(BQ) Part 1 book Civetta, taylor, & kirby’s manual of critical care has contents: Emergency situations, cardiovascular monitoring - invasive and noninvasive, techniques, procedures, and treatment, essential physiologic concerns, modulating the response to injury,.... and other contents.
P1: Trim: 8.375in × 10.875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 Civetta, Taylor, & Kirby’s MANUAL OF CRITICAL CARE Andrea Gabrielli, MD, FCCM Mihae Yu, MD, FACS Professor of Anesthesiology and Surgery Division of Critical Care Medicine Section Head, NeuroCritical Care University of Florida College of Medicine Medical Director, Cardiopulmonary Service and Hyperbaric Medicine Shands Hospital at the University of Florida Gainesville, Florida Professor of Surgery University of Hawaii John A Burns School of Medicine Vice Chair of Education University of Hawaii Surgical Residency Program Program Director of Surgical Critical Care Fellowship Program Director of Surgical Intensive Care The Queen’s Medical Center Honolulu, Hawaii A Joseph Layon, MD, FACP Director, Critical Care Medicine Geisinger Health System Danville, PA i 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 Acquisitions Editor: Brian Brown Product Manager: Nicole Dernoski Production Manager: Bridgett Dougherty Senior Manufacturing Manager: Benjamin Rivera Marketing Manager: Angela Panetta Design Coordinator: Teresa Mallon Production Service: Aptara, Inc © 2012 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business Two Commerce Square 2001 Market Street Philadelphia, PA 19103 USA LWW.com All rights reserved This book is protected by copyright No part of this book may be reproduced in any form by any means, including photocopying, 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 Printed in China Library of Congress Cataloging-in-Publication Data Gabrielli, Andrea Civetta, Taylor, and Kirby’s manual of critical care / Andrea Gabrielli, A Joseph Layon, Mihae Yu – 1st ed p ; cm Manual of critical care Includes bibliographical references and index ISBN 978-0-7817-6915-0 (alk paper) I Layon, A Joseph II Yu, Mihae III Civetta, Joseph M IV Title V Title: Manual of critical care [DNLM: Critical Care–Handbooks Intensive Care Units–Handbooks WX 39] 616.02 8–dc23 2011035304 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication Application of the information in a particular situation remains the professional responsibility of the practitioner The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions This is particularly important when the recommended agent is a new or infrequently employed drug Some drugs and medical devices presented in the publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320 International customers should call (301) 223-2300 Visit Lippincott Williams & Wilkins on the Internet: at LWW.com Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to pm, EST 10 ii 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 D E D I C AT I O N To the memory of my father and mother, Pietro and Giuliana: They would have been proud to see the results of my efforts —Andrea Gabrielli To my best friend and partner Susana E Picado—who makes me better To those who, in service to our people, struggle for justice and peace; Giuliana and Pietro were two —A Joseph Layon To my dad, General Jae Hung Yu, and the Seventh Division for their sacrifices and changing history for the better To my Mom, the late Esang Yoon who was the wind beneath our wings To the late Dr Thomas J Whelan Jr who continues to mentor me in the practice of Surgery and Code of conduct To Joe and Judy Civetta who sparked my continuing love for Critical Care and being the guiding light for all Peepsters And to my late daughter Pearl (and CD) who has the Master Key to All —Mihae Yu iii 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 iv 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 ■ CONTRIBUTING AUTHORS The authors would like to gratefully acknowledge the efforts of the contributors of the original chapters in Civetta, Taylor, and Kirby’s Critical Care, Fourth Edition Steven G Achinger, MD Maher A Baz, MD Gareth Adams, MD Elizabeth Cordes Behringer, MD Olufemi Akindipe, MD Giuseppe Bello, MD Serge Alfandari, MD, MSc Rinaldo Bellomo, MBBS, MD, FRACP, FJFICM Adrian Alvarez, MD Howard Belzberg, MD, FCCM Marcelo Amato, MD Ira M Bernstein, MD Giuditta Angelini Rebecca J Beyth, MD