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POSTOPERATIVE INFECTION IN AN EYE HOSPITAL
338 POSTOPERATIVE INFECTION IN AN EYE HOSPITAL SiR,-It seems clear from correspondence (June 11 and 25, July 2 and 23) that some ambiguity has arisen out of my joint article. The position at this hospital is that all solutions which are used for intraocular operations are autoclaved in their final containers, and these containers are used to provide single doses. There is difficulty, however, in providing single-dose eye-drops autoclaved in their final containers for all the patients
given intravenously. Since a satisfactory circulation wasn,. maintained, after five minutes the left chest was opened.B bleeding occurred, and the heart was seen to be grosslp ,, tended and in asystole. Within a minute the heart had bet massaged into normal size, and regular rhythm was establish; ’.
The oatient made a raoid and uneventful recovery. Royal National Orthopaedic Hospital, Brockley Hill, JUNE Stanmore, Middlesex.
SQUIRE
who attend the hnsnitat.
Birmingham and Midland Eye Hospital, Church Street, Birmingham 3.
M. J. ROPER-HALL. Chairman, Medical Staff Committee.
POSTOPERATIVE HYPOXÆMIA SiR,-Your leading article (July 23) suggests collapse of alveoli in the basal regions of the lung as an important mechanism of postoperative hypoxsmia. On p. 203 of the same issue, we describe a physiological basis for basal collapse-namely, a decrease in alveolar size from upper to lower regions of the lung such that the alveoli in the dependent zone may have only one-quarter of the resting volume of those above. These alveoli and their small airways will be unstable and the first to collapse during prolonged shallow breathing or general anaesthesia. Since the dependent regions of the lung have the greatest blood-flow, hvooxaemia would then be inevitable. J. B. GLAZIER J. M. B. HUGHES Clinical Respiratory Physiology Research Group, Postgraduate Medical School, London W.12.
J. E. MALONEY M. C. F. PAIN
J. B. WEST.
HEPATIC CIRRHOSIS AND THE LUNGS SiR,ňIwas interested to read your annotation.2 Apparently my joint article,3 on cirrhosis of liver simulating congenital cyanotic heart-disease, has escaped your notice. I have demonstrated numerous tiny arteriovenous aneurysms in the lungs in these cases, which account beyond any doubt for the severe desree of desaturation. R. C. HANSOTI. Bombay.
*** It is highly probable that no single pulmonary change is responsible for the central type of cyanosis shown by some patients with hepatic cirrhosis. As we wrote, an increase in pulmonary vascularity was found by Berthelot et al. in the 13 cases they studied post mortem, but apart from some spider naevi in the pleura arteriovenous anastomoses were absent. They did, however, observe some nodularity in the base of the lungs similar to that described by Dr. Hansoti in his joirit article, but neither by injection nor by microscopic examination could this be identified as due to arteriovenous anastomoses. But Dr. Hansoti and Dr. Shah, by pulmonary angiography, have interpreted as such anastomoses the similar shadows in 3 of their patients.-ED. L.
PHYTOHÆMAGGLUTININ IN APLASTIC ANÆMIA SIR,-We have treated a patient with idiopathic aplast anaemia by a method similar to that of Astaldi et al.l Leucr. cytes from 20 ml. peripheral blood were cultured in it. presence of phytohæmagglutinin (P.H.A.) (Difco) using Nowell method,2 as modified by Prof. R. J. V. Pulvertaft. The lymphocytes from our patient appeared refractory to the actior of P.H.A., and cultures died on three occasions without any evidence of blastic transformation. After 4 days, however, the transformed lymphocytes from surviving cultures were counted washed in two changes of phosphate-buffered saline, and injected directly into the marrow cavity of the iliac crests ot the patient. A total of 40 x 106 transformed autologous lymphocytes were injected on eight occasions over a period of 2 months Our patient, a 10-year-old Nigerian girl, was referred to thk hospital with the history of progressive tiredness, fever, insomnia, and frequent loose stools with blood and mucus fo a week. The parents denied giving any medication before th; onset of illness. The patient was well developed, with gros: pallor of the palms of the hands and mucous membranes. Her temperature was 1036°F; the pulse was collapsing and the rate was 140 per minute. There was a diffuse cardiac impulse and cardiomegaly. A moderately loud systolic murmur was present over the entire precordium. Stool culture yielded Shigella dysenterice 2. Blood-cultures were negative. Hb was 28 g. per 100 ml., and packed-cell