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(BQ) Part 1 book “Decision making in emergency critical care” has contents: Emergency critical care, tissue oxygenation and cardiac output, noninvasive hemodynamic monitoring, arterial blood pressure monitoring, the central venous and pulmonary artery catheter,… and other contents.

Decision Making in Emergency Critical Care An Evidence-Based Handbook EDITOR John E Arbo, MD Assistant Professor of Emergency Medicine and Critical Care Medicine New York-Presbyterian Hospital/Weill Cornell Medical Center New York, New York ASSOCIATE EDITORS Stephen J Ruoss, MD Professor of Pulmonary and Critical Care Medicine Co-Chief, Division of Pulmonary and Critical Care Medicine Stanford University Medical Center Stanford, California Geoffrey K Lighthall, MD Associate Professor of Anesthesia and Critical Care Medicine Stanford University Medical Center Stanford, California Michael P Jones, MD Assistant Professor of Emergency Medicine Associate Program Director – Jacobi/Montefiore Emergency Medicine Residency Program Albert Einstein College of Medicine New York, New York SPECIAL EDITOR: NEUROLOGY SECTION Joshua Stillman, MD, MPH Assistant Professor of Medicine Emergency Medicine Director of the Stroke Center at New York-Presbyterian Hospital/Columbia University Medical Center New York, New York Acquisitions Editor: Jamie M Elfrank Product Development Editor: Ashley Fischer Production Project Manager: David Orzechowski Manufacturing Manager: Beth Welsh Marketing Manager: Stephanie Manzo Design Coordinator: Teresa Mallon Production Service: SPi Global Copyright © 2015 Wolters Kluwer 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 978-1-4511-8689-5 1-4511-8689-4 Library of Congress Cataloging-in-Publication Data available upon request 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 6 pm, EST 1 0 9 8 7 6 5 4 3 2 1 To John and Marlene for a lifetime of support, to Rani for her editorial genius, and to Morgan for never letting me forget the bigger picture CONTRIBUTORS Darryl Abrams, MD Assistant Professor of Medicine Division of Pulmonary, Allergy, and Critical Care Department of Medicine Columbia University Medical Center Assistant Attending Physician Division of Pulmonary, Allergy, and Critical Care Department of Medicine New York-Presbyterian Hospital New York, New York Cara Agerstrand, MD Assistant Professor of Medicine Department of Medicine Columbia College of Physicians and Surgeons and the New York-Presbyterian Hospital New York, New York John E Arbo, MD Assistant Professor of Clinical Medicine Department of Medicine Weill Cornell Medical College Attending Physician Division of Emergency Medicine and Pulmonary Critical Care Medicine New York-Presbyterian Hospital/Weill Cornell Medical College New York, New York Anne-Sophie Beraud, MD, MS Consulting Instructor Division Cardiovascular Medicine Stanford University School of Medicine Stanford, California Staff Cardiologist Cardiovascular Medicine Clinique Pasteur Toulouse, France Rana Biary, MD Assistant Professor Department of Emergency Medicine Division of Medical Toxicology New York University Medical Center New York, New York Nicole Bouchard, MD, BSc Assistant Clinical Professor Director of Medical Toxicology Division of Emergency Medicine New York-Presbyterian Hospital/Columbia University Medical Center New York, New York Daniel Brodie, MD Associate Professor of Medicine Department of Medicine Columbia College of Physicians and Surgeons and the New York-Presbyterian Hospital New York, New York Carlos Brun, MD Clinical Instructor Department of Anesthesiology, Perioperative, and Pain Medicine Stanford University School of Medicine Stanford, California Attending and Intensivist Anesthesiology and Perioperative Care Service VA Palo Alto Health Care System Palo Alto, California Carla M Carvalho, MD Surgical Critical Care Fellow Stanford University Medical Center Stanford, California Betty C Chen, MD Acting Instructor Division of Emergency Medicine Department of Medicine University of Washington School of Medicine Attending Physician Division of Emergency Medicine Department of Medicine Harborview Medical Center Seattle, Washington Glenn Chertow, MD, MPH Norman S Coplon/Satellite Healthcare Professor of Medicine Chief, Division of Nephrology Stanford University School of Medicine Palo Alto, California Jey K Chung, MD Fellow Division of Pulmonary and Critical Care Medicine Stanford University Medical Center