Djillali Annane, MD, PhD Indermeet S Bhullar, MD Massimo Antonelli, MD Luca M Bigatello, MD Juan Carlos Ayus, MD, FACP, FASN Thomas P Bleck, MD, FCCM Keri A Baacke, MD Ernest F.J Block, MD, MBA Sean M Bagshaw, MD, MSc, FRCPC Eric L Bloomfield, MD Philip S Barie, MD, MBS, FCCM, FACS Karen L Booth, MD Claudia L Barthold, MD Karen Bordson, DO Robert H Bartlett, MD Adrien Bougle, MD Miho K Bautista, MD Philip Boysen, MD v 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM vi Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 Contributing Authors James E Calvin, Jr., MD Clifford S Deutschman, MS, MD, FCCM William G Cance, MD Karen E Doucette, MD, MSc Lawrence J Caruso, MD Quan-Yang Duh, MD Juan C Cendan, MD Stephanie H Dunlap, DO Cherylee W.J Chang, MD, FACP Herbert L DuPont, MD Marianne E Cinat, MD, FACS Soumitra R Eachempati, MD, FACS Cornelius J Clancy, MD Rodney K Edwards, MD, MS Michael Coburn, MD Elamin M Elamin, MD, MSc, FACP, FCCP Giorgio Conti, MD Timothy C Fabian, MD, FACS Jamie B Conti, MD, FACC, FHRS Samir M Fakhry, MD, FACS Timothy J Coons, RRT, MBA Kevin J Farrell, MD Mark S Cooper, BM, BCh, PhD Robert J Feezor, MD C Clay Cothren, MD, FACS Niall D Ferguson, MD, FRCPC, MSc Douglas B Coursin, MD Sebastian Fernandez-Bussy, MD Claudia Crimi, MD Joseph Ferreira, BS, CPTC, CTOP II Kristina Crothers, MD Henry E Fessler, MD Gohar H Dar, MD Jay A Fishman, MD Rabih O Darouiche, MD Timothy C Flynn, MD Elizabeth Lee Daugherty, MD, MPH Michael A Frölich, MD, MS David A Decker, MD Brian Fuehrlein, PhD Leonardo De Luca, MD Andrea Gabrielli, MD, FCCM Demetrias Demetriades, MD, PhD, FACS Robert Peter Gale, MD 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 Contributing Authors George D Garcia, MD Charles W Hoopes, MD Achille Gaspardone, MD, Mphil Ramona O Hopkins, PhD Dany E Ghannum, MD David B Hoyt, MD, FACS Lewis R Goldfrank, MD Laurence Huang, MD Shankar P Gopinath, MD Thomas S Huber, MD, PhD Dietrich Gravenstein, MD Ahamed H Idris, MD J.S Gravenstein, MD Steven R Insler, DO David M Greer, MD, MA Felicia A Ivascu, MD Jeffrey S Groeger, MD James C Jackson, PsyD Jonathan Haft, MD Sridivya Jaini, MD, MS Stephen B Hanauer, MD Michael A Jantz, MD, FCCP Ikram U Haque, MD Edgar Jimenez, MD, FCCM Cathleen Harris, MD Aaron Joffe, MD Kevin W Hatton, MD Raja Kandaswamy, MD George Hatzakis, MSc, PhD Scott R Karlan, MD Steven O Heard, MD Paraskevi A Katsaounou, MD Alan W Hemming, MD, MSc Robin D Kim, MD Dean R Hess, PhD, RRT Craig S Kitchens, MD Zoltan G Hevesi, MD Charles T Klodell, MD Thomas L Higgins, MD, MBA Marin H Kollef, MD Brian L Hoh, MD Meghavi S Kosboth, DO M Barbara Honnebier, MD, PhD Andreas H Kramer, MD, FRCPC vii 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM viii Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 Contributing Authors Anand Kumar, MD Jerome H Modell, MD Aseem Kumar, PhD Ernest E Moore, MD Franco Laghi, MD Frederick A Moore, MD, FACS A Joseph Layon, MD, FACP Sharon E Moran, MD Marc Leone, MD, PhD Jan S Moreb, MD Olivier Y Leroy, MD Alison Morris, MD, MS David M Levi, MD Thomas C Mort, MD Lawrence Lottenberg, MD, FACS David W Mozingo, MD, FACS Harrinarine Madhosingh, MD Susanne Muehlschlegel, MD Michael E Mahla, MD Deane Murfin, MBBCh, DA(SA), FCA(SA) Patrick T Mailoux, DO Michael J Murray, MD, PhD Daniel R Margulies, MD, FACS Neil A Mushlin, DO Paul E Marik, MD, FCCm, FCCP Ece A Mutlu, MD, MBA Claude Martin, MD Gökhan M Mutlu, MD Larry C Martin, MD Bhiken I Naik, MBBCh(Wits), DA(SA) Mali Mathru, MD Minh-Hong Nguyen, MD S Anjani D Mattai, MD Minh-Ly Nguyen, MD Kristin L Mekeel, MD Jennifer A Oakes, MD Richard J Melker, MD, PhD Nimisha K Parekh, MD, MPH Scott T Micek, PharmD Robert I Parker, MD William M Miles, MD David A Paulus, MD Taro Mizutani, MD, PhD V Ram Peddi, MD 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 Contributing Authors Kevin Y Pei, MD Sherry J Saxonhouse, MD Carl W Peters, MD Thomas M Scalea, MD Frederic M Pieracci, MD, MPH Denise Schain, MD Michael R Pinsky, MD, CM, Drhc, FCCP, FCCM Carten M Schmalfuss, MD F Elizabeth Poalillo, RN, MSN, ARNP, CCRN Eran Segal, MD Andrew Pollak, MD Allen M Seiden, MD, FACS David T Porembka, DO, FCCM Steven A Seifert, MD, FACMT, FACEP Raymond O Powrie, MD, FRCP, FACP Hani Seoudi, MD Issam I Raad, MD Christoph N Seubert, MD, PhD Amin Rahemtulla, PhD, FRCP David Shade, BA, JD S Sujanthy Rajaram, MD Stephen D Shafran, MD, FRCPC H David