KINESIOL 1Y03 Chapter 12: Acute liver failureCHECK SLIDES!

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Acute liver failure
= the result of severe and extensive damage to hepatocytes leading to loss of hepatic
function in a previously healthy liver
= syndrome with a wide range of symptoms
high mortality, but is completely reversible
characterized by jaundice, followed by encephalopathy
Classification
-depends on length of time between jaundice and encephalopathy (fulminant hepatic
failure) - O’grady, 1993:
TYPE
DURATION
BETWEEN
JAUNDICE AND
ENCEPHALOPATHY
SURVIVAL WITH
SUPPORTIVE CARE
Hyperacute hepatic failure 0-7 days 36%
Acute hepatic failure 8-28 days 7%
Subacute hepatic failure 4 – 12 weeks 14%
 subacute has slightly higher survival than acute due to decreased risk of cerebral oedema
Causes
1) Infection: Enteric: Hep A and Hep E
Parenteral: Hep B, Hep D and CMV
Unknown non Hep A non Hep B (viruses we haven’t discovered)
2) Toxins: paracetemol, amanita phalloides (mushrooms), bacillus cereus (rice)
3) Disease of pregnancy: Hep E (worse in preganancy), hepatic infarction (as more prone to
thrombosis), AFLOP (acute fatty liver of pregnancy), HELLP (high enzyme low platelets)
4) Idiosyncratic drug reactions: Isoniazid , NSAIDs, valproate
AND Drug combinations: amoxicillin + clavulanic acid, trimethoprim + suplhamethoxazole,
rifampicin + isoniazid
5) Vascular diseases: ischaemic hepatitis, post-OLT hepatic thrombosis, post-arrest
6) Metabolic causes: Wilson’s disease, Reye’s syndrome (‘dispirin’ – aspirin in children)
 paracetemol is commonest, then non-A non-B viruses, then hep B, then hep A, then
halothane
 more commonly now recreational drugs like ecstasy and methedrone
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