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• W4250460639 abstract "Review ArticlesAcute Liver Failure Mohammad Sultan KhurooMD, DM, FACP, FRCP(Edin) Mohammad Sultan Khuroo Address reprint requests and correspondence to Professor Khuroo: Department of Medicine (MBC-46), King Faisal Specialist Hospital and Research Centre, P.O. Box 3354, Riyadh 11211, Saudi Arabia. From the Department of Medicine, Section of Gastroenterology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia. Search for more papers by this author Published Online::1 Jul 1998https://doi.org/10.5144/0256-4947.1998.318SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutIntroductionMS Khuroo, Acute Liver Failure. 1998; 18(4): 318-326Acute liver failure (ALF) is a dramatic and challenging syndrome in clinical medicine. Although an uncommon disorder, it is usually fatal. At present there is no universally accepted criteria for diagnosis of ALF. However, for practical purposes, it is defined as the occurrence of encephalopathy in a previously healthy person, within six months from onset of severe liver disease.1,2 This syndrome is subdivided into fulminant hepatic failure, if onset of encephalopathy is within eight weeks, and late onset hepatic failure, if the onset of encephalopathy is 8-24 weeks from the onset of liver disease. The definition usually includes the absence of preexisting liver disease, however, ALF may be the presentation of Wilson's disease, autoimmune chronic active hepatitis, and chronic hepatitis B infection.3–7 ALF has been subdivided into a number of syndromes by various investigators, based on the duration between onset of jaundice to onset of encephalopathy (Table 1).8–13 These syndromes differ from each other in etiology, disease course, complications and survival, and should help in defining treatment strategies. Hepatic encephalopathy of ALF must be differentiated from hepatic encephalopathy in patients with chronic liver disease, the so-called portosystemic encephalopathy (Table 2).14,15Table 1. The various syndromes of acute liver failure and their characteristics.Table 1. The various syndromes of acute liver failure and their characteristics.Table 2. The differentiating features of encephalopathy in acute liver failure and chronic liver disease (portosystemic encephalopathy).Table 2. The differentiating features of encephalopathy in acute liver failure and chronic liver disease (portosystemic encephalopathy).EPIDEMIOLOGYThere is little information on the epidemiology of ALF in various regions of the world. Crude estimates suggest that there are approximately 2000 deaths per year from ALF related to viral hepatitis in the United States.1 In contrast, ALF caused by hepatitis E is a national health problem in the developing countries. Hepatitis E causes large-scale epidemics of hepatitis in the Indian subcontinent, involving hundreds of thousands of cases with high mortality.16ETIOLOGYALF can result from diverse etiological agents (Table 3).17,18 Of these, hepatitis viruses, acetaminophen overdose and idiosyncratic drug reactions constitute the bulk of cases. Metabolic and vascular liver diseases (Figure 1), liver diseases unique in pregnancy (Figure 2) and a number of miscellaneous liver diseases causes a small number of the remaining cases.Figure 1A. Acute liver failure caused by hepatic vein thrombosis. This 30-year-old woman developed abdominal pain, ascites, jaundice and progressive encephalopathy during 36 weeks of her pregnancy. She died with massive gastrointestinal bleeding and cerebral edema two weeks after the onset of her illness. Abdominal computed tomographic scan after oral and intravenous administration of contrast medium, showing extensive hypodense areas suggestive of hepatic congestion.Download FigureFigure 1B. Photograph of sliced liver at autopsy revealing extensive hemorrhage in the liver parenchyma.Download FigureFigure 1C. Microphotograph of liver revealed multiple thrombi in hepatic veins, extensive centrilobular hemorrhagic necrosis and a few islands of surviving liver cells.Download FigureFigure 2A. Acute liver failure caused by hepatic infarction in a pregnant woman. Abdominal computed tomographic scan: nonenhanced scan (right panel) revealed a large hypodense area in the right lobe of liver with irregular hyperdense area around the lesion suggestive of calcification. The contrast enhanced scan (left panel) revealed the large hypodense lesion with marked contrast enhancement of the surrounding liver.Download FigureFigure 2B. Microphotograph of needle biopsy of liver revealing