Reines, MD Jack D Shannon, MD Zaccaria Ricci, MD Marc J Shapiro, MD, MS, FACS, FCCM Winston T Richards, MD Takeru Shimizu, MD, PhD Claudia S Robertson, MD William C Shoemaker, MD Steven A Robicsek, MD, PhD Marc A Simon, MD, MS, FACC Claudio Ronco, MD Jennifer A Sipos, MD Amy F Rosenberg, PharmD Lee P Skrupky, PharmD, BCPS Stephen J Roth, MD, MPH Robert N Sladen, MBChB, MRCP(UK), FRCP(C), FCCM Daniel T Ruan, MD Matthew S Slater, MD Steven Sandoval, MD Danny Sleeman, MD, FACS, FRCS Stephanie A Savage, MD Wendy I Sligl, MD ix 13:18 P1: Trim: 8.375in × 10.875in LWBK937-FM x Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2011 Contributing Authors Arthur S Slutsky, MD Kimi R Ueda, PharmD Eric S Sobel, MD, PhD Kürsat Uzun, MD Howard K Song, MD, PhD Johannes H van Oostrom, PhD Edward D Staples, MD Thomas C Vary, PhD John K Stene, MD, PhD Theordoros Vassilakopoulos, MD Deborah Stern, MD, MPH George C Velmahos, MD, PhD, MSEd Andrew Stolbach, MD J Matthias Walz, MD R Todd Stravitz, MD, FACP, FACG Hsiu-Po Wang, MD Kathirvel Subramaniam, MD Michael F Waters, MD, PhD Murat Sungur, MD Carl P Weiner, MD, MBA, FACOG David E.R Sutherland, MD, PhD Eelco F.M Wijdicks, MD Maria Suurna, MD Robert D Winfield, MD Sankar Swaminathan, MD Charles C.J Wo, BS Danny M Takanashi, Jr., MD, FACS Linda L Wong, MD Christopher D Tan, PharmD, BCPS Gregory W Woo, MD Jamie Taylor, MD Kenneth E Wood, DO Lisa Thannikary, MD Jean-Pierre Yared, MD S Rob Todd, MD, FACS Mihae Yu, MD, FACS Krista L Turner, MD Arno L Zaritsky, MD Andreas G Tzakis, MD, PhD Janice L Zimmerman, MD 13:18 P1: Trim: 8.375in × 10.875in LWBK937-58-60 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 CHAPTER 58 ■ PANCREATIC TRANSPLANTATION sPancreas transplantation offers selected diabetic patients the prospect of glucose control, avoiding—and, in some cases, reversing—the devastating complications of the disease Most pancreata are transplanted simultaneously with a kidney (SPK), although a significant fraction are transplanted alone (PTA) or at some time after a kidney (PAK) transplant Deceased donor pancreas remains a relatively underutilized organ resource; only 19% of available deceased donor pancreata are recovered and transplanted A few percent are procured, processed, and transplanted as islet cell transplants The reasons for this underutilization are multifactorial, and include regional variation in the number of potential recipients, donor and organ quality, and competition for kidneys with other patients sIn 2005, 903 SPK transplants, 344 PAK transplants, and 195 PTA transplants were performed These totals have changed little over the last several years Figure 58.1 depicts the trend for SPK transplants over the past decade Similarly, patient and graft survival has improved, with 5-year patient survival approaching 90% sThere are three broad categories of recipients: SPK, PAK, and PTA sSPK transplants: Most SPK transplants have been done with both organs coming from the same cadaveric donor Because a large number of patients are waiting for a kidney, unless priority is given to SPK candidates, waiting times tend to be long (years) Thus, to avoid two operations and a long wait, a simultaneous kidney and segmental pancreas transplant from a living donor can be done Only a few centers offer this option There has been a report from Japan of successful islet transplantation from a live donor Therefore, a simultaneous living-donor islet kidney transplant may become a viable option in the future If a living donor is suitable for or only willing to give a kidney, another option is a simultaneous living-donor kidney and cadaveric pancreas transplant For these options, the living kidney donor usually must be available on a moment’s notice (the same as for the recipient), as the cadaveric pancreas must be transplanted soon after procurement Alternatively, a recipient of a scheduled living-donor kidney transplant could also receive a cadaveric pancreas simultaneously if one became available fortuitously If not, and only a kidney is transplanted, the recipient becomes a PAK candidate sPAK transplants: For nephropathic diabetic patients who have already undergone a kidney transplant from a living or a cadaveric donor, a PAK transplant can be performed Most PAK transplants today are done in patients who previously received a living-donor kidney because suitable uremic diabetic patients