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REGISTRATION OF CAUSES OF STILLBIRTH
455
REGISTRATION OF CAUSES OF STILLBIRTH SIR,-Causes of stillbirth have been registered in England and Wales since Oct. 1, 1960. I would be grateful if you would allow me to comment on one particular aspect of the first three months’ results which is causing some concern. During this period, out of a total of 3737 stillbirths registered, the certificate was given by a doctor in only 2360, or 63% of cases. In the remaining 37% the certificate was given by a midwife. The proportion is very little different for births at home or in hospital. It is possible that some doctors may not be aware of the requirements of the Population (Statistics) Act 1960 which makes it obligatory on every medical practitioner who was either present at the birth of a stillborn child, or who examined the body of such a child, to give a certificate which includes a statement of the cause of death. Only if no doctor was present or examined the body may the certificate be given by a midwife. The Registrar-General for Scotland has reported1 that in that country midwives complete stillbirth certificates in only 0-6% of cases. General Register Office, London, W.C.2.
M. A.
HEASMAN,
Acting Chief Medical Statistician.
BRONCHIOLITIS IN INFANTS SIR,—Iobtained good results in bronchiolitis in infants (discussed in your annotation 2) by treatment with chloramphenicol combined with an age-adjusted dose of a diuretic like chlorothiazide. The distressing symptoms (dyspnoea, grunting respirations, and rib recession) diminish within 48 hours, the temperature drops, and respiration becomes freer and more even. Obviously bronchiolitis is an entity-probably an infection associated with some lung cedema-but more information is clearly needed about its xtiology. T. M. SUSAI. TERSAVID IN ANGINA PECTORIS
SIR,-Dr. Murphy, Dr. Barber, and Dr. Kilpatrick (Jan. 21) are to be congratulated on their concise and conclusive paper on the effects of ’Tersavid ’ in angina pectoris. Their results are in keeping with the findings of Phear and Walker,3 and with my own more modest experience of tersavid.4 In a preliminary study using a sequential procedure I discontinued the trial after 17 patients had been assessed. Out of 14 choices, 9 preferred the placebo as against 5 who chose tersavid. Side-effects, especially gastric, were troublesome and may well have prejudiced patients towards the placebo; in fact, 1 patient with an ulcer history had a hxmatemesis. I was most interested in their recent conclusions, especially as my own disappointing results were obtained at the same time as their original report of improvement in 65% of their cases.55 At the time I could not understand this at all. But I do feel that monoamine-oxidase inhibitors should not all be condemned because of the experience with one drug; other compounds should be given a controlled trial. The results of Dr. Allanby and his colleagues (Jan. 21) with nialamide, and Mackinnon et al.with pheniprazine hydrochloride (’ Cavodil ’) suggest that further work is required. Furthermore, in a condition so difficult to assess as angina, patients may be helped by a drug, but side-effects may still lead to an inconclusive or adverse opinion unless relief is dramatic. It would, therefore, Report of Registrar-General for Scotland, 1959, p. 55. H.M. Stationery Office. 2. Lancet, 1960, ii, 806. 3. Phear, D., Walker, W. C. Brit. med. J. 1960, ii, 995. 4. Grant, A. P., Irish J. med. Sci. 1960, no. 418, 466. 5. Murphy, F. M., Barber, J. M. Cardiologia, Basle, 1960, 37 suppl. 2, 117. 6. Mackinnon, J., Anderson, D. E., Howitt, G. Brit. med. J. 1960, i, 243. 1. Annual
be helpful in future to know in addition to bare statistical details whether there were other reasons for the patients’ choice besides reduction of anginal pain. In these days of figures the final mathematical masterpiece should not make us forget clinical criteria originally chosen. Belfast City Hospital, Northern Ireland.
A. P. GRANT.
PROTEIN-LOSING ENTEROPATHY IN THE SPRUE SYNDROME his SIR,-In paper (Dec. 24) Dr. Parkins states that he failed to find a correlation in his patients between the serum-protein level and the fxcal excretion of radioiodine-labelled polyvidone (131I-P.V.P.). We investigated 8 patients with severe steatorrhcea of various aetiologies with Gordon’s 131I-p.v.p. test. In all cases with an abnormal 1311-p.v.p. excretion the total serum protein and especially the serum-albumin were markedly decreased. Of course, not all the investigated patients with steatorrhoea and hypoproteinaemia displayed a pathological level of excretion of 131I-p.v.p. We agree with Dr. Parkins that the protein disturbances in the sprue syndrome are complex (protein malabsorption, protein loss, and also decreased albumin synthesis by a fatty liver). Some of our findings have been published. 12
P. VESIN H. RENAULT R. CATTAN.
Hôpital Saint-Antoine, Paris, 12e.
