Acute liver failure

Author(s):  
Daniel Marks ◽  
Marcus Harbord

Definitions of acute liver failure Aetiology Presentation Investigation Initial management Subsequent management Markers of disease severity Paracetamol overdose Acute presentations of Wilson’s disease Acute-on-chronic liver failure Hepatic encephalopathy Criteria for emergency liver transplantation Acute liver failure (ALF) is defined as potentially reversible severe liver injury with impaired synthetic function (INR 〉1.5) and hepatic encephalopathy, developing within 28d from the onset of jaundice, in the absence of pre-existing liver disease or with well-compensated chronic liver disease (...

2020 ◽  
pp. 3089-3100
Author(s):  
Jane Macnaughtan ◽  
Rajiv Jalan

Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury, with hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Acute-on-chronic liver failure is characterized by hepatic and/or extrahepatic organ failure in patients with cirrhosis associated with an identified or unidentified precipitating event. The commonest causes of acute liver failure are acute viral hepatitis and drugs. Acute-on-chronic liver failure is most commonly precipitated by infection, alcohol abuse, and superimposed viral infection. The main clinical manifestations are hepatic encephalopathy, coagulopathy, jaundice, renal dysfunction, and haemodynamic instability. Infection and systemic inflammation contribute to pathogenesis and critically contribute to prognosis. Specific therapy for the underlying liver disease is administered when available, but this is not possible for most causes of liver failure. Treatment is predominantly supportive, with particular emphasis on (1) correction or removal of precipitating factors; (2) if encephalopathy is present, using phosphate enemata, nonhydrolysed disaccharide laxatives, and/or rifaximin; (3) early detection and prompt treatment of complications such as hypoglycaemia, hypokalaemia, cerebral oedema, infection, and bleeding. The onset of organ failure should prompt discussion with a liver transplantation centre. The mortality of acute liver failure (without liver transplantation) is about 40%. Patients with acute liver failure who do not develop encephalopathy can be expected to recover completely. Those who recover from an episode of acute-on-chronic liver failure should be considered for liver transplantation because otherwise their subsequent mortality remains high.


2020 ◽  
Vol 46 (06) ◽  
pp. 656-664 ◽  
Author(s):  
Lara N. Roberts ◽  
William Bernal

AbstractHistorically, liver disease has been associated with a bleeding tendency. Global hemostatic assays have demonstrated that hemostasis is overall rebalanced, in both acute liver failure and chronic liver disease. It is now recognized that many bleeding events in chronic liver disease are mediated by portal hypertension rather than an underlying hemostatic defect. This is acknowledged in recent guidelines, which recommend against coagulation testing prior to low risk procedures in this patient group, with avoidance also of attempts at correction of prolonged coagulation times. Over time, the incidence of bleeding events has decreased in both chronic liver disease and acute liver failure, with improved supportive care, targeted treatments for underlying cause of liver disease, and the advent of liver transplantation. Concurrently, there has been increased recognition of the risk of thrombosis in chronic liver disease, with a predilection for the splanchnic vasculature. This review describes the incidence of bleeding and thrombosis in chronic liver disease and acute liver failure, including the periprocedural and liver transplantation setting.


2020 ◽  
pp. 3080-3089
Author(s):  
Paul K. Middleton ◽  
Debbie L. Shawcross

Hepatic encephalopathy (HE) is a significant complication of both acute and chronic liver disease, causing much morbidity and mortality. It is a complex neuropsychological condition, associated with hyperammonaemia and systemic inflammation, with a wide spectrum of symptoms. The West Haven criteria describe grades of severity from 0 (subclinical) and I (changes in awareness, mood, attention, cognition, and sleep pattern) through to IV (coma). It is further classified by the underlying aetiology: type A, due to acute liver failure; type B, secondary to portosystemic shunting; and type C, occurring in chronic liver disease in association with precipitating factors including infections, gastrointestinal bleeding, and electrolyte disorders, particularly hyponatraemia. There is no definitive test or set of diagnostic criteria to establish a diagnosis of HE, which remains primarily a clinical diagnosis of exclusion in patients with a history or clinical evidence of liver disease. Management depends on the type of HE, but for type C (the commonest type) typically includes lactulose and rifaximin. Patients with cirrhosis with ongoing overt HE despite optimal medical management have a dismal outlook and should be considered promptly for liver transplantation.


Author(s):  
George F. Mells ◽  
Graeme J.M. Alexander

Case History—A 53 yr old man, known to have alcoholic liver cirrhosis, now presenting with jaundice, ascites and deteriorating renal function. Case History—A 62 yr old man presenting with confusion and ascites. Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury. Acute liver failure is the syndrome of hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Chronic liver failure is characterized by a chronic liver injury with one or more features of liver failure....


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