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Acute Liver Failure Acute Liver Failure ••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••• When liver failure occurs in a previou ly healthy individual, it onset is often o rapid that it take experienced physicians by WILLIAM M. LEE surprise. Terms such a hyperacute or fulminant hepatic necrosis have been u ed to emphasize the rapidity and everity of the JULIE POLSON condition. The onset of acute liver failure is heralded by an altered mental state, often with agitation and confusion that may proceed to coma, and by evidence of coagulopathy [1 - 4]. The diagno is of acute liver failure require that these symptom develop in a patient without preexisting chronic liver disease. Although not all observers agree on precise definitions, it is generally accepted that onset of liver-related illness (usually, but not always, accompanied by jaundice) les than 8 weeks before patient presentation with altered mentation and coagulopathy fits the designation of acute liver failure. Development of these signs within a week of onset of liver disease and as much as 6 months from the first sign of illness is sometimes referred to as hyperacute and ubacute liver failure, respectively. An immediate challenge in managing sud1 patients is deter­ mination of the cause of acute liver failure in each case. Wherea certain factors, such a extent of encephalopathy and development of various complications, have an impact on outcome, the underlying etiology best determines the likeli­ hood of spontaneous survival or the need for urgent liver trans­ plantation [3,4]. The primary cause of acute liver failure vary in prevalence in different region of the world, and include drug toxicity and viral infections; there i also a large category of cases in which the pecific etiology cannot be determined. Other less common but important cau es include autoimmune hepatitis, Wilson di ea e, ischemic injury secondary to cardiac dysfunction or to drug effects, the Budd-Chiari syndrome, malignant infiltration, and fatty liver of pregnancy [3-9). Whatever the cause, the resulting disea e process involves exten­ sive loss of hepatocyte mass and functional capacity. Unique clinical features of acute liver failure include altered mental status with evolution of cerebral edema ensuing in many patients [2,3,10 ]. II ere, a stark contra t exists with W. C. Maddrey (ed.), Atlas of the Liver © Springer Science+Business Media New York 2004 cirrhotic liver disease, in which cerebral edema is rarely seen. tion. Such cases will most frequently be due to hepatitis B or, The hypotension and peripheral vasodilation seen in less often, to hepatitis A. Occasionally, acute hepatitis D may cirrhosis, however, are observed in patients with acute liver be diagnosed in a hepatitis B-positive individual. Hepatitis C failure. Loss of intravascular fluid volume into the interstitial alone does not appear to cause true acute liver failure. tissues results in renal failure and lactic acidosis if volume Hepatitis E is a significant cause of acute liver failure in some status cannot be carefully maintained. Bleeding from the developing countries, and tends to be more severe in preg­ gastrointestinal tract, increased susceptibility to a variety of nant women [15-17]. nosocomial infections, occasional cardiac arrhythmias, adult The hallmark of treatment consists of good intensive care respiratory distress syndrome, and the multiple organ and support because no specific therapy has yet been discov­ dysfunction syndrome are observed, testifying to the wide­ ered that provides the required rapid hepatic regeneration. spread organ involvement engendered by the sudden loss of Attention to careful fluid management, surveillance for infec­ hepatocyte function [2]. tion and prompt resuscitation for evidence of gastrointestinal Liver biopsy in these critically ill patients is generally not bleeding are important. Platelets and plasma may be required feasible because of coagulopathy, but a transjugular approach but are usually administered only with evidence of hemor­ may be used with less bleeding risk. When tissue is available, rhage. Elevation of intracranial pressure may lead to brain­ the typical findings are massive necrosis of hepatocytes with stem herniation and death. Specific therapy with intravenous varying degrees of inflammation. Biopsy is especially valuable mannitol may be used to abort signs of intracranial hyperten­ when tumor infiltration is suspected, since this diagnosis sion, such as decerebrate posturing, pupillary dilatation, and precludes consideration of transplantation. respiratory pattern changes. Risk of gastrointestinal bleeding In addition to determination of likely etiology, initial diag­ can be minimized with prophylactic use of histamine-2- nostic