Document gD277L8pY8ZjJd7551v6N2jEG

PROCEEDINGS OF THE Mine Medical Officers' Association of S.A. VOLUME LXII - NUMBER 431 JANUARY - DECEMBER, 1983 ADVENTURES WITH NITROUS OXIDE Mark Gillman WHAT IS SILICOSIS? R.L. Cowie FORTY YEARS OF PHYSIOTHERAPY FOR BLACK PATIENTS Alfred Rothberg VALEDICTORY ADDRESS 0. Martiny EPIDEMIOLOGY : A PERSPECTIVE R.L. Cowie SYMPOSIUM ON RECONSTRUCTIVE SURGERY CHAMBER OF MINES ISSUED BY THE ASSOCIATION HOLLARD STREET JOHANNESBURG Proceedings of the Mine Medical Officers' Association 21 CLINICAL MEETING, 10th FEBRUARY, 1983 A Clinical Meeting of members of the Asso ciation was held at the Rand Mutual Hospital, Johannesburg, on Thursday, 10th February, 1983, at 14h00, with Dr. O. Martiny in the Chair. Adventures with Nitrous Oxide by Dr. Mark Gillman The title of this lecture, "Adventures with Nitrous Oxide", may appear flippant, but this work has been an adventure for me and will, I hope, be so for you after today. What prompted my interest in N2O? As a dentist, I use N2O in analgesic doses and noticed that some patients became euphoric, lost their anxiety and enjoyed a measure of analgesia following this procedure. I enrolled as a post-graduate student in Pharmacology at Potchefstroom in order further to investigate these effects. Here we carried out experiments based on Berkowitz's hypothesis that naloxerie reversed the analgesic effect of N2O. Painful stimuli were applied to patients given N20 and naloxene and to our surprise the anal gesic effect was reversed. This indicates to us that there must be two systems, the first affec ted by N20 and the second by naloxene. Having decided that one system suppressed pain and the other increased plain, we believe that there must be a line between pain and pleasure. We then consulted a neurosurgeon who, following a morphine saturation iest, performs operations for the relief of pain by inserting brain implants. The experiment which followed, using morphine followed by narcan, showed an increased response, which is para doxical and these results have been published. We then looked at the pleasure response to see whether this could be manipulated with N20 and naloxene. N20 was used to stimulate sexual fantasies and the narcan was given in small doses to potentiate orgasm. This in fact happened, and these results have been pub lished in the American Journal of Sex Re search. We are at present experimenting on yogic states as well as addiction, and preliminary results, by independent observers, indicate that 100 per cent oxygen relieves the symp toms and signs associated with alcohol with drawal in addicts. N2O is also effective, im proving mainly the affective symptoms. We postulate that the withdrawal of alcohol re sults in an 02 debt as well as overacting on the cholinergic and adrenergic systems. We now believe that N20 in analgesic doses stimulates the opiate system and can safely be used to investigate psychiatric ill nesses and we have, in fact, been doing this for eighteen months, working particularly with depressive states. Recently, we have shown that patients given N20 and narcan developed a flat EEC tracing (technical errors have been excluded) while continuing to breathe normally. We hypothesise that brain death is over-activity of the opiate system, and these results have been published in The Lancet. Finally, nitrous oxide used correctly is ex tremely safe, and myeloncuropathy following N20 occurs only in addicts. Reversible megalo blastic anaemia may also occur following long operations, but this is a clinical curiosity. This lecture has been summarised by the Hon. Editor. CLINICAL MEETING, 14th APRIL, 1983 A Clinical Meeting of members of the Asso ciation was held at the Rand Mutual Hospital. Johannesburg, on Thursday, 14th April, 1983, at 14h00, with Dr. O. Martiny in the Chair. The meeting took the form of a discussion on the theme "Problems Arising from the Re-employ ment of Treated Silicotics and Tuberculotics", introduced by Drs. F. Wiles and R.L. Cowie. What is Silicosis? by Dr. R.L. Cowie The new regulations1 concerning silicosis require us to take a more thoughtful look at this disease. In the past, a suspicion of silicosis set us automatically upon a statutory, inflexible course which required neither thought, dis cretion nor knowledge beyond crude recog nition on the part of the Mine Medical Officer. We are now called upon to use our pro 22 Proceedings of the Mine Medical Officers' Association fessional judgement in our patient population with silicosis. With this new dispensation it behoves us to know about silicosis, its likely effect upon our patient and the risks of further exposure to silica-containing dust, and with that knowledge to take the best decision for each affected employee in our care. WHAT IS SILICOSIS? Silicosis as we see the disease in the gold mining industry in South Africa is synonymous with chronic silicosis which is also referred to as simple silicosis. This is usually recognised by a typical chest radiograph with predominantly upper zone nodularity which is usually of gradual onset and slowly progressive with in creasing profusion and size of nodule. The nodules do not exceed 10 mm in diameter. Hilar nodes are often prominent and occa sionally show the typical egg-shell calcification. Such a chest radiograph can be considered to represent chronic silicosis if the man has been exposed to silica-containing dust for a period exceeding 15 years. The term "silicosis" also encompasses other forms of the disease which are not usually seen in our employees but which need to be dis tinguished from chronic silicosis for different management. In accelerated silicosis a similar