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At least 19 recordsLinked to original sources
PubMed1999

Acute liver failure.

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.

Age Distribution↗
PubMed1998

[Prognostic factors in acute liver failure].

Acute liver failure is defined as acute severe, potentially reversible hepatic failure complicated by cerebral dysfunction. The high mortality rate of between 50% and 90% justifies early transfer to a specialised centre with the possibility of orthotopic liver transplantation to ensure adequate intensive care monitoring and treatment, 57 patients with acute liver failure (34 female, 23 male, aged 6 to 87 years, median 33 years) treated at our intensive care unit during the past 10 years were analysed retrospectively. Various factors and laboratory data were analysed in respect to their prognostic value. Depending on the aetiology, the survival rate in acute liver failure under conservative treatment ranges from 79% (amanita intoxication) to 10% (cryptogenic genesis). The most important predictive parameter is the extent of cerebral dysfunction. The extent of cerebral dysfunction is a determining factor of the survival rate under conservative treatment; it ranges from 94% (patients with hepatic encephalopathy grade I) to 11% (patients with hepatic encephalopathy grade IV). The occurrence of complications such as infections, cerebral oedema, respiratory failure or renal failure is also associated with an unfavourable outcome. Additionally, various laboratory parameters have a predictive ability. The mortality rate of our patients with acute liver failure has decreased from 56% to 32% since early intensive care monitoring and treatment and the possibility of acute orthotopic liver transplantation were established.

Adolescent↗
PubMed2002

Splanchnic circulation and metabolism in patients with acute liver failure.

Acute liver failure is associated with mortality of around 50%. The aim of the present studies was to examine the circulatory and metabolic state of the splanchnic region in acute liver failure. This had not been studied previously and it could be expected that improved understanding of the pathophysiology of acute liver failure could lead to improved therapy. Hepatic plasma flow was estimated in patients with acute liver failure after development of hepatic encephalopathy grade III, by the use of liver vein catheterization and continuous infusion of sorbitol. The method was evaluated against the prerequisites of Fick's principle. Hepatic plasma flow could be estimated with sorbitol but not in all patients and the standard error of the estimated hepatic blood flow was higher than in other patient groups. In 20 patients with acute liver failure, mean hepatic blood flow was increased. At the same time, the systemic and the peripheral hemodynamics were examined. The ratio hepatic blood flow/cardiac output was increased in many patients. Lower extremity blood flow was within normal limits. Thus, low systemic vascular resistance index in acute liver failure was likely to be a consequence of vasodilatation in the muscular resistance vessels and, in particular, in the splanchnic resistance vessels. Intervention with high-volume plasmapheresis changed systemic and splanchnic hemodynamics differently, suggesting that the splanchnic vasodilatation in liver failure may by caused by a specific mechanism different from the one that leads to peripheral vasodilatation. Infusion of dopamine increased mean arterial pressure, cardiac output, and hepatic blood flow in acute liver failure. The splanchnic exchange of substrates for oxidative metabolism was examined. Splanchnic oxygen consumption was increased. The ratio splanchnic oxygen consumption/systemic oxygen consumption indicated that 1/3 of the oxygen used in the whole body in acute liver failure was used in the splanchnic region. The splanchnic metabolism of fuel substrates was abnormal. Lactate and pyruvate was released and there were no detectable gradients of free fatty acids or of the sum of amino acids. There was a small release of ketone bodies. The data suggested that the energy needs of the failing liver was covered by intracellular fat. The hypothesis of splanchnic tissue hypoxia was examined from different approaches. The normal hepatic venous oxygen saturation, the splanchnic release of both lactate and pyruvate, and a normal hepatic venous pyruvate/lactate ratio in the presence of low acetoacetate/hydroxybutyrate ratio rather indicated high substrate turnover than splanchnic tissue hypoxia. Amino acid and ammonia metabolism was examined. It was observed that arterial ammonia concentration measured after institution of mechanical ventilation was associated with cerebral herniation 1-5 days later. The background for hyperammonemia was that ammonia was released from the splanchnic circulation. The data implied that glutamine was deamidated in the gut and alanine and ammonia was released into the portal vein as during normal circumstances. Then due to severely decreased hepatic function the liver was unable to remove ammonia and alanine as it normally would. Further, the data implied that urea synthesis was impaired. Exchange of ammonia in muscle tissue was studied in 7 patients with acute liver failure and muscle tissue seems to play a major role in ammonia detoxification in acute liver failure. Treatment with high-volume plasmapheresis decreased arterial ammonia, which was likely due to increased urea production or stimulation of glutamine synthesis in muscle tissue. These findings add to our understanding of the pathophysiology and have implications for the management of acute liver failure.

