in septic patients with MODS, so it should be avoided and studied urther. Most guidelines recommend against the use o anti brinolytic agents, such as gamma aminocaproic acid and tranexamic acid. T ese drugs block already suppressed brinolysis and may urther compromise tissue per usion. Anticoagulation with heparin of ers no signi cant survival bene t, although it has been studied in several large trials. Anticoagulatin has the potential or catastrophic thrombotic complications, so is generally avoided. T at said, i the risk o bleeding is low and the patient has purpura ulminans, aortic aneurysm, or metastatic carcinoma, heparin administration is generally accepted due to bene t outweighing the risk.

99 C

Fibrinolysis Raj Parekh, MD, and Vinh Nguyen, DO

Fibrinolysis is a biological process that aims to degrade clot ormation. T is is done in balance with coagulation, which aims to induce clot ormation. Many pathologic conditions occur when the balance between these two systems is altered, usually leading to the extremes o their respective purposes, that is, severe bleeding or severe clotting. On the other hand, coagulation, or clotting, is the process in which blood transitions rom a liquid state to gel, leading to hemostasis. T is is usually done when the endothelium tissue su ers an injury. Coagulation prevents bleeding and activates the repair system o cells. Coagulation is executed by platelet aggregation and brin ormation. Fibrin is ormed via two pathways: tissue actor pathway (extrinsic) and contact activation pathway (intrinsic). Both pathways rely on series o coagulation actors that work in synchrony to eventually activate brin at the necessary site within the vasculature. Factor X is the coagulation actor that unites both pathways onto a common pathway to ultimately convert prothrombin into activated thrombin. In turn, thrombin is now active and converts brinogen into brin. Fibrin then auto-polymerizes into several brin strands to stabilize the clot ormation, with the aid o platelet aggregation.

E R

Plasmin continues to cleave brin into FDP, thus degrading the clot, until other proteases begin inactivating plasmin. T ese enzymes include alpha 2-macroglobulin and alpha 2-antiplasmin. Both enzymes are produced and secreted by the liver. Interestingly, alpha 2-macroglobulin also inhibits thrombin as well. Aside rom the t-PA and u-PA activation o plasmin, there are several other endothelial molecules that aid in promoting an anticoagulant state within the body. Some o these molecules include prostacyclin and nitric oxide. Both are well known to act as power ul endothelial vasodilators; however, they also appear to play a role in preventing coagulation by opposing the e ects o thromboxane and thus preventing platelet aggregation. Antithrombin III (A III), protein C, and protein S are proteins that unction to prevent the coagulation pathways rom activating thrombin. Antithrombin inactivates thrombin ( actor IIa), thus preventing the ormation o a stable clot. Proteins C and S both aid in inhibiting actor V and VIII o the coagulation pathway. De ciencies o any o these proteins, either acquired or inherited, would lead to prothrombotic state o variable severity.

PHARMACOLOGIC FIBRINOLYSIS PHYSIOLOGY OF FIBRINOLYSIS Once a stable clot is ormed within the vasculature, the balance can begin to shi towards stimulation o brinolysis. Plasminogen is released rom the liver, where it is produced, and imbeds itsel into the stable clot. Even though plasminogen can bind to the clot, it is unable to cleave it until it is converted into plasmin. Over several days during the clot li espan, damaged endothelium begins to secrete urinary plasminogen activator (also re erred to as u-PA or urokinase) and tissue plasminogen activator (t-PA). T ese two enzymes convert plasminogen into its active orm, plasmin. Plasmin then degrades brin into brin degradation products (FDP). A positive eedback loop ensues as FDP leads to urther upregulation o urokinase and t-PA. However, both enzymes, u-PA and t-PA, are inhibited by plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) (Figure 99-1).

Myocardial Infarction T e use o brinolytics (or thrombolytics) has become one o the oundations o treatment in patients su ering rom S elevation myocardial in arction (S EMI). T is is particularly true in areas where percutaneous coronary intervention is not readily available. T e quicker patients receive brinolytic therapy, the higher the survival rates. Highest survival rates occur when the brinolytic agent is given within 4 hours o symptom onset and survival rates are especially high i given within 70 minutes. Several studies have shown a bene t o thrombolytic therapy within 12 hours o symptom onset. However, again, survival rates precipitously drop when the time between symptom onset and thrombolytic agent is administered increases. Even though brinolytic therapy has shown to be very ef cacious in treating S EMI, especially in the early onset o symptoms, early percutaneous coronary intervention 371

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PART III Organ-Based Advanced Sciences

Endo the lial c e lls

PAI-1 PAI-2

Plas mino g e n α 2 -AP

t-PA Plas min

Fibrin

S mo o th mus cle c e lls /mac ro phag es

FIGURE 99 -1

Fibrinolysis. (Reproduced with permission from Brunton L, Chabner BA, Knollmann BC, eds. Goodman &Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York, NY: McGraw-Hill Education, Inc.; 2011: Fig. 30-3.)

(PCI) per ormed by an experienced operator is still the superior treatment option or S EMI. T e common brinolytic agents used are alteplase, reteplase, and tenecteplase. Streptokinase is another popular brinolytic; however, it is not readily available in the United States. Moreover, streptokinase has shown to have a lesser survival rate than other brinolytics such as alteplase. T e drawbacks to using brinolytic agents include: early recurrence o ischemia and risk or major hemorrhagic events such intracranial hemorrhage (ICH). Absolute contraindications to using brinolytic therapy in a S EMI patient include but not limited to: previous ICH, previous stroke in the past three months, active bleeding, i aortic dissection has not been ruled out, or presence o a malignant intracranial cancer.

Cerebrovascular Accident Similar to myocardial in arction, an ischemic stroke also necessitates an immediate and e ective reper usion strategy in order to preserve and protect as much brain unction as possible. Conventional practice has held that thrombolytic therapy is bene cial i given within 3 hours o symptom onset; however, new studies have shown that there may be a bene t with giving thrombolytic therapy within 4.5 hours o symptom onset. T e thrombolytic that has been most studied and most commonly used in the clinical setting is alteplase (t-PA). Similar to S EMI, the bene ciary e ect o brinolysis in an acute stroke precipitously decline as the time between symptom onset and treatment lengthen. T e keys are early recognition o stroke-like symptoms, ruling out hemorrhagic etiology (usually diagnosed with C scan o head), assessing

patient’s comorbid risk actors, then quickly administering thrombolysis, i deemed appropriate. Once the patient with an ischemic stroke arrives in the Emergency Department, the goal is to begin thrombolytic therapy within 60 minutes o arrival. I brinolytic therapy is to be given, it is essential that the blood pressure is controlled at or below 185 mmHg systolic and at or below 110 mmHg diastolic. Intracranial hemorrhage is the most serious and o en times atal complication with administering alteplase in ischemic stroke patients. Several studies have shown that this complication rate is approximately 5%. Other complications include systemic bleeding, such as gum bleeding, and angioedema. T ese complications are rarely atal and rarely necessitate stopping treatment. Inclusion criteria or the use o alteplase include age ≥ 18 years old, clinic nding o some type o neurologic impairment suggesting acute ischemic stroke, and administering the brinolytic within 4.5 hours o symptom onset. Exclusion criteria or using alteplase in ischemic stroke are similar to S EMI exclusion criteria. T ey include but are not limited to current evidence o hemorrhage, previous history o ICH, intracranial neoplasm, active systemic bleeding, and history o stroke or head trauma in the past 3 months.