nodularity is often less obviously of upper zone predominance and is readily distinguished by the history of too short an exposure to silicacontaining dust for the definition of chronic silicosis. The history is usually of exposure for less than 10 years and may be as little as 3 years. An even more rapidly developing and lethal form of silicosis which, for practical purposes, does not occur in the gold-mining industry, is known as acute silicosis or silicoproteinosis. In this disease, which results from massive ex posure over periods of between 6 months to 2 years, nodule formation is not apparent and symptoms of dyspnoea, wasting and weakness are striking, with death following within a matter of months rather than years. It must be clear, therefore, that the disease to which this paper refers is chronic or simple silicosis. It occurs commonly in our South African gold-miners and is characterised by a long history of dust exposure (not less than 1S and usually more than 20 years), and by a readily discernible nodular opacification of the lungs which is seen to develop and progress over years. NATURAL HISTORY OF CHRONIC SILICOSIS It is remarkable but true that the natural his tory of chronic silicosis is not really known. The disease in miners has been known for centuries, with literature dating back to 1556 and first descriptions from South Africa in 1902. It is probable that the lack of data results from failure to separate chronic silicosis from the accelerated and acute forms of the disease. The much higher incidence of complicating tuberculosis which was untreatable until the last 30 years has also made a separate outcome for chronic silicosis difficult to identify. However, through the uncertainty, several authoritative reports2' 3 reflect the view which is steadily gaining support that chronic sili cosis is a disease which results in little or no pulmonary disability. Having said this, most authorities hasten to add that additional work needs to be done to substantiate this benign view of the disease and at least two studies are under way in our industry. For the present, we depend on random samplings which suggest that silicosis, as we see it, is seldom complicated by lung dysfunction, that there is a steady progression of the disease after diagnosis and that continued exposure to silica-containing dust has little effect upon the rate of progression. COMPLICATIONS All the complications of silicosis are far more common in the accelerated and acute forms than in the chronic disease. Pulmonary tuberculosis remains the commonest and probably the only relevant complication in our patient population. The ex cess of pulmonary tuberculosis which can be attributed to silicosis is not known but is steadily falling.3 A recent study4 presents evidence that the complication of tuberculosis in chronic silicosis can be successfully treated using a 100-dose, four-drug regimen5 similar to that which is currently standard in our industry. Prompt diagnosis and treatment of tuber culosis in men with silicosis should prevent any Proceedings of the Mine Medical Officers' Association 23 adverse effect of this complication on the natural progression of their silicosis. This view is, however, implicitly rejected by the official interpretation of the new regulations1 and can not be tested for lack of data. Nevertheless, there is no reason to believe that the natural histoiy of tuberculosis, the success of its treat ment nor the relapse rate after treatment are in any way affected by continued exposure to silica-containing dust. It would seem, therefore, that a mineworker with pulmonary tuberculosis whose general clinical state is satisfactory, should be allowed to resume his previous occu pation irrespective of his stage of treatment, his sputum bacteriology or the presence or absence of underlying chronic silicosis. It is to be hoped that the official view will eventually make such practice permissible. CRITERIA FOR EMPLOYMENT OF CHRONIC SIL1COTICS The fear of pulmonary disability has moti vated previous restrictions for the re-employ ment of employees with silicosis. For this reason, a measurement of lung function must be central to any decision concerning a man with chronic silicosis. As it is known that silicadust exposure leads to lung dysfunction of an obstructive type6 quite independently from silicosis, the vital capacity which is the simplest of the tests for a restrictive lung process such as silicosis, has been chosen to assess the employee with silicosis. To allow for the normal variation about the predicted value for vital capacity, a cut-off level of 75 per cent of the predicted vital capacity is recommended: those whose vital capacities are 75 per cent or less than predicted should not be allowed further exposure to silica-containing dust. It should be emphasised that chronic silicosis will only exceptionally cause a reduction of vital capacity and that such a finding should raise suspicions that the diagnosis of chronic silicosis has been wrongly applied. This leads on to the next criterion for re-employment of an employee in a "risk" occupation; we must be certain that the disease which we have detected through our regular chest radio graphs really is chronic silicosis. Doubt must arise if the pulmonary opacification has developed rapidly, if the duration of service is less than 15 years, if the distribution of the nodules does not emphasise the upper zones and, as noted above, if there is a reduction of the vital capacity. Doubt on any one of these counts should result in a more complete in vestigation with a transbronchial lung biopsy often proving to be the most definitive as