468 gery and

Letters

to

the Editor

HALOTHANE HEPATITIS

SIR,-Professor Sherlock’s Point of View on halothane hepatitis (Aug. 12, p. 364) has an air of deja vu. In the past, appeals have been made to hepatologists and others to act responsibly (because of possibly medicolegal implications) when making statements about halothane which may be open to mis-

interpretation. It is worth emphasising that an "anaesthetic" does not only consist of halothane, but may involve other drugs, cardiorespiratory and cellular changes, as well as the surgical procedure. Any or all of these factors may be involved in postoperative problems. The choice by Sherlock of Peters et al.as a reference source concerning the incidence of hepatic necrosis is unfortunate. These workers both misquote2 the National Halothane Study and also, in their own data, seem confused between halothane and other anaesthetic agents. A more recent source3 relevant to British practice quotes the incidence of severe liver damage associated with halothane as between 1 in 6000 and 1 in 20 000. Reviewing experience in Sweden, Bottinger et al. calculated a risk figure of 1 in 7000 halothane anaesthetics giving rise to hepatic damage, and 1 in 110 000 anaesthetics ending in a fatal reaction. Since halothane-associated hepatitis is rare it was surprising that small prospective studies, such as those in Oxfordand Southamptonapparently yielded positive results. Later prospective trials7 8 of repeated halothane anaathesia have not substantiated the Oxford and Southampton studies. I cannot help feeling that assessing postoperative liver function by changes in transaminases alone is unrewarding. Multiple liver biopsies have both ethical and logistical drawbacks. Furthermore, proper interpretation is only available in a few specialised centres and is rarely done on a blind basis. As far as the mechanism of halothane hepatotoxicity is concerned it is disappointing that Sherlock only mentions oxidative metabolism of halothane and ignores the reductive pathway first described in 19759 and the possible role of enzyme-inducing agents. 10 The concept of an immune reaction being responsible for halothane hepatitis is not new. The example" of the patient described as having acute serum sickness and immune complexes is a bad one. That patient had a breast carcinoma, and immune complexes are often present in such patients and are related to their disease. 12 The relationship between halothane, liver damage, and the immune systems is not clearly established. Sherlock chides anxsthetists for losing contact with their patients in the postoperative period. Equally, however, I must take her to task for her suggestion that it is ill-advised to give halothane for minor surgery. Such advice shows a sad lack of understanding of modern anaesthetic practice. There may be an argument for restricting the use of halothane in major sur1. Peters, R. L., Edmonson, H. A., Reynolds, T. B., Meister, J. C., Curphey, T. J. Am. J. Med. 1969, 47, 748. 2. Simpson, B. R., Strunin, L., Walton, B. in Controversy in Internal Medicine II (edited by F. J. Ingelfinger, R. V. Ebert, M. Finland, and A. S. Relman); p. 580. Philadelphia, 1974. 3. Inman, W. H., Mushin, W. W. Br. med. J. 1974, i, 5. 4. Bottinger, L. E., Dalen, E., Hallen, B. Acta anæsth. scand. 1976, 20, 40. 5. Trowell, J., Peto, R., Crampton-Smith, A. Lancet, 1975, i, 821. 6. Wright, R., Chisholm, M., Lloyd, B., Edwards, J. C., Eade, D. E., Hawksley, M., Moles, T. M., Gardner, M. J. ibid. 1975, i, 817. 7. McEwan, J. Br. J. Anæsth. 1976, 48, 1065 8. Allen, P. J., Downing, J. W. ibid. 1977, 49, 1035. 9. Cohen, E. N., Trudell, J. R., Edmunds, H. N., Watson, E. Anesthesiology,

1975, 43, 392. Sipes, I. G., Brown, B. R. ibid. 1976, 45, 522. Williams, B. D., White, N., Amlot, P. L., Staney, J., Toseland, P. A. Br. med. J. 1977, ii, 159. 12. Hoffken, K., Meredith, I. D., Tobms, R. A., Baldwin, R. W., Davies, C. J., Blarney, R. W. ibid. 1977, ii, 218. 10. 11.

reserving it for the preceding minor procedure, but avoid it in the latter situation implies that there are safer alternatives. This is not the case. Indeed what studies there are of anaesthetic morbidity and mortality suggest that halothane is probably the "safest" agent currently available. Everyone agrees that halothane should be avoided in the patient with unexplained hepatitis after a previous halothane anxsthetic, but this is rare. One might go further and suggest that such patients should not be subjected to any anaesthesia and surgery, except in an emergency, until their hepatitis has resolved since this appears to increase the risk of further liver damage." However, the vast majority of patients who receive repeated halothane ansesthesia do so without ill-effect. It is a matter for judgement, therefore, whether the few cases of halothane hepatitis which might be avoided by not using halothane would be offset by other deaths not from liver damage associated with alternative and perhaps inappropriate anxsthetics. to