extensive areas of hepatic infarction with two foci of parenchymal calcification.Download FigureTable 3. The etiological causes of acute hepatic failure.Table 3. The etiological causes of acute hepatic failure.AcetaminophenThe most common cause of ALF in the United Kingdom is related to acetaminophen toxicity in association with a suicidal or parasuicidal episodes.19,20 Hepatotoxicity has been reported after therapeutic doses in patients who are concurrently taking enzyme-inducing drugs, such as phenytoin, and in patients who are chronic consumers of alcohol. Alcohol acetaminophen syndrome is emerging as an important cause of ALF in the United States. The syndrome is characterized by extremely high transaminase levels and a poor prognosis.21,22Viral HepatitisHepatitis A is a relatively uncommon cause of ALF. This is due to the benign course of illness caused by this agent, with case fatality rates of around 0.1%-0.4%1,14 Hepatitis E is the most common cause of ALF in endemic regions of the world, with high mortality (25%) in pregnant women (Figure 3).23–26 Hepatitis B has a case fatality of around 1.0% and constitutes a significant percent of ALF in various endemic regions of the world.1,13 Chronic hepatitis B can cause ALF during reactivation, especially after immunosuppression therapy.6 Moreover, in about 50% of patients with ALF and chronic hepatitis B positive status, ALF is precipitated by another factor, usually superinfection with hepatitis D virus, hepatitis E virus, or putative non-A-E agent.7 Hepatitis C is a very rare cause of ALF in Europe and the United States,27,28 although a number of series from Japan and India have found evidence of hepatitis C in the non-A, non-B group of patients.24,25,29 The etiology of ALF is unknown in 30%-50% of patients and is presumed to be caused by yet unidentified non-A-E viral agent. This non-A-E agent accounts for 90% of patients with late onset hepatic failure, and identification of this agent is a matter of great priority.30,31Figure 3. Microphotograph of needle biopsy of liver from a patient with acute liver failure caused by hepatitis E virus. This 25-year-old pregnant woman developed acute liver failure during the third trimester of pregnancy. Serum sample collected on her 10th day of illness was reactive for IgM antibody to hepatitis E virus (ELISA) and HEV RNA (PCR). Dominant changes in liver biopsy were panlobular marked intracanalicular cholestasis (bile plugs) with pseudo-ductular formation (arrow), focal necrosis and lobular disarray.Download FigureHepatitis G virus is a newly identified positive-stranded RNA virus, with a genome of 10 KB, and belonging to the member of the Flaviviridae, distinct from hepatitis C virus. It has, though possibly prematurely, received the appellation of hepatitis virus. The clinical implications of hepatitis G virus in causing acute and chronic liver disease are as yet unclear. Of significance are the data that the virus has not been implicated in the etiology of ALF caused by putative non-A-E agent.32 However, in one study, a specific strain of the virus was detected in a high percentage of German and Japanese patients with ALF. These results, though interesting, need to be confirmed by other workers.33Drug ReactionsIdiosyncratic drug reactions resulting in ALF include a wide variety of drugs (Figure 4). Some of the common agents associated with ALF are non-steroidal antiinflammatory drugs and antitubercular drugs. Of perhaps greater concern than single agents is the use of drug combinations which result in ALF.2 These include trimethoprim-sulfamethoxazole; amoxicillin-clavulanic acid (Augmentin), rifampicin-isoniazid and isoniazid acetaminophen.Figure 4A. Acute liver failure caused by L-asparaginase. The clinical and biochemical parameters of a 49-year-old male known to have chronic granulocytic leukemia with recent extramedullary acute transformation (granulocytic sarcoma). He presented with acute liver failure while undergoing induction chemotherapy.Download FigureFigure 4B. Contrast-enhanced computed tomographic scan revealed enlarged liver with general gross hypodense appearance suggestive of diffuse fatty infiltration.Download FigureFigure 4C. Transverse liver biopsy revealed panlobular macrovesicular steatosis.Download FigureThe dominant etiologic agents of ALF have wide geographic variation.16,17 Viral hepatitis is nearly the sole agent of ALF in the Indian subcontinent, the most important cause in Europe and the United States, and comes next to acetaminophen hepatotoxicity as a cause of ALF in the United