Stanford, California Nicholas J Connors, MD Medical Toxicology Fellow Division of Medical Toxicology Department of Emergency Medicine New York University School of Medicine New York, New York J Randall Curtis, MD, MPH A Bruce Montgomery—American Lung Association Endowed Chair in Pulmonary and Critical Care Medicine Division of Pulmonary & Critical Care Medicine University of Washington Professor of Medicine, Section Head Division of Pulmonary & Critical Care Harborview Medical Center Seattle, Washington Christopher Davis, MD, DTMH Assistant Professor Department of Emergency Medicine Altitude Research Center University of Colorado School of Medicine Aurora, Colorado Katy M Deljoui Critical Care Medicine Fellow Department of Pulmonary and Critical Care Medicine University of Maryland Medical Center Baltimore, Maryland Rachel H Dotson, MD Attending Physician Division of Pulmonary and Critical Care Medicine Department of Medicine California Pacific Medical Center San Francisco, California E Wesley Ely, MD, MPH Professor Division of Allergy, Pulmonary, and Critical Care Department of Internal Medicine Vanderbilt University Medical Center Nashville, Tennessee Morgan Eutermoser, MD, DTMH Wilderness Medicine Fellow Department of Emergency Medicine University of Colorado Aurora, Colorado Jose Evangelista III, MD Assistant Professor Department of Emergency Medicine Division of Undersea and Hyperbaric Medicine University of California San Diego San Diego, California Brandon Foreman, MD Clinical Fellow in Neurocritical Care/EEG Division of Neurocritical Care Department of Neurology Columbia University College of Physicians and Surgeons New York-Presbyterian Hospital New York, New York Shai Friedland, MD Assistant Professor Stanford University School of Medicine Staff Physician Gastroenterology Stanford University Hospital and Veteran Affairs Hospital Palo Alto Palo Alto, California Samuel Gerson, MD Assistant Clinical Professor infusion of g/kg body weight) in the treatment of patients with intracranial hypertension (ICP ≥30 mm Hg for >5 minutes) Compared to the 17 patients who did not receive mannitol therapy, those who underwent mannitol infusions had significantly higher overall survival (47.1% vs 5.9%).17 In a randomized controlled trial of 30% hypertonic saline in the management of 45 patients with ALF (using a target serum sodium level of between 145 and 150 mmol/L), a significantly lower incidence of intracranial hypertension was seen among the treatment group.18 For patients requiring mechanical ventilation, hyperventilation to a goal PaCO2 of 25 to 30 mm Hg results in vasoconstriction and decreased ICP and cerebral edema While mechanical hyperventilation has not been proven effective in the prevention of cerebral edema, it is commonly used for treatment of acute rises in ICP/cerebral edema.6,7 The role of hypothermia in the management of ALF patients is complex; it likely affects multiple factors responsible for the development of encephalopathy and intracranial hypertension.19–21 An early clinical study evaluated the role of hypothermia in seven patients with uncontrolled intracranial hypertension despite the aforementioned therapies Patients who were cooled to 32°C demonstrated a significant decline in ICP, from 45 to 16 mm Hg, with subsequent improvements in CPP.21 Other studies have reported that hypothermia used as adjunct to standard therapy may be helpful in patients with persistent uncontrolled intracranial hypertension, especially as a bridge toward liver transplantation19–21; however, well-designed randomized clinical trials for this application are lacking Pharmacologic coma and sedation, another adjunctive therapy, reduce ICP by suppressing cerebral metabolic activity and decreasing CPP Phenobarbital has been traditionally used for this purpose, but propofol has become the preferred sedative agent in many centers.22,23 Hepatic Encephalopathy Hepatic encephalopathy is a neurologic complication of ALF that requires early identification and aggressive treatment Accurate assessment (see grading system, below) of degree of encephalopathy helps inform the decision to initiate definitive ventilatory support and protect the patient's airway; prompt treatment helps prevent worsening cerebral edema Serum ammonia will be elevated in ALF and is hypothesized play a role in the pathogenesis of worsening cerebral edema and intracranial hypertension Lowering ammonia levels with lactulose and early dialysis