Chinese Medical Information Portal Website (Taiwan Medical Network-TMN) - OldDoc Wu's Series
(Established in March 1996)
Dr. Wu's Liver diseases
for professionals (medical students and residents)
(Posted Sep. 16, 1996; Updated May 14, 2009)
Acute liver failure
(Key words: acute liver failure, fulminant hepatitis, fulminant hepatic failure, superacute liver failure, subacute liver failure)
- Acute liver failure is a clinical condition that result from severe and extensive damage of liver cells leading to failure of the liver to fucntion normally and induce mental confusion of various degree.
- It is caused by various kinds of diseases, therefore it is called a syndrome (a similar clinical condition caused by different diseases).
- It is a very severe clinical condition with high mortality rate, but when patients recover, they will recover completely.
- The symptoms are: icterus or jaundice (yellowish change of skin and mucosa color), and mental confusion and loss of different degree.
- The shorter the interval from onset of icterus to onset of mental confusion, the better the outcome appears to be.
- Acute liver failure is a clinical syndrome that results from massive necrosis of livr cells leading to hepatic encephalopathy and severe impairement of hepatic function.
- It is caused by different kinds of diseases, such as viral hepatitis (A, B, C, ...), drugs, intoxication, autoimmne hepatitis, and etc.
- It has diverse clinical courses and etiological factors, therefore, various classifications have been proposed with some degree of overlaps.
Perplexity in Terminology:
- Fulminant Hepatic Failure (FHF)
- Acute liver failure
- "Acute" vs "Fulminant"; "liver" vs "hepatic"
- Lucke and Mallory (1946):
- Two types of acute hepatitis:
- 1) fulminant form with an extremely rapid outcome
- 2) subacute form with a slower course
- Trey (1970; USA):
- Fulminant hepatic failure:
- potentially reversible condition
- consequence of severe liver injury
- with an onset of encepalopathy within 8 weeks of the appearance of the first symptoms
- absence of pre-existing liver disease.
- Bernuau and Benhamou (1986; 1993; Paris):
- Fulminant hepatic failure
- development of encephalopathy within 2 weeks after the onset of jaundice
- Subfulminant liver failure
- cause, age, and prothrombin or factor V level is more accurate than that based only on the interval between the onset of jaundice and encephalopathy
- Bernuau also suggested the term "Severe acute liver failure" for a case with:
- a greater than 50 % decrease in normal coagulation factors concentration without the
development of hepatic encephalopathy.
- as soon as encephalopathy develops, uses the term "fulmiant or subfulminant liver failure"
- O'Grady (1993; London):
- classification: (encephalopathy appears ~wks within or after the onset of the first symptoms)
- Hyperacute liver failure ( within 1 week),
- acute liver failure( 2 to 4 weeks) and
- subacute liver failure ( 5 to 12 weeks).
- survival rate with medical management :
- HALF : ALF : SALF = 36 % : 7 % : 14 %
= incidence of cerebral edema (H : H : L)
- encepahalopathy: mandatory clincal feature
- include cases of pre-existing synptomless chronic liver conditions
- both groups accept the fact that the survival rate is greater in those
cases with a shorter interval between onset of the first symptom and encephalopathy.
- Two groups -- Encephalopathy occur within and over 10 days after onset
- Shorter interval -- better pgognosis
- Acharya SK (1996; India)
- Pregnancy, cause, and rapidity of onset of encephalopathy did not influence survival
- Questions on evaluation of the prognosis of FHF -- to estimate probability of spontaneous recovery
- Completely reversible condition
- FHF case with stage 3~4 encephalopathy -- medical therapy alone -- poor prognosis
- Orthotopic liver transplantation (OLTx) -- survival rate: 60~80% -- lifelong immunosuppressive therapy
- Timing -- when to perform OLTx -- critical for successful OLTx
- Predictive factors for survival:
- Static variables: age, race, gender, cause
- Dynamic variables: degree of come, serum bilirubin, prothrombin time, factor V
- HAV, HBV, HCV, HEV, HDV, HSV, CMV, EBV, HZV, drug-induced, toxic,
concommitant use of enzyme-inducing drugs and chronic alcohol ingestion
aaggravate paracetamol-induced liver injury, afratoxin, herbs,
ischemic liver cell necrosis, hypovolemic or septicemic shock,
hepatic artery thrombosis, Budd-Chiary syndrome, veno-occlusive
disease of the liver, microvesicular steatosis in pregnancy, Ray's
syndrome, liver transplantation.
- Clinical presentation:
- Hepatic encepahlopathy:
- stupor or coma
- fector hepaticus
- flapping remor
- raised blood ammonia.
- Cerebral edema:
- vasogenic - disruption of blood-brain barrier.
- cytogenic edema - loss of capacity of neuroglial cells to
maintain solute and water homeostasis.
- increase of intracranial pressure.
- platelet - decrease
- coagulation factors - decrease (factor V, VII, XIII, fibrinogen)
- antithrombin III, alpha-2 macroblobulin - decrease
- fibrinolysis and DIC
- prothrombin-T, PTT
- Infection and immunity:
- bacteremia, septicemia, endotoxemia.
- cytokines - increase (IL-1, TNF,)
- Biochemical change:
- alpha-fetoprotein - regeneration
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(By Jau-Shin Wu, M.D.; Posted Sep. 16, 1996; Revised May 12, 2009)
(TMN) Since June 09, 2002
(Dr. Wu's Liver D) Since Jan. 01, 2008
(Olddoc)Since Jan. 01, 2008
(TMN) Since Jan. 01, 2008