Kingdom.CLINICAL FEATURESClinical features of ALF can be divided into two broad groups: 1) manifestations of acute hepatic injury, namely, jaundice, shrunken liver, high liver enzymes, deficiency of clotting factors and other synthetic functions of the liver; and 2) multiorgan failure and a wide range of metabolic disturbances.2,17EncephalopathyEncephalopathy is the essential clinical feature of ALF, and is graded on a scale of 1 to 4.15 The grade of encephalopathy has prognostic value and patients with grade 2 encephalopathy, without further progression, have an excellent prognosis. In contrast, patients with grade 3 or 4 coma carry a poor prognosis.2,13–15Cerebral EdemaCerebral edema is one of the most important causes of death in ALF. The pathogenesis of cerebral edema is unclear and may be caused by vasogenic (direct leakage of plasma into the cerebrospinal fluid) or cytotoxic (cellular injury causing increased water uptake) mechanisms. The early clinical signs of cerebral edema are subtle and include changes in pupillary response, bradycardia, hypertension and hyperventilation. Changes in muscle tone, myoclonus, seizures and decerebrate rigidity follow, and may occur unpredictably fast to cause respiratory arrest or irreversible brain damage.34 The management of cerebral edema needs a few simple measures. It has been observed that tactile stimuli, faulty neck position and physical manipulation can precipitate episodes of cerebral edema. Thus patients with ALF need to be nursed in a quiet room, with the head end of the bed elevated, and institution of early mechanical ventilation and muscle paralysis with onset of grade 3 encephalopathy. A high clinical index of suspicion of cerebral edema should be kept and early warning signs detected by careful monitoring. Direct measurement of intracranial pressure is a valuable tool to diagnose and monitor response to therapy in such patients. Intracranial pressure monitoring is indicated in all patients with grade 3 or 4 encephalopathy and those being considered for liver transplantation. The procedure is hazardous and needs experienced hands, and prior correction of coagulopathy by fresh frozen plasma and/or platelet transfusions.35 A standardized approach to treat episodes of cerebral edema includes: 1) hyperventilation to keep pCO2 less than 25 mm Hg, if no response, 2) administration of mannitol (0.5 to 1 g/kg) as a bolus intravenously, which can be repeated if needed in case there is no response; 3) maintaining serum osmolality between 310 to 320 mOsm/L and monitoring urine flow to ensure diuresis. In patients with oliguria, mannitol is administered along with ultrafiltration to remove fluid and to prevent worsening of cerebral edema. If there is no response to mannitol, or if cerebral edema relapses, thiopental sodium coma can be induced, using a bolus of 3 to 5 mg/kg of the drug intravenously and followed by intravenous infusion at a rate of 50-250 mg/h for the next 4 hours.34CoagulopathyALF results in wide qualitative and quantitative defects in platelets, coagulation factors and the fibrinolytic system. Disseminated intravascular coagulation may also play a role, although this syndrome is difficult to distinguish from changes due to failure of hepatic synthesis of coagulation factors and their clearance alone. Prothrombin time is a good guide to prognosis. The coagulopathy presents as bleeding, which may be severe, and may cause or contribute to death in around 30% of patients. The most common site of bleeding is the upper gastrointestinal tract, possibly precipitated by the occurrence of gastric erosions, in addition to coagulopathy. Other important sites of bleeding include the nasopharynx, lungs, kidneys, retroperitoneum and skin (if punctured). H2 receptor antagonists and sucralfate therapy can reduce incidence of gastrointestinal bleeding and improve survival, independent of correction of coagulation factors. Management with blood products is indicated only in manifest bleeding, or to cover periods during invasive procedures.36InfectionsPatients with ALF have increased susceptibility to infections as a result of impaired phagocytic function, reduced complement levels, and the need for invasive procedures. Bacteriologically proven infection is recorded in up to 80% of these patients, and fungal infections (predominantly Candidiasis) in 32%. The predominant bacterial pathogens include Staphylococci aureus, coagulase-negative Staphylococci, Streptococci species and coliform organisms (Escherichia coli and Pseudomonas aeruginosa). The usual sites of infections