may help treat or prevent the development of cerebral edema.1,11,24,25 The U.S Acute Liver Failure Study Group retrospectively evaluated the role of lactulose in the management of encephalopathy among ALF patients.25 While the severity of encephalopathy did not differ between patients in the treated and untreated groups, overall survival was slightly higher for patients receiving lactulose therapy.25 Care should be taken, however, to avoid lactulose therapy–associated dehydration and electrolyte disturbances The role of nonabsorbable antibiotics (e.g., rifaximin) in the management of encephalopathy in patients with ALF is not well studied26; as a result, rifaximin is not considered standard of care, but may be considered on a case-by-case scenario in consultation with the hepatology service Hepatic Encephalopathy Grading System Grade 1—changes in behavior, minimal change in consciousness Grade 2—gross disorientation, drowsiness, asterixis, slowness of mentation Grade 3—marked confusions, incoherent speech, sleeping, arousable to vocal stimuli Grade 4—comatose, unresponsive to pain, decorticate or decerebrate positioning Cardiovascular Complications The systemic inflammation and hormonal dysregulation that result from ALF can lead to systemic vasodilation, contributing to decreased MAP and CPP Adequate maintenance of cardiovascular perfusion directly affects the CPP and overall neurologic complications Initial management with intravascular volume repletion is aimed at maintaining MAP > 80 mm Hg and CPP > 60 mm Hg Patients should be resuscitated with normal saline first and switched to halfnormal saline with 75 mEq/L of sodium bicarbonate if acidosis is present Adjunctive therapy with vasopressor therapy may be needed to maintain/reach MAP and CPP targets Norepinephrine is the vasopressor of choice, with the addition of vasopressin to permit titration of the norepinephrine infusion.1,4 Hematologic Complications Coagulopathy is another common feature of ALF and correlates with a patient's degree of hepatic synthetic dysfunction Aggressive correction of thrombocytopenia and elevated INR is not necessary if there is no evidence of bleeding.27 Prior to invasive diagnostic or therapeutic interventions, however, coagulopathy may be corrected with fresh frozen plasma and platelets; goals for correction, however, are not well established In the setting of active gastrointestinal bleeding, more aggressive transfusion of cryoprecipitate may also be instituted Recombinant factor VIIa is an option for life-threatening bleeding but carries risk of thrombosis.28 Given the increased risk of gastrointestinal tract bleeding in the setting of coagulopathy and the risk of developing stress-induced ulcers, routine prophylactic acid suppression therapy is indicated In a multicenter, randomized placebo-controlled trial of 1,200 mechanically ventilated patients, acid suppression therapy was associated with significantly reduced risk of gastrointestinal bleeding (relative risk 0.44).29 While the study cohort was not limited to patients with ALF, the findings of this study have been used to support the routine use of acid suppression in ALF Renal Complications Acute renal failure is a common complication in ALF Hemodynamic alterations affecting adequate renal perfusion coupled with the direct nephrotoxicity of drugs and toxins such as acetaminophen and amanita poisoning contribute to worsening renal function ALF-induced acidosis, electrolyte abnormalities, and uremia can further contribute to renal impairment The renal failure, in turn, can exacerbate the systemic inflammatory response triggered by the ALF Fluid resuscitation to achieve optimal intravascular volume, coupled with vasopressor therapy to achieve MAP goals, can improve hypoperfusion-induced renal failure Early recognition of renal failure and, when indicated, initiation of renal replacement therapy with continuous venovenous hemodialysis (CVVH) can also assist significantly in the overall management of ALF.30,31 Early initiation of dialysis allows for more aggressive management of encephalopathy and elevated ICP by forced hypernatremia and lowering of blood ammonia levels Furthermore, CVVH has been demonstrated to improve cardiovascular stability in patients with ALF.30,31 In one study, 32 critically ill patients with ALF and acute renal failure were randomized to receive either intermittent or continuous modes of renal replacement therapy.31 Patients treated