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Halothane and Liver Damage Postgrad Med J: first published as 10.1136/pgmj.65.761.129 on 1 March 1989. Downloaded from Postgraduate Medical Journal (1989) 65, 129 - 135 Review Article Halothane and liver damage D. Rosenak, A. Halevy and R. Orda Department ofSurgery 'A', AssafHarofeh Medical Center, Sackler Faculty ofMedicine, Tel Aviv University, Zerifin 70300, Israel. Introduction Halothane was first synthesized by Suckling in 1952 observed in control groups. Minor reversible changes and introduced into clinical practice a few years in liver function are common after surgery regardless later.',2 Its many advantages, such as quick action, of the anaesthetic agent used,36 though in the case of easy administration, non-explosiveness, high potency other agents, the changes noted are of a much lower and low cost, led to its widespread use within a short magnitude than with halothane. The other form of time. liver damage after halothane is severe acute hepatitis, Although initial animal work did not indicate any with histological findings of massive hepatic necrosis. hepatotoxic effect,3`5 the first cases of unexplained This form is sporadic and its frequency varies from hepatitis after exposure to halothane were reported 1:6000 to 1 :3500"2.31,36-40 with a mean frequency only two years after its introduction into clinical use.6'7 around 1:10000. Strunin36 suggested a pyramidal During the following years an increasing number of morbidity model, in which many patients with mild reports dealt with the association between halothane hepatic dysfunction constitute the base, and those exposure and liver damage.8"'6 Despite the accumul- presenting severe liver disease are located at the apex copyright. ation of clinical evidence, there was still considerable of the pyramid. disagreement regarding this association. The con- troversy was based on whether post-anaesthetic hepatic dysfunction could be attributed only to Risk factors halothane or also to other anaesthetic agents. Early clinical research also failed to show a significant rise in Repeated exposure the frequency of liver damage following exposure to Many reports indicate an association between halothane, compared with other anaesthetic agents in repeated exposures to halothane within short inter- http://pmj.bmj.com/ use.11'1724 The difficulty in proving an association vals, and a rise in the rate ofhepatic morbidity, mild or results from the rarity of the phenomenon on the one severe. 6422.28,34,40-43 Seventy seven to 95% of the cases hand, the widespread use ofthe agent on the other and occur after repeated exposures;22'27,3034'38 most often the many other reasons for fever and jaundice follow- (55-80%) repeat exposure took place within a month ing surgery.25 Only during the 1960s and since have or less after the previous one.22 24 27 30,33,38,40 Since the sufficient data accumulated to prove the existence of rate of repeated exposure in uncomplicated halothane 'halothane hepatitis'.22'26-29 anaesthesia is only 7-9%,40 the element of repeated on September 30, 2021 by guest. Protected exposure within a brief period is significant. Frequency Moreover, liver disease after a single exposure is rare. There is a direct relationship between the number of Two forms of hepatic damage following halothane repeated exposures and the severity of hepatic dys- anaesthesia have been described.0 The more frequent function and it has also been found that an inverse one is asymptomatic and expressed by abnormal relationship exists between the number of previous laboratory values only, such as a rise in hepatic exposures and the duration of the latent transaminase levels and other liver enzymes. The period. 1622.30.37'38 It is also well known that most of the incidence ofthis asymptomatic liver dysfunction is not patients who developed massive hepatic necrosis had known.3' Some reports indicate an incidence of up to had a milder reaction when previously exposed to 20% of all patients undergoing halothane anaes- halothane.'6'30 However, patients who have suffered thesia,25'28,32-35 much higher than enzyme changes liver dysfunction following the drug do not necessarily develop a further episode when re-exposed,22'45 and Correspondence: Professor R. Orda, M.D., M.S. there is still no way to predict which patient will Accepted: I November 1988 develop a recurrent reaction.30 (D The Fellowship of Postgraduate Medicine, 1989 130 D. ROSENAK et al. Postgrad Med J: first published as 10.1136/pgmj.65.761.129 on 1 March 1989. Downloaded from Sex operation.25 30 Moreover, the condition may arise even after minor and non-abdominal surgery. It was found Halothane hepatitis is more frequent among females, that 69% of the patients underwent a relatively minor the male/female ratio being 1:2223034 although it seems operation of less than 30 minutes duration (most of that males have a worse prognosis.22'34 Apparently, sex them gynaecological procedures, eye