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Liver failure 

Liver failure

Chapter:
Liver failure
Author(s):

George F. Mells

and Graeme J.M. Alexander

DOI:
10.1093/med/9780199204854.003.152204_update_001

August 28, 2014: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.

Update:

Extensive revisions include (1) definitions of types of liver failure; (2) classification of acute liver failure; (3) causes of acute liver failure; (4) causes of chronic liver failure; (5) grading systems for hepatic encephalopathy; (6) prognostic scoring systems in acute liver failure and chronic liver disease; (7) management of acute and chronic liver failure and their complications.

Two relevant case histories from Oxford Case Histories in Gastroenterology and Hepatology have been added to this chapter.

Updated on 28 Nov 2012. The previous version of this content can be found here.
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date: 23 April 2017

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.

The most common causes of acute liver failure are acute viral hepatitis and drugs. Prevention may be achieved by vaccination against hepatitis B, avoidance of re-exposure to drugs that have previously induced hepatitis, avoidance of poisons (e.g. Amanita mushrooms) and—after exposure to a relevant toxin—the use of specific antidotes, e.g. N-acetylcysteine after paracetamol (acetaminophen) overdose. Chronic liver failure may complicate any progressive chronic liver disease such as cirrhosis.

There are four main manifestations of liver failure. (1) Hepatic encephalopathy—this complex neuropsychiatric syndrome is divided into four stages of increasing severity: stage I, psychiatric and behavioural changes; stage II, drowsiness and lethargy; stage lll, more advanced but reversible somnolence; stage lV, coma. Clinical signs may be non-specific. Asterixis (‘liver flap’) can often be elicited. Raised brain concentrations of ammonia and increased GABA-mediated inhibitory neurotransmission may be important in pathogenesis. (2) Haemorrhagic diathesis—the main factor is portral hypertension but other contributors include impaired synthesis of hepatocyte-derived blood clotting factors and thrombocytopenia. (3) Ascites—see Chapter 15.22.3. (4) Jaundice—see Chapter 15.20. Other features of particular importance include increased susceptibility to infection, cerebral oedema and raised intracranial pressure, hypoglycaemia, hepatorenal syndrome, portopulmonary hypertension, and hepatopulmonary syndrome. Patients with liver failure complicating chronic liver disease may manifest peripheral stigmata, such as liver palms, peripheral oedema, spider naevi, or clubbing.

In patients with chronic liver disease hepatic encephalopathy can be precipitated by a wide range of factors including (1) gastrointestinal disturbance—e.g. bleeding oesophageal varices, constipation; (2) fluid/electrolyte imbalance, especially hyponatraemia and elevated creatinine which may be diuretics-induced; (3) metabolic disturbance—e.g. hypoglycaemia, hypoxia; (4) drugs—particularly sedatives and hypnotics; (5) infection, which is the most common precipitant identified.

Management

Specific and effective therapy for the underlying liver disease is administered when available, but this is not possible for most causes of liver failure. Treatment is therefore predominantly supportive, with particular emphasis on: (1) correction or removal of precipitating factors; (2) if encephalopathy is present, using phosphate enemata to empty the gut and minimizing absorption of nitrogenous substances from the gut by administration of a nonhydrolysed disaccharide laxative (e.g. lactulose, lactitol) or—more recently—oral rifaxamin; (3) very careful monitoring of clinical status and laboratory data to facilitate early detection and prompt treatment of complications, such as hypoglycaemia, hypokalaemia, cerebral oedema, infection, and bleeding.

All patients with acute or subacute liver failure should be considered to have potentially reversible disease. Nevertheless, when a patient develops stage II encephalopathy intensive supportive care should be instituted and transfer of the patient to a unit with the potential for undertaking orthotopic liver transplantation is recommended.

Course and prognosis

Patients with acute liver failure who do not develop encephalopathy can be expected to recover completely. The mortality of acute liver failure (without liver transplantation) is about 40%. A number of models in both acute and subacute liver failure predict survival without transplantation to aid clinical decision-making: these include the ‘King’s criteria’ and factor V measurement, favoured in France. The most important determinant of mortality in chronic liver disease is the severity of liver failure, and scoring systems such as UKELD and MELD based on prothrombin time, bilirubin. and renal function predict 1 to 2 year mortality.

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