efforts are directed at confirming the presence of coag­ receptor blockers or proton pump inhibitors [4, 18]. Hepatic ulation changes, elevated ammonia levels, and a central transplantation produces dramatic patient rescues; 1-year nervous system-mediated respiratory alkalosis. Not only survival rates have been reported at greater than 70% [19,20]. prognosis but also potential treatment decisions hinge on Unfortunately, difficulties in timing of transplantation and in diagnosis of certain causes of acute liver failure. Historical predicting prognosis, as well as a lack of readily available evidence of ingestion of excessive amounts of acetamino­ donor organs, continue to limit the use of this often lifesaving phen, either as an intended suicidal overdose or the inadver­ technique. Various liver-support devices are continually being tent use of supertherapeutic amounts of pain medications, tested as potential bridges to transplantation, but as yet none should be of paramount concern because timely administra­ has provided reliable improvement in outcome [4,21-23]. tion of N-acetylcysteine may prove to be lifesaving [11,12]. It The crisis that so rapidly evolves in acute liver failure can should be remembered that significant hepatotoxicity may quickly dissipate once the failing liver begins to recover its occur even when recommended doses of acetaminophen are own intrinsic function. The most recent data show that as ingested in the presence of chronic alcohol abuse or other many as two thirds of patients with acute liver failure from poor nutritional states [13]. Similarly, mushroom poisoning acetaminophen overdose recover spontaneously. The fact must be specifically indicated in the history so that proper remains, however, that some groups, such as cases of idiosyn­ antidotes may be given [14]. In the absence of clear toxin cratic drug toxicity and those of indeterminate etiology, still overdose or other immediately evident etiology, hepatitis have less than 25% survival without liver transplantation; such serologies are generally indicated to look for acute viral infec- numbers highlight the gravity of this relatively rare condition. ifpi Atlas of the Liver EPIDEMIOLOGY AND ETIOLOGY . , • Acetammophen Hepatitis A •HepalltisB United Kingdom India United States United States D Drug (1983-1995) (1998-2002) Other FIGURE 7-1 . Estimated prevalence of common causes of acute liver failure account for more than 50% of patient hospital admissions for worldwide. Great variation is observed between the United acute liver failure in certain urban areas 12, 13]. Furthermore, Kingdom (high prevalence of acetaminophen toxicity) and India significant numbers of unintentional acetaminophen poisoning (predominantly hepatitis B and others, including a large cases are being recognized, in which the medication is taken to percentage of hepatitis E cases) 124]. An increasing proportion of relieve pain, without suicidal intent. Whether ethanol abuse is a acute liver failure in the United States is attributable to acetamino­ cofactor in these cases is not entirely clear. phen. Although generally with better outcomes, these cases may TABLE 7-1. TABLE 7-1. PRINCIPAL CAUSES OF ACUTE acute liver failure. Cause of acute liver failure is LIVER FAILURE Principal causes of important because it determines prognosis. In some instances, initial management must be directed at the specific cause. Disease­ Drug-related hepatotoxicity specific treatments include antidotes to acetaminophen and mush­ room poisoning that must be given immediately on patient admis­ Acetaminophen sion to the hospital. Identification of severe heart failure as the Idiosyncratic drug reactions cause indicates proper resuscitation and correction of any fluid Indeterminate etiology balance disturbance. Likewise, recognition of acute fatty liver of Viral hepatitis pregnancy leads to consideration of delivery of the mother as the logical treatment for this condition. Patients with fulminant Acute hepatitis 8 Wilson disease carry such a poor prognosis that urgent listing for Acute hepatitis A transplantation must be immediately undertaken once this diag­ Others (hepatitis E, others rare) nosis is made, although therapy with trientine or penicillamine is Autoimmune hepatitis often initiated. Ischemic liver inJury Cardiogenic "shock" Other (eg, cocaine, methamphetamines, ephedrine) Miscellaneous causes Wilson disease Budd-Chiari syndrome Acute fatty liver of pregnancy Malignancy Veno-occlus1ve disease Acute Liver Failure IQI FIGURE 7-2. Reactivation of inactive hepatitis B after chemotherapy. Patients It is not clear whether these mutations are directly related to the with fulminant hepatitis B infection often clear the virus rapidly, fulminant course. presumably as the result
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