with CVVH had improved overall cardiovascular parameters, as measured by cardiac output and tissue oxygen delivery Infectious Complications Ninety percent of ALF patients develop some degree of infection, a result of the confluence of invasive monitoring and immune system dysfunction Severe bacterial or fungal infections can preclude liver transplantation and/or complicate the posttransplantation recovery.1,32–35 Pneumonia is the most common infection experienced by ALF patients, followed by urinary tract infections and catheter-related infections Gram-positive organisms are the most common infectious culprits, followed by gram-negative organisms and fungi.34,35 Surveillance cultures of blood, urine, and sputum and chest radiography should be routinely evaluated in patients with ALF In the absence of suspected infection, empiric prophylactic antibiotic or antifungal therapy has not been shown to provide a survival benefit.32,33 In one study, ALF patients without evidence of acute infection were randomized to receive or not to receive prophylactic parenteral and enteral antimicrobial therapy.33 While the treated group showed a significant reduction in the development of infections, overall survival was not significantly different between the treated and untreated groups Gut decontamination with poorly absorbable antibiotics has also not been shown to improve survival outcomes among ALF patients.36 Antibiotic or antifungal therapy should, however, be initiated if there is a clinical suspicion of infection or deteriorating clinical status (e.g., worsening hepatic encephalopathy or systemic inflammatory response syndrome) Metabolic Complications Severe metabolic and electrolyte abnormalities are common in patients with ALF, a result of multiorgan dysfunction Early recognition and correction of these derangements can prevent further deterioration.1 Some of the common metabolic complications that result from ALF include the following: Acidemia and alkalemia: Both are important predictors of mortality and need for liver transplantation Acid–base status is also an important component of the King's College criteria (Table 25.4),37 which is used to guide prognostication in patients with ALF Hypoglycemia: Patients with ALF experience hypoglycemia because of impaired glucose metabolism When hypoglycemia is identified, a continuous glucose infusion (e.g., 5% dextrose, half-normal saline) should be administered Hypophosphatemia, hypokalemia, and hypomagnesemia: These electrolyte disturbances are commonly encountered in the ALF Frequent monitoring of electrolytes with prompt repletion is needed to avoid associated complications Inadequate nutrition: As with other ICU patients, early initiation of enteral nutrition is preferred over parenteral nutrition in patients with ALF.40 TABLE 25.4 King's College Criteria for Assessment of Liver Failure Prognosis From O'Grady JG, Alexander GJM, Hayllar KM, et al Early indicators of prognosis in fulminant hepatic failure Gastroenterology 1989;97:439–455 Patients meeting the criteria are identified has having a poor prognosis MANAGEMENT GUIDELINES Acetaminophen Acetaminophen toxicity is by far the most common cause of ALF in the United States, accounting for over 50% of all cases in the United States.1,3,5 A detailed patient history is essential to diagnosing a deliberate or accidental overdose, especially given the multitude of both prescription and nonprescription medications that include acetaminophen Acetaminophen-related hepatotoxicity is a dose-related adverse event; while ingestion of >10 to 15 g over a period of 24 hours is typically needed to induce ALF, concurrent disease or individual variations in hepatic metabolism may allow significant damage from ingestion of only 3 to 4 g.41–43 In toxic acetaminophen ingestions, aminotransferase levels are characteristically elevated several hundred-fold above normal values, with a peak in the rise of aminotransferases typically occurring 48 to 72 hours following ingestion Use of the Rumack-Matthew acetaminophen nomogram can assist in prognosticating the risk of ALF in patients with less severe aminotransferase abnormalities.3,43 The nomogram plots the serum concentration of acetaminophen against last known ingestion time in an attempt to prognosticate hepatotoxicity and guide administration of therapy with Nacetylcysteine (NAC) Recently, acetaminophen–protein adducts, which have a longer half-life than acetaminophen, have been