Amino Acids↗
PubMed2005

Acute liver failure.

Acute liver failure is a complex multisystemic illness that evolves quickly after a catastrophic insult to the liver leading to the development of encephalopathy. The underlying aetiology and the pace of progression strongly influence the clinical course. The commonest causes are paracetamol, idiosyncratic drug reactions, hepatitis B, and seronegative hepatitis. The optimal care is multidisciplinary and up to half of the cases receive liver transplants, with survival rates around 75%-90%. Artificial liver support devices remain unproven in efficacy in acute liver failure.

Humans↗
PubMed2003

[Acute liver failure].

Acute liver failure is characterized by a dynamic clinical course associated with high mortality. The main prognostic determinant is the development of extrahepatic complications. Close monitoring is mandatory, and prophylactic measures to avoid complications should be initiated. In case of complications, early and aggressive treatment is indicated. To date, artificial liver support devices are still in the experimental phase. Liver transplantation should be considered in patients with predictors of a poor spontaneous prognosis. Therefore, a transplant center should be contacted in every case of acute liver failure.

Emergencies↗
PubMed2006

[Specific therapy in acute liver failure].

Acute liver failure is defined as hepatic insufficiency (icterus and coagulopathy), hepatorenal syndrome and encephalopathy, associated with a high mortality. A number of conditions can cause this sudden severe liver failure, which finally triggers a multi-organ response. Its etiology shows considerable geographic variation, with viral hepatitis being the most common cause worldwide, whilst drugs, especially acetaminophen-induced hepatotoxicity, form the most common precipitant in many developed countries. The essential feature of a wide variety of agents is apoptosis and/or necrosis of liver cells which is associated with liver injury and insufficiency. Based on new experimental data, the identification of target molecules involved in apoptosis may offer new therapeutic options and improvement of prognosis scores in patients with acute liver failure.

Animals↗
PubMed2003

Molecular neurobiology of acute liver failure.

Acute liver failure results in encephalopathy and brain edema that is characterized by astrocytic cell swelling. Molecular biological techniques have led to the identification of alterations in expression of several genes coding for key astrocytic proteins in acute liver failure. Such proteins include amino acid transporters, structural proteins, the endothelial cell glucose transporter GLUT-1, the mitochondrial "peripheral-type" benzodiazepine receptor, and the water channel protein aquaporin IV. Magnetic resonance spectroscopic studies reveal increased brain lactate concentrations that are positively correlated with severity of encephalopathy and brain edema in acute liver failure, suggesting a deficit of cellular oxidative capacity and impending brain energy failure. Mild hypothermia prevents brain edema in acute liver failure, and mechanisms responsible for this beneficial effect include reduced blood-brain ammonia transfer as well as normalization of astrocytic amino acid transport and brain energy metabolism. Further elucidation of the molecular mechanisms responsible for brain edema and encephalopathy in acute liver failure will undoubtedly lead to novel treatment strategies for these complications.

Astrocytes↗
PubMedDate not supplied

[Acute liver failure].

Acute liver failure, also called fulminant hepatic failure, is characterized by sudden hepatic synthetic dysfunction associated with coagulopathy and hepatic encephalopathy. Acute liver failure has most recently been defined based on the timing from onset of jaundice to encephalopathy as follows: 1) hyperacute (1-7 days); 2) acute (8-28 days), and 3) subacute (29-60 days). Rapid onset of encephalopathy in hyperacute liver failure is paradoxically associated with highest rate of spontaneous recovery, and subacute liver failure is associated with worst prognosis. The etiology of liver failure is established by history, serologic assays, and exclusion of alternative causes. Acute liver failure is most frequently caused by drug hepatotoxicity, including acetaminophen toxicity and idiosyncratic drug reactions, with viral hepatitis playing a lesser role in recent surveys. A substantial number of cases have an indeterminate etiology. Major complications of acute liver failure that require active intervention include metabolic disorders, coagulopathy, cerebral edema, renal failure, and infection. The focus of management of acute liver failure is comprehensive supportive care in an intensive care unit and assessment of the need for liver transplantation.

Humans↗
PubMed2000

Prognostic value of abdominal CT scanning and hepatic histopathology in patients with acute liver failure.

