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(BQ) Part 1 book “A practical approach to obstetric anesthesia” has contents: Physiologic changes of pregnancy, local anesthetics and toxicity, obstetric medications, ethical and legal considerations in obstetric anesthesia, nonobstetric surgery during pregnancy, fetal assessment and monitoring,… and other contents.
Acquisitions Editor: Keith Donnellan Product Development Editor: Nicole Dernoski Editorial Assistant: Kathryn Leyendecker Marketing Manager: Dan Dressler Production Project Manager: Marian Bellus Design Coordinator: Stephen Druding Manufacturing Coordinator: Beth Welsh Prepress Vendor: Absolute Service, Inc 2nd edition Copyright © 2016 Wolters Kluwer Copyright © 2009 Lippincott Williams & Wilkins, a Wolters Kluwer business All rights reserved This book is protected by copyright No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews Materials appearing in this book prepared by individuals as part of their official duties as U.S government employees are not covered by the above-mentioned copyright To request permission, please contact Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at permissions@lww.com, or via our website at lww.com (products and services) 9 8 7 6 5 4 3 2 1 Printed in China Library of Congress Cataloging-in-Publication Data Names: Baysinger, Curtis L., editor | Bucklin, Brenda A., editor | Gambling, David R., editor Title: A practical approach to obstetric anesthesia / editors, Curtis L Baysinger, Brenda A Bucklin, David R Gambling Description: 2nd edition | Philadelphia : Wolters Kluwer Health, [2016] | Preceded by A practical approach to obstetric anesthesia / editors, Brenda A Bucklin, David R Gambling, David Wlody c2009 | Includes bibliographical references and index Identifiers: LCCN 2015046281 | ISBN 9781469882864 Subjects: | MESH: Anesthesia, Obstetrical | Pregnancy Complications | Labor, Obstetric Classification: LCC RG732 | NLM WO 450 | DDC 617.9/682—dc23 LC record available at http://lccn.loc.gov/2015046281 This work is provided “as is,” and the publisher disclaims any and all warranties, express or implied, including any warranties as to accuracy, comprehensiveness, or currency of the content of this work This work is no substitute for individual patient assessment based on healthcare professionals’ examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data, and other factors unique to the patient The publisher does not provide medical advice or guidance, and this work is merely a reference tool Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources When prescribing medication, healthcare professionals are advised to consult the product information sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things, conditions of use, warnings and side effects and identify any changes in dosage schedule or contraindications, particularly if the medication to be administered is new, infrequently used, or has a narrow therapeutic range To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property, as a matter of products liability, negligence law or otherwise, or from any reference to or use by any person of this work LWW.com Dedication To the memory of Dr Geraldine O’Sullivan Preface A PRACTICAL APPROACH TO OBSTETRIC ANESTHESIA, 2ND EDITION There is certainly no shortage of obstetric anesthesia texts currently available, from introductory handbooks to encyclopedic treatises What has been lacking is a book that straddles the middle ground between those extremes, a book that would serve to supply both experienced and novice clinicians with guidance for managing routine and complicated parturients, as well as providing an explanation of the physiologic and pharmacologic principles underlying clinical care We think that A Practical Approach to Obstetric Anesthesia has achieved this goal by assembling and reviewing the most up-to-date information relevant to the practice of obstetric anesthesiology The book is a portable user-friendly reference that gives easy-to-follow guidance in an outline format The table of contents is divided into six sections: Pharmacology and Physiology, Antepartum Considerations, Labor and Delivery, Postpartum Issues, Disease States, and Guidelines from National Organizations The book contains 33 chapters that have been organized within a particular section Key points are noted at the beginning of each chapter Clinical Pearls are embedded within the text Each chapter also contains a list of current and relevant references The use of color in this edition highlights important sections to improve readability This book would not have been possible without the commitment and hard work of more than 40 contributors as well as the production staff at Wolters Kluwer Acknowledgments I would like to dedicate this book to the memory of Sol Shnider, who started me on my career in obstetric anesthesia; to my parents, Roy and Mary Lee, whose resources and encouragement