without a living donor will undergo a cadaveric pancreas transplant Although a PAK means a uremic diabetic patient requires two operations to achieve both a dialysis-free and insulin-independent state, the two 368 transplants done separately are smaller procedures than a combined transplant The interval between the living-donor kidney and cadaveric pancreas transplant depends on several factors, including recipient recovery from the kidney transplant and donor availability, but the outcome is similar for all intervals more than month PAK is the largest pancreas transplant category at the University of Minnesota sPTA: For recipients with adequate kidney function, a solitary pancreas transplant can be performed from either a living or a cadaveric donor Because the waiting time for a cadaveric pancreas is relatively short at the present time, living-donor pancreas transplants are done infrequently, but are particularly indicated if a candidate has a high panelreactive antibody and a negative cross-match to a living donor Most PTA candidates have problems with glycemic control, hypoglycemic unawareness, and frequent insulin reactions A successful PTA not only obviates these problems, but also improves the quality of life, and may ameliorate secondary complications, thus increasing the applicability of PTA PERIOPERATIVE CARE OF PANCREAS TRANSPLANTATION sAfter an uncomplicated pancreas transplant, the recipient is transferred to the postanesthesia care unit or the surgical intensive care unit Centers that have a specialized monitored transplant unit (with central venous and arterial monitoring capabilities) transition the postoperative recipients through the postanesthesia care unit to the transplant unit Others transfer directly to the surgical intensive care unit for the first 24 to 48 hours Care during the first few hours after transplant is similar to care after any major operative procedure Careful monitoring of vital signs, central venous pressure, oxygen saturation, and hematologic and laboratory parameters is crucial The following factors are unique to pancreas recipients and should be attended to: sBlood glucose levels: Any sudden, unexplained increase in glucose levels should raise the suspicion of graft thrombosis An immediate ultrasound examination must be done to assess blood flow to the graft Maintenance of tight glucose control (50% of a lymphocyte panel, retransplantation, African American race, and recipient age younger than 16 years The classic clinical features associated with acute rejection are fever, oliguria, weight gain, edema, hypertension, and the presence of an enlarged, tender graft However, these features are frequently absent, and the most common presentation may be an asymptomatic rise in serum creatinine An increase in serum creatinine >20% is often the cardinal feature of rejection Percutaneous needle biopsy of the allograft is the most reliable method of diagnosis of acute rejection The principles and the management of acute rejection include rapid diagnosis, accurate classification, and prompt administration of antirejection therapy Chronic Rejection sChronic rejection is characterized clinically by a progressive decline in renal function, persistent proteinuria, and hypertension The course of chronic rejection is slow and insidious Chronic rejection often occurs in conjunction with other histologic causes of allograft dysfunction: acute rejection, calcineurin inhibitor nephrotoxicity, and recurrent or de novo glomerular diseases There is no treatment for chronic rejection at the present time Urologic Complications sUrologic problems have been reported in between 2% and 20% of all renal transplantations These complications can include urinary retention, urine leak, and ureteral stenosis Vascular Complications sVascular complications including vessel thrombosis or steno- TA B L E Medical Acute Rejection Other drug toxicities Infection BK virus nephropathy De novo/recurrent disease Renal artery stenosis Ureteric obstruction Urine leak Vascular thrombosis sis have been reported in 2% to 12% of all renal transplants Vascular complications in general are significantly associated with ATN and graft loss Early graft dysfunction should be evaluated for vascular complications with ultrasound with Doppler Lymphocele sA lymphocele is a collection of lymphatic fluid around the allografted kidney that can