HYPERFIBRINOLYSIS Hyper brinolysis is a medical condition where there is increased and unchecked activity o the brinolytic pathway. T is leads to an unbalance between brinolysis and coagulation, thus leading to marked increased bleeding. At times, the bleeding can be severe enough to cause death. Congenital

CHAPTER 99

hyper brinolysis is rare and is usually due de ciencies in alpha 2-antiplasmin or plasminogen activator inhibitor-1 (PAI-1): •

•

PAI-1 def ciency is quite rare and only seems to mani est itsel clinically i the patient is a homozygous or the de cient gene. Heterozygote patients do not appear to have abnormal bleeding. Homozygous patients will typically present with prolonged bleeding in the post-operative phase or trauma. Clinically, emale patients may complain o menorrhagia and post-partum hemorrhage. Alpha 2-antipla smin def ciency is also a rare disorder o hyper brinolysis. For the most part, patients with the enzyme de ciency are asymptomatic. Only a er an event that causes bleeding does the patient begin showing signs o impaired coagulation. T e most common event is usually trauma leading to massive blood loss.

Fibrinolysis

373

Acquired hyper brinolysis is usually secondary to liver disease. T is occurs due to the delayed clearance o t-PA and decreased protein synthesis and alpha 2-antiplasmin. Other common causes o acquired hyper brinolysis are disseminated intravascular coagulation (DIC) and malignancy. Acquired hyper brinolysis can also occur secondary to trauma, known as trauma-induced coagulopathy ( IC). Hyper brinolysis is thought to occur here due to depletion o coagulation actors at a rate greater than brinolytic actors, dilution o blood secondary to volume repletion, and enzyme inactivation rom acidemia secondary to ischemia. Diagnosis is dif cult to elucidate due to the act that many o the biomarkers o hyper brinolysis are nonspeci c and can be elevated in many other conditions. D-dimer, a product o brin degradation, and t-PA have increased activity in hyper brinolysis.

100 C

Hemoglobinopathies Vinh Nguyen, DO

T e red blood cell is a vehicle that utilizes hemoglobin to acilitate the delivery o oxygen to vital organs or tissue. Hemoglobin is a tetrameric protein composed o two α- and two β-molecules. Hemoglobinopathies are a result o various types o mutation within either the α or β genes. T is mutation a ects transcription, translation, and ultimately protein ormation. T e mutated globin proteins lead to the lack o production, deletion, or dys unctional hemoglobin subunits.

SICKLE CELL DISEASE Sickle cell disease (SCD), or hemoglobin S (HbS), is the most common inherited hemoglobinopathy. T e genetic mutation occurs at the sixth amino acid position o the β-chain. Glutamic acid, a negatively charged amino acid, is substituted or valine, a nonpolar amino acid. T e loss o a negative charge group produces radical change, compromising the integrity o the hemoglobin structure causing instability and rapid degradation. In a low oxygen environment, HbS polymerizes, becomes insoluble, and orms a precipitate. Furthermore, the accelerated hemoglobin breakdown causes extensive cell membrane damage and dehydration. As a result, the shape o the red cell morphs to the characteristic “sickle” appearance. T e second consequence o sickling causes a widespread vascular in ammation. T e instability o the HbS releases iron into the circulation causing direct oxidative cell membrane damage locally and systemically. T e circulating iron binds to endogenous nitric oxide (NO), thus consuming ree nitric oxide and impairing normal physiologic transport o nitric oxide by erythrocytes. T is chronic hemolysis will lead to a chronic state o NO de ciency and in ammatory vasculopathy. T e clinical eatures o SCD are one o evolving organ damage. It can a ect multiple di erent organs su ering early organ dys unction and death ( able 100-1). Pulmonary and neurologic diseases are the leading causes o morbidity and mortality but chronic renal ailure can be an additional contributing actor. Pain crises or vasoocclusive crises are noted in lumbar spine, abdomen, emoral sha , and knee in the majority o the cases. Acute chest syndrome (ACS) is de ned as new pulmonary in ltrates involving at least one complete lung segment. Ultimately, ACS will lead to chronic progressive

E R

lung damage. It may start as airway hyperreactivity to brosis and progressive restrictive de ect. Stoke in SCD can be due to hemorrhage due to chronic damaged and weakened arteries, whereas in arction is secondary to intimal hyperplasia and progressive occlusion o large and small arteries. Nephropathies include papillary necrosis and glomerular disease. As a result, these potential organs damage can lead to devastating complications and debilitation. T e anesthetic management o SCD patient relies on adequate perioperative screening, vigilant intraoperative management, and avoiding precipitating actors postoperatively. T e incidence o an acute sickle cell exacerbation has been examined base on the type o procedure, patient age and preexisting actors. Exacerbation was commonly observed in 0% or tonsillectomy, 2.9% or hip surgery, 3.9% or myringotomy, 7.8% or intra-abdominal nonobstetric surgery, 16.9% or cesarean section and hysterectomy, and 18.6% or dilation and curettage. Perioperative management depends on an adequate history to establish speci c organ damage and requency and

TABLE 100-1

Clinical Features of Sickle Cell Anemia

Complications Neurological • Pain crisis • Stroke • Proli erative retinopathy • Peripheral neuropathy • Chronic pain syndrome

Genitourinary • Chronic renal insu ciency • Urinary tract in ection • Priapism • Hyposthenuria • Pregnancy

Pulmonary • Acute chest syndrome • Airway hyperreactivity • Restrictive lung disease

Gastrointestinal • Cholelithiasis • Liver disease • Dyspepsia

Hematological Hemolytic anemia Acute aplastic anemia Splenic enlargement/ brosis

Immunological • Immune dys unction • Erythrocyte auto/ alloimmunization • Hemolytic trans usion reactions

Orthopedic • Osteonecrosis • Dactylitis • Osteomyelitis

Vascular • Leg ulcers

375

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PART III Organ-Based Advanced Sciences

TABLE 100 -2

Guideline for the Use of Perioperative Prophylactic Erythrocyte Transfusion

Transfusion Goal

Low Perioperative

Moderate Perioperative

Hematocrit 180

ANESTHETIC INDUCTION Smooth induction o general anesthesia is crucial or these patients. A preoperative arterial line is placed under local anesthesia to acutely assess and address blood pressure swings. Premedications may be given to acilitate invasive line placement and patient com ort. Nitroglycerin, nitroprusside, phentolamine, and a variety o beta-blockers should be available. Any medications that may provoke a histamine or

catecholamine release like ketamine, atracurium, or morphine should be avoided. Once standard monitors are placed and adequate preoxygenation achieved, propo ol, rocuronium, and entanyl may be used to acilitate intubation. Etomidate while providing a cardiovascularly stable induction causes pain on injection and myoclonus both o which may cause a catecholamine surge. Succinycholine while providing a rapid relaxation may cause generalized asciculations that may unintentionally squeeze the tumor. Once the patient is asleep, a lidocaine spray may be considered to reduce the reaction to endotracheal tube placement. I the patient is amenable, central access should be placed prior to induction. However, i the patient is unable to tolerate it, central access should be placed immediately a er induction. T e central line will help with volume resuscitation and provide a route or the vasoactive in usions. At least two large bore IVs should be placed in addition to a central access. With chronic sympathetic stimulation, these patients have a near-complete inhibition o the renin, angiotensin, aldosterone cascade. As such, they constantly diurese, causing a volume contracted state. T ese patients require strict electrolyte corrections during and a er an adrenalectomy.