Acute liver failure has extremely high mortality without liver transplantation. We attempted to determine the value of abdominal CT scanning and liver biopsy in its management. A retrospective analysis of patients with acute liver failure was performed; demographic, clinical, radiologic and histopathologic features were noted. Over a period of 13 years, 177 patients were evaluated. The mean age was 39 years and 63% were females. The patients were divided into three groups. Fourteen percent survived with medical management (group I), 37% died (group II), and 49% had liver transplantation (group III). Most patients showed diffuse low density of the liver on CT scanning and the proportions were similar in the three groups. Moderate to large ascites was not present in group I but occurred in 31% of patients in group II and in 15% in group III. Mean hepatic volumes were similar in the three groups; however, 97% of the patients with a liver volume of less than 1000 ml either died or required liver transplantation. Liver biopsies among patients with spontaneous recovery (group I) were distinguished by the presence of regenerative changes and a hepatic parenchymal necrosis of less than 50%. These results suggest that in patients with acute liver failure a liver volume of less than 1000 ml and/or hepatic parenchymal necrosis of greater than 50% is indicative of a poor prognosis. This information may assist decision making in such patients, in particular, regarding the need for liver transplantation.

Adolescent↗
PubMed1996

Management of acute liver failure.

Acute liver failure (ALF) constitutes a medical emergency requiring the prompt response of experienced clinicians. As it is relatively infrequent, and tends to evolve rapidly, decisions concerning care and prognosis must be made promptly. Determining etiology is vital since prognosis is largely determined by the cause of the illness, and the use of antidotes may be lifesaving. Estimating the severity of the liver failure is also important, because if liver transplantation is necessary, it must be undertaken quickly. No treatment thus far is better than good general care of the comatose patient, with attention to the special problems associated with acute liver failure: cerebral edema, infection, circulatory collapse. A number of issues have been debated recently, including use of prostaglandins and N-acetylcysteine for treatment of all forms of acute liver failure, and the use of extracorporeal liver assist machines, however, the efficacy of non-specific treatments for this complex syndrome has not been proven.

Drug-Related Side Effects and Adverse Reactions↗
PubMed1994

Acute liver failure.

Acute liver failure is a multiorgan syndrome with dramatic clinical features and, often, a fatal outcome. It is characterized by the onset of coma and coagulopathy within 6 months, and usually in < 6 weeks, from onset of illness. Viral hepatitis, drug-related liver injury, and the alcohol-acetaminophen syndrome are the most common etiologies. Altered mental status accompanied by jaundice is a hallmark of acute liver failure. A unique feature is the evolution of increased intracranial pressure due to cerebral edema. The resulting cerebral ischemia and brainstem herniation account for approximately 50% of deaths in patients with acute liver failure. Mannitol therapy may successfully treat most patients with high intracerebral pressure. Most patients demonstrate features of the multiple organ failure syndrome, including a shock-like state, renal failure, and occasionally respiratory distress syndrome. Close monitoring of volume status is necessary, since administration of large quantities of fluid may be required. Infection is also common; most pathogens are gram-positive, and fungal infections are also seen. Because an optimum therapy for acute liver failure does not yet exist, liver transplantation should be considered early, before advanced levels of coma develop. Alternative, experimental treatment modalities include heterotopic liver grafting, administration of hepatocyte growth factor, use of an extracorporeal liver-assist device, and liver cell transplantation, but none of these has attained widespread use.

Humans↗
PubMed2005

Anaplastic T-cell lymphoma presenting as fatal acute liver failure.

Acute liver failure (ALF) is an uncommon manifestation of liver disease and constitutes a medical emergency for which early identification is necessary. Hepatic involvement by hematologic malignancies although frequent, rarely causes severe hepatic dysfunction. Even more, acute hepatic failure as the first manifestation of a hematologic malignancy is extremely uncommon, although some cases have been reported in the literature. We describe the case of a 61 y/o puertorrican veteran who developed acute hepatic failure secondary to massive infiltration of the liver by a recurrent non-Hodgkin's lymphoma.

Fatal Outcome↗
PubMedDate not supplied

Management of acute liver failure.

Acute liver failure represents one of the most challenging conditions in gastroenterology. In most cases, there is no effective therapy making supportive intensive care the most important management tool. These patients frequently develop multi-organ failure, placing them at risk of systemic infections, cerebral edema, hemodynamic instability, coagulopathy and various renal and metabolic complications. Successful management of the patient with acute liver failure requires an understanding of the pathophysiology and management of these complications. An overview of acute liver failure and its most common complications is presented.

Hepatic Encephalopathy↗
PubMed2002

Acute liver failure.