helped make my career in medicine a reality; to my children, Charles and Katherine, who have honored me by pursuing careers as physicians; and to my wife Mary, whose love and support I receive daily Curtis L Baysinger I would like to dedicate this book to my husband, Uli, my parents, and all of the learners who study obstetric anesthesiology Brenda A Bucklin I would like to acknowledge two important mentors, Professor Graham McMorland and Professor Joanne Douglas, who facilitated my understanding of obstetric anesthesia I dedicate this book to the memory of my father Gordon and to acknowledge the love and support of my wife Kimberley; my children Carwyn, Jake, and Samantha; and my mother Sadie David R Gambling Contributors Bryan S Ahlgren, DO Assistant Professor University of Colorado School of Medicine Aurora, Colorado Mrinalini Balki, MB, BS; MD Associate Professor University of Toronto Department of Anesthesia and Pain Management Department of Obstetrics and Gynaecology Mount Sinai Hospital Toronto, Ontario, Canada Curtis L Baysinger, MD Professor of Anesthesiology Division of Obstetric Anesthesia Department of Anesthesiology Vanderbilt University School of Medicine Nashville, Tennessee Yaakov Beilin, MD Professor of Anesthesiology and Obstetrics Gynecology and Reproductive Science Vice Chair for Quality Department of Anesthesiology Director, Obstetric Anesthesiology Icahn School of Medicine at Mount Sinai New York, New York Jessica Booth, MD Assistant Professor Discontinuation of chest compressions is indicated when the heart rate is greater than 80 bpm and the pulse remains palpable I Umbilical vein catheterization Cannulation of the umbilical vessels allows for both prompt administration of resuscitation drugs and hemodynamic monitoring In addition, they provide a reliable conduit for the administration of epinephrine and/or fluids The umbilical artery can be cannulated when frequent assessment of systemic blood pressure or arterial blood gases is necessary A 3.5 or 5 French catheter is sterilely inserted into the vein at the stump of the umbilical cord The catheter is advanced 2 to 3 cm, at which point aspiration of blood should be possible The catheter must remain infrahepatic because hepatic infusion of drugs or hypertonic solutions can cause hepatic necrosis or portal vein thrombosis The tip of the umbilical artery catheter should be positioned above the bifurcation of the aorta and below the celiac, renal, and mesenteric arteries In a term infant, advancement of the catheter between 9 and 12 cm generally allows for optimal positioning Radiographic verification of the tip position is indicated if the catheter is to remain in place for an extended period J Medications Epinephrine In approximately 1 in 2,000 deliveries where the heart rate remains less than 60 bpm despite adequate ventilation and 30 seconds of chest compressions, epinephrine is the vasopressor of choice (see Fig 17.3) Administration of epinephrine leads to increased myocardial blood flow from α-adrenergicmediated vasoconstriction and a subsequent increase in coronary perfusion pressure a Intravascular epinephrine is given at doses of 0.01 to 0.03 mg per kg and can be repeated every 3 to 5 minutes until the heart rate is greater than 60 bpm (see Table 17.8) Adequate ventilation must be established prior to its administration because the α-and β-adrenergic activity of epinephrine increases oxygen consumption and can lead to myocardial damage in the setting of hypoxemia b The endotracheal route for epinephrine administration is controversial In one report, only 32% of neonates experienced a return of spontaneous circulation after administration of endotracheal epinephrine.44 Several factors may impede neonatal alveolar drug absorption, including the persistence of the fetal circulation, dilution of the drug due to alveolar fluid remaining in the lungs after delivery, and reduction of pulmonary blood flow due to pulmonary vasoconstriction Although some animal studies demonstrate a positive result with high-dose endotracheal epinephrine,45 more conventional doses fail to show an effect.46 These higher doses of epinephrine are associated with exaggerated hypertension, a decrease in myocardial function, and poor neurologic outcome Because the use of medications during neonatal resuscitation is an uncommon event, determination of the most effective epinephrine regimen has been difficult CLINICAL PEARL Adequate ventilation is required before epinephrine can be administered Administration via an endotracheal tube is controversial Volume expanders for the treatment of shock Although neonatal cardiorespiratory depression is most often secondary to hypoxemia and acidosis, in rare situations, it is the result of significant hypovolemia a The most common cause of neonatal shock is acute compression of the umbilical cord A tight nuchal cord may result in placental trapping of fetal blood as flow continues through the