INTRAOPERATIVE MANAGEMENT Close communication with the surgeon is essential during the dissection o the tumor. Minimal mechanical stimuli to the adrenal masses may trigger catecholamine surges. o avoid unexpected or prolonged elevations in blood pressure, the surgeon needs to communicate when they are manipulating the tumor. T e anesthesiologist should preemptively treat these anticipated manipulations with short-acting medications. It is critical to maintain euvolemia while monitoring the volume status o the patient. T ese patients will o en present with decreased intravascular volumes due to chronic diuresis. Furthermore, with an inhibition o the sympathetic tone by anesthetic agents, pro ound drops in blood pressure are also possible. Colloid volume expanders such as albumin should be available or this purpose. However, these expanders should be held until a er the adrenal gland is ligated. Arterial blood gases should be ollowed regularly or several reasons. T ey will identi y any instances o underper usion with elevated lactate levels. Glucose levels may f uctuate with catecholamine surges and need to be treated to avoid prolonged hyperglycemic periods. Electrolytes should be ollowed and idealized, as dysrhythmias are o en already present. A er the dissection is complete, the adrenal veins are ligated. T is cuts o the supply o catecholamines to the systemic circulation and can result in a sudden hypotension. A moderate f uid bolus can be given or this hypotension. I a signi cant amount o blood has been lost during the dissection, blood products could be substituted or albumin.

CHAPTER 111

A continuous in usion o phenylephrine or norepinephrine is o en needed at this point to maintain an adequate blood pressure.

POSTOPERATIVE MANAGEMENT T ree main complications persist in the postoperative period: hypertension, hypotension, and hypoglycemia. Paradoxically, even with the decrease in catecholamine supply, up to 50% o patients may experience hypertension or a ew days a er the surgery. T is hypertension rom residual catecholamine levels must be di erentiated rom that caused by residual adrenal tissue. T is can be achieved with ollow-up tests. Most patients receive a ollow-up urine test 1–2 weeks a er the surgery. I the levels are normal, the resection is considered complete and the patient has yearly checks. Longterm beta-blockade used be ore the surgery should be tapered

Pheochromocytoma

413

o slowly to avoid a severe rebound hypertension episode. I the urine tests are positive, then the patient needs to be reimaged via C and MRI to assess or the presence o residual adrenal tissue. Persistent hypotension a er the surgery should be considered care ully. Although the most likely cause is the sudden drop in sympathetic tone, surgical bleeding should be considered in the immediate postoperative period. Serial CBC checks and CVP measurements should help distinguish between hypovolemia rom bleeding and the expected postadrenalectomy decrease in sympathetic tone. In either situation, vasopressor support will be required. Hypoglycemia results rom an increase in insulin levels. Catecholamines are responsible or suppressing pancreatic beta-cell activity, and with their sudden absence, the pancreatic cells produce an excess o insulin. T is insulin increase is exacerbated by a decrease in lipolysis and glycogenolysis rom the absence o alpha adrenergic activity.

112 C

Carcinoid Syndrome Michael J. Berrigan, PhD, MD

Carcinoid tumors are slow-growing neoplasms arising rom enterochroma n cells. Because they originate rom neuroendocrine cells, they are capable o secreting vasoactive substances, notably serotonin, kinin peptides, and histamine. I these substances reach the systemic circulation in su cient quantity, they may produce the “carcinoid syndrome” which has important rami cations to the anesthesiologist.

PATHOPHYSIOLOGY T e tumors arise rom di erent embryonic divisions o the gut and their classi cation is based on the site o origin and histological characteristics. T e sites are o en the gastrointestinal tract (68%) and the bronchopulmonary system (25%). T e amount o a metabolite o serotonin, 5-hydroxyindoleacetic acid (5-HIAA), in a 24-hour urine collection provides a measurement o the disease process. T is test is highly speci c, but has a sensitivity o 73%. Another marker o disease progression is the level o serum chromagra n A. T e 5-year survival o patients with no metastases is approximately 71%; however, this is reduced to 38% in those patients with metastases. Only a small subset (10%) o patients with a carcinoid tumor will develop the carcinoid syndrome. T is is explained by the ability o the liver to metabolize the tumor’s secreted vasoactive substances. Vasoactive substances secreted by tumors in the gut will pass through the liver via the hepatic portal vein and be metabolized be ore they can reach the systemic circulation. However, tumors arising in other locations, or those that originate in the liver (or liver metastases), can produce important systemic e ects. T e most requent clinical eatures are cutaneous f ushing and intestinal hypermotility (which may lead to dehydration and metabolic acidosis). Approximately 18% o patients with carcinoid syndrome may exhibit wheezing. Carcinoid heart disease occurs in about two-thirds o patients with carcinoid syndrome and is associated with perioperative complications. T e right heart is typically a ected and exhibits a thickened endocardium with mixed tricuspid and pulmonary valve disease. A severe mani estation o the syndrome, “carcinoid crisis,” is characterized by hemodynamic instability, bronchospasm, and pro ound f ushing.

E R

ANESTHETIC MANAGEMENT T e two greatest areas o concern in the perioperative care o these patients are as ollows: 1. Complications related to carcinoid heart disease 2. Potential or unpredictable vasoactive substance release T e severity o preoperative symptoms does not predict the severity o intraoperative complications. Likewise, the levels o 5-HIAA, although ref ecting disease progression, do not reliably predict the incidence o intraoperative events. A cardiovascular history and examination should ocus on the possibility o the presence o right or biventricular heart ailure. Signs and symptoms o reduced exercise tolerance, orthopnea, paroxysmal dyspnea, and peripheral edema should be investigated. Excessive uncontrolled release o vasoactive substances may occur in response to anesthetic or surgical stimuli and hemodynamic variation. T e possibility o either hypotension or hypertension exists, leading to hemodynamic instability. Importantly, hemodynamic collapse may be unresponsive to conventional therapy with inotropes and pressors. Indeed, catecholamine administration may stimulate vasoactive substance secretion causing a paradoxical worsening o hypotension. It is important that tumor “activity” is decreased prior to surgery because o the increased risk o uncontrolled vasoactive substance release during surgical manipulation. T is can be achieved by the administration o octreotide. Octreotide is a synthetic analog o somatostatin that blocks hormonal release and inhibits the action o circulating peptides. Its hal li e is 1.5–2 hours given subcutaneously and 50 minutes given intravenously, much longer than somatostatin’s hal -li e o 1–3 minutes. Important side e ects are Q prolongation, gastrointestinal upset, and bradycardia. Various regimens or preoperative octreotide have been reported. One regimen, or example, suggests giving octreotide 100 mcg subcutaneously three times a day or 2 weeks preoperatively and 100 mcg be ore induction o anesthesia. Even with pretreatment, it is di cult to predict intraoperative carcinoid events; additional 415

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octreotide doses o 50–200 mcg IV have been e ective in reversing severe hypotension and bronchospasm. In addition to standard monitors, it is prudent to place an arterial line prior to anesthetic induction. Care should be taken to suppress the sympathetic response to induction and intubation, but hypotension needs to be avoided. T e use o succinylcholine has been debated (because o increased intraabdominal pressure), but it has been used without adverse e ects. Opioids are not associated with increased substance release. Close and clear communication with the surgeon is important. Should manipulation o the tumor cause hemodynamic instability, the surgeon should cease the manipulation

until the instability is corrected. Bronchospasm is less common than cardiovascular events; however, when it occurs, it may be severe and resistant to treatment. Beta-adrenergic receptor agonists may increase substance release and worsen the bronchospasm. Again, octreotide is use ul in this situation.

