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DELAYED CLOSURE OF PULMONARY VALVE
386
CLOSURE OF PULMONARY VALVE SIR Dr. Honey has reported an interesting case of acquired stenosis of the larger branches of the pulmonary artery due,, recurrent pulmonary emboli.1 He drew attention to wid; splitting of the second heart-sound, a sign which occurred very commonly in the series of patients with congenital bilateral stenosis of the larger branches of the pulmonar; trunk reported by me and my former colleagues at Coo Country Children’s Hospital, Chicago. Phonocardiograh tracings were available in 14children with bilateral stenos,
medicine, and hygiene-used to describe work that has or should . have a common scopeand purpose. Otherwise it will be difficult to elevate this work academically on the lines envisaged by Dr. White5 in his proposal for a " dean of health studies ". Social medicine as it has been defined by Professor Pemberton 6 could be applied equally well in an urban or, rural, temperate or tropical, setting provided the practitioner is acquainted with the behaviour, customs, and motivation of the community he is working in. Hence the importance of including or upgrading sociology and psychology in the medical curriculum, a point emphasised by the Annis Gillie report.’7 West
Chiltington,
Pulborough, Sussex.
DELAYED
A. M. ROBERTSON
of the pulmonary-artery branches unassociated with other anomalies, and in them maximum splitting of the secon,, heart-sound varied from 40 to 80 milliseconds. The explanation for the typical pulmonary-artery pressurs curve put forward by Dr. Honey is very similar to tha advanced by the Cook County Hospital group in their arigina] descrintion of this characteristic nressure curve.’ Lokmanya Tilak General Hospital and Municipal Medical College, I. A. D’CRUZ. Sion, Bombay 22.*
.
ÆTIOLOGY OF JAMAICAN CARDIOMYOPATHY SIR,-In the practice of cardiology in the West Indies, patients are frequently seen who9are suffering from congestive heart-failure and cardiomegaly. The clinical picture of these patients is that of a chronic cardiomyopathy, and Sutton and I have suggested that the patients seen in Trinidad had Chagas’ disease because of positive complement-fixation. tests against antigens prepared from Trypahosoma cruzi.8 No aetiology has been suggested for the illness of similar patients from Jamaica.9 During a recent visit to Jamaica I was able to examine a few patients with congestive heart-failure and cardiomegaly, under the care of Dr. S. Suite, at the Spanish Town Hospital. The clinical picture that some of these patients presented conformed to that already described 8 9 in cardiomyopathy. Dr. Suite has kindly sent me five sera which were tested for the presence of complement-nxing’antibodies, by the plastic-plate technique of Fulton and Dumbell,1O against antigen prepared from T. cruzi isolated in Trinidad from triatomid bugs.ll One serum showed a denifite positive reaction (fixing more than two units of complement in the presence of antigen), and one serum was negative. The remaining three sera were received in poor condition and showed moderate to strong anticomplementary activity. In order to reduce their anticomplementary activity .these sera were treated for twenty minutes with an equal volume of 25% w/v suspension of kaolin in physiological saline solution. The kaolin was then removed by centrifugation. The supernatant fluids were tested again by the cOIÌ1plement fixation reaction, and one of them proved to be positive. Thus two of the five sera examined were found to contain antibodies against T. cruzi. In my own practice I would accept the finding of a positive serology in conjunction with the clinical- picture of cardiomyopathy as positive indication that chronic infection by T. cruzi is responsible for the cardiac disability. In Trinidad, ,. both triatomid bugs 11 and wild mammals 12 have been found to be infected by T. cruzi. No similar studies have yet been carried out in Jamaica, where at least two species of triatomid bugs are known to occur (Triatoma rubrofasciata and Nesotriatoma obscura).13 In the light of these ’findings I feel that it is important to determine whether T. cruzi is to be found in Jamaica, arid, if so, what part it plays in the aaiology of Jamaican cardiomyopathy. =
‘
I wish to thank Dr. S. Suite for allowing me to examine patients in his care and for sending me sera for testing. This work was part of a study on trypanosomiasis in Trinidad, in progress at the present time, which is supported by a grant from were the Ministry of Overseas Development. Laboratory made available to me at the Trinidad Regional Virus Laboratory of the University of the West Indies.