volume (P.c.v.) 8%, and I reticulocytes were less than 1 % ;white-cell count was 2700 per , c.mm. (neutrophils 17%, eosinophils 1%, lymphocytes 77° iI monocytes 5%); platelets were less than 10,000 per c,mm,; ’, the red cells showed anisocytosis and slight poikilocytosis, with occasional ovalocytes and spherocytes. Bone-marrow aspirate: from both iliac crests showed fatty hypoplastic tissue, witha relative excess of reticulum cells; no megakaryocytes were seen Treatment started with prednisolone 60 mg. per day, ani testosterone 40 mg. per day. After 5 weeks the white cells rose over the period of a week to 3800 per c.mm., the platelets K ! ’ 21,000 per c.mm., and the reticulocytes to 10%, but at the sam: time, following blood-transfusion, the p.c.v. fell from 200" ICi 13 %. This slight improvement of the peripheral-blood counts was not maintained. Prednisolone dosage was decreased aftera further 4 weeks and finally stopped, but testosterone 11’2’ continued. 12 weeks after her first admission to hospital, the patient was given her first injection of transformed autologous leucocytes On the 4th day the white-cell count had risen from 1600 to 25l’ per c.mm., the lymphocytes from 40 to 92%, and the reticula cytes from less than 1 to 65%. These counts returned’ their original low levels, and there were no other alterations the peripheral-blood counts. No primitive lymphocytes B,,:, seen in the peripheral blood. No significant changes were observed after the next seven injections. After eight injections it was decided to abandon the treatment because of the lack of response and the discomfort of repeated marrow punctures 11 months after her first admission the peripheral-blood counts still show no improvement (p.e.v. 11%,white-cell count 136 per c.mm., platelets 11,000 per c.mm.). Treatment = -
CARDIOPULMONARY RESUSCITATION SIR,-In support of Mr. Harley’s arguments (July 2) for early use of internal cardiac massage when external cardiac massage has failed, I report here the following case. A fit 18-year-old boy was to have a Kuntscher nail inserted for a fractured femur. After uneventful induction of general anaesthesia he was turned on his side, and then cardiac arrest occurred. External cardiac massage was started, the lungs were inflated with oxygen and 8-4% sodium bicarbonate solution 1. 2. 3.
Ayliffe, G. A. J., Barry, D. R., Lowbury, E. J. L., Roper-Hall, M. J., Walker, W. M. Lancet, i, 1113. Lancet, 1966, i, 968. Hansoti, R. C., Shah, N. J. Circulation, 1966, 33, 71.
testosterone and
supportive
measures
continues.
The difficulty in culturing this patient’s 1.
2.
lymphocytes.
Astaldi, G., Airo, R., Sanli, S., Costa, G. Lancet, 1965, Astaldi, G., Airo, R., Costa, G., Sanli, S. 10th European Congress Hæmatology at Strasbourg, Aug. 23-28, 1965. See Br. med. J ii, 754. Nowell, P. C. Cancer Res. 1960, 20, 462.
given intravenously. Since a satisfactory circulation wasn,. maintained, after five minutes the left chest was opened.B bleeding occurred, and the heart was seen to be grosslp ,, tended and in asystole. Within a minute the heart had bet massaged into normal size, and regular rhythm was establish; ’.
The oatient made a raoid and uneventful recovery. Royal National Orthopaedic Hospital, Brockley Hill, JUNE Stanmore, Middlesex.
SQUIRE
who attend the hnsnitat.
Birmingham and Midland Eye Hospital, Church Street, Birmingham 3.
M. J. ROPER-HALL. Chairman, Medical Staff Committee.
POSTOPERATIVE HYPOXÆMIA SiR,-Your leading article (July 23) suggests collapse of alveoli in the basal regions of the lung as an important mechanism of postoperative hypoxsmia. On p. 203 of the same issue, we describe a physiological basis for basal collapse-namely, a decrease in alveolar size from upper to lower regions of the lung such that the alveoli in the dependent zone may have only one-quarter of the resting volume of those above. These alveoli and their small airways will be unstable and the first to collapse during prolonged shallow breathing or general anaesthesia. Since the dependent regions of the lung have the greatest blood-flow, hvooxaemia would then be inevitable. J. B. GLAZIER J. M. B. HUGHES Clinical Respiratory Physiology Research Group, Postgraduate Medical School, London W.12.
J. E. MALONEY M. C. F. PAIN
J. B. WEST.
HEPATIC CIRRHOSIS AND THE LUNGS SiR,ňIwas interested to read your annotation.2 Apparently my joint article,3 on cirrhosis of liver simulating congenital cyanotic heart-disease, has escaped your notice. I have demonstrated numerous tiny arteriovenous aneurysms in the lungs in these cases, which account beyond any doubt for the severe desree of desaturation. R. C. HANSOTI. Bombay.