SUGGESTED READING Mancuso K, et al. Carcinoid syndrome and perioperative anesthetic considerations. J Clin Anesth. 2011;23:329–341.

113 C

Diabetes Mellitus Matthew deJesus, MD

Diabetes mellitus is an endocrinologic disorder in which carbohydrate metabolism is compromised by either reduced insulin production or sensitivity, resulting in hyperglycemia. In 2013 there were 382 million estimated cases o diabetes worldwide. ype 1 diabetes, also known as insulin-dependent diabetes mellitus (IDDM), accounts or 5%–10% o all cases. It is a chronic autoimmune disorder in which the beta cells o the pancreas are a ected, resulting in the cessation o insulin production. Exogenous insulin is the primary therapy or type 1 diabetes. Onset is typically acute. Initial symptoms due to hyperglycemia may include polydipsia, polyuria, hyperphagia, weight loss, atigue, and blurred vision. I untreated, coma rom ketoacidosis may be the diagnostic presentation. ype 2 diabetes starts as insulin resistance. Insulin production may initially increase in an attempt to overcome this resistance, but eventually it is inadequate. T erapy may include weight reduction via exercise and diet, oral hypoglycemic medications, and exogenous insulin. T e diagnosis o diabetes mellitus requires ul lling at least one o the ollowing criteria: • • • •

Fasting blood glucose > 125 mg/dL on more than one occasion Random blood glucose > 199 mg/dL along with symptoms o polyuria, polydipsia, or weight loss 75 g glucose tolerance test with a 2 h value > 199 mg/dL HA1C > 6.4 %

Prolonged hyperglycemia leads to complications associated with diabetes in two orms: microvascular and macrovascular disease processes. Microvascular complications include retinopathy, nephropathy, and neuropathy. Peripheral sensory neuropathy may lead to a propensity or oot wounds. Autonomic neuropathy can cause hemodynamic uctuations, gastroparesis, and silent cardiac ischemia. Macrovascular disease processes associated with diabetes include coronary artery disease, cerebrovascular disease, and peripheral vascular disease. Hypertension and dyslipidemia are comorbidities that requent diabetics. Nonenzymatic glycosylation o hemoglobin by plasma glucose can be quanti ed via the blood test hemoglobin

TABLE 113-1 HA1C (%)

E R

Hemoglobin A1C and Blood Glucose Average Blood Glucose (mg/dL)

5.0

6.0

120

7.0

150

8.0

180

9.0

210

10.0

240

A1C (HA1C). T e li espan o a red blood cell is approximately 90 days; thus, HA1C levels give a 90 day average o glycemic control. Higher HA1C levels correlate with a higher average blood sugar and thus more hyperglycemia complications ( able 113-1). 1. Oral hypoglycemics—T ere are seven main classes o oral hypoglycemic medications ( able 113-2). T ese medications are prescribed to type 2 diabetics, and not use ul or patients who no longer make insulin. T ey may be used in combination and with or without exogenous insulin administration. 2. Insulin—Insulin is a hormone made in the β-cells o the islets o Langerhans in the pancreas. It is released into the blood stream in response to an elevation in plasma glucose. Insulin acilitates a number o anabolic processes, including glucose uptake into muscle and adipose cells, promotion o glycogen ormation, and protein and atty acid synthesis. It inhibits catabolic processes such as gluconeogenesis, glycogenolysis, lipolysis, ketogenesis, and protein breakdown. Insulin also increases plasma potassium uptake into cells and thus can cause hypokalemia or be used in the treatment o hyperkalemia. A basal level o insulin is required to keep the body in a homeostatic metabolic state. T e average basal insulin production in an otherwise healthy adult is about 40–50 U/d, about 1 U/h, increasing 5–10 old ollowing carbohydrate ingestion. In the absence o insulin, catabolism takes precedence leading to mobilization o energy stores. I the 417

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TABLE 113-2

Oral Hypoglycemic Agents

Class

Action

Example

Biguanides

Reduces hepatic glucose output and increases insulin sensitivity

Met ormin (Glucophage)

Sul onylureas

Stimulates beta cells to secrete insulin

Glimepiride (Amaryl)

Meglitinides

Stimulates insulin release via dif erent binding site than sul onylureas

Repaglinide (Prandin)

Improve insulin sensitivity

Pioglitazone (Actos)

Alpha-glucosidase inhibitors

Delay the absorption o glucose

Acarbose (Precose)

Incretins

Analogues o GLP-1 which stimulates insulin and inhibits glucagon release

Exenatide (Byetta)

DPP-4 inhibitors

Inhibit degradation o GLP-1, leading to stimulation o insulin and reduction o glucagon secretion

Sitaglitin (Januvia)

Thiazolidinediones

DIABETIC KETOACIDOSIS

lack o insulin is prolonged, it may lead to ketogenesis, and then to ketoacidosis. T e standard insulin concentration is U100 (100 U/mL). Dosages should be checked appropriately as its high concentration can lead to dose miscalculation. All insulins can be administered subcutaneously either via bolus or via continuous subcutaneous in usion (i.e., an insulin pump). Insulin pumps typically use rapid-acting insulin to allow easier titration. Discontinuation o an insulin pump containing rapid-acting insulin can lead to acute

TABLE 113-3

Diabetic ketoacidosis (DKA) is a metabolic emergency occurring predominately in type 1 diabetics. It is typically preceded by illness, in ection, or discontinuation o insulin, leading to ketogenesis and the ormation o the ketone bodies acetoacetic acid and beta-hydroxybutyric acid. As ketones accumulate, they cause an anion gap acidosis. Elevated blood sugar will cause the patient to be polyuric and polydipsic, and may lead to pro ound dehydration and electrolyte abnormalities. Symptoms are lethargy, nausea, abdominal pain, and can progress to coma and death. Patients may have a ruity or acetone smell to their breath. ests to con rm DKA include elevated blood sugar (greater than 250 mg/dL), anion gap acidosis, and plasma or urine ketone bodies. reatment or DKA involves IV insulin in usion, IV hydration, electrolyte correction, and correction o the inciting actor. Despite a possible perceived hyperkalemia, the body may be relatively hypokalemic. As insulin is administered, plasma potassium will re-enter cells, requiring correction. Overzealous glucose correction should be avoided and most recommend glucose-containing uids once glycemic control is reasonable. In ection or dehydration in type 2 diabetics can lead to a hyperosomlar hyperglycemic state (HHS), a medical emergency similar to DKA. Blood sugar may exceed 600 mg/dL.

Exogenous Insulins

Type

Name

Brand Name

Onset *

Peak*

Duration *

Rapid acting

Lispro Aspart Glulisine

Humalog NovoLog Apidra

10–15 min

30–90 min

3–5 h

Intermediate acting

NPH (Neutral Protamine Hagedorn)

Novolin N, Humulin N

60–90 min

6–8 h

10–18 h

Short acting

Regular

Novolin R, Humulin R

30–60 min

2–4 h

4–8 h

Long acting

Glargine

Lantus

1–2 h

No peak

Up to 24 h

Detemir

Levemir

Times apply or subcutaneous administration. All times are estimates.

hyperglycemia. Regular insulin is the only type that can be administered e ectively intravenously ( able 113-3). It can be given as a bolus dose, or via IV in usion. Intravenous regular insulin has an action pro le similar to rapidacting insulin. 3. Glucagon—Glucagon is a peptide hormone produced in the pancreatic alpha cells that has e ects opposite to that o insulin: increase in gluconeogenesis, increase in glycogenolysis, and inhibiting glycogen synthesis, all resulting in the mobilization o glucose into the bloodstream.