well as the quickest and easiest of the available investigations. In my experience, doubt about the diagnosis of chronic silicosis has resulted in diagnoses of sarcoidosis, of disseminated tuber culosis and of accelerated silicosis. Further criteria for re-employment of silicotic employees in "risk" work relate to their length of previous dust exposure which, in turn, reflects the chronicity of the^process, as does their age, with^the older man likely to have had longer exposure., Age is also relevant as the older man will have l^ss future exposure, thus the decision to allow a 55-year-old to re turn to, at most, another 5 years of dust ex posure is far less critical than a similar decision in a 40-year-old with a possible 20 years of further exposure. In other words, the vital capacity and duration of exposure, criteria will be less strictly enforced in an older subject than they would in a younger man. In general a his tory of less than 15 years of dust exposure in association with chronic silicosis implies a more aggressive process and would contraindicate further exposure. ,;-izcioo Lastly, it is an essential requirement thafflie silicotic employee be allowed to choose fiirtffer employment in a dusty environment and thit he does so with the knowledge that there are dust-related lesions in his lung. This criterion, with a confident diagnosis of chronic silicosis, and a normal vital capacity, must be seen as the definitive criteria. Age and duration of ex posure are the negotiable criteria for allowing a man with silicosis to continue "risk" work (Table I). TABLE I CRITERIA FOR CONTINUED EXPOSURE TO SILICA-CONTAINING DUST IN A MINEWORKER WITH SILICOSIS 1. Has vital capacity >75 per cent predicted 2. Has chronic (simple) silicosis 3. Is 40 or more years old 4. Has 15 or more years' exposure 5. Makes an informed request for continued exposure 24 Proceedings of the Mine Medical Officers' Association CONCLUSION With the implementation of the new regu lations which permit the continued employ ment of men with silicosis in "risk" work, ex posed to silica-containing dust, it has become necessary for the Mine Medical Officer to re develop clinical skills which the previous legis lation rendered atrophic and rudimentary. The true story of chronic silicosis has yet to emerge, but it is very different from that which prevails in mining mythology and in many of the standard medical texts. In this short paper I have attempted to show that chronic silicosis is a mild disease associated with little or no pulmonary disability, and that it is no longer reasonable to cripple those who develop it by excluding them from their only means of earning a living. I have suggested criteria which may be used to determine which silicotic miners may safely continue with "risk" work. The prevalence of accelerated silicosis is very low but, as is the case with other lung diseases such as sarcoidosis and disseminated tubercu losis, it may mimic chronic silicosis radio logically. An alternative diagnosis should al ways be sought if any feature seems to be in consistent with chronic silicosis. It is my practice to include a vital capacity of 75 per cent or less of the predicted capacity, as an indication for further investigation, which usually includes a transbronchial lung biopsy. Pulmonary tuberculosis is the only compli cation of chronic silicosis with which we need to concern ourselves in the South African gold mining industry. My view of pulmonary tuber culosis with silicosis differs from the official view. I believe that with proper surveillance the disease can be diagnosed before it has destroyed lung and before it has accelerated the silicosis. With a complete course of modern, shortcourse, rifampicin-containing therapy, I believe that the chronic silicotic can again be judged as such and not as a silico-tuberculotic. REFERENCES 1. Occupational Diseases in Mines and Works Act, 1973. Government Gazette. Amend ment of Regulations, 1982. No. 8482 pp. 15-16 2. Morgan, W.K.C., and A. Seaton. Occupa tional Lung Diseases. (W.B. Saunders Co., Philadelphia. 1975. p.80) 3. Ziskind, M., R.N. Jones and H. Weill. Sili cosis. Am. Rev. Respir. Dis. 1976. 113, 643-666 4. Escreet, B.C., M.E. Langton and R.L. Cowie. Short-course Chemotherapy for Silico-tuberculosis. Unpublished Report. 1982 5. Escreet, B.C. and R.L. Cowie. Short-course Chemotherapy for Pulmonary Tubercu losis. S. Afr. Med. J. 1981. 60,951-3 6. Wiles, F.J. and M.H. Faure. Chronic Ob structive Lung Disease in Gold Miners. In: Inhaled Particles IV. (Pergamon, Ox ford, 1977. pp. 727-734) CLINICAL MEETING, 14th JULY, 1983 A Clinical Meeting of members of the Asso ciation was held at the Stilfontein Golf Club on Thursday, 14th July, 1983, at lOhOO, with Dr. D.J. Heydenrych, President, in the Chair. Epidemiology of Cardiovascular Disease in S.A. with Emphasis on the Treatment of Chest Pains with Sudden Onset Dr. H.S. Viljoen South African White males have for some time run a close second to their counterparts in Northern America in deaths due to Coron ary Artery Disease (CAD). The Federal Govern ment embarked, a decade and a half ago, on a vigorous programme to arouse the consciousness of the nation in combating CAD : known causative factors such as over weight. high blood cholesterol, smoking, lack of exercise and a high-flying, competitive, stressinducing environment, were more clearly de fined. There is now enough evidence to show that the reduction or elimination of some of these causative factors results in a significant drop in deaths due to CAD and to a remark able improvement in mental health, thus saving the country in the region of 470 billion dollars