include chest, urinary tract, blood and intravenous cannulae.37 Spontaneous bacterial peritonitis is common in patients with late onset hepatic failure, and occurred in 32% of 82 patients in one study.38 Clinical signs of sepsis, such as high temperature and high leukocyte count, are absent in 30% of cases. Use of prophylactic antibiotics in patients with ALF causes significant decrease in bacterial infections, shortens hospital stay, increases rate of successful liver transplantation and improves overall survival. As usual clinical signs of sepsis may be absent, careful monitoring by regular cultures is important to detect infections early.37–39Metabolic ChangesALF is associated with a number of metabolic changes. Hypoglycemia is common and may precede the onset of grade 3 encephalopathy, resulting in precipitous deterioration in mental state. The hypoglycemia is a consequence of increased circulating insulin levels, impaired gluconeogenesis and inability to mobilize glycogen stores. The clinical signs and symptoms of hypoglycemia are masked in the presence of established encephalopathy, and blood glucose monitoring should be done on an hourly basis and supplement glucose administered intravenously when blood glucose falls below 3.5 mmol/L.40Hyperventilation occurs early in the course of ALF, causing respiratory alkalosis even before grade 3 coma ensues. In addition, hyponatremia, hypokalemia, hypophosphatemia, and hypomagnesia occur frequently, and need regular monitoring and correction. However, acetaminophen-induced ALF can lead to metabolic acidosis in a high percentage of patients early in the clinical course of overdose, and precedes onset of encephalopathy.17Hemodynamic ChangesCirculatory changes resembling septic shock syndrome occur in ALF, and are a result of release of toxic substances from tissue injury and cytokines from activated macrophages.41 ALF is associated with abnormal oxygen supply dependency pattern resulting in oxygen extraction taking place over a wider than normal range of oxygen delivery. Severe peripheral shunting occurs and tissue oxygen extraction is diminished, leading to lactic acidosis. Prostaglandins (PGE1 and PGE2) and N-acetylcysteine have been shown to increase tissue oxygen extraction and improve hemodynamics in such patients, however, whether such therapy can improve survival is not known.42–44 Functional renal failure occurs in about one-third of patients with ALF, as a result of hypovolemia, sepsis and reduced intravascular filling pressures. Oliguric renal failure occurs late in the clinical course of the disease. In contrast, acetaminophen can cause direct renal toxicity, resulting in oliguric renal failure in around 75% of patients. Prevention of hemodynamic changes should be directed at maintaining vascular filling pressure by use of intravenous albumin infusions and aiming at a pulmonary wedge pressure of 12 to 13 mm Hg. Persistent hypotension with adequate intravascular volumes carry poor prognosis and can be managed by vasopressors. Conventional hemodialysis can lead to sudden changes in the circulatory volume and electrolyte balance and may worsen cerebral edema. Thus continuous veno-venous hemofiltration is the preferred option. If not available, continuous arteriovenous hemofiltration may be the next alternative following formation of a temporary shunt in the forearm.17MANAGEMENTIntensive CareManagement of ALF starts from the diagnosis of the syndrome in the emergency room (Table 4). Altered mentation and coagulopathy in a patient with liver disease are hallmarks of the diagnosis, and such patients need admission to the intensive care unit and appropriate monitoring.1,2,9,13Table 4. Steps of management of acute liver failure.Table 4. Steps of management of acute liver failure.Specific TherapyFrom therapeutic considerations, it is imperative to evaluate for etiologies which have specific treatments and/or antidotes (Table 5). ALF caused by HELLP syndrome, fatty liver of pregnancy and Budd-Chiari syndrome following pregnancy, need urgent termination of pregnancy.45–47 Acetaminophen overdose should be treated with N-acetyl cysteine.19,20 Nanograms of serum acetaminophen levels to predict hepatotoxicity are of little value in alcohol-acetaminophen syndrome because of a number of reasons: 1) time of ingestion is frequently not available; 2) ingestion usually occurs over multiple stages; and 3) hepatotoxicity can occur with therapeutic doses and low blood levels in patients with concurrent use of alcohol.2,21,22 Mushroom poisoning caused by the species