Notes

May increase incidence o protamine reaction

May be Q12hr or Q24hr dosing

CHAPTER 113

T e high plasma glucose will act as an osmotic diuretic, urther dehydrating the patient and leading to electrolyte abnormalities. Serum osmolality will be greater than 320 mOsm/ kg. reatment o HHS is similar to DKA, and includes IV insulin in usion, IV hydration, electrolyte correction, and treating the underlying cause.

HYPOGLYCEMIA Hypoglycemia is a medical emergency and can occur secondary to excessive medication (insulin or oral agents) in relation to carbohydrate intake. It can also occur with excessive energy expenditure, such as physical exercise. Symptoms typically occur with blood sugar below 70 mg/dL and include anxiety, diaphoresis, and tachycardia, all associated with a sympathetic response. T ese symptoms may be masked by sympatholytic medications such as beta-blockers or general anesthesia. As the brain is dependent on continuous glucose, neurological symptoms can progress to con usion, neurological de cits (can mimic a stroke), seizures, coma, and death. Once again, these symptoms may be masked by general anesthesia, and patients at risk should have requent blood glucose monitoring. Hypoglycemia should be included in the di erential diagnosis o a diabetic patient with delayed emergence.

PERIOPERATIVE MANAGEMENT Preoperative evaluation should involve a history o recent glycemic control and medication administration. Asking the patient what their insulin dosage or hyperglycemia correction is help ul as patient sensitivity to insulin is variable. Discontinuation o met ormin is advisable due to the risk o lactic acidosis, especially in patients with renal impairment, hypovolemic patients, and patients receiving IV contrast. Many practitioners reduce the dose o intermediate- and longacting insulins as to avoid hypoglycemia during NPO status, and permit mild hyperglycemia. Abrupt discontinuation o

Diabetes Mellitus

419

short-acting insulin via an insulin pump can lead to aggressive hyperglycemia as these patients typically have no long-acting insulin in their system. I the choice is made to stop an insulin pump, starting an IV insulin in usion to meet their basal insulin requirement is recommended. Ideally, diabetic patients should be euglycemic, leading up to surgery as con rmed by normal asting glucose and a reasonable HA1C. Hyperglycemic patients should be evaluated or DKA/HHS, both medical emergencies, and their treatment should precede elective procedures. I a procedure is emergent, treatment o DKA should be initiated as soon as possible. Hyperglycemic patients should also be evaluated or dehydration, electrolyte abnormalities such as hyperkalemia, and underlying in ectious causes. Poorly controlled diabetics may have autonomic dysunction that can cause hemodynamic instability, especially under general anesthesia. esting positive or orthostatic hypotension can suggest autonomic dys unction. Diabetics may also have gastroparesis which may increase the potential or regurgitation and aspiration. Limited joint mobility in diabetics may lead to sti joints, making intubation via laryngoscopy dif cult. T e “prayer sign” and “tabletop test” can help to evaluate the degree o joint immobility. Intraoperative glycemic control should be ollowed with requent blood sugar checks. Insulin therapy can be either via bolus doses or via IV in usion. I bonus administration o insulin is the chosen therapy, allow the dose to reach peak levels be ore considering subsequent doses to avoid iatrogenic hypoglycemia. Diabetics may be at risk or peripheral neuropathy, so pressure points should be well padded and requently checked. Postoperative management should again ocus on euglycemia. Evidence shows that hyperglycemia inhibits woundhealing via multiple modalities, including reduced phagocytic activity. T e stress response o surgery may elevate insulin requirements. Hyperglycemia has been associated with severe head injury, and postoperative glycemic control was ound to be a predictor o outcomes.

114 C

Demyelinating Diseases Juanita M. Villalobos, MD

A demyelinating disease is any disease in which the myelin sheath o the neuron is damaged. Weakening o the transmitted electrical signal ultimately results in impairment in sensation, cognition, and movement or other unctions depending on which nerves are a ected. Classi cation o demyelinating diseases is made on the basis o whether the nerves a ected are o the central nervous system or o the peripheral nervous system ( able 114-1). T e causes o demyelinating diseases are multi actorial. Myelin destruction may be caused by autoimmune reactions (e.g., multiple sclerosis), in ammation (e.g., optic neuritis, transverse myelitis, disseminated encephalomyelitis), or in ectious agents (e.g., Creutz eldt-Jakob viral in ection o oligodendrocytes). In addition, there is a genomic component to demyelinating diseases. Inherited metabolic disorders a ect myelin synthesis/turnover; these diseases are termed leukodystrophies. Other causes o demyelinating diseases involve neuroleptics, and certain chemicals such as organophosphates. Lysophosphatidylcholine or lysolecithins, ound in oods and cosmetics with lecithin treated with the enzyme phospholipase, also cause demyelination.

TABLE 114-1

Classi ication o Demyelinating

Diseases

Central nervous system Optic neuritis Transverse myelitis Multiple sclerosis Schilder’s disease Devic’s disease (neuromyelitis optica) Vitamin B12 de ciency Central pontine myelinolysis Syphilitic myelopathy (tabes dorsalis) Leukoencephalopathies (i.e., progressive multi ocal leukoencephalopathy) Leukodystrophies Peripheral nervous system Guillain–Barré syndrome Chronic in ammatory demyelinating polyneuropathy Charcot–Marie–Tooth disease Anti-MAG peripheral neuropathy Copper de ciency

E R

CENTRAL NERVOUS SYSTEM DEMYELINATING DISEASES Optic Myelitis A condition de ned by demyelinating in ammation o the optic nerve that o en occurs in association with multiple sclerosis and Devic’s disease (neuromyelitis optica). Visual recovery begins within a ew weeks. 30% o adults develop multiple sclerosis within 5 years o presenting with optic myelitis. reatment with intravenous (IV) methylprednisolone is indicated or patients with either severe vision loss or two or more white matter lesions in MRI.

Transverse Myelitis (TM) M is a rare in ammatory disorder causing injury across both sides o one level or segment o the spinal cord, resulting in various degrees o weakness, sensory alterations, and autonomic dys unction. M usually occurs as a postin ectious complication, and presumably results rom an autoimmune process. However, M also can be associated with in ectious, systemic in ammatory, or multi ocal CNS diseases. M a ects people o all ages, with bimodal peaks at 10–19 and 30–39 years and 25% o cases in children. Approximately 70%–90% o cases are monophasic, and a small percentage experience recurrent disease i a predisposing underlying disease is present. reatment or acute idiopathic M is high-dose IV glucocorticoids, such as methylprednisolone or dexamethasone, or 3–5 days. reatment or acute M complicated by motor involvement is steroid plus plasma exchange.