ame ties
Port of
Spain,
BORIS FISTEIN. Trinidad, West Indies. 5. White, T. H. Lancet, 1966, i, 1379. 6. Pemberton, J. ibid. p. 925. 7. The Field of Work of the Family Doctor. Report of the subcommittee of the Standing Medical Advisory Committee. H.M. Stationery Office, 1963. See Lancet, 1963, ii, 721, 727. 8. Fistein, B., Sutton, R. N. P. Lancet, 1963, i, 330. 9. Stuart, K. L., Hayes, J. A. Q. Jl Med. 1963, 32, 99. 10. Fulton, F., Dumbell, K. R. J. gen. Microbiol. 1949, 3, 97. 11. Fistein, B. Trans. R. Soc. trop. Med. Hyg. (in the press). 12. Downs, W. G. J. Parasit. 1963, 49, 50. 13. Maldonado-Capriles, J., Farr, T. H. Proc. ent. Soc. Wash. 1962, 64, 187.
PULMONARY ŒDEMA IN BLOOD-TRANSFUSION SIR,—Iwish to draw attention to a simple manoeuvre thatI, no doubt in common with many others, have used to prevent pulmonary redema during transfusion of blood to aneemic patients. An intravenous injection of frusemide 40 mg, at the outset will produce a diuresis of some 2 litres within 2 hours, m patients with full renal function, and about 1 litre in a similar period in those in whom anaemia has impaired renal function Such a diuretic response will clearly permit administration of at least L litre of blood in a period as short as 2 hours without There will, indeed, be any increment in blood-volume. preferential loss of fluid components and corresponding gain of packed-cell volume in the patient’s blood. Some absolute, as’ well as considerable relative, improvement in fluid-balance will occur. This may be critical in those already presenting an increase of blood-volume, as shown by a raised jugular venous pressure.
The principle of this method,which has been practised successfully over the past few months, deserves recognition. even where the transfusion is restricted carries the risk (certainly where the rate, given of anaemia is severe and packed cells are not available degree in time) of causing pulmonary œdema—still one of the chief among the potentially fatal complications of transfusion. DAVID LEWIS. Leicester General Hospital.
.Conventional management, at a
RHESUS-IMMUNISED MOTHERS AND
DIRECT-COOMBS-TEST-NEGATIVE BABIES SIR,—Iwas interested to read the article by Dr. Weiner and Miss Wingham (July 9), for a similar case occurred here years ago.
’
The mother was a 23-year-old Scottish immigrant, para gravida 2, in excellent general health. Her genotype w& group 0, dce/dce (rr), and her first child had been unaffected by haemolytic disease of the newborn. The present antenatal course had been uneventful apart from a gradually increasing anti-D titre first detected at 16 weeks. Because of prolongt,4 and difficult labour, caesarean section was performed anda 6 lb. 311/2 oz. female infant was delivered. Tests on the cord blood showed the baby’s genotype to be group 0, DCe d (Rlr). The direct Coombs test was negative (’ Ortho’ Coombs serum), and the serum bilirubin was 8-8 mg. per 100 mi. Within 12 hours the baby became listless with increasing jaundice. 48 hours after birth the serum-bilirubin had risento Honey, M. Lancet, 1966, i, 318. D’Cruz, I. A., Agustsson, M. H., Bicoff, J. P., Weinberg, M., A R. A. Am. J. Cardiol, 1964, 13, 441. 3. Agustsson, M. H., Arcilla, R. A., Gasul, B. M., Bicoff, J. P., N S. I., Lendrum, B. L. Circulation, 1962, 26, 421. 1. 2.