occur due to leakage of small lymphatic channels around the iliac vessels at the time of the transplantation The incidence of lymphoceles has been reported from 0.02% up to 26% after renal transplant Consequences of lymphoceles can include distention due to the fluid collection and venous or ureteral obstruction and graft compromise Treatment of lymphoceles can include percutaneous techniques with drainage and sclerosis of the cavity or may include operative marsupialization via the laparoscopic or open technique Laparoscopic techniques are less invasive, have less morbidity, and are generally the first line of therapy 12:54 P1: Trim: 8.375in × 10.875in LWBK937-58-60 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Chapter 60: Critical Care Aspects of Stem Cell Transplantation Stones sCalculi may have been present in the donor kidney or may develop after transplantation Predisposing factors include obstruction, recurrent urinary tract infection, 377 hypercalciuria, hyperoxaluria, internal stents, and nonabsorbable suture material Open removal of a calculus from the transplanted kidney is rarely necessary Complete stone removal is usually possible by standard urologic techniques CHAPTER 60 ■ CRITICAL CARE ASPECTS OF STEM CELL TRANSPLANTATION sBone marrow and blood cell transplants are widely used to treat aplastic anemia, leukemias, lymphomas, myeloma, and immunodeficiency disorders Transplants are also increasingly used to treat other bone marrow disorders such as sickle cell disease and thalassemia Morbidity and mortality associated with transplants usually result from regimen-related toxicity, such as adverse effects of drugs and radiation given pretransplant, complications of graft-versus-host disease (GVHD), and infections resulting from bone marrow failure sPretransplant evaluation of recipients typically includes the following: sMeasurement of the left ventricular ejection fraction, which should be at least 40% sPulmonary function tests, including diffusing capacity (DLCO), and forced vital capacity, which should be more than 50% of predicted sHepatic transaminases, which should be less than twice normal sCreatinine clearance, which should be more than 50 mL/ minute sA pretransplant performance score consistent with an independent life PERIOPERATIVE CARE OF STEM CELL TRANSPLANTATION sIn the setting of allotransplants, the pretransplant conditioning regimen needs to moderate or eliminate recipient immunity to prevent graft rejection When the allotransplant recipient has cancer, the pretransplant conditioning regimen must also eradicate it Most allotransplant conditioning regimens contain cyclophosphamide and busulfan, or totalbody radiation Antilymphocyte antibodies, such as antilymphocyte globulin, antithymocyte globulin, or alemtuzumab (anti-CD52), are often used in reduced-intensity conditioning regimens or in alternative donor transplants In immunodeficiency disorders—for example, severe combined immunodeficiency, pretransplant conditioning is not necessary, as the host is already immune deficient sFor autotransplants, the choice of pretransplant conditioning regimen is based on anticancer effect, a steep dose- response curve, lack of cross-resistance with other drugs, and low non-bone marrow dose-limiting toxicities In general, these regimens contain alkylating drugs, such as melphalan or cyclophosphamide, combined with two or three other drugs Immunosuppression is unnecessary and an unwanted side effect of therapy Radiation is not used in autotransplants, as the effective anticancer doses exceed non-bone marrow dose-limiting toxicity sPretransplant conditioning regimens are typically empirically determined (Table 60.1) BONE MARROW AND BLOOD CELL INFUSION sBone marrow and blood cells may be frozen in dimethyl sulfoxide for later use The intracellular contents of cells destroyed in the freezing and thawing processes—and dimethyl sulfoxide itself—may cause hypotension, anaphylaxis, or dysrhythmias, including transient heart block To avoid complications, subjects are premedicated with diphenhydramine hydrochloride (Benadryl) and methylprednisolone sodium succinate (Solu-Medrol) Intubation equipment and epinephrine should be available at the bedside when cells are infused If hypotension occurs, the infusion is slowed or temporarily interrupted until the blood pressure stabilizes If the bone marrow or blood cells