Educational Case: Acetaminophen hepatotoxicity: Pathophysiology and evaluation of acute liver failure

Author: mycolabadmin
9/9/2024
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Summary

This educational case describes how acetaminophen overdose causes severe liver damage leading to acute liver failure. The toxic form of acetaminophen damages liver cell mitochondria and causes widespread cell death, particularly in the center of liver lobules. Treatment with N-acetylcysteine within 24 hours of overdose significantly improves outcomes, though severe cases require liver transplantation.

Background

Acetaminophen is the most widely used over-the-counter analgesic and antipyretic worldwide. At therapeutic doses, it is safe, but overdoses exceeding 10 g/day can cause severe liver injury and account for 42-46% of acute liver failure cases in developed nations.

Objective

To describe the clinicopathologic features of excessive acetaminophen ingestion, focusing on biochemical pathways, short- and long-term complications, and management strategies including N-acetylcysteine therapy and liver transplantation criteria.

Results

The patient presented with right upper quadrant pain, jaundice, hepatomegaly, hepatic encephalopathy, coagulopathy, and metabolic acidosis consistent with acute liver failure. Serum acetaminophen level was elevated at 22 hours post-ingestion. Liver biopsy showed centrilobular necrosis characteristic of acetaminophen toxicity. The patient met King’s College Criteria for transplantation and recovered post-transplant.

Conclusion

Acetaminophen-induced acute liver failure presents with characteristic centrilobular necrosis due to NAPQI-mediated hepatocyte injury and mitochondrial dysfunction. Early recognition and treatment with N-acetylcysteine within 4-24 hours significantly improves outcomes, and liver transplantation is the definitive treatment for severe cases meeting King’s College Criteria.

Published in:Academic Pathology,
Study Type:Educational Case Study,
Source: PMID: 39309105, DOI: 10.1016/j.acpath.2024.100146