Halothane Hepatotoxicity Clinical Presentation

Updated: Dec 17, 2019
  • Author: Ruben Peralta, MD, FACS; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM  more...
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Type I (mild) halothane hepatotoxicity occurs within hours of halothane exposure. It does not occur after other agents. Type I is characterized by mild, transient elevations in serum transaminase and glutathione S- transferase concentrations. Jaundice is not observed, and no evidence of hepatocellular disease is present.

Type II (fulminant) halothane hepatotoxicity usually occurs 5-7 days following exposure, although it can be delayed by up to 4 weeks. Fever, leukocytosis, and eosinophilia are observed. Nonspecific gastrointestinal upset may be noted. Nausea and vomiting may occur. Patients may report arthralgias. Most prominently, the patient looks and feels unwell. Fulminant liver failure may ensue.

Hepatic dysfunction in the postoperative period has many possible causes. Halothane hepatotoxicity is a diagnosis of exclusion. Other potential causes of liver dysfunction should be considered, including other hepatotoxic medications, hypotension, hypoxia, and infection.


Physical Examination

Physical findings in type II halothane hepatotoxicity include delayed pyrexia (up to 75% of patients). Jaundice can be present 7-10 days after exposure, but it may occur earlier in previously exposed patients. Liver tenderness is common but hepatomegaly is usually mild. A nonspecific rash may be observed.



Fulminant liver failure is possible. In rare cases, cirrhosis may develop following halothane hepatitis. However, in most cases, liver function returns to normal. Halothane given with succinylcholine for induction anesthetic is associated with masseter spasm.