have not been frozen, the risk of anaphylaxis is similar to a standard blood transfusion, and premedication is unnecessary sApproximately 1.2% of cultures obtained during these processes are found to contain bacteria Most cultures show coagulase-negative Staphylococcus spp., which colonize the skin; pathogenic gram-negative bacteria are occasionally present Thus, despite positive culture results, most centers reinfuse the stem cells after appropriate antibiotic coverage FLUIDS AND HYPOTENSION sHigh-dose chemotherapy and radiation damage vascular endothelial cells, resulting in extravascular leakage of fluids Furthermore, GVHD and cytokines such as tumor necrosis 12:54 P1: Trim: 8.375in × 10.875in LWBK937-58-60 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 378 August 12, 2011 Section IX: Organ Transplantation TA B L E TOXICITY OF CONDITIONING REGIMEN DRUGS Drug/dose Extramedullary dose-limiting toxicity BCNU Busulfan CCNU (lomustine) Cyclophosphamide Interstitial pneumonitis Mucositis, VOD Interstitial pneumonitis Heart failure Cytarabine Mucositis, cerebellar ataxia Cisplatin Renal insufficiency, peripheral neuropathy Ototoxicity, hepatitis Mucositis Encephalopathy, renal insufficiency Mucositis Cardiotoxicity Mucositis Mucositis Carboplatin Etoposide Ifosfamide Melphalan Mitoxantrone Paclitaxel Thiotepa Other toxicities Renal insufficiency, encephalopathy, nausea, vomiting, VOD Seizures, rash, hyperpigmentation, nausea, vomiting, pneumonitis Renal insufficiency, encephalopathy, nausea, vomiting, VOD Hemorrhagic cystitis, SIADH, nausea, vomiting, pulmonary edema, interstitial pneumonitis Pulmonary edema, conjunctivitis, rash, fever, hepatitis, toxic epidermal necrolysis Nausea, vomiting, renal tubular acidosis, hypomagnesemia Renal insufficiency, hypomagnesemia, peripheral neuropathy Nausea, vomiting, hemorrhagic cystitis, pneumonia, hepatitis Hemorrhagic cystitis, renal tubular acidosis Nausea, vomiting, hepatitis, SIADH, pneumonitis, renal insufficiency Mucositis Peripheral neuropathy, bradycardia, anaphylaxis Intertriginous rash, hyperpigmentation, nausea, vomiting VOD, veno-occlusive disease; SIADH, syndrome of inappropriate antidiuretic hormone factor, interleukin 2, and interferon-gamma contribute to a posttransplant capillary leak syndrome sIf hypotension develops, emphasis should be placed on early invasive cardiovascular monitoring, inotropic support, and irradiated packed red blood cell transfusion to maintain intravascular oncotic pressure Aggressive hydration may precipitate pulmonary and peripheral edema, even with normal pulmonary artery wedge pressure and right atrial pressure ELECTROLYTE BALANCE sElectrolyte abnormalities are common in transplant recipients, resulting from the underlying disease, prophylactic hydration for hemorrhagic cystitis, diarrhea, parenteral nutrition, renal insufficiency, diuretics, and other medications BLOOD PRODUCT TRANSFUSIONS sSubjects receiving transplants are immunocompromised and at risk for transfusion-associated GVHD All cellular blood products contain white blood cells, including immunecompetent T cells, and should be irradiated (25 Gy) sFurthermore, all allotransplant recipients should receive cytomegalovirus-negative (CMV-negative) blood product transfusions, especially when the recipient is CMVseronegative sIn the allotransplant setting, special consideration is needed regarding ABO compatibility between recipient and donor This complexity of blood product transfusion support should be viewed in terms of whether there is a major or minor ABO incompatibility between the recipient and donor (Tables 60.2 and ( 60.3) Despite using ABO-compatible platelets, many subjects fail to respond to platelet transfusions early after transplant Causes include fever, hepatic veno-occlusive disease (VOD), drugs, infection, disseminated intravascular coagulation, and microangiopathic hemolytic anemia related to cyclosporine and/or GVHD INFECTION PREVENTION sStandards for prevention of infection vary from strict isolation in laminar airflow (LAF) rooms to none In LAF rooms, the subject is in a sterile environment; anyone who enters must be gloved and gowned, and the patient’s food is sterilized or has a low microbial content secondary to autoclave or microwave treatment Prophylactic oral antibiotics are given to destroy enteric pathogens, which not only are reservoirs for