Multiple Sclerosis (MS) MS is an autoimmune demyelinating disorder with a genetic predisposition characterized by distinct episodes o neurological de cits that a ect the brain and spinal cord. MS is disseminated in time attributable to white matter lesions that are separated in space. Females are twice as a ected as males. Incidence is unknown, but 15 times greater i present in rst degree relative. Disease is initiated by CD4+ h1 and h17 -cells that react against sel -myelin antigens and secrete cytokines, which activate 421

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macrophages and recruit leukocytes, the latter which is responsible or demyelination. Clinical eatures include optic neuritis, retrobulbar neuritis—unilateral visual impairment, ataxia, or nystagmus, motor and sensory impairment o trunk and limbs, spasticity, and dif culty with bladder control. reatment ocuses on strategies to minimize ares, manage symptoms, and reduce progression since no cure exists. Approved drugs used to treat attacks or relapses include teri unomide, inter eron β-1a, inter eron β-1b, glatiramer acetate, ngolimod, mitoxantrone, dimethyl umarate and natalizumab, and corticosteroids. Most o these drugs are immunosuppressive with signi cant toxicities: nephrotoxicity, hepatotoxicity, thrombocytopenia, as well as pulmonary damage. o treat symptoms, plasmapherisis, ampyra, baclo en, tizanidine, and amantadin are indicated.

Schilder’s Disease It is a rare, progressive demyelinating disorder that begins in childhood. Symptoms include dementia, aphasia, seizures, personality changes, poor attention, tremors, balance instability, incontinence, muscle weakness, headache, vomiting, and vision and speech impairment. Schilder’s disease is a variant o multiple sclerosis. reatment generally ollows established standards as with multiple sclerosis and includes corticosteroids, β-inter eron or immunosuppressive therapy, and symptomatic treatment. For some patients the disorder is progressive with a steady, unremitting course; others may experience signi cant improvement and even remission.

Malabsorption o B12 rom the small intestine, due to disease or surgical resection, is the usual cause o vitamin B12 de ciency. Vitamin B12 de ciency is also commonly caused by an autoimmune disease and results in pernicious anemia. Other causes include poor dietary intake, malabsorption syndromes, and tapeworm in ection. In addition to megaloplastic anemia, vitamin B12 de ciency also causes gastrointestinal symptoms, Hunter’s glossitis (atrophic tongue), and neurological dys unction. Neurological symptoms appear as bilateral peripheral neuropathy, gait ataxia, depression, and in some cases as psychotic symptoms. Vitamin B12 de ciency results in degeneration o the lateral and posterior columns o the spinal cord, and symmetrical paresthesias with loss o proprioceptive and vibratory sensations, especially in the lower extremities. A ected individuals have an unsteady gait with diminished deep tendon re exes. reatment is parental administration o vitamin B12.

Central Pontine Myelinolysis (CPM) CPM is a loss o myelin in the nerve cells o the brainstem (pons). T e most common cause is an abrupt change in the serum sodium levels, particularly hyponatremia that has been rapidly corrected. Risk actors include liver disease, alcoholism, and malnutrition. Symptoms are con usion, delirium, reduced alertness, dif culty swallowing, speech changes, tremor, and weakness (bilateral). T ere is no known cure, and the nerve damage caused by CPM is long-lasting and can cause serious chronic disability.

Devic’s Disease (Neuromyelitis Optica) Devic’s disease leads to the development o synchronous (or near synchronous) bilateral optic neuritis and spinal cord demyelination. wo-thirds women and one-third men are a ected, 80% o patients relapse, and generally regarded as non amilial. Neuromyelitis optica is more common in Asians than Caucasians. reatment includes a short course o highdose IV corticosteroids such as methylprednisolone. Plasmapheresis can be an e ective treatment with progressive disease or or patients who do not respond to corticosteroid treatment. Residual signs and disability may persist a er therapy, sometimes severely; 20% o patients with monophasic disease have permanent visual loss, while 30% have permanent paralysis in one or both legs. Among patients with relapsing disease, 50% have paralysis or blindness within 5 years. In some patients (30%), transverse myelitis in the cervical spinal cord results in respiratory ailure and subsequent death.

Syphilitic Myelopathy (Tabes Dorsalis) abes dorsalis, or neurosyphillis, is a mani estation o the tertiary stage o syphilis and is seen in 10% o patients with untreated in ection. abes dorsalis is also known as syphyllitic myelopathy, which is a slow degeneration resulting in demyelination o the nerves primarily in the dorsal columns o the spinal cord. T e dorsal column helps maintain proprioception, vibration, and discriminative touch. Symptoms include impaired joint position sense and resultant ataxia, loss o pain sensation causing skin and joint damage (charcot joints), and sensory disturbances. reatment is penicillin IV; associated pain can be treated with opiates, valproate, or carbamazepine plus physical therapy. Untreated tabes dorsalis can lead to paralysis, dementia, blindness.

Vitamin B12 De ciency

Progressive Multi ocal Leukoencephalopathy (PML)

Vitamin B12 is crucial or the ormation o red blood cells, as well as or the health o nerve tissue. Megaloplastic anemias are o en due to de ciencies in vitamin B12 or vitamin B9 ( olic acid). Both o these vitamins must be supplied by diet. Absorption o vitamin B12 is dependent on the glycoprotein “gastric intrinsic actor,” which is produced by the gastric parietal cell.

PML is a rare disorder that damages the myelin in the white matter in the brain. PML is caused by the Creutz eldt–Jakob (CJ) virus. Most people, generally by age 10, have been in ected with the virus but remain asymptomatic. Immunosuppressed individuals are at the greatest risk o developing PML. Symptoms include clumsiness, memory loss, vision

CHAPTER 114

problems, headaches, aphasia, loss o coordination, weakness, and sometimes personality changes. De nitive diagnosis can be made via brain biopsy or by the detection o the CJ virus in spinal uid. reatment is strengthening the immune system. PML has a 30%–50% mortality rate, and individuals that survive PML can be le with severe neurological disabilities.

Leukodystrophies T ese are rare diseases characterized by the degeneration o the white matter in the brain. T e leukodystrophies are caused by imper ect growth or development o myelin. Symptoms are progressive loss in body tone, movement, gait, speech, vision, ability to eat, hearing, and behavior. ypes include adrenoleukodystrophy, metachromatic leukodystrophy, adrenomyeloneuropathy, and hereditary CNS demyelinating diseases: Krabbe disease, Pelizaeus–Merzbacher disease, Canavan disease, leukoencephalopathy with vanishing white matter, also known as childhood ataxia with CNS hypomyelination (CACH), and Alexander disease. Re sum disease and cerebrotendineous xanthomatosis are additional types.

PERIPHERAL NERVOUS SYSTEM DEMYELINATING DISEASES Guillain–Barré Syndrome (GBS) GBS, also known as acute idiopathic polyneuritis or acute in ammatory polyneuropathy, is a disorder in which the body’s immune system develops an immunological reaction against peripheral nerves. It usually presents several weeks a er a relative benign respiratory or gastrointestinal illness with complaints o proximal muscle weakness o the lower extremities. T e weakness progresses to involve the arms, truncal muscles, cranial nerves, and muscles o respiration. GBS also has autonomic system changes such as orthostatic hypotension, acial ushing, anhydrosis, diaphoresis, and extreme variations in heart rate and blood pressure. reatment is supportive plus immunomodulation, such as intravenous immunoglobulin (IVIG) and plasma exchange. Ninety percent o patients make a ull recovery within a ew months, while 10% may have a long-term disability.

