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SEVERE RESPIRATORY DISTRESS IN BABIES
204 may be related to the age of the patient, since the levels of plasma and platelet enzymes seem to be higher in childhood. None of these patients had been previously treated with acetylsalicylic acid, so that these abnormalities cannot be related, as suggested by Evans et al.,7 to this drug. Our findings support the existence of a new congenital disease. Further work is in progress and will be reported elsewhere. Laboratoire d’Hémostase, JACQUES P. CAEN
Institut de Recherches sur les Maladies du Sang, Hôpital Saint-Louis, Paris 10e.
YVETTE SULTAN
MARIE-JOSETTE
LARRIEU.
SEVERE RESPIRATORY DISTRESS IN BABIES SIR,-In reply to Dr. Wiles’ letter (Dec. 30, p. 1423), we should like to point out that the facts she asks for were given in our paper,8 in which the duration of illness in all the patients was clearly stated, using the best criterion that we could think of-i.e., need for added oxygen. As regards opinions, we would, despite her criticisms, stick to our own-that it is important to make a clear distinction between clinical respiratory distress and pathological hyaline-membrane disease, and that the so-called aspiration syndrome is not an entity, there being no better proof that it is due to aspiration than in the case of the respiratory-distress syndrome proper. What she asks for Ňa clearer delineation of the different types of respiratory distress based on measurable criteria-is exactly what we were attempting to provide. We would also point out that in the babies who died the postmortem findings were those of hyaline-membrane disease; and that in our opinion radiological findings are not a good guide to the prognosis in clinical respiratory distress. Could we not now drop the ponderous and confusing term idiopathic respiratory-distress syndrome of the premature infant, substituting respiratory distress (clinical) and hyalinemembrane disease (pathological) and leaving open the question of how well these correlate ? Department of Child Health, St. Mary’s Hospital, Manchester 13. J. A. DAVIS. Nuffield Neonatal Research Unit, Hammersmith Hospital, London W.12.
ASPIRIN AND PLATELET AGGREGATION SIR,-Dr. Evans and his colleaguesimply that perhaps the minor hxmorrhagic syndrome I provisionally reported2 as the " Portsmouth syndrome " could be due to aspirin ingestion. The ten patients I reported2 with minor bleeding have all recently been asked how many tablets containing aspirin they had ingested during the month of December, 1967. The results were: one patient 50 tablets, two 25, one 15, and six 0. The proportion of aspirin eaters is high but not appreciably higher than that found in a sample of 141 people in the same population group who have lately been questioned. Since the pattern of casual aspirin ingestion remains roughly constant, the amount ingested in the summer of 1967 was probably not much less. The four aspirin eaters and two of the patients who ate none failed in the summer of 1967 to give the normal second wave of aggregation with adrenaline and responded incompletely and poorly to tendon extract. The second wave with adrenaline and the completeness of the response to
tendon extract were not considered part of the syndrome but the " slope " of the aggregation with tendon extract was. Furthermore it has since been shown that eating aspirin has no effect on the result of passing blood through my glass-bead column,3 yet all the ten patients gave abnormal results. Thus all the reported tests were uninfluenced by aspirin, except the slope of aggregation with tendon extract, which on average
N. R. C. ROBERTON.
SPIRAMYCIN PROPHYLAXIS IN SURGERY
SIR, The paper by Mr. Macfarlane and his colleagues (Jan. 6, p. 1) will probably encourage others to use spiramycin prophylaxis in surgery. Although the results of treatment seem encouraging, however, they are not conclusive. A four-year trial carried out at this hospital showed 9 that
staphylococcal wound infection was closely related to the number of nasal carriers admitted to the wards. In our experience this was very variable; Mr. Macfarlane and his colleagues cannot safely assume that the risk of infection when they did not use prophylaxis was the same as in the next year when prophylaxis was given. Moreover, this is only one of many possible variables between the two years. A controlled trial, in which at the same time half the patients in the same ward are given prophylaxis and the others an inactive preparation, should yield convincing evidence of the benefit or otherwise of treatment. Although few spiramycin-resistant strains were encountered during the trial of Mr. Macfarlane and his colleagues, it would be extraordinary if resistant strains did not become dominant after further treatment. There are indications for antibiotic prophylaxis in surgery but none that I know of for routine prophylaxis. University College Hospital, Department of Clinical Pathology, London W.C.1.
