ENDOMYOCARDIAL FIBROSIS

ENDOMYOCARDIAL FIBROSIS

657 Can we accept this as a serious contribution to the relief of pain in labour when there is a British method, internationally used, which minimises...

204KB Sizes 3 Downloads 96 Views

657 Can we accept this as a serious contribution to the relief of pain in labour when there is a British method, internationally used, which minimises discomfort and therefore analgesia ; which shortens la,bour ; which time and money ; which relieves the pressure on and eases nurses’ work ; and which has many other advantages we need not enumerate at length? Surely it is wiser to extend the use of this method rather than search for new drugs with which to hide our own saves

hospital beds .

failures. Petersfield,

Hants.

GRANTLY DICK READ.

ENDOMYOCARDIAL FIBROSIS SIR,—The paper by Dr. Ball and his colleagues in your issue of May 22, and the recent correspondence, prompt me to make the following comments. Thrombosis is always prone to occur in dilated heart chambers. A natural sequel to the lodgment of thrombus on the endocardial surface of the heart is that the thrombus acquires a covering of endothelium and becomes, in the phraseology of the pathologist, organised. Pibrous proliferation in the African, moreover, is exuberant, a characteristic to which the frequency of cheloid bears witness. I suggest that endomyocardial fibrosis is the end-result of endocavitory thrombosis in a previously dilated heart. That the heart in its final form may not be enlarged in no way conflicts with this, for the heart being a collapsible as well as a distensible organ, neither its weight nor its volume post mortem is a measure of its size in the dynamic living state. And endocardial sclerosis may be expected to contract a previously dilated heart. Apart from this argument, however, a reasonable interpretation of figs. 1 and 4 in the paper by Dr. Ball and his colleagues is that they illustrate

organised mural of myocardium.

thrombus without discernible fibrosis A pertinent observation in this context is that the apical part of the left ventricular wall is thin, no less so naturally than it is in these illustrations. It is not alone in Africa that one encounters congestive heart-failure that does not conform to established ætiological patterns. Cases of this kind are apt to be included in the comprehensive files of ischaemic (or arteriosclerotic) heart-disease (and, to rationalise the diagnosis, coronary atherosclerosis and some fibrosis of the myocardium can alwaysbe found in adult hearts in chronic congestive failure) or hypertensive heart-disease - despite the absence of hypertension. (In Africans, incidentally, as in other races, arterial pressure rises progressively with age.) But in South Africa it has, I believe, been established that a significant proportion of heart-failure is caused by malnutrition existing in varying degree over the major part of a lifetime. The heart in these circumstances is a dilated, hypodynamic one in which endocavitory thrombosis is relatively common. This form of thrombosis is a tragically frequent cause of systemic arterial embolism and a commoner cause of pulmonary embolism than peripheral venous thrombosis. If the patient survives these hazards the endocardial thrombus becomes organised, blending with the endocardium to produce a thick membrane or persisting as a polypoid fibrous excrescence. In either event, but more commonly in the latter, fibrous strands spread fanwise from the mural attachment of the thrombus into the substance of the myocardium beyond. This in minor degree is common. I have only once seen endomyocardial fibrosis of the gross degree described by Dr. Ball and his colleagues, but in that instance the basic relationship between thrombus and endomyocardial fibrosis was, I believe; recognisable. The heart is relatively invulnerable to chronic malnutrition ; other organs, notably the liver, usually fail before it does. The precise physiological relationship

between the liver and the heart is fascinatingly problematical, but there is impressive evidence that the liver exercises a dominant role in the metabolism of the heart and that, in certain circumstances, heart-failure may be a consequence of hepatocellular failure. (It may be of interest that in South Africa the combination of hepatocellular failure and disease of the central nervous system, especially extrapyramidal disease, is a frequent

one.) That an individual is obese does not necessarily imply that lie is not malnourished. And oedema may obscure emaciation. Malnutrition in South Africa is often attributable to a diet containing a disproportionately. large amount of carbohydrate at the expense of protein and fat (a diet which may encourage fat storage and clinical obesity), and the individual’s metabolism is geared accordingly. Spontaneous hypoglycaemic symptoms including coma are common. Intravenous injection of glucose causes prompt recovery from coma but, as in Mann’s hepatectomised dogs, successive episodes of coma become less responsive, and eventually irreversible. In the presence of hypoglycæmia of this degree the liver, as judged by needle biopsy, is replete with glycogen, which is not mobilisable by injection of potent adrenaline, a combination of circumstances that is reminiscent of Oral glucose, adrenaline, and von Gierke’s disease. insulin tolerance tests, applied to a large number of malnourished Africans, reveal bizarre but constant patterns that are (by our standards) grossly abnormal. It is notoriously difficult to extract from an African (as I have known him) the details ofwhat he is in the habit of eating. He will readily answer with a fanciful account of what he regards as socially acceptable fare by the white man’s standards as he understands them. It will take no less than an hour of diligent questioning and patient listening to get the true story. And after that the wise investigator will check his information before accepting it as fact. Royal Infirmary, A. D. GILLANDERS. Edinburgh. DEATHS DURING ANÆSTHESIA

SiR.,-In your annotation last week you refer to Beecher and Todd’s statistical analysis1 of some 600,000

operations-an analysis which reveals that the mortalitynearly sixfold when muscle relaxants were used. You say that you can see no evidence to justify putting blame so squarely on the muscle relaxants. I would go much further and say that the evidence they present indicts not the relaxant drugs but the technique of the majority of the anaesthetists involved. rate increased

The introduction of the muscle relaxants constituted possibly the most important advance in the history of anaesthesia. These drugs which were welcomed with open arms by British anaesthetists transformed our techniques and are now very widely used and regarded as an indispensable part of major anaesthetic procedures. In this hospital, for example, apart from those administered to outpatients, over 85% of all anaesthetics given during 1953 incorporated some specific relaxant. I maintain flatly that these drugs are extremely safe provided always that -normal pulmonary ventilation is2 maintained. As long ago as 1946, Gray and Halton pointed out the necessity for augmenting respiration when using curare. It should be unnecessary at this date to labour this point for obviously if neuromuscular blocking agents are administered in amounts which will cause partial paralysis of, for example, abdominal muscles, they will at the same time cause partial paralysis of the muscles of respiration, and pulmonary ventilation * will necessarily be reduced. Beecher and Todd’s figures show that American anaesthetists use muscle relaxants much less widely than

1.

Beecher, H. K., Todd, D. P. Ann. Surg. 1954, 140, 1. 2. Proc. R. Soc. Med. 1946, 39, 400.