Acute hepatic failure (AHF) in India almost always presents with encephalop
athy within 4 weeks of the onset of acute hepatitis. Further subclassificat
ion of AHF into hyperacute, acute and subacute forms may not be necessary i
n this geographical area, where the rapidity of onset of encephalopathy doe
s not seem to influence survival. Viral hepatitis is the cause in approxima
tely 95-100% of patients, who therefore constitute a more homogeneous popul
ation than AHF patients in the West. In India, hepatitis E (HEV) and hepati
tis B (HBV) viruses are the most important causes of AHF; approximately 60%
of cases are caused by to these viruses. Hepatitis B virus core mutants ar
e very important agents in cases where hepatitis B results in AHF in this c
ountry. Half of the patients with AHF admitted to our centre are female, on
e-quarter of whom are pregnant. Therefore, pregnant females who contract vi
ral hepatitis constitute a high-risk group for the development of AHF. Howe
ver, the outcome of AHF in this group is similar to that in non-pregnant wo
men and men. No association with any particular virus has been identified a
mong sporadic cases of AHF.
In our centre, approximately one-third of AHF patients survive with aggress
ive conservative therapy, whereas two-thirds of deaths occur within 72 h of
hospitalization. Cerebral oedema and sepsis are the major fatal complicati
ons. Both fungal and Gram-negative bacteria are major causes of sepsis. Amo
ng patients with AHF, despite the presence of sepsis, its overt clinical fe
atures (i.e. fever, leucocytosis) may be absent and objective documentation
of the presence of sepsis in such patients is achieved by repeated culture
of various body fluids. It should be possible to develop simple, clinical
prognostic markers for AHF in this geographical region, in order to identif
y patients suitable for liver transplantation. (C) 2000 Blackwell Science A
sia Pty Ltd.