Acute liver failure K72.0

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 31.01.2023

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Acute hepatic failure, acute liver failure; ALV; Liver failure acute

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Severe clinical picture characterized by a loss of liver function in patients who previously showed no signs of chronic liver disease (Trey C et al. 1970; O'Grady JG et al. 1989)

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The current definition of the American "Acute Liver Failure Study Group" places coagulopathy (INR > 1.5) in the foreground and differentiates between the temporal occurrence of coagulopathy and encephalopathy (Lee WM et al. 2008):

  • hyperacute liver failure (< 7 days)
  • acute liver failure (7 to 28 days)
  • subacute or prolonged liver failure (>28 days to 6 months)

A longer latency is associated with an increased mortality rate of 86%. A clear differentiation of ALV from acute-on-chronic or acute-on-cirrhosis liver failure is necessary, especially from a clinical-prognostic point of view, since the latter two are associated with a significantly worse prognosis.

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Incidence: 200 cases/year

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In earlier years, acute hepatitis B virus (HBV) infection was considered the most important trigger for ALV. Toxic liver damage has now increased through the use of acetaminophen (paracetamol). In the USA, Great Britain and Scandinavia, paracetamol intoxication is stated as the most frequent cause with over 40%. Viral hepatitides are the cause with 10 %. 20 % of cases remain unclear. In Southern Europe, Africa and Asia, acute viral hepatitis dominates. In the Mediterranean region, about 40 % of ALV cases are caused by hepatotropic viruses, especially HBV; about 20 % by intoxications (Escorsell A et al. 2007).

Among the rarer causes are toxic damage, mainly caused by tuberculostatics (e.g. isoniazid); furthermore by antibiotics, drugs (e.g. ectasy), tuber leaf fungi, phytopharmaceuticals (e.g. kava kava, Chinese green tea, St. John's wort) or chemicals (carbon tetrachloride).

Frequently, reactivation of a latent HBV infection under immunosuppressive therapy (especially anti-CD20 antibodies) can lead to fulminant liver failure. A fulminant initial manifestation of Wilson's disease can also cause ALV. (Eisenbach C et al. 2007), as well as autoimmune hepatitis (5% of cases) or pregnancy (3% of cases) (Canbay Ali et al. 2011).

Clinical features
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Hepatic encephalopathy (clouding of consciousness somnolence to coma), jaundice, foetor hepaticus, liver decay with decreasing liver size, hemorrhagic diathesis due to failure of liver function, disseminated intravascular coagulation (DIC), arterial hypotension, hyperventilation (ammonia effect).

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Analysis of laboratory parameters that measure the severity of liver cell damage (GOT, GPT, AST, GLDH), cholestasis (gamma-GT, AP, bilirubin) and the extent of liver synthesis (INR/Quick, albumin) and excretory function (ammonia). In addition, laboratory values that record the accompanying organ complications (blood gas analysis, lactate, differential blood count, creatinine, urea).


Toxicological screening (amphetamines, barbiturates, benzodiazepines, cannabinoids, ecstasy, cocaine, metamphetamines, opiates, tricyclic antidepressants),

virus diagnostics (HAV, HBV, HCV, HEV, HIV, HSV, CMV, EBV, VZV),

Indications of genetic causes (caeruloplasmin, ferritin, transferrin saturation, alpha1-antitrypsin)

Autoimmune parameters (ANA, SMA, AMA, ANCA)

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Anamnesis, an essential diagnostic measure is the laparoscopic liver biopsy. Furthermore, laboratory parameters and imaging procedures (duplex sonography).

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Hepatic encephalopathy: One of the major symptoms (and causes of death) in liver failure is hepatic encephalopathy.

Acute renal failure in acute liver failure: The incidence of acute renal failure caused by ALV may be as high as 80%. This may be caused by the direct toxic effects of paracetamol, aflatoxin or non-steroidal anti-inflammatory drugs, but also by acute tubular necrosis due to hypotension or ischaemia.

Furthermore, gastrointestinal bleeding, hypoglycemia, respiratory infections.

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Liver transplantation (LTx): Already during the diagnosis of ALV, potential candidates for LTx must be quickly selected and connected to a transplant centre. After exclusion of contraindications such as florid alcohol or drug abuse, systemic organic ischemia or an unfavorable social prognosis regarding the required compliance post transplantation and careful medical evaluation of the overall medical situation, a positive decision in favor of a LTx should be followed by an immediate listing of the patient for transplantation (Bernal W et al. 2004).

Conservative therapy: The high-dose administration of N-acetylcysteine (NAC = Fluimucil®) has been established as a specific therapy for paracetamol-induced ALV, but has also proved successful for other causes of ALV (NAC over a period of 72 h in 3 steps of decreasing dosage (150 mg/kg/h i.v. over 1 h, then 12.5 mg/kg/h over 4 h, then 6.25 mg/kg/h over 67 h (Koch A et al. 2010).

In addition, intensive care therapies to stabilize hemodynamics, secure the airways and early mechanical ventilation are mandatory for clouded patients. Furthermore, measures to prevent brain edema (elevation of the upper body, compensation of hyponatremia, osmotic therapy with mannitol) as well as the monitoring and early management of infections (Canbay Ali et al. 2011).

Otherwise, special therapy depending on the cause of ALV (e.g. detoxification measures when hepatotoxins are ingested); in pregnancy-associated acute liver failure: termination of pregnancy. In case of tuber leaf fungus intoxication: high-dose i.v. administration of the antidote silicin (Legalon® SIL)

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Depending on aetiology and age. Most frequent cause is cerebral edema; mild encephalography with good prognosis. 50% of ALV patients require liver transplantation.

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Most paracetamol intoxications with ALV are suicidal. Comorbidities and/or use of other substances as well as alcohol consumption increase the chances of ALV.

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  1. Bernal W et al (2004) Liver transplantation in adults with acute liver failure. J Hepatol 40: 192-197.
  2. Canbay Ali et al (2011) Acute Liver Failure-a Life-Threatening Disease. German Arztebl Int 108: 714-720
  3. Eisenbach C et al (2007) Diagnostic criteria for acute liver failure due to Wilson disease. World J Gastroenterol 13: 1711-1714
  4. Escorsell A et al (2007) Acute liver failure in Spain: analysis of 267 cases. Liver Transpl 13: 1389-1395.
  5. Hadem J et al (2008): Prognostic implications of lactate, bilirubin, and etiology in German patients with acute liver failure. Clin Gastroenterol Hepatol 6: 339-345.
  6. Jochum C et al (2009) Hepatitis B-associated acute liver failure: immediate treatment with entecavir inhibits hepatitis B virus replication and potentially its sequelae. Digestion 80: 235-240.
  7. Koch A et al (2010) N-acetylcysteine on its way to a broader application in patients with acute liver failure. Hepatology 51: 338-340.
  8. Lee WM et al (2008): Acute liver failure: Summary of a workshop. Hepatology 47: 1401-1415.
  9. O'Grady JG et al (1989) Early indicators of prognosis in fulminant hepatic failure. Gastroenterology 97: 439-445.
  10. Trey C et al (1970): The management of fulminant hepatic failure. Prog Liver Dis 3: 282-98.
  11. Wei G et al.: Acute liver failure in Sweden: etiology and outcome. J Intern Med 2007; 262: 393-401.


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Last updated on: 31.01.2023