proposed as a means of identifying the cause of ALF in patients presenting without an identifiable etiology or undetectable acetaminophen levels.43,44 A recent study evaluated sera from 110 subjects with indeterminate ALF enrolled in the Acute Liver Failure Study Group.43 The sera of these patients, along with 199 positive controls of sera from patients with known acetaminophen-related ALF, were evaluated for acetaminophen–cysteine adducts Over 94.5% of controls demonstrated levels of adducts that confirmed acetaminophen toxicity; 18% of the indeterminate cases tested positive, which confirmed previous reports citing the high prevalence of unrecognized acetaminophen toxicity among patients with indeterminate liver failure.43 If ingestion occurs within 3 to 4 hours, administration of activated charcoal at a dose of g/kg orally may be of some benefit,45 however, NAC therapy remains the most beneficial intervention.46,47 One of the original studies evaluating the benefit of NAC in the treatment of acetaminophen-related ALF described the outcomes of 2,540 acetaminophen-toxic patients treated with oral NAC.47 Patients treated with oral NAC had significantly lower rates of hepatotoxicity and significantly reduced mortality; patients treated within hours of last ingestion had better outcomes that those who were treated at later intervals NAC can be administered orally or intravenously; however, the intravenous route is preferred given the lower risk of aspiration The dosing regimen for both oral and intravenous NAC is presented in Table 25.2 Nonacetaminophen Drug/Toxins Given the multitude of potentially hepatotoxic prescription and nonprescription drugs, a thorough patient history is essential Common culprits of mixedetiology ALF include antibiotics, antifungals, antituberculosis medications, sulfa-containing drugs, and psychiatric and neurologic medications including antiepileptics In addition to pharmaceutical agents, nutritional and herbal supplements need to be carefully evaluated for potential hepatotoxicity Early identification and removal of the offending agent, along with supportive care, are the mainstay of therapy in these cases.48,49 While NAC therapy has demonstrated greatest utility in patients with acetaminophen toxicity, it may also benefit patients with non–acetaminophenrelated ALF.50 In a prospective, double-blinded trial of 173 ALF patients without evidence of acetaminophen toxicity, a 72-hour infusion of NAC was compared to placebo (dextrose) in affecting survival outcomes While there was no statistically significant difference in overall 3-week survival seen between the NAC group and the placebo group (70% vs 66%), patients treated with NAC had significantly better 3-week transplant-free survival (40% vs 27%).50 The survival advantage was, however, limited to patients with less severe hepatic encephalopathy (grade 1 to 2) Mushroom poisoning with Amanita toxin is a potentially lethal cause of ALF As there is no serologic test to confirm exposure, a careful patient/observer history is essential, both to identify the fungus and to estimate the timing of exposure Patients presenting with recent ingestion may benefit from nasogastric lavage to attempt removal of remaining toxic material Silibinin and penicillin are accepted antidotes to mushroom poisoning While greater evidence supports the efficacy of silibinin, this treatment is not available as a licensed drug in the United States.51,52 However, when Amanita poisoning is suspected, an application to the Food and Drug Administration for emergency use of this agent is possible Silibinin is administered orally or intravenously at a dose of 30 to 40 mg/kg/d for to days Penicillin is an acceptable alternative in conjunction with NAC treatment Amanita toxin is excreted in the bile, and the use of nasobiliary drainage or aspiration of the second portion of the duodenum (ideally performed in an ICU) may decrease enterohepatic circulation of the toxin.53 Viral Hepatitis Acute viral hepatitis accounts for approximately 12% of all cases of ALF in the United States.54,55 Several viruses have the potential to induce liver failure, each with its own unique risk factors, routes of transmission, diagnostic workup, and targeted treatment regimen Acute hepatitis A infection (HAV) is a common ailment spread primarily through fecal–oral transmission The diagnosis can be confirmed with positive anti-HAV IgM Most HAV infections resolve with supportive therapy