Acute liver failure (ALF) is a rare condition in the pediatric population. Patients who present with severe failure of liver synthetic function have a high mortality with medical therapy alone. The main causes of death are cerebral edema, hemorrhage, renal failure and sepsis. The etiology of ALF is age specific, with a significant number due to inborn errors of metabolism especially in neonates and infants. Treatment of children with ALF is supportive, aimed at preventing and managing associated complications until the native liver recovers or liver transplantation. Sedation should not be administered unless a decision for artificial ventilation has been made. As all children are potential transplant candidates, transfer to and management in a liver transplant centre is recommended. Prognostic criteria for mortality are less well defined compared to the adult population, although a significantly elevated INR > or = 4 carries a high chance of death, and liver transplantation should be considered at this stage. Auxiliary transplantation is an attractive option in selected individuals and provides the chance to stop immunosuppression should sufficient hepatic regeneration occur. The use of various liver assist devices and hepatocyte transplantation as a bridge to liver transplantation show promise, although when used in isolation, they do not have an impact on overall patient survival.

Child↗
PubMed2004

Acute liver failure.

Acute liver failure is a rare and life-threatening clinical syndrome following severe hepatic injury. Depending on the rapidity of its development, two distinct complications contribute to a high mortality: in hyperacute liver failure, rapid development of massive hepatic necrosis and apoptosis gives rise to severe hyperammonemia, hepatic encephalopathy and life-threatening cerebral edema. The high risk of cerebral herniation requires early listing for emergency liver transplantation. Patients with hyperacute liver failure surviving the initial episode of cerebral edema have a substantial potential for hepatic recovery. If progressive hepatic failure develops more slowly, astrocytic osmoregulation prevents cerebral herniation in most instances. Unfortunately, these patients have a small potential of hepatic regeneration and transplantation should be performed before renal failure, sepsis or multiorgan failure emerge. Experimental treatment methods including detoxification by artificial or bioartificial liver support or by stimulating hepatic regeneration are currently evaluated. Recognition of ammonia toxicity has stimulated the search for early ammonia-lowering strategies and strongly renewed the interest in dialytic therapies. Anti-apoptotic interventions are among the most promising pharmacological options for the near future.

Brain Edema↗
PubMed1998

Review article: the management of acute liver failure.

Acute liver failure (ALF) is a relatively uncommon but dramatic clinical syndrome with high mortality rates, in which a previously normal liver fails within days or weeks. Paracetamol overdose remains the major cause of ALF in the UK, while viral hepatitis is the commonest cause world-wide. Cerebral oedema is the leading cause of death in patients with ALF. Despite advances in intensive care and the development of new treatment modalities, ALF remains a condition of high mortality best managed in specialist centres. Orthotopic liver transplantation is the only new treatment modality that has made a significant impact in improving outcome. Bioartificial liver support systems and hepatocyte transplantation are new promising treatment options that may change the management of ALF in the future.

Animals↗
PubMed2001

Acute liver failure.

Acute liver failure (ALF) is defined as hepatic encephalopathy complicating acute liver injury. The most common etiologies are acute viral hepatitis A and B, medication overdose (e.g., acetaminophen), idiosyncratic drug reactions, ingestion of other toxins (e.g., amanita mushroom poisoning), and metabolic disorders (e.g., Reye's syndrome). Despite advances in intensive care management, mortality continues to be high (40-80%) and is partly related to ALF's complications, such as cerebral edema, sepsis, hypoglycemia, gastrointestinal bleeding, and acute renal failure. Several prognostic models have been developed to determine which patients will spontaneously recover. Treatment is directed at early recognition of the complications and general supportive measures. The only proven therapy for those who are unlikely to recover is liver transplantation. Therefore, recognition of ALF is paramount, and urgent referral to a transplant center is critical to assess transplantation status.

Brain Edema↗
PubMed2005

Drug-induced acute liver failure.

Acute liver failure is the most severe expression and represents the first cause of fatalities related to drugs. As a consequence, it is also the first cause of drug withdrawal from the pharmaceutical market. The incidence of drug-induced hepatotoxicity in the general population has been recently estimated to be around 14/100,000 inhabitants in a Western country. Drugs appear to be responsible for 10-52% of all causes of acute liver failure. In Western countries, paracetamol (acetaminophen) represents the first cause of all liver failures. The contribution of non-paracetamol drugs given at normal doses is equivalent to that of combined viral hepatitis A and B. The natural prognosis varies between drugs. The spontaneous mortality rate ranges from 32% to 50% for paracetamol intoxication and more than 75% for other drugs. The preventive occurrence of drug hepatotoxicity and the course to acute liver failure is rather limited. It is recommended to stop the administration of a suspected drug when alanine aminotransferase levels increase to more than 3-5 times the upper limit of normal. In paracetamol intoxication, the rapid administration of N-acetylcysteine is a classical antidote. At the stage of liver failure, treatment is mostly supportive. Since irreversible damage is unpredictable, early transfer to a transplantation centre should be considered.

Acetaminophen↗