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Identification of factors contributing to hepatomegaly in severely burned children
Robert E Barrow1, Hal K Hawkins, Asle Aarsland
1Shriners Hospitals for Children, Galveston, Texas 77550, USA. rbarrow@utmb.edu
Insights
Postmortem hepatomegaly in burned children is primarily caused by enlarged liver cells containing significant intracellular fat. This finding helps understand liver changes after severe burns.
Area of Science:
- Pathology
- Pediatric Burn Injury
- Hepatology
Background:
- Hepatomegaly (enlarged liver) is frequently observed postmortem in severely burned children.
- Autopsy findings include hepatocyte fat deposition, congestion, necrosis, and cholestasis.
Purpose of the Study:
- To determine the primary causes of postmortem hepatomegaly in severely burned children.
- To investigate the relationship between liver size and histopathological findings.
Main Methods:
- Review of 41 pediatric postmortem cases with severe burns.
- Histopathological examination of liver tissue.
- Analysis of liver enzymes, density, and wet/dry weight ratios.
Main Results:
- Intrahepatocytic fat droplets and cholestasis significantly contribute to hepatomegaly.
- Hepatomegaly correlated with increased hepatocyte volume and total fat content.
- Triglycerides increased with hepatomegaly severity; saturated fatty acids decreased.
Conclusions:
- Hepatocyte enlargement with substantial intracellular fat (up to 19%) accounts for 85-90% of postburn hepatomegaly.
- Minor contributions may come from extracellular protein, glycogen, and fluid accumulation.
Abstract:
Hepatomegaly is a common postmortem observation in severely burned children, with the liver often tripling in size when compared with normal livers for age, weight, and sex. Lesions identified at autopsy include deposition of large and small fat droplets in the hepatocyte, congestion, centrilobular necrosis, and cholestasis. The present study was designed to identify the primary causes of hepatomegaly in severely burned children postmortem. For this purpose, 41 autopsies were reviewed and, when available, blood and tissue samples were studied. Histopathologic findings showed that large intrahepatocytic fat droplets within hepatocytes and cholestasis were important contributors to hepatomegaly. Liver density and wet/dry weight ratios significantly decreased with increasing liver size. Hepatocyte volume increased with increasing liver size (P < 0.001) as did total fat content (P < 0.001). The liver enzymes, alanine aminotransferase and aspartate aminotransferase, remained normal except within 5 to 10 days of injury and 5 to 10 days of death. Triglycerides made up 4% to 70% of the total fat, with the percentage of triglycerides increasing with the severity of hepatomegaly. Saturated fatty acids represented about 85% of the total fatty acids in normal-sized livers, whereas in the largest livers (400% of predicted), only 25% of the fatty acids were saturated. This study provides evidence that 85% to 90% of the hepatomegaly observed in severely burned children postmortem is associated with hepatocyte enlargement, which includes up to 19% intracellular fat. Increases in extracellular protein, intracellular glycogen, and fluid accumulation may make a minor contribution to postburn hepatomegaly.
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