Urgent considerations
See Differentials for more details
Acute liver failure
Acute liver failure (fulminant hepatic failure) can occur following hepatocellular injury. It is rapidly progressive and severe. Deteriorating functional capacity of the liver leads to hepatic encephalopathy, metabolic disturbances (including acidosis and hypoglycaemia), and an increased bleeding tendency. Rapid elevation of aminotransferases, prolongation of prothrombin time, and onset of jaundice are characteristic.
Acute liver failure is defined by onset of the following in a person with no prior history of liver disease:
Jaundice
Hepatic encephalopathy
Coagulopathy.
It may be seen in association with many causes, including:
Drugs and other toxins (e.g., paracetamol poisoning)
Viral hepatitis (e.g., hepatitis viruses A, B, and E)
Autoimmune diseases
Vascular causes (e.g., Budd-Chiari syndrome, shock)
Wilson's disease
Pregnancy-related liver disease (e.g., haemolysis, elevated liver enzymes, low platelets [HELLP] syndrome; acute fatty liver of pregnancy).
All drugs suspected as a possible cause should be discontinued immediately. Patients with acute liver failure require management with continuous renal replacement therapy for management of hyperammonaemia in an intensive care unit.[51] Urgent intervention, including transplant evaluation, needs to be considered, based on the patient's clinical condition (e.g., grade of encephalopathy) and laboratory parameters (e.g., prothrombin time, international normalised ratio, serum creatinine, and blood pH).[52] Treatment is time-sensitive (e.g., transfer to a liver transplant centre, initiation of liver transplant evaluation, promptly giving acetylcysteine in both paracetamol and non-paracetamol acute liver failure).
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