surgery or hormones play a role in the ability to reduce or wound debridment), and only 32% underwent a major increase the metabolism rate of halothane, and procedure (4% of the patients underwent biliary thereby influence the accumulation rate of toxic operations).30 The presence of previous biliary or metabolites, as was shown in laboratory animals.' compensated liver disease has not increased the risk,21 but one must keep in mind the fact that any type of Age anaesthesia may affect liver function adversely in a patient suffering from active liver disease.54 The condition is extremely rare in children and is most Other factors such as hypoxia, hypotension, impair- frequent in middle age.22'30 According to one series, ment of hepatic blood flow during the operation, 68% of the patients were in the age group of 41-70 hypothyroidism, starvation, alcoholism, and enzyme years.22 The mean age for morbidity is 56.5-57.273034 inductors, do not increase morbidity rate, although The rarity of this condition in childhood results most exposure to one of these factors or a combination of probably from the absence of the immunological them has been shown to be significant in laboratory and/or metabolic mechanisms necessary for halothane animals.364'48,49,55-57 to induce liver damage47 and from the fact that less surgery (and probably less repeated surgery) is done in children. Only two cases of liver damage following Pathogenesis halothane anaesthesia have been described among patients under 20 years, and even in those, the Two different mechanisms have been proposed to diagnosis was doubtful.22 explain the liver damage following halothane exposure in man. Obesity copyright. The metabolic mechanism; (bio-transformation) The liver complication is most frequent in the obese.22'34'" In one series, two thirds of patients with About 20% ofhalothane undergoes metabolism either liver dysfunction following halothane exposure were in an oxidative or non-oxidative ('reductive') path- fat.30 This phenomenon can be explained by the ability way, producing a number of intermediate products, ofthe adipose tissue to act as a reservoir for halothane, especially chlorides, bromides, and trifluoro-acetic which delays its release into the circulation and acid (TFAA).58 62As in the case ofother hepatotoxins, prolongs its presence in the body.3' It may also be halothane is metabolized by cytochrome P450 andhttp://pmj.bmj.com/ conjectured that obesity exposes to intra-operative other liver enzymes.63 It has been postulated that the hypoxia which was demonstrated to be a risk factor in intermediate products generated in the non-oxidative laboratory animals."'48 51 pathway, especially under hypoxic conditions, play a major role in the hepatotoxicity44'48'49'55 probably due A history ofatopic diseases or allergy to other drugs to their tendency to bind to the fatty and protein macromolecules in the microsomal fractions of the There is a link between known history of hypersen- hepatocytes. Other intermediate products, such as free on September 30, 2021 by guest. Protected sitivity and morbidity, as was indicated in some radicals, may also be implicated by a direct reports.22'27'34 In one series, a third of the patients had mechanism.65 However, it should be emphasized that history of drug allergy.30 all the theories related to this metabolic mechanism arise from experiments in laboratory animals and are HLA andgeneticpredisposition of doubtful applicability to human beings.59'66 Some studies show a tendency for certain races" or The immunological mechanism families3' to develop liver dysfunction following halothane exposure. Perhaps genetic factors pre- Evidence that liver damage following halothane dispose to this sensitivity by an immunological and/or exposure is activated by a hypersensitivity mechanism metabolic mechanism.35'52 There is evidence that to halothane or its metabolites, is supported by the specific HLA types are more prone to develop liver following findings: dysfunction with halothane.53 (a) The disease is extremely rare after a single No correlation has been shown between the mor- exposure and the latent period, the severity and bidity rate and the type, duration or location of the frequency of appearance are directly related to the HALOTHANE AND LIVER DAMAGE 131 Postgrad Med J: first published as 10.1136/pgmj.65.761.129 on 1 March 1989. Downloaded from number of previous exposures, the explanation being exposure.32 70 In some cases, atypical lymphocytes idiosyncrasy which is not dose related.6'22'30'37'38 The were also found.'6 fact that the event can occur, though very rarely, after In summary, the pathogenesis of the liver damage a single exposure, can be explained on the basis of caused by halothane is still not fully understood. It is non-specific hyper-sensitivity. possible that both mechanisms play a role in the (b) Many patients with massive hepatic necrosis pathogenesis.
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