that includes fluid resuscitation and correction of electrolyte disturbances However, any signs of hepatic dysfunction, including encephalopathy or coagulopathy, or signs of multiorgan dysfunction (e.g., renal failure or respiratory failure) require hospital admission and monitoring for development of ALF Acute hepatitis B infection (HBV) most often occurs as a result of intravenous drug use or sexual transmission Acute HBV is confirmed by the presence of anti-HBV core Ab IgM HBV antigen and HBV viral DNA may also be present As in acute HAV, patient evaluation in acute HBV centers on assessment of organ function and identification of early symptoms of ALF that would require hospital admission Following an initial diagnostic workup and appropriate resuscitation in the ED, inpatient treatment is generally guided by the hepatology service First-line treatment for HBV consists of tenofovir 300 mg/d or entecavir 0.5 mg/d.56 A randomized, placebo-controlled trial of patients with ALF secondary to HBV demonstrated that treatment with tenofovir was associated with significantly lower HBV viral DNA levels and improved liver disease severity, as measured by the model for end-stage liver disease (MELD) score and Child-Pugh score.56 In addition, patients who were treated with tenofovir had significantly higher 3-month survival compared to patients who received placebo (57% vs 15%).56 Acute hepatitis C infection (HCV) in the United States is associated primarily with intravenous drug use in the United States; the diagnosis can be confirmed with anti-HCV Ab and HCV viral RNA ALF secondary to acute HCV is rare The timing of antiviral therapy for acute HCV is unclear; current studies lack definitive data, and recently developed anti-HCV therapies have not undergone well-designed clinical trials In patients with uncomplicated acute HCV, monitoring for spontaneous clearance of HCV RNA over a 12- to 16-week period is reasonable The evidence for antiviral therapy in the setting of HCVinduced ALF is less clear, and general supportive measures should be instituted instead.57 Acute hepatitis D infection (HDV) is rare and occurs either as a coinfection with HBV or as superimposed acute HDV in a patient with chronic HBV Diagnosis is conferred with the anti-HDV Ab and HDV antigen; supportive care occurs concurrently with treatment of the HBV infection Acute hepatitis E infection (HEV) is transmitted via fecal–oral route, and diagnosis is confirmed with anti-HEV IgM and IgG Treatment is supportive With all the acute viral hepatitis infections, the initial evaluation and management in the ED focus on supportive care, including fluid and electrolyte resuscitation The appropriate laboratory workup as previously described should be initiated; treatment is usually guided by the diagnosis and initiated by the inpatient team Autoimmune Hepatitis Autoimmune hepatitis can present with a wide spectrum of clinical disease severity While it is often diagnosed in the workup of mild elevations in aminotransferase levels and vague systemic complaints, autoimmune hepatitis can also present in a fulminant course with ALF.58,59 A suspicion for autoimmune hepatitis is gleaned from a complete patient history of potential comorbid autoimmune disease states Initial evaluation in the ED should include antinuclear antibodies (ANA), anti–smooth muscle antibodies (ASMA), and total serum IgG A thorough workup to exclude viral hepatitis and alcoholic liver disease further supports the diagnosis of autoimmune hepatitis In patients with negative serologic markers in whom the suspicion for this etiology remains, liver biopsy may help to confirm diagnosis Once ALF secondary to autoimmune hepatitis is confirmed, timely initiation of immunosuppressive therapy is critical and may reduce the progression of disease and need for liver transplantation.59 The initial evaluation in the ED should focus on ensuring that the diagnostic workup is sufficient to evaluate for this process Wilson Disease Wilson disease is a rare cause of liver disease; it is caused by a defect in copper metabolism and characterized by Kayser-Fleischer rings (secondary to copper deposition at the corneoscleral junction of the eye) and neuropsychiatric disease (secondary to copper deposition in the brain) Coombs-negative hemolytic anemia is a common associated presentation A characteristic biochemical finding is an extremely low alkaline phosphatase (ALK) in the setting of marked elevation of