Amanita phalloides needs urgent gastric lavage and penicillin 300,000 to 1,000,000 units/kg/day intravenously in divided doses, plus silibinin (a water-soluble form of silymarin) 20 to 50 mg/kg/day intravenously.14Table 5. The clinical manifestations of acute liver failure and suggested treatment strategies.Table 5. The clinical manifestations of acute liver failure and suggested treatment strategies.Metabolic diseases of liver, namely, Wilson's disease and autoimmune chronic active hepatitis, need specific therapies.3–5,48 Hepatic venous outflow obstruction (Budd-Chiari syndrome) responds well to anticoagulation and urgent portacaval shunts performed at surgery, or through creation of a transjugular intrahepatic portosystemic shunt.49–52Liver TransplantationThe successful use of liver transplantation has had the single greatest impact on the management of ALF.1,53,54 The selection of patients, appropriate timing of the transplant, the difficulty of making donor liver available within a short period of time, and postoperative course of these sick patients make the transplantation for ALF a very challenging field. Over the years, ALF has constituted between 6% to 7% of total liver transplantation performed in the United States. ALF patients undergoing liver transplantation were more likely to be younger, on life support (status 4), to receive incompatible blood systems, and have considerably shorter waiting time than those undergoing transplantation for other causes. In view of these disadvantages, patients with ALF had a lower one-year rate of patient (63%) and graft (53%) survival than patients transplanted for other causes (78% and 70%, respectively).1,50 Liver transplant should be offered to patients with ALF before severe irreversible brain damage has ensued, and prior to performing the transplant a careful assessment of the brain function needs to be done to exclude irreversible brain damage.17,53,54The majority of patients with ALF have received orthotopic liver transplantation, however, the possibility of eventual recovery makes auxiliary liver transplantation an attractive option. The advantages of auxiliary liver transplantation are temporary requirement of immunosuppression drugs until the host liver recovers and the relative ease of surgery. Two types of auxiliary liver support are possible: heterotopic transplantation, in which the liver graft is placed in the right upper quadrant beside the native liver, and auxiliary orthotopic liver transplantation, where the portion of native liver is removed and replaced by the reduced size graft.55–59PROGNOSTIC INDICATORSCritical in the decision to use liver transplantation is the assessment of the likelihood of spontaneous recovery. A number of transplant centers in the West have defined prognostic criteria in ALF, and these criteria can be applied to estimate the probability of spontaneous recovery in a given patient.60–63 The criteria include static variables, such as age, sex and etiology, and dynamic variables, such as grade of encephalopathy, serum bilirubin, prothrombin time, etc. The prognostic model proposed by King's College Hospital in London is the most popular for reference.60 This model divides ALF into two broad etiological groups, acetaminophen and non-acetaminophen. In the acetaminophen group, arterial pH of <7.3, prothrombin time of >100 sec., and serum creatinine of >300 mmol/L were bad prognostic variables. In the non-acetaminophen group, etiology (non-A-E agents or drugs), age (<10 or >40 years), pre-encephalopathy period (>7 days), serum bilirubin (>300 mmol/L), and prothrombin time (>50 sec.) were bad prognostic variables (Table 6). By contrast, French workers rely primarily on factor V levels, with a value of less than 20% (30% in those over 30 years), leading to transplantation. Factor V estimations were found to less sensitive but more specific than the King's College criteria when determined 48 hours before transplantation. Recent data published from India have shown that these prognostic indicators may not be valid for other geographical regions, in view of the differences in the etiological causes, behavior and clinical profile of ALF.25 Thus, such prognostic indicators need to be defined for different geographical regions and validated by application into prospective studies.63Table 6. Prognostic model developed at King's College Hospital to select patients with acute liver failure for liver transplantation.Table 6. Prognostic model developed at King's College Hospital to select patients with acute liver failure for liver