Chronic Inf ammatory Demyelinating Polyneuropathy (CIPD) CIPD is also known as chronic relapsing polyneuropathy. It is characterized by progressive weakness and impaired sensory unction in the legs and the arms, loss o deep tendon re exes, atigue, and abnormal sensations. CIPD is caused by damage to the myelin o the peripheral nerves. CIPD closely resembles Guillain–Barré syndrome and is considered the chronic counterpart o that acute disease. It is more common in young adults and in men than women. reatment includes corticosteroids, alone or combined with other immunosuppressant drugs, plasmapherisis, and immunoglobulin therapy.

Demyelinating Diseases

423

Charcot–Marie –Tooth Disease (CMT) CM , a group o inherited neurological disorders, is also known as hereditary sensory and motor neuropathy (HMSN) or peroneal muscular atrophy. CM is composed o a group o disorders that a ect the peripheral nerves. It is caused by mutations in genes that produce proteins involved in the structure and unction o the myelin sheath or the nerve axon. T is results in degeneration o motor nerves, muscle weakness, and atrophy o the extremities, and in some cases degeneration o sensory nerves, resulting in decreased ability to eel cold, heat, and pain. Mutations can be autosomal dominant or recessive, or inherited in an X-linked ashion.

Anti MAG Peripheral Neuropathy Anti-myelin-associated (MAG) neuropathy is an antibodymediated demyelinating neuropathy. Monoclonal immunoglobulin M anti-MAG antibodies are characteristic o this condition. Immunoglobulin M deposits at the site o MAG localization and causes demyelination and axonal degeneration. Individuals with this condition show distal and symmetric, mainly sensory, neuropathy. reatment aims to reduce the antibody concentration, blocking the e ector mechanism and depleting the monoclonal B cells. Rituximab, the drug o choice, is a monoclonal antibody that suppresses B-cell clones.

Copper De ciency Copper de ciency is a very rare neurological and hematological disease. It can mani est alone or with other nutritional de ciencies such as vitamin B12. Copper is required in the diet in very small amounts. Copper is involved in multiple enzymatic reactions, and these enzymes catalyze reactions or iron transport, oxidative phosphorylation, antioxidant and ree radical scavenging, and neurotransmitter synthesis. Copper de ciency can cause many hematological mani estations, such as anemia, myelodysplasia, leukopenia, and neutropenia. Neurological mani estations o copper de ciency include dorsal column dys unction, muscle weakness, peripheral neuropathy, myelopathy, progressive numbness, paresthesia, spastic gait, and sensory ataxia. reatment requires supplementation. T e progression o neurological symptoms can be stopped, but o en results with residual neurological disability.

ANESTHETIC CONSIDERATIONS Many demyelinating diseases a ect multiple organ systems, and preoperative management is best accomplished by a multidisciplinary approach. Current medications should be reviewed to maintain current stability and to avoid untoward drug interactions. Some o the more common a ected organ systems are listed in able 114-2.

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PART III Organ-Based Advanced Sciences

TABLE 114-2

Organ Systems Commonly A ected by Demyelinating Diseases

Nervous system

Developmental delay, chronic pain, spasticity, progressive loss o unction, demyelination, atrophy, mood disorders

Cardiovascular

Autonomic dys unction, arrhythmias, cardiomyopathy

Respiratory

Impaired cough re ex, bulbar muscle weakness, respiratory muscle weakness

It is not known whether M has relapses a er pregnancy, but there are several reported cases o M ollowing a neuraxial technique and general anesthesia. Demyelinated bers may be more susceptible to neurotoxicity with neuraxial blocks, spinal more than epidural anesthesia. Succinylcholine leads to signi cant hyperkalemia due to increased expression o nicotinic neuromuscular acetylcholine receptors in denervated skeletal muscle.

Gastrointestinal

Impaired swallowing, delayed gastric emptying, dys unctional motility, impaired nutritional status

Endocrine

Chronic steroid use and glucose intolerance, and need or stress dose steroids to avoid adrenal insuf ciency

Preoperative A detail discussion with the patient and amily should take place, and should include the possibility o neurological deterioration, prolonged ventilation, and any possible untoward e ects. Assess aspiration risk by determining the degree o impaired cough, gastrointestinal hypomobility, and pharyngeal muscle weakness. Premedication may cause exaggerated sedation and respiratory depression. Documentation o baseline neurological de cits, disease severity, and progression should occur.

Intraoperative Autonomic instability may present as hypotension, absent baroreceptor responses, or hypertension with stimulation. It is recommended to use direct-acting vasopressors. Hyperkalemia is possible in response to succinylcholine and should there ore be avoided. Response to nondepolarizing muscle relaxants is increased and in some cases unpredictable. Consider the need or corticosteroid supplementation.

Postoperative Per orm neurological exam. May need postoperative ventilatory support and continued ECG monitoring.

SPECIFIC ANESTHETIC CONSIDERATIONS (TABLE 114-3) Optic Neuritis Avoid intraoperative external pressure on the ocular globe and minimize microemboli during cardiopulmonary bypass. In addition, maintenance o adequate per usion pressure is necessary and steps should be taken to avoid severe anemia.

Surgical stress is associated with MS exacerbation, independent o drug or technique. As little as 0.5°C increase in temperature can cause exacerbation o MS symptoms. Clinical and historical data show no absolute contraindications to general or regional anesthesia. Peripheral nerve blocks are also probably sa e. Worsening o symptoms is experienced by 20%–30% o women in the postpartum period. When perorming epidural or regional anesthesia, recommendations are to use the minimum dose necessary and to use shorter acting drugs and less concentrated local anesthetics. Spinal anesthesia should be avoided in patients with MS. With muscle wasting, succinylcholine is contraindicated because o the potential hyperkalemic e ect. Lower and shorter duration nondepolarizing muscle relaxants should be used, i absolutely needed.

GBS Pharyngeal muscle weakness and oral secretion intolerance leads to aspiration risk. Autonomic dys unction results in hypotension with changes in posture, blood loss or positive airway pressure, hypertension with noxious stimulation, and exaggerated response to an indirect-acting vasopressor. Arterial blood pressure monitoring tracks blood pressure variations or acute management. Possible hyperkalemia in response to succinylcholine extends beyond disease resolution. Depending on the stage, patients may be resistant or hypersensitive to nondepolarizing muscle relaxants. Anticipate need or postoperative mechanical ventilatory support.

Vitamin B12 De ciency As with any anemia, supplemental oxygen is indicated. Avoid nitrous oxide. Active vitamin B12 contains cobalt in its reduced orm (Co+). Nitrous oxide produces irreversible oxidation to the Co++ and Co orms, which renders vitamin B12 inactive. Vitamin B12 (cyanocobalamin) is an integral component o two biochemical reactions in man: the conversion o L-methylmalonyl coenzyme A into succinyl coenzyme A and the ormation o methionine by methylation o homocysteine. T e transmethylation reaction is essential to DNA synthesis and to the maintenance o the myelin sheath by the

CHAPTER 114

TABLE 114-3

Key Concerns or Surgery in Patients with Demyelinating Diseases Aspiration risk secondary to bulbar muscle weakness or vocal cord paralysis Autonomic dys unction with orthostatic hypotension Weak respiratory muscles requiring postoperative mechanical ventilation Succinylcholine should be avoided because o denervation atrophy, which may result in severe hyperkalemia and subsequent cardiac arrest Unpredictable nondepolarizing muscle relaxant response, but most exhibit sensitivity Avoid spinal anesthesia with multiple sclerosis Neither general nor regional anesthesia exacerbates the course o the disease (with the exception o spinal anesthesia in multiple sclerosis)

methylation o myelin basic protein. T ere have been ew cases unsuspected o having vitamin B12 de ciency who developed subacute combined degeneration o the spinal cord ollowing nitrous oxide anesthesia. Patients with vitamin B12 de ciency are exceedingly sensitive to neurologic deterioration ollowing nitrous oxide anesthesia.