Department of Anæsthetics, King’s College Hospital and Medical School, London SE5 9RS

LEO STRUNIN

SIR,-Although I would not resist the possibility that halothane could have toxic effects on the liver, I would be reluctant to accept Professor Sherlock’s point of view (Aug. 12, p. 364) that it seems ill-advised to give halothane to patients for minor surgery. No anxsthetic is without a mechanical or pharmacological risk in minor or major surgery, and unless all risks are taken into account the choice of halothane or an alternative method cannot sensibly be made. The Southampton study cited by Sherlock did not provide comparative data on the morbidity in general associated with halothane or non-halothane anaesthesia. It would be regrettable if anaesthetic specialists, aware of many of the hazards of anxsthesia, were unduly influenced in their choice of agents and in their advice to trainee anxsthetists, by the opinion of specialists in other medical fields. Sherlock’s point of view, if generally accepted, might even have legal implications not only for anxsthetists but for those who continue to manufacture and market halothane. Wessex Cardiac & Thoracic Centre Southampton Western Hospital, Southampton SO9 4WQ

J. M. MANNERS

NITROGEN-OXYGEN SATURATION THERAPY IN DECOMPRESSION SICKNESS

SIR,-We read the paper by Dr Miller and colleagues (July 22, p. 169) with considerable interest because twice during the past two years we have converted an atmosphere of air to one of helium and oxygen during therapeutic recompression in order to provide a means of safe decompression after prolonged exposure to an air atmosphere at 50 metres (6 atmospheres absolute). We were aware of the possible problems, but facilities for conversion to a controlled nitrogen and oxygen atmosphere were not available. The patient’s condition did not worsen after conversion on either occasion. On the first occasion, a pneumothorax delayed decompression ; the patient had spent ten hours at 50 metres by the time the chamber had been rigged for a heliox saturation mode. A chest drain was inserted before conversion of the atmosphere, and the patient was successfully decompressed on a standard heliox saturation decompression schedule. In the second case, serious neurological signs (paraplegia) worsened during attempts to decompress a diver from 50 metres after standard treatment at that depth. The patient had already been exposed to hyperbaric oxygen during initial standard therapy at 18 metres. While awaiting the rigging of the chamber to a heliox 13. Strunin, L. The Liver and Anæsthesia. London, 1977.

469 saturation mode, the diver was returned to 50 metres for a further two hours. Symptoms did not worsen during the subsequent heliox saturation decompression schedule. The patient improved, regaining considerable motor and sensory function with daily treatment with standard oxygen therapeutic tables1 at 18 metres and with adjuvant therapy. When last seen at our centre, the diver had a residual limp. We are aware of a third case of conversion from air to heliox done recently, when nitrogen was not available. Again there was no apparent worsening of the patient’s condition. We have not experienced difficulties converting from air to heliox, but agree that conversion to a controlled nitrogen/ oxygen atmosphere is a more logical choice, especially when nitrogen becomes as freely available at the work site as helium is now. Like Miller et al., we have found that only a minority of cases fail to respond to standard therapy, and any remaining neurological signs may be resolved by further daily recompression with oxygen (as shown in case 1 of their paper). We have also found that after a course of treatment, neurological signs and symptoms resolve without further specific therapy (as in case 3 of their paper). Although all three of their cases received adjuvant therapy (dexamethasone and dextran infusion), Miller et al. do not discuss its relevance to the results obtained, although attempts to treat difficult cases, to which they refer, lacking the benefit of these more recent additions to the treatment of decompression sickness, achieved only poor results. From the case descriptions, it seems that only case 2 tests the hypothesis that a sufficient time at depth allows the complete resolution of the manifestations of decompression sickness. Certainly cases 1 and 3 show that the schedule described provides a safe method of decompression from 30 metres in a controlled nitrogen/oxygen atmosphere. The result achieved by treatment in case 2 is certainly impressive: in due course such treatment may well become a useful addition to current therapy. We realise that it is difficult to design a satisfactory comparative study of the treatment of decompression sickness, but these studies are necessary for the assessment of new therapy. In view of the implications of their new regimen for the management of cases in operational conditions, we feel that Miller et al. should have discussed their results more fully.