transplantation.FUTURE DEVELOPMENTSIn recent years, there has been considerable interest in the use of newer forms of support system or transplantation in patients with ALF that may provide a bridge until the native liver recovers its functions spontaneously, or until an appropriate donor is available (Table 7).63–78 Some of these developments may also address the issue of difficulty in finding a donor liver and use of alternative/innovative forms of transplantation.1 Such approaches would avoid major surgery, allow use of live related donors, have feasibility of multiple courses of treatments and could be used for temporary support without committing the patient to life-long immunosuppression.Table 7. Future developments for treatment of acute liver failure.Table 7. Future developments for treatment of acute liver failure.Artificial hepatic support systems are cell-based extracorporeal system incorporating hepatocytes, which take up various excretory and synthetic hepatic functions until the liver regenerates.64–68 Two bioartificial devices have already been used clinically in the treatment of ALF: bioartificial liver (BAL), based on pig hepatocytes attached to microcarriers, and the extracorporeal liver assist devices (ELAD), which contain a human liver-derived tumor cell line (C3A cells). Hepatocyte transplantation uses hepatocytes rather than the whole organ for transplantation.69–75 The procedure would be ideal for transfer of genes to individuals with genetic diseases, such as familial hypercholesterolemia, Griggler-Najjar syndrome, etc. Extracorporeal liver (ECL) support system involves the diversion of patient's circulation through a liver outside the body.76,77 The organ used for cross-circulation may be human or from another species. Xenotransplantation uses baboon or pig liver to perform human hepatic functions. Anecdotal reports of the use of the above devices in humans with ALF appear in the literature, but such devices need further refinements to be evaluated by controlled clinical trials for proper evaluation.78ARTICLE REFERENCES:1. Hoofnagle JH, Carithers RL., Shapiro C, Ascher N. Fulminant hepatic failure: summary of a workshop . Hepatology. 1995; 21: 240–52. Google Scholar2. Lee WM. Acute liver failure . Am J Med. 1994; 96 (Suppl A): 3–9. Google Scholar3. Nazer H, Ede RJ, Mowat AP, Williams R. Wilson's disease: clinical presentation and use of prognostic index . Gut. 1986; 27: 1377–81. Google Scholar4. Walia BN, Singh S, Marwaha RK, Bhusnurmath SR, Dilawari JB. Fulminant hepatic failure and acute intravascular haemolysis as presenting manifestations of Wilson's disease in young children . J Gastroenterol and Hepatol. 1992; 7: 370–3. Google Scholar5. Maggiore G, Porta G, Bernard O, Hadchouel M, Alvarez F, Homberg JC, et al. Autoimmune hepatitis with initial presentation as acute liver failure in young children . J Pediatr. 1990; 116: 280–2. Google Scholar6. Flowers MA, Heathcote J, Wanless IR, Morris S, Reynold WJ, Cameron J, et al. Fulminant hepatitis as a consequence of reactivation of hepatitis B virus infection after discontinuation of low-dose methotrexate therapy . Ann Intern Med. 1990; 112: 381–2. Google Scholar7. Saracco G, Macagno S, Rosina F. Serologic markers with fulminant hepatitis in persons positive for hepatitis B surface antigen. A worldwide epidemiological and clinical survey . Ann Intern Med. 1988; 108: 380–3. Google Scholar8. Trey C, Davidson CS. The management of fulminant hepatic failure. In: Popper H, Schaffner F, editors. Progress in liver failure. New York: Grune and Stratton, 1970: 292–8. Google Scholar9. Gimson AES, O'Grady J, Ede RJ, Portmann B, Williams R. Late onset hepatic failure: clinical, serological and histological features . Hepatology. 1986; 6: 288–94. Google Scholar10. Khuroo MS, Dar MY. Subacute hepatic failure: experience at Institute of Medical Sciences, Srinagar . Ind J Gastroenterol. 1993; 12 (Suppl): 7–10. Google Scholar11. Tandon BN. Subacute hepatic failure: definition, nomenclature and criteria for diagnosis . Ind J Gastroenterol. 1993; 12 (suppl): 5–6. Google Scholar12. O'Grady JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes . Lancet. 1993; 352: 273–5. Google Scholar13. Bernuau J, Rueff B, Benhamou JP. Fulminant and subfulminant liver failure: definition and causes . Semin Liver Dis. 1986; 6: 97–106. Google Scholar14. Sherlock S, Dooley J. Diseases of the liver and biliary system. 