The concept of anaphylaxis originates from the observations by the French physiologist Charles Richet in 1902 of the effects of actinotoxins on the blood pressure of dogs [1]. Anaphylactic shock is the classic example of the immediate type of hypersensitivity reaction; it may be defined as the failure of the peripheral circulation induced by an antigen-antibody reaction [2]. The circulatory collapse may be primary, if the circulatory reaction is the primary event, or secondary, if the circulatory collapse is the consequence of an initial respiratory insufficiency.

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Hepatic histopathology and clinical-pathologic correlations were studied in 77 patients who met clinical criteria for halothane hepatotoxicity. They were divided into groups based on the type of surgery (minor or major) and outcome (nonfatal, biopsy group or fatal, autopsy group). The two nonfatal groups (minor surgery and major surgery) and the two fatal groups (minor surgery and major surgery) were comparable with regard to age, time of onset from exposure, peak aminotransferase values and peak bilirubin determinations. A spectrum of histologic patterns was identified in these patients. It ranged from panlobular and multifocal spotty necrosis resembling viral hepatitis through submassive confluent zonal necrosis to massive necrosis. Progression of severity of injury from spotty to massive necrosis was more closely related to multiple exposures to halothane (and especially repeated exposure within less than three months), than to the extensiveness of the associated surgical procedures.