Their paper states that changing from a nitrogen-oxygen mixture to a helium-oxygen mixture has "occasionally been associated with complications". Their first reference’ gives little evidence for this statement for the cases referred to had minor symptoms after an isobaric change of gases-i.e., no compression was involved. Their second reference3 refers to a helium-oxygen diver who had paraplegia after recompression on air. This is precisely the opposite situation to that argued in the paper. The paraplegia was quickly and totally resolved by further compression and a return to breathing helium-oxygen, in marked contrast to the three cases quoted in their paper where each patient emerged from the treatment with serious symptoms. The advantages of using helium are that the patient may be recompressed further, possibly as the authors suggest, to the depth of relief; pure helium is generally more readily available than pure nitrogen in the diving industry; and there are proven decompression tables for helium-oxygen saturation from depths in excess of 165 ft. The reduction of the partial pressure of oxygen is clearly advisable if pulmonary oxygen toxicity is appearing but the authors suggest that this has been the main reason for not remaining on air at 165 ft (50 m). However, another reason would appear to be the lack of proven therapeutic tables for an exposure greater than 1 h at that depth. Finally, the authors cite a paper in which three of them stated ... "Yet our recent experience indicates that decompression sickness may be more refractory to recompression therapy if nitrogen is employed rather than helium". This seems to contradict the recommendations in their Lancet article. We agree, however, with their subsequent statement that a comprehensive study of treatment procedures is needed, but this should include the substitution of helium for nitrogen and vice versa, with and without further compression. Wolfson Institute of Occupational Health, University of Dundee, Ninewells, Dundee

P. B. JAMES

University of Texas Medical Branch

B. A. HILLS

Oceaneering

International Inc.

R. H. HOLLAND

North Sea Medical Centre,

Sussex Road, Gorleston, Great Yarmouth NR31

6QB

C. H. BROOKINGS N. K. I. MCIVER

SIR,-Dr Miller and colleagues (July 22, p. 169) correctly draw attention to some of the problems faced when cases of compressed-air decompression sickness do not respond to conventional treatment. Unfortunately the academic discussion and the cases presented do not, in our opinion, provide adequate support for the recommendation to adopt nitrogenoxygen saturation. We feel it is important to broaden the debate, particularly in view of the practical and legal consequences for the diving industry. Their paper highlights the fact that normally the standard procedures result in complete relief. However, tissue damage due to hypoxia, which is likely to result from a delay before recompression, may not be reversible regardless of the pressure used. It is therefore surprising to find the statement "If the breathing medium is changed from air to an appropriate helium-oxygen mixture in order to go deeper, it is possible to recompress to the depth of relief". This clearly, is not correct in all cases and advocating a helium and oxygen breathing mixture would appear to contradict later arguments in their paper. The phrase "in order to go deeper" merits closer scrutiny : the adoption of a nitrogen-oxygen mixture rules out the use of additional pressure because nitrogen narcosis would worsen.

1.

Therapeutic Table No.

5. U.S.

Navy Diving Manual; p. 8. 1975.

MORTALITY FROM CARCINOMA OF THE CERVIX

SIR Yule3reported that in England and Wales between 1970 and 1976 the number of deaths in women under 35 years of age from carcinoma of the cervix had almost doubled. After commenting on the earlier onset of sexual activity in the young and the increased use of non-barrier contraceptives, he suggested that, although increasingly large numbers of young women were being screened, "such screening is relatively ineffective in detecting pre-cancerous lesions leading to the prevention of death from invasive carcinoma". Nevertheless he concluded that in younger women "the detection of pre-cancerous conditions of the cervix must be ensured by widespread and frequent cyto-testing" in contradistinction to the encouragement of the screening of older women by the payments from the Department of Health and Social Security to general practitioners. In contrast, in the same issue MacGregor and Teperafter analysing the experience in Aberdeen up to 1976 and having pointed out that "The absolute number of young women with abnormal smears is increasing, although the proportion with abnormal smears has not risen", concluded that "Routine well-women screening need not be carried out on women under 25". 1. Miller, J. N., Fagraeus, L., Bennett, P. B. Undersea biomed. Res. 1977, A48. 2. Barnard, E. E. P., Elliot, D. H. Br. med. J. 1966, ii, 809. 3. Yule, R. Lancet, 1978, i, 1031. 4. MacGregor, E., Teper, S. ibid. p. 1029.

4,

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Nitrogen-oxygen saturation therapy in decompression sickness.

468 gery and Letters to the Editor HALOTHANE HEPATITIS SIR,-Professor Sherlock’s Point of View on halothane hepatitis (Aug. 12, p. 364) has an ai...
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