*** It is highly probable that no single pulmonary change is responsible for the central type of cyanosis shown by some patients with hepatic cirrhosis. As we wrote, an increase in pulmonary vascularity was found by Berthelot et al. in the 13 cases they studied post mortem, but apart from some spider naevi in the pleura arteriovenous anastomoses were absent. They did, however, observe some nodularity in the base of the lungs similar to that described by Dr. Hansoti in his joirit article, but neither by injection nor by microscopic examination could this be identified as due to arteriovenous anastomoses. But Dr. Hansoti and Dr. Shah, by pulmonary angiography, have interpreted as such anastomoses the similar shadows in 3 of their patients.-ED. L.
PHYTOHÆMAGGLUTININ IN APLASTIC ANÆMIA SIR,-We have treated a patient with idiopathic aplast anaemia by a method similar to that of Astaldi et al.l Leucr. cytes from 20 ml. peripheral blood were cultured in it. presence of phytohæmagglutinin (P.H.A.) (Difco) using Nowell method,2 as modified by Prof. R. J. V. Pulvertaft. The lymphocytes from our patient appeared refractory to the actior of P.H.A., and cultures died on three occasions without any evidence of blastic transformation. After 4 days, however, the transformed lymphocytes from surviving cultures were counted washed in two changes of phosphate-buffered saline, and injected directly into the marrow cavity of the iliac crests ot the patient. A total of 40 x 106 transformed autologous lymphocytes were injected on eight occasions over a period of 2 months Our patient, a 10-year-old Nigerian girl, was referred to thk hospital with the history of progressive tiredness, fever, insomnia, and frequent loose stools with blood and mucus fo a week. The parents denied giving any medication before th; onset of illness. The patient was well developed, with gros: pallor of the palms of the hands and mucous membranes. Her temperature was 1036°F; the pulse was collapsing and the rate was 140 per minute. There was a diffuse cardiac impulse and cardiomegaly. A moderately loud systolic murmur was present over the entire precordium. Stool culture yielded Shigella dysenterice 2. Blood-cultures were negative. Hb was 28 g. per 100 ml., and packed-cell volume (P.c.v.) 8%, and I reticulocytes were less than 1 % ;white-cell count was 2700 per , c.mm. (neutrophils 17%, eosinophils 1%, lymphocytes 77° iI monocytes 5%); platelets were less than 10,000 per c,mm,; ’, the red cells showed anisocytosis and slight poikilocytosis, with occasional ovalocytes and spherocytes. Bone-marrow aspirate: from both iliac crests showed fatty hypoplastic tissue, witha relative excess of reticulum cells; no megakaryocytes were seen Treatment started with prednisolone 60 mg. per day, ani testosterone 40 mg. per day. After 5 weeks the white cells rose over the period of a week to 3800 per c.mm., the platelets K ! ’ 21,000 per c.mm., and the reticulocytes to 10%, but at the sam: time, following blood-transfusion, the p.c.v. fell from 200" ICi 13 %. This slight improvement of the peripheral-blood counts was not maintained. Prednisolone dosage was decreased aftera further 4 weeks and finally stopped, but testosterone 11’2’ continued. 12 weeks after her first admission to hospital, the patient was given her first injection of transformed autologous leucocytes On the 4th day the white-cell count had risen from 1600 to 25l’ per c.mm., the lymphocytes from 40 to 92%, and the reticula cytes from less than 1 to 65%. These counts returned’ their original low levels, and there were no other alterations the peripheral-blood counts. No primitive lymphocytes B,,:, seen in the peripheral blood. No significant changes were observed after the next seven injections. After eight injections it was decided to abandon the treatment because of the lack of response and the discomfort of repeated marrow punctures 11 months after her first admission the peripheral-blood counts still show no improvement (p.e.v. 11%,white-cell count 136 per c.mm., platelets 11,000 per c.mm.). Treatment = -
CARDIOPULMONARY RESUSCITATION SIR,-In support of Mr. Harley’s arguments (July 2) for early use of internal cardiac massage when external cardiac massage has failed, I report here the following case. A fit 18-year-old boy was to have a Kuntscher nail inserted for a fractured femur. After uneventful induction of general anaesthesia he was turned on his side, and then cardiac arrest occurred. External cardiac massage was started, the lungs were inflated with oxygen and 8-4% sodium bicarbonate solution 1. 2. 3.
Ayliffe, G. A. J., Barry, D. R., Lowbury, E. J. L., Roper-Hall, M. J., Walker, W. M. Lancet, i, 1113. Lancet, 1966, i, 968. Hansoti, R. C., Shah, N. J. Circulation, 1966, 33, 71.
testosterone and
supportive
measures
continues.
The difficulty in culturing this patient’s 1.
2.
lymphocytes.
Astaldi, G., Airo, R., Sanli, S., Costa, G. Lancet, 1965, Astaldi, G., Airo, R., Costa, G., Sanli, S. 10th European Congress Hæmatology at Strasbourg, Aug. 23-28, 1965. See Br. med. J ii, 754. Nowell, P. C. Cancer Res. 1960, 20, 462.