PERITONEAL DIALYSIS IN RENAL FAILURE

PERITONEAL DIALYSIS IN RENAL FAILURE

1385 of bath fluid, each of 100 litres, and blood-flow 250-300 ml. During and after this prolonged hsemodialysis there was no change in the general co...

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1385 of bath fluid, each of 100 litres, and blood-flow 250-300 ml. During and after this prolonged hsemodialysis there was no change in the general condition and in the neurological state of the patient. The tachycardia also remained unchanged (140 per minute). Four to six hours later the patient developed intercostal and diaphragmatic paralysis, which was rapidly progressive, and she died within two hours from respiratory insufficiency. per minute.

2nd Department of Internal Medicine, Medical School of Athens University, and Hippocration Hospital, Athens, Greece.

HIPPOCRATES YATZIDIS.

PERITONEAL DIALYSIS IN RENAL FAILURE SIR,-May we reply to the letters of Dr. Kennedy and his colleagues and Dr. Flynn last week (p. 1330) ? First we should like to deal with a number of points which are not in dispute, and which obviously arise from a misinterpretation of our intentions in writing our article (June 3, p. 1188). Patients with hypercatabolic acute renal failure must, of course, be managed in experienced renal units, and nowhere in our article was the contrary suggested. The free choice of the " physician or surgeon in the light of local resources and experience " was a reference to the fact that although most renal units are headed by physicians, some are run exclusively by surgeons. The writers of both letters seem to have interdoctor with preted our article as an incentive to the isolated " no haemodialysis facilities to " have a go at treating hypercatabolic acute renal failure, but by the description of the high mortality and extreme difficulties encountered we intended to indicate that the problem is an exacting one. It was never our intention to deal with the whole " complex problem " of acute renal failure, nor are we so naive (as Dr. Flynn may be thought to imply) as to think that control of the blood-urea is the whole question. Having managed a number of patients in this fashion for two years, we set out to examine a specific question from our data: how well can the blood-urea and other metabolic products be controlled ? We were careful to distinguish both in the paper and in the summary, between control of uraemia and mortality. The answer to the question, When must one perform hxmodialysis? may well be different from the answer to the question, When should one perform

haemodialysis ? Next, we come to points on which there are grounds for disagreement, beginning with those in Dr. Flynn’s letter. In our hands, peritoneal dialysis is as reliable as htmodialysis and no more expensive; the benefits of speed and efficiency carry with them the dangers of disequilibrium between intracellular and extracellular water, as described by Dr. Kennedy and his colleagues. If " effort " has to be put into running a peritoneal dialysis then it is being misapplied. Dr. Flynn also suggests that we have misrepresented two papers: his own with Dr. Bowden,! and that of Stewart et al.2 Dr. Flynn represents his paper as a plea for flexibility in the treatment of acute renal failure as a whole ", but to ignore peritoneal dialysis altogether even in discussion could scarcely be less flexible. Reading the paper will confirm that it categorically recommends hxmodialysis for catabolic renal failure, which is what we quoted it as suggesting. Again, data of Stewart et awl.2 were not misrepresented; they stated that in most patients with acute renal failure mortality and morbidity were approximately the same whichever mode of dialysis is used. Finally, to compare results on two different groups of patients managed in different units is quite meaningless, although the data on Dr. Flynn’s patients are of course of interest; we do not see the road-accident trauma leading to renal failure that

But how many units have actually tried to evaluate the two techniques, side by side, in these patients ? At the Hammersmith Hospital, something approaching this has been done: in 1961-65 23 patients with acute renal failure following trauma were treated, 15 with haemodialysis and 8 with peritoneal dialysis 3; 11of the haemodialysis and 3 of the peritonealdialysis groups died. Of course, one cannot be sure that the patients were comparable, but in the absence of any true comparative data we should prefer to regard the issue as not proven. It is important to emphasise that hxmodialysis and peritoneal dialysis are complementary techniques in the treatment of acute renal failure, and not rival systems; personal preference and experience will always play a part in selection of technique. It may be that the development of really simple reliable machines of the type described by Mr. Simpson and his colleagues (June 10, pp. 1244 and 1247) will make peritoneal dialysis less necessary. Some problems, however, will remain; less doctor-time, at a lower level of skill, is required, to set up peritoneal dialysis than to insert a hxmodialysis shunt. It takes only a tiny fraction of the time required to train a competent hsmodialysis nurse to show her the simple techniques of peritoneal dialysis. Most renal units which have accepted intermittent-haemodialysis patients are overcrowded and understaffed. Some (like ours) have temporarily turned over acute-renal-failure units to chronic beds, and no longer wish to mix acute and chronic patients in the same area. Peritoneal dialysis has much to offer in liberating both space and staff time. J. S. CAMERON C. S. OGG Guy’s Hospital, London S.E.1 J. R. TROUNCE.

patient.

HÆMATOLOGICAL EFFECTS OF ORAL CONTRACEPTIVES SIR,-Dr. Burton (May 6, p. 978) reports definite rise in packed-cell volume (P.c.v.) but only doubtful rise in hxmoglobin in a series of women using oral contraceptives. I have seen a woman of 67 who had been treated elsewhere for carcinoma of body of uterus for some months with benefit by’Enavid’ (norethynodrel 30 mg. and mestranol [ethinylcestradiol-3-methyl ether] 0-45 mg. daily, six times the contraceptive dose of ’Conovid ’). On admission here, because of deterioration, she had polycythaemia with haemoglobin 18.6 g. per 100 ml., P.c.v. 55%, white cells 7400 per c.mm., and platelets 200,000 per c.mm. Blood-film was normal. She improved with general care and a further increase in dose of enavid, and was discharged. This case, showing that the rise in haemoglobin observed on smaller doses by Dr. Burton may be real, has been reported to the Dunlop Committee. Since I reported a case of hereditary haemorrhagic telangiectasia4have diagnosed two more. One needed no treatment but the other is relevant to Dr. Burton’s findings.

"

he does at Halton, and cannot comment upon its management. Dr. Kennedy and his colleagues mention their own feelings, and those of the Leeds and King’s College Hospital, London, groups that haemodialysis is preferable in the hypercatabolic 1. 2.

Flynn, C. T., Bowden, C. H. Br. med. J. 1966, ii, 1109. Stewart, J. K., Tuckwell, L. A., Sinnett, P. F., Edwards, Whyte, H. M. Q. Jl Med. 1966, 35. 407.

K. D.

G.,

A woman of 81 had had iron-deficiency anaemia for years. Several exhaustive investigations had revealed nothing beyond melxna, until a fuller history from relatives uncovered repeated epistaxes, which the patient concealed from all her medical advisers by swallowing the blood. Her father had frank epistaxis daily. Ethinyloestradiol 0-5 mg. daily5 increased her haemoglobin in only 9 days from 8-7 to 12.2 g. per 100 ml. (large doses of iron had never brought it above 9-6 g. per 100 ml. before). This remarkable rise was hard to account for solely by the haemostatic properties of ethinylaestradiol,6 but now seems less improbable. I am indebted to Dr. R. W. Parnell, who first suspected, on clinical grounds, the polycythasmia in the first case, for permission to report these two cases. Summerfield

Hospital, Birmingham 18. 3. 4. 5. 6.

ROBERT

J. HETHERINGTON.

Mehl, R. Proc. Eur. Dial. Transpl. Ass. 1966, 3, 330. Hetherington, R. J. Lancet, 1965, ii, 237. Harrison, D. F. N. Q. Jl Med. 1964, 33, 25. Hetherington, R. J. Lancet, 1966, ii, 855.