rigid, muscular umbilical arteries but is inhibited through the compliant umbilical vein Less frequent causes of neonatal hypovolemia include placental abruption, placenta previa, vasa previa, and fetomaternal hemorrhage b Despite the various potential causes of neonatal blood loss during delivery, volume infusions are rarely indicated and in many situations are detrimental In a recent retrospective study of approximately 38,000 deliveries, only 1:12,000 term infants needed volume therapy after birth.47 According to the current AHA guidelines, volume expansion may be indicated if the infant is not responding to intensive resuscitation and there is evidence of blood loss.1 In the presence of hypovolemia, volume expansion may be achieved with either isotonic crystalloid or O- negative blood An initial dose of 10 mL per kg over 5 to 10 minutes may be repeated, if necessary (see Table 17.8) There is no benefit of albumin over isotonic crystalloid for the treatment of hypotension in neonates.48 c The inappropriate infusion of fluid may contribute to continued cardiac and neurologic compromise Unfortunately, in the absence of obvious blood loss, it is difficult to distinguish a hypovolemic infant from a normovolemic, asphyxiated infant Both will exhibit cyanosis, weak pulses, and delayed capillary refill Because the neonatal heart has a relatively fixed stroke volume, increased preload can be detrimental in a normovolemic, asphyxiated infant with decreased myocardial function and reduced cardiac output Furthermore, the cerebral microcirculation of an asphyxiated neonate is particularly vulnerable to injury from rapid volume expansion Infants receiving volume infusions early during cardiopulmonary resuscitation have shown decreased Apgar scores at 10 minutes, lower cord arterial pH, larger base deficits, and longer resuscitation periods.47 CLINICAL PEARL Hypovolemia is a rare cause of neonatal acidosis The administration of large volumes of fluid is detrimental in the normovolemic depressed neonate Sodium bicarbonate Although acidemia impairs myocardial performance and may attenuate the hemodynamic response to catecholamines, the benefit of sodium bicarbonate infusions has been refuted by several studies in adults and neonates.49 a Among 19 retrospective adult studies examining mortality rates and other outcomes, none demonstrated benefit: 11 showed no difference in outcomes, and 8 suggested a deleterious effect of sodium bicarbonate administration during cardiopulmonary resuscitation.50 One randomized controlled trial of sodium bicarbonate use in neonatal resuscitation demonstrated no difference in mortality rates or neurologic outcomes.51 Recent AHA guidelines highlight the adverse neurologic and cardiac effects linked to bicarbonate administration.52 b Exogenously administered sodium bicarbonate is readily converted into carbon dioxide It diffuses into myocardial and cerebral cells and paradoxically contributes to intracellular acidosis and reduced cellular function The extracellular alkalosis created by sodium bicarbonate shifts the oxyhemoglobin saturation curve, further worsening the intracellular acidosis by impeding oxygen release to the tissues Sodium bicarbonate infusions also hinder cerebral and coronary perfusion by reducing SVR The strong relationship between intracranial hemorrhage and rapid infusions of hyperosmolar sodium bicarbonate further argue against its routine use The administration of sodium bicarbonate is no longer recommended during initial neonatal resuscitation CLINICAL PEARL The administration of sodium bicarbonate during initial resuscitation is not recommended K Discontinuation of resuscitative efforts In addition to providing guidelines for neonatal resuscitation, the AHA has recommendations on when it is appropriate to terminate resuscitative efforts.1 Most infants with Apgar scores of 0 after 10 minutes after adequate resuscitative measures will expire during the immediate neonatal period from multiorgan failure; those who survive will almost invariably suffer severe hypoxic-ischemic encephalopathy and devastating neurologic sequelae.53 It is therefore acceptable to withhold or interrupt resuscitation after 10 minutes if the neonate shows no evidence of life V Special resuscitation circumstances A Meconium-stained amniotic fluid Meconium is the breakdown product of amniotic fluid, gastrointestinal cells, and intestinal secretions Passage of meconium normally occurs after delivery; however, intrapartum fetal distress can stimulate colonic activity, resulting in meconium-stained amniotic fluid (MSAF) in 10% to 15% of all deliveries.54 Intrapartum hypoxic stress may trigger deep, agonal gasping, leading to meconium aspiration and the development of meconium aspiration syndrome (MAS) in 5% of infants delivered through MSAF.55 The consequences of severe MAS include inflammation of lung tissue, obstruction of the small airways, release of vasoactive substances