aminotransferases Early identification is important for prompt initiation of liver transplant evaluation Initial diagnostic tests that can be sent from the ED include serum ceruloplasmin and routine liver function tests Further diagnostic testing with urinary copper levels and liver biopsy with quantitative copper concentration in patients with high suspicion of Wilson disease can help confirm the diagnosis The hepatology service should be consulted to evaluate the need for liver biopsy In the setting of ALF, treatment in the ED should be supportive while the patient is rapidly evaluated for liver transplantation.1 Vascular Disease “Shock liver” is a relatively common syndrome of ischemic hepatitis, characterized by acute elevation of aminotransferase levels Precipitated by severe hypotension or hypovolemia resulting in hepatic ischemia, this syndrome is common in patients with underlying cardiac disease or severe congestive heart failure Post–cardiac arrest patients who experience a period of hepatic hypoperfusion will often present with some degree of ischemic hepatitis Correction of the underlying etiology and prompt initiation of cardiovascular support generally lead to recovery of hepatic function and usually prevent the need for liver transplant.1,60 Overall prognosis, however, depends on the etiologies that precipitate the ischemic event Budd-Chiari syndrome is a rare disease precipitated by hepatic venous outflow obstruction resulting in hepatic decompensation and ALF.60,61 Hepatic vein obstruction is generally secondary to thrombosis, and an underlying hypercoagulable state should be evaluated for Acute abdominal pain, new-onset ascites, and marked hepatomegaly are often found on clinical presentation The diagnostic approach relies on radiographic evidence of obstructive disease, preferably obtained through abdominal ultrasonography with Doppler flow Contrast-enhanced computed tomography and magnetic resonance venography are alternative diagnostic tools, but should be used with caution, as many patients presenting with ALF have impaired renal function A diagnosis of Budd-Chiari requires a comprehensive workup to determine the underlying prothrombotic disorder Potential culprits include hematologic disorders and hematologic malignancy (which, if diagnosed, may preclude the option of transplantation) Anticoagulation therapy and venous decompression (i.e., transjugular intrahepatic portosystemic shunting) have a role in the management of Budd-Chiari syndrome, but patients presenting with ALF as a result of this disease have a poorer prognosis, and liver transplantation may be the preferred therapeutic option.60,61 In the ED, initial workup involves early resuscitation and the initiation of appropriate laboratory and radiographic diagnostic evaluation Pregnancy-Related Disease Pregnancy-related liver disease is relatively rare, and the development of ALF in pregnant patients is even more rare.62 Both acute fatty liver of pregnancy and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) generally occur during the third trimester of pregnancy and can result in progressive hepatic injury leading to liver failure In addition to abnormal aminotransferase levels and thrombocytopenia, jaundice, coagulopathy, preeclampsia, and hypoglycemia are often seen in the setting of pregnancyrelated ALF Treatment is supportive, and prompt delivery of the fetus in consultation with a high-risk obstetrics team generally results in rapid recovery of hepatic function.62 While rare, liver transplantation may need to be considered in postpartum patients with persistent or progressively worsening hepatic dysfunction CONCLUSION ALF is a significant cause of morbidity and mortality in the United States Prompt recognition of ALF is important to initiate the appropriate diagnostic workup and to triage the patient toward an appropriate critical care setting While the diagnostic evaluation and subsequent management of ALF are complicated, the emergency physician plays a key role in assessing the severity of disease and initiating the appropriate diagnostic testing required to confirm the underlying etiology Severely ill ALF patients should always be admitted to an ICU or transferred to a liver transplantation center as needed LITERATURE TABLE CI, confidence interval; RR, relative risk REFERENCES Lee WM, Stravitz RT, Larson AM Introduction to the revised American Association for the Study of Liver Diseases Position Paper on acute liver failure 2011 Hepatology 2012;55(3):965–967 Lee WM, Squires RH Jr., Nyberg SL, et al Acute liver failure: summary of a workshop Hepatology 2008;47:1401–1415 Ostapowicz GA, Fontana RJ, Schiodt FV, et al Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States Ann Intern Med 2002;137:947–954 Stravitz RT, Kramer DJ Management of acute liver failure Nat Rev Gastroenterol Hepatol 2009;6:542–553 Larson AM, Polson J, Fontana RJ, et al.; for the Acute Liver Failure Study Group Acetaminopheninduced acute liver failure: results of a United States multicenter, prospective study Hepatology 2005;42:1364–1372 Strauss G, Hansen BA, Knudsen GM, et al Hyperventilation restores cerebral blood flow autoregulation in patients with acute liver failure J Hepatol 1998;28:199–203 Ede RJ, Gimson AE, Bihari D, et al Controlled hyperventilation in the prevention of cerebral oedema in fulminant hepatic failure J Hepatol 1986;2:43–51 Stravitz RT, Kramer AH, Davern T, et al.; for the Acute Liver Failure Study Group Intensive care of patients with acute liver failure: recommendations of the U.S Acute Liver Failure Study Group Crit Care Med 2007;35:2498–2508 Frontera JA, Kalb T Neurological management of fulminant hepatic failure Neurocrit Care 2011;14:318–327 10 Vaquero J, Chung C, Cahill ME, et al Pathogenesis of hepatic encephalopathy in acute liver failure Semin Liver Dis 2003;23:259–269 11 Bernal W, Hall C, Karvellas CJ, et al Arterial ammonia and clinical risk factors for encephalopathy and intracranial hypertension in acute liver failure Hepatology 2007;46:1844–1852 12 Munoz SJ Difficult management problems in fulminant hepatic failure Semin Liver Dis 1993;13:395–413 13 Vaquero J, Fontana RJ, Larson AM, et al Complications and use of intracranial pressure monitoring in patients with acute liver failure and severe encephalopathy Liver Transpl 2005;11:1581–1589 14 Munoz SJ, Robinson M, Northrup B, et al Elevated intracranial pressure and computed tomography of the brain in fulminant hepatocellular failure Hepatology 1991;13:209–212 15 Lidofsky SD, Bass NM, Prager MC, et al Intracranial pressure monitoring and liver transplantation for fulminant hepatic failure Hepatology 1992;16:1–7 16 Larsen FS, Hansen BA, Ejlersen E, et al Cerebral blood flow, oxygen metabolism and transcranial Doppler sonography during high-volume plasmapheresis in fulminant hepatic failure Eur J Gastroenterol Hepatol 1996;8:261–265 17 Canalese J, Gimson AES, Davis C, et al Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure Gut 1982;23:625–629 18 Murphy N, Auzinger G, Bernal W, et al The effect of hypertonic sodium chloride on intracranial pressure in patients with acute liver failure Hepatology 2002;39:464–470 19 Stravitz RT, Larsen FS Therapeutic hypothermia for acute liver failure Crit Care Med 2009;37:S258–S264 20 Jalan R, Damink SWMO, Deutz NE, et al Moderate hypothermia prevents cerebral hyperemia and increase in intracranial pressure in patients undergoing liver transplantation for acute liver failure Transplantation 2003;75:2034–2039 21 Jalan R, Olde Damink SW, Deutz NE, et al Moderate hypothermia in patients with acute liver failure and uncontrolled intracranial hypertension Gastroenterology 2004;127:1338–1346 22 Forbes A, Alexander GJ, O'Grady JG, et al Thiopental infusion in the treatment of intracranial hypertension complicating fulminant hepatic failure Hepatology 1989;10:306–310 23 Wijdicks EF, Nyberg SL Propofol to control intracranial pressure in 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A single center experience with 50 patients Hepatology 1995;21:1337–1344 62 Hay JE Liver disease in pregnancy: a review Hepatology 2008;47:1067–1076 ... in critical care medicine following fellowship training Decision Making in Emergency Critical Care: An Evidence-Based Handbook is a portable guide to diagnosis and treatment in emergency critical care for the... rational clinical decision making in the challenging—and changing—world of emergency critical care John E Arbo, MD CONTENTS Contributors Preface: From The Editor Section 1 Introduction Chapter 1 Emergency Critical Care... government employees are not covered by the above-mentioned copyright Printed in China 978 -1- 4 511 -8689-5 1- 4 511 -8689-4 Library of Congress Cataloging -in- Publication Data available upon request Care has been taken to confirm the accuracy of the information presented and to describe generally

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