E.
JOAN STOKES,
7. Evans, G., Mustard, J. F., Packham, M. A. Lancet, 1967, ii, 724. 8. Roberton, N. R. C., Hallidie-Smith, K. A., Davis, J. A. ibid. p. 1108 9. Stokes, E. J., Hall, B. M., Richards, J. D. M., Reilly, D. J. ibid. 1965, ii, 197.
Duration of inhibition of second wave of adrenaline response after different single doses of aspirin (on left) taken at 9 a.m. on day 0.
No second wave. Ň Ň.Ň Ň Not studied. N indicates normal double response.
return to a
aspirin will be prohibited for a week before the tests are carried out. Dr. Weiss and Dr. Aledort4 report that 3 g. of aspirin a day decreases the platelet response to connective-tissue fragments, and Zucker and Peterson that 1-3 g. inhibits secondary platelet aggregation following the addition of adenosine diphosphate (A.D.P.). I can confirm these findings and in addition have now shown that the secondary wave of platelet aggregation produced in most people by adrenaline6 is also inhibited by aspirin. Eighteen volunteers were tested on day 0 to show that their citrated platelet-rich plasma (P.R.P.) gave a double wave of aggregation with strong adrenaline (5 M x 10-4). They then ate the dose of soluble aspirin noted in the
may have been. In future
1. 2. 3. 4. 5. 6.
Evans, G., Mustard, J. F., Packham, M. A. Lancet, 1967, ii, 724. O’Brien, J. R. ibid. p. 258. O’Brien, J. R., Heywood, J. B. J. clin. Path. 1967, 20, 56. Weiss, H. J., Aledort, L. M. Lancet, 1967, ii, 495. Zucker, M. B., Peterson, J. Proc. Soc. Exp. Biol. Med. (in the press). O’Brien, J. R. Nature, Lond. 1963, 200, 763.
Institut de Recherches sur les Maladies du Sang, Hôpital Saint-Louis, Paris 10e.
YVETTE SULTAN
MARIE-JOSETTE
LARRIEU.
SEVERE RESPIRATORY DISTRESS IN BABIES SIR,-In reply to Dr. Wiles’ letter (Dec. 30, p. 1423), we should like to point out that the facts she asks for were given in our paper,8 in which the duration of illness in all the patients was clearly stated, using the best criterion that we could think of-i.e., need for added oxygen. As regards opinions, we would, despite her criticisms, stick to our own-that it is important to make a clear distinction between clinical respiratory distress and pathological hyaline-membrane disease, and that the so-called aspiration syndrome is not an entity, there being no better proof that it is due to aspiration than in the case of the respiratory-distress syndrome proper. What she asks for Ňa clearer delineation of the different types of respiratory distress based on measurable criteria-is exactly what we were attempting to provide. We would also point out that in the babies who died the postmortem findings were those of hyaline-membrane disease; and that in our opinion radiological findings are not a good guide to the prognosis in clinical respiratory distress. Could we not now drop the ponderous and confusing term idiopathic respiratory-distress syndrome of the premature infant, substituting respiratory distress (clinical) and hyalinemembrane disease (pathological) and leaving open the question of how well these correlate ? Department of Child Health, St. Mary’s Hospital, Manchester 13. J. A. DAVIS. Nuffield Neonatal Research Unit, Hammersmith Hospital, London W.12.
