There have been very few reports dealing with liver failure transplantations performed in our center. 3,4 There have been very few reports dealing specifically with HAV-induced liver related to hepatitis A in children. Moreover, the criteria usually used for selecting patients with fulminant hepatitis A failure in children, including one main series of 20 children from Chile. 5,6 We thus report the results of the retrospective for liver transplantation have not been evaluated in children. Therefore, the current study was conducted retrospectively study of 24 children with liver failure because of hepatitis A treated in a single center, as a reminder of the potential in a single French urban pediatric liver transplantation center to serve as a reminder of the potential severity of hepatits A severity of hepatitis A in children and as an attempt to identify prognostic indicators for liver transplantation. in children and to identify predictors of outcome. Children were selected by chart review using a data base system and were grouped according to outcome for analyses purposes.
PATIENTS AND METHODS
Over a 15-year period, 24 children with hepatitis A showed
Patients were retrospectively identified by chart review using a evidence of liver failure, including 6 children who did not data base system. Between 1980 and 1995, 24 children (13 boys) develop hepatic encephalopathy, 7 children in whom encephaaged 17 years or below, were admitted to Bice Λtre hospital for liver lopathy occurred but resolved spontaneously, and 11 children failure related to HAV infection. Diagnosis of hepatitis A was estab- in whom death or liver transplantation was the outcome. The lished by the detection of immunoglobulin M anti-HAV antibodies mean age at onset was 6.5 years. Those with the most rapid in serum samples of all children on admission; no children had onset of liver failure from onset of jaundice had the best evidence of pre-existing liver disease. Infection with other hepato- tropic viruses (hepatitis B virus, hepatitis C virus [since 1991], chance of recovery without developing encephalopathy. Oth-Epstein Barr virus, and cytomegalovirus), autoimmune hepatitis, erwise, no predictive factors of outcome were found at onset and Wilson's disease were excluded. Signs of liver failure, defined of liver failure. Among the 18 children who developed encephas a decrease in prothrombin time (PT) and plasma level of clotting alopathy, the best early prognostic indicator of a poor outcome factor V (FV) below 50% of normal, were present in all children. irrespective of the grade of encephalopathy, appeared to be a FLF was applied to patients in whom hepatic encephalopathy develprothrombin time level below 21% of normal combined with oped within 8 weeks of the onset of jaundice. 7 a serum bilirubin level above 400 mmol/L. Therefore, these All children who developed encephalopathy were transferred in two prognostic indicators may be helpful in deciding liver the pediatric intensive care unit. The standard classification of en- transplantation in children with hepatitis A-induced fulmicephalopathy was adapted to children according to the following nant liver failure. (HEPATOLOGY 1997;26:1018-1022.)
grades of severity: grade 1, child is confused and has mood changes; grade 2, child is drowsy and displays inappropriate behavior; grade 3, child is stuporous but obeys simple commands; grade 4a, child Abbreviations: HAV, hepatitis A virus; FLF, fulminant liver failure; PT, prothrombin All patients were given standard supportive care, as previously time; FV, clotting factor V; OLT, orthotopic liver transplantation. described. 3 No sedative drugs were administered. Fresh frozen From the 1 Service d'He Β΄patologie Pe Β΄diatrique,