stimulating pulmonary vasoconstriction, and inhibition of surfactant function MAS may be complicated by the need for prolonged mechanical ventilation, the development of pulmonary air leaks, or persistent pulmonary hypertension This severe respiratory compromise results in a mortality rate among infants with MAS as high as 5%.55 The management of infants delivered through MSAF has evolved over the past several decades a In the 1970s, MAS was presumed to be a postnatal event initiated by the aspiration of meconium at the time of the first breath Early investigations suggested that meticulous suctioning of the fetal oropharynx and trachea at delivery decreased the rate of MAS.56,57 With reports of 100% survival in infants born through MSAF who subsequently underwent tracheal intubation and suctioning,56 a combined approach was introduced involving suctioning of the upper airway at the perineum followed by tracheal suctioning after delivery.57 Although the clinical significance of these earlier studies was questionable, until recently, the combined two-step approach was universally adopted b MAS is no longer considered to be an exclusively postnatal disorder Recent studies suggest aspiration of meconium by itself is insufficient to produce the histologic or physiologic changes of severe MAS.58,59 Evidence of long-standing stress in infants with MAS, including pulmonary hypertension and vascular hypertrophy, suggests this is a complex, multifactorial disorder with antenatal as well as intrapartum factors It is likely that aspiration of meconium is an event predating labor, and severe MAS is caused by pathologic processes occurring in utero, primarily chronic asphyxia and infection.60 c Therapeutic interventions that have traditionally been advocated, including oropharyngeal suctioning prior to delivery of the thorax and tracheal suctioning after delivery, have questionable benefit in altering the outcome of severe MAS.61–64 In an international, prospective randomized controlled trial involving 2,514 infants, suctioning of the oropharynx and nasopharynx prior to delivery of the thorax caused no difference in the incidence of MAS, mechanical ventilation, duration of supplemental oxygen use, or mortality.61 Other investigators have found that vigorous, meconium-stained infants with a heart rate >100 bpm, spontaneous ventilation, and reasonable muscle tone do not benefit from tracheal suctioning.62,63 The benefit of tracheal suctioning in depressed infants born through MSAF has yet to be determined d It is imperative to recognize that tracheal suctioning may actually cause complications, including: (1) vagal stimulation resulting in bradycardia and apnea; (2) irritation to mucous membranes, causing increased mucus production and nasal congestion; (3) tissue trauma, resulting in a break in the natural barrier against infection, thereby increasing the risk of transmission of infection.65 The Neonatal Resuscitation Program (NRP) and the ACOG no longer recommend routine intrapartum oropharyngeal and nasopharyngeal suctioning in the presence of MSAF; in vigorous infants, tracheal suctioning is advocated only for depressed neonates (see Fig 17.6) CLINICAL PEARL Intrapartum oropharyngeal and tracheal suctioning is recommended only for the depressed infant born with MSAF B Premature infants Although the survival rate of premature infants has steadily increased over the past few decades,66,67 long-term morbidity and mortality is still common in neonates less than 28 weeks’ gestational age.68 Appropriate resuscitation of this subset of newborns requires an understanding of their unique physiologic limitations Although premature infants are at higher risk for problems with multiple organ systems, the pulmonary and cerebral systems deserve special consideration Fetal lung development during the third trimester is characterized by the saccular development of terminal bronchioles and the formation of surfactant by type II pneumocytes The reduction in pulmonary surface area and surfactant production characteristic of immature lungs contributes to difficulty in ventilation and increases vulnerability to barotrauma during positive pressure ventilation In addition, the antioxidant defense system develops late in gestation, and premature neonates may be more susceptible to the adverse effects of excess oxygen In one study, preterm infants resuscitated with 30% oxygen had less oxidative stress, inflammation, and chronic lung disease compared to those resuscitated with 100% oxygen.69 However, room air appears to be insufficient for the resuscitation of most neonates born at less than 28 weeks’ gestation.70–72 In another study, attempts to titrate oxygen concentrations in preterm infants initially receiving room air left several babies with uncertain or dangerously low levels of oxygenation at 9 minutes of life.72 In an attempt to ensure oxygenation while avoiding the complications of hyperoxia, neonates