HÆMOLYTIC DISEASE OF THE NEWBORN
has been shown that some serum-proteins in man) are transmitted from mother to foetus in utero in primates.3 In man the so-called " incomplete " " or albumin " antibodies can injure the foetus in utero in saline contrast to the " complete " or agglutinins. At present, hxmolytic disease of the newborn is a less important cause of infant mortality than in the past. Improved
SIR,-It (antibodies
"
results of treatment
are
due, in part,
"
to more accurate means
of
diagnosis by testing the blood of the mother before delivery, and to the skilful use of replacement transfusion in the newborn. Means exist for identifying the sex and the ABO group of the unborn child by examining the amniotic fluid; it may not be long before the rhesus state of the child still in utero can be discovered by similar methods. When all these modern methods are exploited to the full, a hard core of mothers still remain with high-titre anti-Rh agglutinins, who eventually will be delivered of an infant with hydrops, icterus gravis, or severe hasmolytic disease of the newborn. Many of those severely affected are hopeless cases stillborn. There is clinical evidence that an Rh-positive foetus may be adversely affected as early as the 27th week of pregnancy by the anti-Rh agglutinins in the mother’s circulation. According to Dr. Ludwig Mond, the only important calculation women ever have to make in their whole lives they invariably get wrong. Fortunately, there are clinical methods which enable the antenatal age of the child to be estimated more accurately. I would like to suggest that some of these stillbirths and hopeless cases due to Rh-sensitisation of the mother, might possibly be salvaged by treatment of the mother with steroids, in a hospital, under supervision, from, say, the 26th week of pregnancy to the 32nd or 33rd week, when the foetus may be just viable. It would be necessary to guard the mother against intercurrent infection with great care; and the six or seven weeks of the mother’s steroid treatment might not harm the adrenals of the foetus, though some fear that adrenal atrophy might result. or are
1. Vesin, P., Troupel, S., Acar, J., Renault, H., Desbuquois, G., Cattan, R. Bull. Soc. méd. Hôp. Paris, 1960, 76, 261. 2. Vesin, P., Troupel, S., Acar, J., Bismuth, V., Renault, H., Cattan, R. ibid. p. 410. 3. Bangham, D. R., Hobbs, K. R., Tee, D. E. H. Lancet, 1960, ii, 1173.
REGISTRATION OF CAUSES OF STILLBIRTH SIR,-Causes of stillbirth have been registered in England and Wales since Oct. 1, 1960. I would be grateful if you would allow me to comment on one particular aspect of the first three months’ results which is causing some concern. During this period, out of a total of 3737 stillbirths registered, the certificate was given by a doctor in only 2360, or 63% of cases. In the remaining 37% the certificate was given by a midwife. The proportion is very little different for births at home or in hospital. It is possible that some doctors may not be aware of the requirements of the Population (Statistics) Act 1960 which makes it obligatory on every medical practitioner who was either present at the birth of a stillborn child, or who examined the body of such a child, to give a certificate which includes a statement of the cause of death. Only if no doctor was present or examined the body may the certificate be given by a midwife. The Registrar-General for Scotland has reported1 that in that country midwives complete stillbirth certificates in only 0-6% of cases. General Register Office, London, W.C.2.
M. A.
HEASMAN,
Acting Chief Medical Statistician.