CMT Patients may present with a restrictive respiratory de ect secondary to respiratory muscle weakness. Some subtypes may

Demyelinating Diseases

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present with vocal cord paralysis and diaphragm dys unction. T ey may also have higher incidence o obstructive sleep apnea. Exhibit caution or aspiration, and increased sensitivity to sedatives and nondepolarizing muscle relaxants. Due to an increased incidence o mitral valve prolapse and arrhythmias, a medical history o palpitations, dizziness, and/or chest pain requires a preoperative ECG.

Copper De ciency Consider perioperative in ections with immunosuppression. T e existing neuropathy may increase the risk o neurological injury or patients undergoing neuraxial anesthesia. In patients with polyneuropathy, succinylcholine is contraindicated. Patients may also have increased sensitivity to nondepolarizing muscle relaxants resulting in prolonged blockade.

SUGGESTED READINGS Hebl JR, Horlocker , Schroeder DR. Neuraxial anesthesia and analgesia in patients with preexisting central nervous system disorders. Anesth Analg. 2006;103(1):223–228. Naguib M, Flood P, McArdle JJ, Brenner HR. Advances in neurobiology o the neuromuscular junction. Anesthesiology. 2002;96(1):202–231.

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Primary Neuromuscular Diseases Angela Lee, MD

MUSCULAR DYSTROPHIES: TYPES Muscular dystrophies are a varied group o genetic disorders a ecting the skeletal, smooth, and even cardiac muscles.

Duchenne’s and Becker’s Muscular Dystrophies Duchenne’s and Becker’s muscular dystrophies are a result o an X-linked recessive mutation in the dystrophin gene. In Duchenne’s muscular dystrophy (DMD), dystrophin in usually absent; in Becker’s muscular dystrophy (BMD), dystrophin is partially unctional. Dystrophin is ound in skeletal, smooth, and cardiac muscles, as well as the brain. It maintains muscle membrane integrity. DMD is more severe and more common than BMD. T e onset o DMD begins in early childhood, with the majority presenting by age 4. Li e expectancy is in the 30s; death results primarily rom respiratory ailure. In BMD, the onset o symptoms is in the teens or twenties, and patients can live into their early 40s. In both DMD and BMD, there is progressive weakness and wasting o proximal muscles. Presenting symptoms in DMD include a waddling walk and di culty climbing stairs. T e classic Gower maneuver describes using both arms to assist in getting rom a sitting to a standing position. T e disease a ects the heart in 90% o DMD and BMD patients, although there is no correlation between the severity o skeletal muscle and severity o cardiac muscle involvement. Echocardiogram may be normal or show wall motion abnormalities. Dilated cardiomyopathy is seen as the disease progresses. Cognitive impairment is also o en seen in a ected patients.

Limb Girdle Dystrophy Limb girdle dystrophy is similar to DMD and encompasses a heterogeneous group o disorders. Anesthetic considerations are similar to those with DMD/BMD.

Myotonic Dystrophy Myotonic dystrophy is characterized by progressive muscle weakness. Aspiration occurs secondary to smooth muscle

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weakness, and cardiac arrhythmias contribute to increased mortality. Mitral valve prolapse is present in about a f h o patients. Succinylcholine is contraindicated and can lead to sustained contractions that are not responsive to nondepolarizing muscle relaxants. Other triggers or myotonia include hypothermia, shivering, and mechanical/electrical stimulation. Myotonic reactions respond to treatment with phenytoin or quinine.

Myotonia Congenita Myotonia congenita has two orms: one with autosomal recessive and the other with autosomal dominant inheritance. It is characterized by uncontrolled temporary muscle excitability due to mutations in the chloride channel gene. Succinylcholine can lead to severe masseter muscle spasm in these patients. Dantrolene is usually e ective. Patients should be kept normothermic because shivering can trigger myotonia.

MUSCULAR DYSTROPHIES: ANESTHETIC CONSIDERATIONS DMD and BMD require care ul preoperative evaluation, with close attention paid to the cardiopulmonary systems. Preoperative workup should include an EKG and echocardiogram. Patients are at risk o aspiration due to involvement o the bulbar and laryngeal muscles. Postoperatively, DMD patients are at risk o respiratory compromise. Scoliosis may urther compromise respiratory status. Pulmonary unction tests can aid in postoperative planning; patients with a vital capacity o greater than 30% predicted value can usually be success ully extubated a er surgery. Succinylcholine is contraindicated due to the risk o hyperkalemic cardiac arrest and rhabdomyolysis. T e Food and Drug Administration has issued a warning against the routine use o succinylcholine in pediatric patients because o clinically latent muscular dystrophies. Nondepolarizing muscle relaxants will have an increased potency and a prolonged duration o action. Opioids should be used gingerly to avoid respiratory depression. Other intravenous agents 427

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should be chosen in light o organ system involvement, such as the extent o cardiac compromise. Although some reports have suggested a relationship between malignant hyperthermia and primary muscular diseases, there is no true association. T e disorders truly known to be associated with malignant hyperthermia are Evans myopathy, King syndrome, and central core disease. However, there is some controversy regarding the use o volatile anesthetics in patients with muscular dystrophy. T ey should be used cautiously, i at all, since volatile anesthetic use in the absence o succinylcholine may be associated with severe rhabdomyolysis in this population.

and/or echocardiogram in patients who show signs o impaired cardiac unction or conduction abnormalities. Both propo ol and barbiturates inhibit the electron transport chain. For this reason, some clinicians avoid propo ol. However, anesthesia, including local anesthetics and volatile agents, impacts mitochondrial unction, and no anesthetic is absolutely contraindicated in this population. T ere is no association between malignant hyperthermia and mitochondrial myopathies. Opioids and sedatives should be used cautiously because respiratory depression can lead to respiratory acidosis in addition to the metabolic acidosis already present. Any condition that increases basal metabolic requirements such as hypoxia, shivering and prolonged asting should be avoided.

MITOCHONDRIAL MYOPATHIES Mitochondrial myopathies are a group o biochemically heterogeneous disorders that a ect the respiratory chain o mitochondrial metabolism. T ey are characterized by proximal muscle weakness and increased lactic acid levels. Histologically, “ragged red f bers” are seen in a ected muscles. A thorough preoperative evaluation may include an EKG

SUGGESTED READINGS Gurnaney H, Brown A, Litman RS. Malignant hyperthermia and muscular dystrophies. Anesth Anal. 2009;109(4):1043–1048. Ross AK. Muscular dystrophy versus mitochondrial myopathy: the dilemma o the undiagnosed hypotonic child. Pediatr Anesth. 2007;17:1–6.

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Myasthenic Syndromes Brian S. Freeman, MD

T e “myasthenic” disorders all share the primary characteristic o muscle weakness that uctuates in severity and recovery. T ese diseases target the three components o synaptic transmission in the neuromuscular junction: presynaptic region, synaptic basal lamina, and postsynaptic receptors. T e underlying de ects are either autoimmune or genetic in nature.

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Classification of Myasthenia Gravis

Type

Anesthesiology Core Review Part Two-ADVANCED Exam 2016 - VSIP.INFO (2023)