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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-.

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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].

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Last Update: January 1, 2018.



Halothane is a potent volatile halogenated anesthetic gas that has been linked to many cases of idiosyncratic acute liver injury that are frequently severe. The potential of halothane to cause hepatotoxicity and the greater safety of newer anesthetics has led to a decrease in its use, currently limited to special situations, particularly in children. Because halothane is relatively inexpensive it continues to be used in developing countries.


Halothane (hal' oh thane) is a volatile anesthetic that was used widely in major surgery between its introduction in 1956 and falling out of favor in the mid 1990s. It is nonflammable, potent and well tolerated. Halothane is administered to produce end tidal concentrations of 0.7% to 1%. It has a somewhat slow onset of action and, therefore, like other halogenated inhalational anesthetics, it is used to maintain anesthesia after induction with other agents. Halothane is no longer available in the United States, but is still used in developing countries, particularly in pediatric patients. Halothane must be administered in a controlled situation by a properly trained and credentialed anesthesiologist or nurse anesthetist and is typically given in concentrations up to 1% with oxygen.


Prospective, serial blood testing often demonstrates minor transient elevations in serum aminotransferase levels in the 1 to 2 weeks after major surgery and anesthesia with halothane and other halogenated anesthetics. Appearance of ALT levels above 10 times the upper limit of normal, however, is uncommon and points to significant hepatotoxicity. Clinically apparent, severe hepatic injury from halothane is rare, occurring in ~1/15,000 cases after initial exposure, but in ~1/1,000 cases after repeated exposures. The injury is marked by acute elevations in serum aminotransferase levels (5- to 50-fold) and appearance of jaundice within 2 to 14 days of surgery. There are usually minimal increases in alkaline phosphatase levels. Fever occurs before onset of jaundice in a high proportion of patients and eosinophilia in up to 30%. Rash and arthralgias can also accompany the onset of hepatic injury. The acute liver injury may be self-limited and resolve within 4 to 8 weeks, but can be severe and lead to acute liver failure. A strong risk factor is previous exposure to any of the halogenated anesthetics and particularly a history of halothane hepatitis or unexplained fever and rash after anesthesia with one of these agents. Other risk factors are hypotension, older age, obesity and concurrent use of CYP 2E1 inducers. The differential diagnosis of acute liver injury after surgery and anesthesia is sometimes difficult, and a clinical picture similar to halothane hepatitis can be caused by shock or ischemia, sepsis, other idiosyncratic forms of drug induced liver injury and acute viral or herpes hepatitis. Indeed, many cases of severe liver injury arising soon after surgery and attributed to halothane or other halogenated anesthetics in the literature probably represent liver injury from shock and ischemia. Factors favoring the diagnosis of ischemic hepatitis are rapid onset after surgery, extremely high values for ALT, AST and LDH, and subsequent rapid fall in serum enzymes.

Likelihood score: A (well known cause of clinically apparent liver injury).

Mechanism of Injury

The mechanism of halothane hepatotoxicity is suspected to be immunoallergic, caused by creation of reactive intermediates of the anesthetic. Approximately 60% to 80% of halothane is eliminated unchanged by the lungs, but a proportion is biotransformed by hepatic microsomal enzyme CYP 2E1 to a trifluoroacetic acid which can be detected in the urine, but which also can trifluoroacetylate hepatic proteins, some of which may be immunogenic and induce cytotoxic reactions. The clinical pattern of injury is suggestive of an allergic hepatitis with rapid onset of injury, fever, eosinophilia and accelerated and more severe injury with reexposure. Patients with halothane hepatitis often have antibodies to trifluoroacetylated proteins. On the other hand, the clinical and histological pattern of halothane hepatic injury also resembles chloroform induced liver damage with centrolobular somewhat bland necrosis, suggesting that toxic intermediates of reductive halothane metabolism may cause the injury by direct injury.

Outcome and Management

Severity ranges from mild and transient aminotransferase elevations without symptoms or other evidence of liver injury, to a self limited symptomatic acute hepatitis-like reaction, to a severe, acute hepatic failure. The severity and prognosis may relate in part of patient age, being more severe in the elderly and both milder and less common in children. Obesity may also be both a predisposing factor and predictor of outcome. Chronic liver injury from repeated halothane exposure has been described in health care workers repeatedly exposed to the agent, but the injury does not appear to lead to a chronic hepatitis if the exposure is terminated. Patients with halothane induced hepatitis should be cautioned against future exposure to a fluorinated hydrocarbon anesthetic such as isoflurane, enflurane, desflurane or sevoflurane.

Drug Class: Halogenated Anesthetics

Other Drugs in the Class: Desflurane, Enflurane, Isoflurane, Sevoflurane



Halothane – Generic, Fluothane®


Anesthetics, Halogenated


Product labeling at DailyMed, National Library of Medicine, NIH


Halothane 151-67-7 C2-H-Br-Cl-F3
Halothane chemical structure


References updated: 01 January 2018

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