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Natural history and risk factors in fulminant hepatic failure
U Poddar1, B R Thapa, A Prasad
1Division of Pediatric Gastroenterology, Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. ujjalpoddar@hotmail.com
Insights
Fulminant hepatic failure (FHF) in children is often caused by viral hepatitis. Spontaneous bacterial peritonitis (SBP) in FHF patients with ascites indicates a worse prognosis and requires investigation.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Infectious Diseases
Background:
- The natural history of fulminant hepatic failure (FHF) in children, particularly without liver transplantation, remains poorly understood.
- Identifying prognostic factors is crucial for managing pediatric FHF cases.
Purpose of the Study:
- To investigate the natural history of FHF in Indian children.
- To determine prognostic factors, focusing on the impact of ascites and spontaneous bacterial peritonitis (SBP).
Main Methods:
- Sixty-seven children (<=12 years) diagnosed with FHF between August 1997 and December 2000 were studied.
- Clinical data, investigations, and outcomes were recorded.
- Viral markers (Hepatitis A, E, B, C) and SBP (defined by ascitic fluid neutrophil count) were assessed.
Main Results:
- Viral markers were positive in 94% of cases, with Hepatitis A being the most common.
- Mortality was 25% overall, significantly higher in patients with ascites (32%) compared to those without (18%).
- Among patients with ascites, mortality was highest in those with SBP (78%).
Conclusions:
- Age, encephalopathy grade, ascites, and SBP are key determinants of FHF outcome in Indian children.
- SBP presence in FHF patients with ascites is a strong indicator of a poor prognosis.
- Investigating SBP is recommended for all FHF cases presenting with ascites.
Background:
The natural history of fulminant hepatic failure (FHF) without liver transplantation is not well known.
Aims:
To study the natural history and prognostic factors, especially the presence of ascites and spontaneous bacterial peritonitis (SBP), in children with FHF.
Methods:
FHF was defined by the onset of encephalopathy within 12 weeks of onset of jaundice. From August 1997 to December 2000, 67 children (< or =12 years) were diagnosed with FHF. Their clinical features, investigations and outcome were noted. Viral markers A to E (IgM, anti-HAV; IgM, anti-HEV, HBsAg, and anti-HCV) were determined by ELISA. SBP was defined by the presence of > or =250 neutrophils with or without a positive culture in ascitic fluid.
Results:
Mean age of the children was 5.8 years with an almost equal sex distribution. Viral markers were positive in 63 (94%) cases: hepatitis A in 34 (54%), E in 17 (27%), A+E in seven (11%), and B in five (8%). Thirty one children presented with grade I or II encephalopathy and all recovered, whereas 17 of 36 children who had grade III or IV encephalopathy died. Ascites was detected (both clinically and ultrasonically) in 34 (51%) cases, nine (26%) of which had SBP. Overall mortality was 25%. Mortality was higher in those who had ascites than in those who did not (32% v 18%); among those with ascites it was maximum in those who had SBP (78% v 16%). Total serum bilirubin and grade of encephalopathy were significantly higher, serum albumin was significantly lower, and prothrombin time was significantly prolonged in those who died than in those who recovered.
Conclusion:
The natural history of FHF in Indian children depends on age, grade of encephalopathy, ascites, and SBP. SBP depicts worse outcome. In all cases of FHF with ascites, the presence of SBP should be investigated.