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[Fulminant hepatic failure in children]
J Cordero1, J Baeza, J Zacarías
1Unidade de Tratamiento Intensivo, Hospital Luis Calvo Mackenna, Santiago de Chile.
Insights
Fulminant liver failure in children is often viral, with jaundice and encephalopathy common. Complications and mortality rates are similar to adults, particularly in severe coma cases.
Area of Science:
- Pediatric Hepatology
- Critical Care Medicine
- Viral Hepatitis
Background:
- Fulminant liver failure (FLF) in children presents unique etiological considerations compared to adults.
- Understanding the clinical course and outcomes is crucial for effective management.
Purpose of the Study:
- To describe the clinical characteristics and outcomes of pediatric patients with fulminant liver failure.
- To identify factors associated with mortality in this cohort.
Main Methods:
- Retrospective analysis of 38 children diagnosed with fulminant liver failure.
- Serologic screening for viral etiologies (Hepatitis A and B).
- Clinical data collection including age, symptoms, disease progression, complications, and survival.
Main Results:
- A viral etiology was identified in 19 of 25 tested patients (17 Hepatitis A, 2 Hepatitis B).
- Common complications included hypoglycemia, seizures, gastrointestinal bleeding, respiratory failure, and severe infections.
- Overall mortality was 42%, significantly higher (83%) in patients presenting with stage 3 or 4 coma.
Conclusions:
- Viral infections are a primary cause of FLF in children.
- Pediatric FLF shares similar high mortality rates and complications with adult FLF, especially in severe cases.
- Prompt recognition and management are vital for improving outcomes in pediatric fulminant liver failure.
Abstract:
We report the clinical characteristics and course of 38 children with fulminant liver failure. A viral etiology was demonstrated in 19 patients out of 25 with serologic screening (virus A in 17 patients, B in 2 patients). One patient had toxic liver damage from ingestion of a caustic substance. Mean age was 4 years and 6 months. Jaundice was present in all but 2 patients at admission. Encephalopathy developed at a mean of 13 days and 17 children were admitted with stage 3 or 4 coma. Evidence of severe liver failure was present in every patient. A lower prothrombin time and higher bilirrubin concentration were shown by non survivors. Hypoglycemia developed in 37% of patients, seizures in 37%, gastrointestinal bleeding in 45%, respiratory failure in 32% and severe infection in 32%. Overall mortality rate was 42% raising to 83% in patients with stage 3 coma at admission. Thus, although the etiology of fulminant liver failure differs in children as compared to adults, mortality rate and complications are similar.