CLOSURE OF PULMONARY VALVE SIR Dr. Honey has reported an interesting case of acquired stenosis of the larger branches of the pulmonary artery due,, recurrent pulmonary emboli.1 He drew attention to wid; splitting of the second heart-sound, a sign which occurred very commonly in the series of patients with congenital bilateral stenosis of the larger branches of the pulmonar; trunk reported by me and my former colleagues at Coo Country Children’s Hospital, Chicago. Phonocardiograh tracings were available in 14children with bilateral stenos,
medicine, and hygiene-used to describe work that has or should . have a common scopeand purpose. Otherwise it will be difficult to elevate this work academically on the lines envisaged by Dr. White5 in his proposal for a " dean of health studies ". Social medicine as it has been defined by Professor Pemberton 6 could be applied equally well in an urban or, rural, temperate or tropical, setting provided the practitioner is acquainted with the behaviour, customs, and motivation of the community he is working in. Hence the importance of including or upgrading sociology and psychology in the medical curriculum, a point emphasised by the Annis Gillie report.’7 West
Chiltington,
Pulborough, Sussex.
DELAYED
A. M. ROBERTSON
of the pulmonary-artery branches unassociated with other anomalies, and in them maximum splitting of the secon,, heart-sound varied from 40 to 80 milliseconds. The explanation for the typical pulmonary-artery pressurs curve put forward by Dr. Honey is very similar to tha advanced by the Cook County Hospital group in their arigina] descrintion of this characteristic nressure curve.’ Lokmanya Tilak General Hospital and Municipal Medical College, I. A. D’CRUZ. Sion, Bombay 22.*
.
ÆTIOLOGY OF JAMAICAN CARDIOMYOPATHY SIR,-In the practice of cardiology in the West Indies, patients are frequently seen who9are suffering from congestive heart-failure and cardiomegaly. The clinical picture of these patients is that of a chronic cardiomyopathy, and Sutton and I have suggested that the patients seen in Trinidad had Chagas’ disease because of positive complement-fixation. tests against antigens prepared from Trypahosoma cruzi.8 No aetiology has been suggested for the illness of similar patients from Jamaica.9 During a recent visit to Jamaica I was able to examine a few patients with congestive heart-failure and cardiomegaly, under the care of Dr. S. Suite, at the Spanish Town Hospital. The clinical picture that some of these patients presented conformed to that already described 8 9 in cardiomyopathy. Dr. Suite has kindly sent me five sera which were tested for the presence of complement-nxing’antibodies, by the plastic-plate technique of Fulton and Dumbell,1O against antigen prepared from T. cruzi isolated in Trinidad from triatomid bugs.ll One serum showed a denifite positive reaction (fixing more than two units of complement in the presence of antigen), and one serum was negative. The remaining three sera were received in poor condition and showed moderate to strong anticomplementary activity. In order to reduce their anticomplementary activity .these sera were treated for twenty minutes with an equal volume of 25% w/v suspension of kaolin in physiological saline solution. The kaolin was then removed by centrifugation. The supernatant fluids were tested again by the cOIÌ1plement fixation reaction, and one of them proved to be positive. Thus two of the five sera examined were found to contain antibodies against T. cruzi. In my own practice I would accept the finding of a positive serology in conjunction with the clinical- picture of cardiomyopathy as positive indication that chronic infection by T. cruzi is responsible for the cardiac disability. In Trinidad, ,. both triatomid bugs 11 and wild mammals 12 have been found to be infected by T. cruzi. No similar studies have yet been carried out in Jamaica, where at least two species of triatomid bugs are known to occur (Triatoma rubrofasciata and Nesotriatoma obscura).13 In the light of these ’findings I feel that it is important to determine whether T. cruzi is to be found in Jamaica, arid, if so, what part it plays in the aaiology of Jamaican cardiomyopathy. =
‘
I wish to thank Dr. S. Suite for allowing me to examine patients in his care and for sending me sera for testing. This work was part of a study on trypanosomiasis in Trinidad, in progress at the present time, which is supported by a grant from were the Ministry of Overseas Development. Laboratory made available to me at the Trinidad Regional Virus Laboratory of the University of the West Indies.