ASPIRIN AND PLATELET AGGREGATION SIR,-Dr. Evans and his colleaguesimply that perhaps the minor hxmorrhagic syndrome I provisionally reported2 as the " Portsmouth syndrome " could be due to aspirin ingestion. The ten patients I reported2 with minor bleeding have all recently been asked how many tablets containing aspirin they had ingested during the month of December, 1967. The results were: one patient 50 tablets, two 25, one 15, and six 0. The proportion of aspirin eaters is high but not appreciably higher than that found in a sample of 141 people in the same population group who have lately been questioned. Since the pattern of casual aspirin ingestion remains roughly constant, the amount ingested in the summer of 1967 was probably not much less. The four aspirin eaters and two of the patients who ate none failed in the summer of 1967 to give the normal second wave of aggregation with adrenaline and responded incompletely and poorly to tendon extract. The second wave with adrenaline and the completeness of the response to
tendon extract were not considered part of the syndrome but the " slope " of the aggregation with tendon extract was. Furthermore it has since been shown that eating aspirin has no effect on the result of passing blood through my glass-bead column,3 yet all the ten patients gave abnormal results. Thus all the reported tests were uninfluenced by aspirin, except the slope of aggregation with tendon extract, which on average
N. R. C. ROBERTON.
SPIRAMYCIN PROPHYLAXIS IN SURGERY
SIR, The paper by Mr. Macfarlane and his colleagues (Jan. 6, p. 1) will probably encourage others to use spiramycin prophylaxis in surgery. Although the results of treatment seem encouraging, however, they are not conclusive. A four-year trial carried out at this hospital showed 9 that
staphylococcal wound infection was closely related to the number of nasal carriers admitted to the wards. In our experience this was very variable; Mr. Macfarlane and his colleagues cannot safely assume that the risk of infection when they did not use prophylaxis was the same as in the next year when prophylaxis was given. Moreover, this is only one of many possible variables between the two years. A controlled trial, in which at the same time half the patients in the same ward are given prophylaxis and the others an inactive preparation, should yield convincing evidence of the benefit or otherwise of treatment. Although few spiramycin-resistant strains were encountered during the trial of Mr. Macfarlane and his colleagues, it would be extraordinary if resistant strains did not become dominant after further treatment. There are indications for antibiotic prophylaxis in surgery but none that I know of for routine prophylaxis. University College Hospital, Department of Clinical Pathology, London W.C.1.
E.
JOAN STOKES,
7. Evans, G., Mustard, J. F., Packham, M. A. Lancet, 1967, ii, 724. 8. Roberton, N. R. C., Hallidie-Smith, K. A., Davis, J. A. ibid. p. 1108 9. Stokes, E. J., Hall, B. M., Richards, J. D. M., Reilly, D. J. ibid. 1965, ii, 197.
Duration of inhibition of second wave of adrenaline response after different single doses of aspirin (on left) taken at 9 a.m. on day 0.
No second wave. Ň Ň.Ň Ň Not studied. N indicates normal double response.
return to a
aspirin will be prohibited for a week before the tests are carried out. Dr. Weiss and Dr. Aledort4 report that 3 g. of aspirin a day decreases the platelet response to connective-tissue fragments, and Zucker and Peterson that 1-3 g. inhibits secondary platelet aggregation following the addition of adenosine diphosphate (A.D.P.). I can confirm these findings and in addition have now shown that the secondary wave of platelet aggregation produced in most people by adrenaline6 is also inhibited by aspirin. Eighteen volunteers were tested on day 0 to show that their citrated platelet-rich plasma (P.R.P.) gave a double wave of aggregation with strong adrenaline (5 M x 10-4). They then ate the dose of soluble aspirin noted in the
may have been. In future
1. 2. 3. 4. 5. 6.
Evans, G., Mustard, J. F., Packham, M. A. Lancet, 1967, ii, 724. O’Brien, J. R. ibid. p. 258. O’Brien, J. R., Heywood, J. B. J. clin. Path. 1967, 20, 56. Weiss, H. J., Aledort, L. M. Lancet, 1967, ii, 495. Zucker, M. B., Peterson, J. Proc. Soc. Exp. Biol. Med. (in the press). O’Brien, J. R. Nature, Lond. 1963, 200, 763.