Acute Liver Failure

By | January 21, 2014
  • 10 cases per million persons per year
  • most often occurs in patients who do not have preexisting liver disease
  • clinical presentation includes hepatic dysfunction, abnormal liver biochemical values, coagulopathy (body's ability to clot blood is impaired), sometimes encephalopathy (brain dysfunction), multiorgan failure and death in half the cases

Definition and Presentation

  • severe liver injury, potentially reversible in nature and with the onset of hepatic encephalopathy within 8 weeks of the first symptoms in the absence of pre-existing liver disease
  • development of encephalopathy after the onset of symptoms may be a week or less in hyperacute cases, mostly the result of acetaminophen toxicity or viral infection


  • in the undeveloped world, viral infections (hepatitis A, B, and E) are the predominant causes
  • in the developed world, drug-induced liver injury is the predominant cause
  • other causes include herpes simplex virus, cytomegalovirus, Epstein-Barr virus, and parvoviruses

Drug-induced liver injury

  • responsible for 50% of acute liver failure in the U.S., some of which is dose-dependent and predictable
  • acetominophen-induced hepatotoxicity is the most common
  • malnourished and alcoholic patients are at higher risk

Other causes

  • acute ischemic hepatocelullar injury, or hypoxic hepatitis, may occur in critically ill patients with cardiac or respiratory failure
  • other drugs, in addition to acetominophen, such as MDMA (ecstasy) and cocaine
  • neoplastic infiltration, acute Budd-Chiari syndrome, heat-stroke, mushroom ingestion, metabolic diseases such as Wilson's disease

Focus of Critical Care

Initial Care

  • restoration of intravascular volume and systemic perfusion may mitigate the severity of organ failure
  • in patients with acetaminophen poisoning, treatment with acetylcysteine is vital (it has complex antioxidant and immunologic effects that may even effect patients without acetaminophen acute liver disease)
  • high standards of infection control should be practiced to minimize the risks of nonsocomial sepsis

Subsequent care

  • dependent on the cause of the acute liver disease; specific therapies exist


Cardirespiratory dysfunction

  • circulatory dysfunction and hypotension
  • if hypotension continues despite volume repletion, norepinephrine is the preferred vasopressor


  • dependent on the location of the encephalopathy; the goal of early care is to reduce the onset of encephalopathy and reduce the risk of cerebral edema
  • intracranial hypertension from severe cerebral edema is a leading cause of death among patients with acute liver disease
  • increased levels of circulation ammonia may cause encephalopathy; sedation and prophylactic osmotherapy is used to reduce levels of ammonia


  • substantial renal dysfunction occurs in 50% of cases; more common in elderly and acetaminophen-induced acute liver disease
  • therapy may be used to control hyperammonemia and other biochemical and acid-base disturbances


Metabolic and nutritional support

  • therapies to achieve overall metabolic and hemodynamic stability
  • large volume infusions of hypotonic fluids should be avoided (they result in hyponatremia and cerebral swelling)
  • control protein loads by measuring ammonia levels

Prognostic evaluation & transplantation

  • candidates for transplantation should be identified as quickly as possible
  • there is no universal acceptance criteria for transplantation consideration
  • rates of survival after transplantation are 79% at year 1 and 72% at year 5
  • most deaths after transplantation are within 3 months and due to infection

Other therapies

  • hepatocyte transplantation involves intraportal or intraperitoneal infusion of isolated human hapatocytes to augment liver function
  • high-volume plasma exchange
Lee, William M. "Acute liver failure." New England Journal of Medicine 329.25 (1993): 1862-1872.
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