9th edition. Oxford: Blackwell Scientific Publications, 1993. Google Scholar15. Riordan SM, Williams R. Treatment of hepatic encephalopathy . N Eng J Med. 1997; 337: 473–8. Google Scholar16. Khuroo MS, Khuroo N. Hepatitis E: global epidemiology with special reference to impact of the disease in India and the South East of Asia. In: Rizzetto M, Purcell RH, Gerin JL, Verme G, editors. Viral hepatitis and liver disease. Turin: Edizioni Minerva Medica, 1997: 601–8. Google Scholar17. O'Grady JG, Portmann B, Williams R. Fulminant hepatic failure. In: Schiff L, Schiff ER, editors. Diseases of the liver. Philadelphia: Lippincott Company; 1993: 1077–90. Google Scholar18. Mahler H, Pasi A, Kramer JM, Schulte P, Scoging AE, Bar W, Krahenbuhl S. Fulminant liver failure in association with the emetic of Bacillus cereus . N Eng J Med. 1997; 336: 1142–8. Google Scholar19. Bray GP. Liver failure induced by paracetamol . Brit Med J. 1993; 306: 157–8. Google Scholar20. Vale JA, Proudfoot AT. Paracetamol (acetaminophen) poisoning . Lancet. 1995; 346: 547–52. Google Scholar21. Zimmerman HJ, Maddrey WC. Acetaminophen (paracetamol) hepatotoxicity with regular intake of alcohol: analysis of instances of therapeutic misadventure . Hepatology. 1995; 22: 588–97. Google Scholar22. Schi⊘dt FV, Rochling FA, Casey DL, Lee WM. Acetaminophen toxicity in an urban county hospital . N Engl J Med. 1997; 337: 1112–7. Google Scholar23. Khuroo MS, Teli MR, Skidmore S, Sofi MA, Khuroo ML. Incidence and severity of viral hepatitis in pregnancy . Am J Med. 1981; 70: 252–5. Google Scholar24. Nanda SK, Yalchinkaya K, Panigrahi AK, Acharya SK, Jameel S, Panda SK. Etiological role of hepatitis E virus in sporadic fulminant hepatitis . J Med Virol. 1994; 42: 133–7. Google Scholar25. Acharya SK, Dasarathy S, Kumer TL, Sushma S, Prasanna KSU, Tandon A, et al. Fulminant hepatitis in a tropical population: clinical course, cause, and early predictors of outcome . Hepatology. 1996; 23: 1448–55. Google Scholar26. Khuroo MS. Acute liver failure in India . Hepatology. 1997; 26: 244–6. Googl" @default.
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• W4250460639 cites W1608215573 @default.
• W4250460639 cites W1615493023 @default.
• W4250460639 cites W1889960934 @default.
• W4250460639 cites W1966425198 @default.
• W4250460639 cites W1966439015 @default.
• W4250460639 cites W1967347732 @default.
• W4250460639 cites W1978504328 @default.
• W4250460639 cites W1979315534 @default.
• W4250460639 cites W1980852639 @default.
• W4250460639 cites W1981003987 @default.
• W4250460639 cites W1983231842 @default.
• W4250460639 cites W1986637042 @default.
• W4250460639 cites W2004249771 @default.
• W4250460639 cites W2007000551 @default.
• W4250460639 cites W2011709012 @default.
• W4250460639 cites W2011803714 @default.
• W4250460639 cites W2013359336 @default.
• W4250460639 cites W2015633825 @default.
• W4250460639 cites W2015943523 @default.
• W4250460639 cites W2018920931 @default.
• W4250460639 cites W2019305472 @default.
• W4250460639 cites W2022354174 @default.
• W4250460639 cites W2022445393 @default.
• W4250460639 cites W2027012879 @default.
• W4250460639 cites W2028946541 @default.
• W4250460639 cites W2032180141 @default.
• W4250460639 cites W2033681968 @default.
• W4250460639 cites W2034964537 @default.
• W4250460639 cites W2038360824 @default.
• W4250460639 cites W2038623213 @default.
• W4250460639 cites W2040944339 @default.
• W4250460639 cites W2043300139 @default.
• W4250460639 cites W2055733550 @default.
• W4250460639 cites W2060442730 @default.
• W4250460639 cites W2062602912 @default.
• W4250460639 cites W2069514277 @default.
• W4250460639 cites W2069910690 @default.
• W4250460639 cites W2080053963 @default.
• W4250460639 cites W2081924433 @default.
• W4250460639 cites W2082251370 @default.
• W4250460639 cites W2088954626 @default.
• W4250460639 cites W2099918136 @default.
• W4250460639 cites W2105202913 @default.
• W4250460639 cites W2136476961 @default.
• W4250460639 cites W2139728745 @default.
• W4250460639 cites W2147578628 @default.
• W4250460639 cites W2158736090 @default.
• W4250460639 cites W2162333553 @default.
• W4250460639 cites W2313265919 @default.
• W4250460639 cites W2318383157 @default.
• W4250460639 cites W2333929473 @default.
• W4250460639 cites W2333982488 @default.
• W4250460639 cites W2334982407 @default.
• W4250460639 cites W2337873021 @default.
• W4250460639 cites W2339231535 @default.
• W4250460639 cites W2395663099 @default.
• W4250460639 cites W2413840422 @default.
• W4250460639 cites W2460383015 @default.
• W4250460639 cites W4230097184 @default.
• W4250460639 cites W4230570388 @default.
• W4250460639 cites W4246649438 @default.
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