infection, but also may function as superantigens that increase the severity of GVHD sThe minimal standards to prevent bacterial infections include the following: sA transplant unit set aside from general hospital, patients, and visitor traffic sHigh-efficiency particulate air filtration to prevent iatrogenic Aspergillus species infection sCareful handwashing before entering a patient’s room sA diet without fresh salads, vegetables, or fruits, as these may be contaminated with gram-negative bacteria, or without pepper, as this may be contaminated with an Aspergillus species Bacterial prophylactic measures are generally discontinued when the neutrophil count is >0.5 × 109 cells/L sTactics to prevent fungal infections include the use of oral triazoles such as itraconazole or fluconazole, given orally or intravenously for the first month after transplant sSubjects with prior aspergillus infection are at high risk of recurrence, especially in the presence of the following: sProlonged neutropenia after transplant sA more advanced cancer state sA 6-week or shorter interval from beginning systemic antiAspergillus therapy to the transplant sSevere acute GVHD 12:54 P1: Trim: 8.375in × 10.875in LWBK937-58-60 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Chapter 60: Critical Care Aspects of Stem Cell Transplantation 379 TA B L E DONOR-RECIPIENT ABO INCOMPATIBILITY Major ABO incompatibility Minor ABO incompatibility Major and minor ABO incompatibility Recipient has antibody to donor Donor has antibody to recipient Recipient has antibody to donor and donor has antibody to recipient Immediate hemolysis Prevent by RBC depletion of marrow Prevent by plasma depletion of marrow Prevent by RBC and plasma depletion of marrow Delayed hemolysis Occurs 2–4 weeks after SCT + Direct antiglobulin test Risk increased with high recipient isohemagglutinin titer Occurs day 9–day 16 after SCT + Direct antiglobulin test Risk increased with T cell–depleted marrow + Direct antiglobulin test Delayed erythropoiesis Plasma exchange, erythropoietin, steroids Plasma exchange, erythropoietin, steroids RBC, red blood cell; SCT, stem cell transplantation; +, positive sPersons with prior aspergillosis should receive amphotericin, voriconazole, or caspofungin early after transplant sHerpes simplex reactivation is usually prevented by using intravenous or oral acyclovir for the first month after transplant Treatment thereafter results in frequent acyclovir resistance and delays the development of natural immunity FEVER AND NEUTROPENIA sIn transplant recipients with fever—temperature ≥38◦ C— and a neutrophil count 34 μmol/L = 2.0 mg/dL Hepatomegaly Ascites Weight gain sVOD, with a reported incidence of 1% to 56%, is a clinical diagnosis suggested by elevated bilirubin, weight gain, ascites, and tender hepatomegaly (Table 60.4) Therapy for VOD is predominantly supportive, but its prognosis is poor when bilirubin is more than 15 to 20 mg/dL RESPIRATORY FAILURE sTransplant recipients who develop respiratory failure and require mechanical ventilation have a poor prognosis Respiratory failure within the first 30 days is usually caused by pretransplant conditioning, regimen-related epithelial cell damage, and/or infection sEarly in the course of respiratory distress, efforts should be directed to preventing intubation Although not evaluated in prospective studies and therefore of unproven benefit, management may include early invasive hemodynamic monitoring, red blood cell transfusions to maintain hemoglobin more than 12 g/dL, ultrafiltration to decrease intravascular volume, and anticytokine monoclonal antibodies or cytokine receptor antagonists Use of high-dose corticosteroids is controversial Transplant recipients are especially susceptible to pulmonary infections because of bone marrow failure, immunosuppressive drugs, mucositis, aspiration, and bronchial epithelial cell damage with impaired ciliary motility Gram-negative and -positive pneumonias are common in the first 30 days after transplantation Fungal infections of the lung also occur early after transplant, and isolation of Aspergillus species in a nasal or sputum culture should prompt initial therapy with amphotericin, voriconazole, or caspofungin TA B L E GRAFT-VERSUS-HOST DISEASE, GRAFT FAILURE, AND DISEASE-FREE SURVIVAL FOR TRANSPLANTS WITH SIBLING-MATCHED OR UNRELATED DONORS Degree of HLA match GVHD grade