ame ties
Port of
Spain,
BORIS FISTEIN. Trinidad, West Indies. 5. White, T. H. Lancet, 1966, i, 1379. 6. Pemberton, J. ibid. p. 925. 7. The Field of Work of the Family Doctor. Report of the subcommittee of the Standing Medical Advisory Committee. H.M. Stationery Office, 1963. See Lancet, 1963, ii, 721, 727. 8. Fistein, B., Sutton, R. N. P. Lancet, 1963, i, 330. 9. Stuart, K. L., Hayes, J. A. Q. Jl Med. 1963, 32, 99. 10. Fulton, F., Dumbell, K. R. J. gen. Microbiol. 1949, 3, 97. 11. Fistein, B. Trans. R. Soc. trop. Med. Hyg. (in the press). 12. Downs, W. G. J. Parasit. 1963, 49, 50. 13. Maldonado-Capriles, J., Farr, T. H. Proc. ent. Soc. Wash. 1962, 64, 187.
PULMONARY ŒDEMA IN BLOOD-TRANSFUSION SIR,—Iwish to draw attention to a simple manoeuvre thatI, no doubt in common with many others, have used to prevent pulmonary redema during transfusion of blood to aneemic patients. An intravenous injection of frusemide 40 mg, at the outset will produce a diuresis of some 2 litres within 2 hours, m patients with full renal function, and about 1 litre in a similar period in those in whom anaemia has impaired renal function Such a diuretic response will clearly permit administration of at least L litre of blood in a period as short as 2 hours without There will, indeed, be any increment in blood-volume. preferential loss of fluid components and corresponding gain of packed-cell volume in the patient’s blood. Some absolute, as’ well as considerable relative, improvement in fluid-balance will occur. This may be critical in those already presenting an increase of blood-volume, as shown by a raised jugular venous pressure.
The principle of this method,which has been practised successfully over the past few months, deserves recognition. even where the transfusion is restricted carries the risk (certainly where the rate, given of anaemia is severe and packed cells are not available degree in time) of causing pulmonary œdema—still one of the chief among the potentially fatal complications of transfusion. DAVID LEWIS. Leicester General Hospital.
.Conventional management, at a
RHESUS-IMMUNISED MOTHERS AND
DIRECT-COOMBS-TEST-NEGATIVE BABIES SIR,—Iwas interested to read the article by Dr. Weiner and Miss Wingham (July 9), for a similar case occurred here years ago.
’
The mother was a 23-year-old Scottish immigrant, para gravida 2, in excellent general health. Her genotype w& group 0, dce/dce (rr), and her first child had been unaffected by haemolytic disease of the newborn. The present antenatal course had been uneventful apart from a gradually increasing anti-D titre first detected at 16 weeks. Because of prolongt,4 and difficult labour, caesarean section was performed anda 6 lb. 311/2 oz. female infant was delivered. Tests on the cord blood showed the baby’s genotype to be group 0, DCe d (Rlr). The direct Coombs test was negative (’ Ortho’ Coombs serum), and the serum bilirubin was 8-8 mg. per 100 mi. Within 12 hours the baby became listless with increasing jaundice. 48 hours after birth the serum-bilirubin had risento Honey, M. Lancet, 1966, i, 318. D’Cruz, I. A., Agustsson, M. H., Bicoff, J. P., Weinberg, M., A R. A. Am. J. Cardiol, 1964, 13, 441. 3. Agustsson, M. H., Arcilla, R. A., Gasul, B. M., Bicoff, J. P., N S. I., Lendrum, B. L. Circulation, 1962, 26, 421. 1. 2.