BRONCHIOLITIS IN INFANTS SIR,—Iobtained good results in bronchiolitis in infants (discussed in your annotation 2) by treatment with chloramphenicol combined with an age-adjusted dose of a diuretic like chlorothiazide. The distressing symptoms (dyspnoea, grunting respirations, and rib recession) diminish within 48 hours, the temperature drops, and respiration becomes freer and more even. Obviously bronchiolitis is an entity-probably an infection associated with some lung cedema-but more information is clearly needed about its xtiology. T. M. SUSAI. TERSAVID IN ANGINA PECTORIS
SIR,-Dr. Murphy, Dr. Barber, and Dr. Kilpatrick (Jan. 21) are to be congratulated on their concise and conclusive paper on the effects of ’Tersavid ’ in angina pectoris. Their results are in keeping with the findings of Phear and Walker,3 and with my own more modest experience of tersavid.4 In a preliminary study using a sequential procedure I discontinued the trial after 17 patients had been assessed. Out of 14 choices, 9 preferred the placebo as against 5 who chose tersavid. Side-effects, especially gastric, were troublesome and may well have prejudiced patients towards the placebo; in fact, 1 patient with an ulcer history had a hxmatemesis. I was most interested in their recent conclusions, especially as my own disappointing results were obtained at the same time as their original report of improvement in 65% of their cases.55 At the time I could not understand this at all. But I do feel that monoamine-oxidase inhibitors should not all be condemned because of the experience with one drug; other compounds should be given a controlled trial. The results of Dr. Allanby and his colleagues (Jan. 21) with nialamide, and Mackinnon et al.with pheniprazine hydrochloride (’ Cavodil ’) suggest that further work is required. Furthermore, in a condition so difficult to assess as angina, patients may be helped by a drug, but side-effects may still lead to an inconclusive or adverse opinion unless relief is dramatic. It would, therefore, Report of Registrar-General for Scotland, 1959, p. 55. H.M. Stationery Office. 2. Lancet, 1960, ii, 806. 3. Phear, D., Walker, W. C. Brit. med. J. 1960, ii, 995. 4. Grant, A. P., Irish J. med. Sci. 1960, no. 418, 466. 5. Murphy, F. M., Barber, J. M. Cardiologia, Basle, 1960, 37 suppl. 2, 117. 6. Mackinnon, J., Anderson, D. E., Howitt, G. Brit. med. J. 1960, i, 243. 1. Annual
be helpful in future to know in addition to bare statistical details whether there were other reasons for the patients’ choice besides reduction of anginal pain. In these days of figures the final mathematical masterpiece should not make us forget clinical criteria originally chosen. Belfast City Hospital, Northern Ireland.
A. P. GRANT.
PROTEIN-LOSING ENTEROPATHY IN THE SPRUE SYNDROME his SIR,-In paper (Dec. 24) Dr. Parkins states that he failed to find a correlation in his patients between the serum-protein level and the fxcal excretion of radioiodine-labelled polyvidone (131I-P.V.P.). We investigated 8 patients with severe steatorrhcea of various aetiologies with Gordon’s 131I-p.v.p. test. In all cases with an abnormal 1311-p.v.p. excretion the total serum protein and especially the serum-albumin were markedly decreased. Of course, not all the investigated patients with steatorrhoea and hypoproteinaemia displayed a pathological level of excretion of 131I-p.v.p. We agree with Dr. Parkins that the protein disturbances in the sprue syndrome are complex (protein malabsorption, protein loss, and also decreased albumin synthesis by a fatty liver). Some of our findings have been published. 12
P. VESIN H. RENAULT R. CATTAN.
Hôpital Saint-Antoine, Paris, 12e.
HÆMOLYTIC DISEASE OF THE NEWBORN
has been shown that some serum-proteins in man) are transmitted from mother to foetus in utero in primates.3 In man the so-called " incomplete " " or albumin " antibodies can injure the foetus in utero in saline contrast to the " complete " or agglutinins. At present, hxmolytic disease of the newborn is a less important cause of infant mortality than in the past. Improved
SIR,-It (antibodies
"
results of treatment
are
due, in part,
"
to more accurate means
of
diagnosis by testing the blood of the mother before delivery, and to the skilful use of replacement transfusion in the newborn. Means exist for identifying the sex and the ABO group of the unborn child by examining the amniotic fluid; it may not be long before the rhesus state of the child still in utero can be discovered by similar methods. When all these modern methods are exploited to the full, a hard core of mothers still remain with high-titre anti-Rh agglutinins, who eventually will be delivered of an infant with hydrops, icterus gravis, or severe hasmolytic disease of the newborn. Many of those severely affected are hopeless cases stillborn. There is clinical evidence that an Rh-positive foetus may be adversely affected as early as the 27th week of pregnancy by the anti-Rh agglutinins in the mother’s circulation. According to Dr. Ludwig Mond, the only important calculation women ever have to make in their whole lives they invariably get wrong. Fortunately, there are clinical methods which enable the antenatal age of the child to be estimated more accurately. I would like to suggest that some of these stillbirths and hopeless cases due to Rh-sensitisation of the mother, might possibly be salvaged by treatment of the mother with steroids, in a hospital, under supervision, from, say, the 26th week of pregnancy to the 32nd or 33rd week, when the foetus may be just viable. It would be necessary to guard the mother against intercurrent infection with great care; and the six or seven weeks of the mother’s steroid treatment might not harm the adrenals of the foetus, though some fear that adrenal atrophy might result. or are
1. Vesin, P., Troupel, S., Acar, J., Renault, H., Desbuquois, G., Cattan, R. Bull. Soc. méd. Hôp. Paris, 1960, 76, 261. 2. Vesin, P., Troupel, S., Acar, J., Bismuth, V., Renault, H., Cattan, R. ibid. p. 410. 3. Bangham, D. R., Hobbs, K. R., Tee, D. E. H. Lancet, 1960, ii, 1173.