III or IV (%) Acute Chronic GVHD (%) Graft failure (%) DFS-AML or all in remission (%) DFS-CML in chronic phase (%) DFS-AML or all in relapse (%) DFS-CML in transformation (%) DFS-AA (%) Sibling 6/6 Related 5/6 Related 4/6 Haplo-identical Unrelated 6/6 7–15 25–30 45–50 50–100 45–50 30–35 50 50 >50 55 500 mL/d Diarrhea >1,000 mL/d Diarrhea >1,500 mL/d Diarrhea >2,000 mL/d or severe abdominal pain with or without ileus AST, aspartate transaminase 381 12:54 P1: Trim: 8.375in × 10.875in LWBK937-58-60 382 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Section IX: Organ Transplantation TA B L E OVERALL GRADE OF GRAFT-VERSUS-HOST DISEASEa Grade I II III IV Skin Gut +1 to +2 +1 to +3 +2 to +4 +2 to +4 +1 to +2 +2 to +4 +2 to +4 and/or and/or and/or Liver ECOG performance +1 to +2 +2 to +4 +2 to +4 0 to to 3 to ECOG, Eastern Cooperative Oncology Group If no skin disease, the overall grade is the higher single organ grade Adapted from Glucksberg H, Storb R, Fefer A, et al Clinical manifestations of graft versus host disease in human recipients of marrow from HL-A-matched sibling donors Transplantation 1974;18:295–304 a T cells, which recognizes recipient tissues as foreign The incidence and severity of acute GVHD increase with increasing recipient age and human leukocyte antigen (HLA) and nonHLA disparity between the recipient and donor (Tables 60.5 and 60.6) sSkin involvement in acute GVHD results in a maculopapular, erythematous rash, often beginning on the palms and soles and which may become systemic In severe cases, acute GVHD with skin involvement may be pruritic with bullae The skin involvement in acute GVHD may be precipitated by exposure to sunlight and/or drugs Histologically, one can see the dermal-epidermal border disrupted by vacuolar degeneration of epithelial cells, dyskaryotic bodies, acantholysis (i.e., separation of cell–cell contact), epidermolysis (separation of the epidermal and dermal layers), and lymphocytic infiltration These clinical and histologic findings are not unique to acute GVHD and may occur from drug allergy or the effects of the high-dose chemotherapy and radiation used in the pretransplant conditioning regimen sGastrointestinal involvement with acute GVHD results in diarrhea, often accompanied by cramping abdominal pain In severe cases, the diarrhea may be bloody or associated with a paralytic ileus Histologically, lymphocytes and apoptotic cells are present, and intestinal crypts are lost, which leads to epithelial denudation Evaluation of gastrointestinal tract signs and symptoms should include stool cultures for bacteria, fungi, and viruses, especially CMV Sigmoidoscopy with biopsy may be helpful if the diagnosis is in doubt and platelet levels are sufficient Acute GVHD with hepatic involvement presents as jaundice and an elevated alkaline phosphatase with or without elevated transaminases The differential diagnosis includes VOD or infections with CMV or Candida spp and may require a transjugular liver biopsy for accurate diagnosis In acute GVHD, the liver biopsy may show T-cell infiltration of the portal triad, with apoptosis of epithelial cells lining the biliary tree sAcute GVHD and infections from immunosuppression are major causes of early death after allotransplant Consequently, acute GVHD prophylaxis is needed for all allotransplant recipients sClinical staging of acute GVHD considers individual tissue/organ involvement scores, which are combined for an overall grade (Tables 60.7 and 60.8) Grade acute GVHD is not clinically important and requires no specific therapy Grades through acute GVHD are typically treated with corticosteroids such as methylprednisolone, to mg/kg/day, with or without cyclosporine Acute GVHD unresponsive to this approach has a poor prognosis 12:54 ... Cardiovascular Care Circulation 2005 ;11 2[24]SIV -1 IV- 211 16 :8 P1: Trim: 8.375in × 10 .875in LWBK937- 01 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2 011 Section I: Emergency Situations... volume ratio 12 :1 P1: Trim: 8.375in × 10 .875in LWBK937-02-05 10 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 11 , 2 011 Section I: Emergency Situations FIGURE 2 .1 Demonstration of the “sniffing... (mihaey@hawaii.edu) Honolulu, Hawaii xi 13 :18 P1: Trim: 8.375in × 10 .875in LWBK937-FM Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 27, 2 011 xii 13 :18 P1: Trim: 8.375in × 10 .875in LWBK937-FM Top: