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A Guide to Managing Acute Liver Failure

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A Guide to Managing Acute Liver Failure REVIEW CME EDUCATIONAL OBJECTIVE: Readers will recognize and manage acute liver failure appropriately CREDIT TAVANKIT SINGH, MD NANCY GUPTA, MD NAIM ALKHOURI, MD WILLIAM D. CAREY, MD IBRAHIM A. HANOUNEH, MD Department of Internal Medicine, Department of Internal Medicine, Department of Gastroenterology and Department of Gastroenterology Minnesota Gastroenterology, P.A., Medicine Institute, Westchester Medical Center, Hepatology, and Department of Pediatric and Hepatology, Digestive Disease Minneapolis, MN Cleveland Clinic New York Medical College, Gastroenterology, Digestive Disease Institute, Cleveland Clinic; Professor, Valhalla, NY Institute, Cleveland Clinic; Assistant Cleveland Clinic Lerner College of Professor, Cleveland Clinic Lerner College Medicine of Case Western Reserve of Medicine of Case Western Reserve University, Cleveland, OH University, Cleveland, OH A guide to managing acute liver failure ABSTRACT hen the liver fails, it usually fails Wgradually. The sudden (acute) onset of Nearly 2,000 cases of acute liver failure occur each year liver failure, while less common, demands in the United States. This disease carries a high mortality prompt management, with transfer to an in- rate, and early recognition and transfer to a tertiary medi- tensive care unit, specific treatment depend- cal care center with transplant facilities is critical. This ing on the cause, and consideration of liver article reviews the definition, epidemiology, etiology, and transplant, without which the mortality rate management of acute liver failure. is high. This article reviews the definition, epide- KEY POINTS miology, etiology, and management of acute liver failure. In the United States, the most common cause of acute liver failure is acetaminophen toxicity, followed by viral ■ DEFINITIONS hepatitis. Acute liver failure is defined as a syndrome of acute hepatitis with evidence of abnormal co- Testing for the cause of acute liver failure needs to start agulation (eg, an international normalized ra- as soon as possible so that specific treatment can be initi- tio > 1.5) complicated by the development of ated and the patient can be placed on the transplant list mental alteration (encephalopathy) within 26 if needed. weeks of the onset of illness in a patient without a history of liver disease.1 In general, patients Acetylcysteine and either a proton pump inhibitor or have no evidence of underlying chronic liver disease, but there are exceptions; patients with a histamine H2 receptor blocker should be given to all patients with acute liver failure. Liver transplant is the Wilson disease, vertically acquired hepatitis B cornerstone of therapy in patients not responding to virus infection, or autoimmune hepatitis can present with acute liver failure superimposed other treatments. on chronic liver disease or even cirrhosis. The term acute liver failure has replaced There are a number of prognostic scores for acute liver older terms such as fulminant hepatic failure, failure, but each has limitations. hyperacute liver failure, and subacute liver fail- ure, which were used for prognostic purposes. Patients with hyperacute liver failure (defined as development of encephalopathy within 7 days of onset of illness) generally have a good prognosis with medical management, whereas those with subacute liver failure (defined as de- velopment of encephalopathy within 5 to 26 Dr. Alkhouri has disclosed membership on advisory committees or review panels for Bristol-Myers Squibb, Gilead Sciences, and Intercept. Dr. Carey has disclosed ownership interest in Gilead Sci- weeks of onset of illness) have a poor prognosis ences and Pfizer. without liver transplant.2,3 doi:10.3949/ccjm.83a.15101 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 83 • NUMBER 6 JUNE 2016 453 Downloaded from www.ccjm.org on October 1, 2021. For personal use only. All other uses require permission. ACUTE LIVER FAILURE Metabolism and hepatotoxicty of acetaminophen Acetaminophen Acetaminophen is generally safe, but excessive doses and conditions that overwhelm its normal metabolic pathways can lead to liver damage. + Glucuronic acid Acetaminophen Higher glucuronide doses (excreted in urine) Glucuronidation, sulfation, and subsequent renal excretion normally remove 90% of a therapeutic dose, but these pathways can become Acetaminophen saturated after an acetaminophen overdose. + Sulfates sulfate (excreted in urine) (CYP2E1) (CYP1A2) Cytochrome P450 metabolism produces a toxic metabolite, N-acetyl-p-benzoquinone (CYP3A4) imine (NAPQI). This pathway produces more NAPQI after higher doses, or when the (CYP2A6) relevant cytochrome P450 (CYP) enzymes are induced by other drugs or chronic alcohol consumption. NAPQI is toxic to the liver. Mercapturic acid + Glutathione (excreted in urine) Conjugation of sulfhydryl groups of glutathione normally detoxifies NAPQI. However, glutathione can become depleted after large doses of acetaminophen Liver damage or in malnourished people, allowing this toxic metabolite to accumulate. FIGURE 1. Reprinted from Schilling A, Corey R, Leonard M, Eghtesad B. Acetaminophen: old drug, new warnings. Cleve Clin J Med 2010; 77:19–27. ■ NEARLY 2,000 CASES A YEAR with acute liver failure.1 Nearly half of them There are nearly 2,000 cases of acute liver present after intentionally taking a single failure each year in the United States, and it large dose, while the rest present with unin- tentional toxicity while taking acetamino- accounts for 6% of all deaths due to liver dis- phen for pain relief on a long-term basis and ease.4 It is more common in women than in ingesting more than the recommended dose.6 men, and more common in white people than After ingestion, 52% to 57% of acetamin- in other races. The peak incidence is at a fairly ophen is converted to glucuronide conjugates, young age, ie, 35 to 45 years. and 30% to 44% is converted to sulfate conju- gates. These compounds are nontoxic, water- ■ CAUSES soluble, and rapidly excreted in the urine. The most common cause of acute liver fail- However, about 5% to 10% of ingested ure in the United States and other Western acetaminophen is shunted to the cytochrome countries is acetaminophen toxicity, followed P450 system. P450 2E1 is the main isoenzyme by viral hepatitis. In contrast, viral hepatitis is involved in acetaminophen metabolism, but the most common cause in developing coun- 1A2, 3A4, and 2A6 also contribute.7,8 P450 tries.5 2E1 is the same isoenzyme responsible for eth- anol metabolism and is inducible. Thus, regu- Acetaminophen toxicity lar alcohol consumption can increase P450 Patients with acetaminophen-induced liver 2E1 activity, setting the stage under certain failure tend to be younger than other patients circumstances for increased acetaminophen 454 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 83 • NUMBER 6 JUNE 2016 Downloaded from www.ccjm.org on October 1, 2021. For personal use only. All other uses require permission. SINGH AND COLLEAGUES metabolism through this pathway. TABLE 1 Metabolism of acetaminophen through the cytochrome P450 pathway results in pro- Advice to patients taking acetaminophen duction of N-acetyl-p-benzoquinone imine Acetaminophen is used to treat pain and fever. Overall, it is safe, but if (NAPQI), the compound that damages the you take too much (more than 4,000 mg per day), it can damage the liver. NAPQI is rendered nontoxic by bind- liver. If you are taking it, please do the following: ing to glutathione, forming NAPQI-glutathi- Read the label. Many medicines contain acetaminophen, so you one adducts. Glutathione capacity is limited, could be taking too much without knowing. however. With too much acetaminophen, glu- tathione becomes depleted and NAPQI accu- Don’t drink. Drinking alcohol increases the likelihood of acetamino- mulates, binds with proteins to form adducts, phen-induced liver toxicity. and leads to necrosis of hepatocytes (Figure Get help. If you or your child may have taken too much acetamino- 1).9,10 phen, call the American Association of Poison Control Centers hotline Acetylcysteine, used in treating acetamin- at 1-800-222-1222 right away. ophen toxicity, is a substrate for glutathione Keep acetaminophen (and all drugs) out of the hands of children. synthesis and ultimately increases the amount of glutathione available to bind NAPQI and prevent damage to hepatocytes.11 Statins can also cause acute liver failure, Acetaminophen is a dose-related toxin. especially when combined with other hepato- Most ingestions leading to acute liver failure toxic agents.16 exceed 10 g/day (> 150 mg/kg/day). Moder- The herbal supplements and weight-loss ate chronic ingestion, eg, 4 g/day, usually leads agents Hydroxycut and Herbalife have both to transient mild elevation of liver enzymes been reported to cause acute liver failure, with in healthy individuals12 but can in rare cases patients presenting with either the hepatocel- cause acute liver failure.13 lular or the cholestatic pattern of liver injury.17 Whitcomb and Block14 retrospectively The exact chemical in these supplements that identified 49 patients who presented with ac- causes liver injury has not yet been determined. etaminophen-induced hepatotoxicity in 1987 The National Institutes of Health main- Acetylcysteine through 1993; 21 (43%) had been taking ac- tains a database of cases of liver failure due is the main etaminophen for therapeutic purposes. All 49 to medications and supplements at livertox. patients took more than the recommended nih.gov. The database includes the pattern of drug used for limit of 4 g/day, many of them while fasting hepatic injury, mechanism of injury, manage- treating and some while using alcohol. Acute liver fail- ment, and outcomes. acetaminophen ure was seen with ingestion of more than 12 g/ day—or more than 10 g/day in alcohol users. Viral hepatitis toxicity The authors attributed the increased risk to Hepatitis B virus is the most common viral cause of acute liver failure and is responsible activation of cytochrome P450 2E1 by alcohol 18 and depletion of glutathione stores by starva- for about 8% of cases. tion or alcohol abuse. Patients with chronic hepatitis B virus in- Advice to patients taking acetaminophen fection—as evidenced by positive hepatitis B is given in Table 1.
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