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SIDS, surfactant, and temperature
690
and infiltration and were firm to the touch. 2 patients had an annular or multi-annular erythematous patch with a slightly irregular margin. 23 patients complained of itching, 5 had pain or tenderness, and 5 were symptom free. Blood samples were obtained from 9 patients for measurement of immunoglobulins. Mean IgG (1440.0 [419’1] mg/dl) and IgM (242-5 [93’7] mg/dl) concentrations were increased, but IgA, C3, C4, CHso, and CIC were normal. Skin biopsy was done in 7 patients and revealed focal or diffuse parakeratosis, microabscesses (composed of neutrophils) in the subcomeum and the upper stratum spinosum, acanthosis, intracellular and extracellular oedema, reticular degeneration, and exocytosis of the lymphoid cells in the epidermis. Moreover, swelling of the vascular endothelial cells and focal or areolar perivascular infiltration, with neutrophils, lymphoid cells, histiocytes, eosinophils, or some nuclear dust were seen in the upper and middle reticular layer of the dermis. These findings were compatible with cutaneous vasculitis. Skin samples from 2 patients showed deposition of IgG and/or IgM in the parakeratotic cells. After erythema was diagnosed the drug was withdrawn immediately and steroid creams were given. 15 patients also received oral prednisone 15-30 mg daily, the dose being dependent on the severity of the lesion and the original disease. Complete recovery occurred within 3-15 days, in all but 1 patient, who had skin necrosis at the centre of the lesion and whose course of treatment was continued for one month. Such skin reactions are often neglected. In the patients reported here the reactions seem to be attributable to the drugs because they appeared soon after injection, and sooner after a second injection in 4 patients. In addition, all but 1 patient responded to prednisone, and IgG and IgM concentrations indicated an immune response. Most of the women were obese and lesions were seen only at the injection site. The cause and pathogenesis of such reactions need to be further investigated. Department of Dermatology, Suzhov No 2 People’s Hospital, Suzhou, Ziangsu,
People’s Republic of China 1. Sanders MN, Winkelmann RK. Cutaneous reactions to vitamin Dermatol 1988; 19: 699-704.
KAI SHEN K. J
Am Acad
SIDS, surfactant, and temperature SIR,-Fleming and co-workers’ suggestion that temperature is a factor in sudden infant death syndrome (SIDS) recalls Clements" statement that "temperature has an exponentially increasing effect on the instability of the alveolar structure". Goerke and Gonzales3 showed that films of the surfactant type have a critical temperature above which they become increasingly weaker-not necessarily exponentially so, but certainly abruptly. The process has been compared to the melting point of wax. This critical temperature for the main constituent of surfactant, dipalmitoylphosphatidylcholine (DPPC) is about 45°C. The critical temperature is sensitive to changes in the fatty acid components on the DPPC. The substitution of one myristoyl chain for one of the palmitoyl chains on the DPPC molecule reduces this temperature to about 33°C, and substitution of both chains to about 29°C. The critical temperature is also reduced by inclusion of other chemical species in the film. The critical temperature for the normal lung surfactant cocktail is about 37°C, which is probably functionally important. Morley et al4 noted a disparity between the constituents of the lung lining layer in SIDS and in controls, and Gibson and McMurchies found a reduction in the disaturated form of the phosphatidylcholine component of lung surfactant in SIDS. Such defects would reduce the transition temperature, rendering the alveolar lining layer more fluid and liable to collapsed Consequently functional residual capacity (FRC) would be reduced and the rate of loss of FRC between deep breaths would increase, with smaller alveoli becoming vulnerable to closure,’ and normal respiratory control might be deranged.6 Thus if a proportion of SIDS deaths are respiratory in origin survival will be increased if air temperature is reduced and the defective surfactant made more rigid. Similarly, any manoeuvre that aids rather than hinders lung inflation will help children retain
adequate FRC, though neither measure will have any effect on those with normal surfactant. On this basis high air temperature and respiratory restriction would not be causes of cot death; their avoidance should perhaps be thought of as a precautionary measure to provide some assistance in rare cases of a respiratory disease not yet understood.
an
Royal Postgraduate Medical School, Institute of Obstetrics and Gynaecology, Queen Charlotte’s Hospital for Women,
D. G. TALBERT
London W6 OXG, UK
1.
2
Fleming PJ, Gilbert R, Azaz Y, et al. Interaction between bedding and sleeping position m the sudden infant death syndrome: a population based case-control study. Br Med J 1990; 301: 85-89. Clements JA. The alveolar lining layer In: de Reuck AVS, Porter R, eds. Ciba Foundation symposium proceedings: development of the lung. London: Churchill,
1967: 203-37. 3. Goerke J, Gonzales
J. Temperature dependence of dipalimtoyl phosphatidylcholine monolayer stability. J Appl Physiol 1981, 51: 1108-14. 4. Morley CJ, Hill CM, Brown BD, Barson AJ, Davies JA. Surfactant abnormalities in babies dying from sudden infant death syndrome. Lancet 1982; i: 1320-23. 5. Gibson RA, McMurchie EJ. Changes in lung surfactant lipids associated with sudden infant death syndrome. Aust Paediatr J 1986; 22 (suppl 1): 77-80. 6. Southall DP, Talbert DG. Sudden atelectasis apnea braking syndrome. In Hollinger MA, ed. Current topics in pulmonary pharmocology. New York: Elsevier, 1987 210-81
Birth of second twin SiR,—Your Aug 4 editorial reminds obstetricians of the contribution that twin pregnancy makes to perinatal morbidity and mortality statistics. We are all too well aware that a brain-damaged second twin may be a greater family tragedy than a stillbirth. On occasion such damage may occur before labour, especially if this takes place after the 38th week, but a traumatic delivery can cause irreversible damage. Skilled delivery can and does save life, as shown by the report from the Birmingham Matemity Hospital But such delivery may tax the obstetrician’s and anaesthetist’s skill. Internal version and breech extraction may be very satisfying but in the grand multigravida may be fraught with the hazards of uterine rupture, catastrophic haemorrhage, hysterectomy, and ureteric injury. A more recent problem is the management of the second twin lying transversely in a secundigravida with a previous caesarean section scar. Uterine rupture can follow when external version has failed to correct a transverse lie and internal version is done. It is therefore worth considering elective section for twin pregnancy in a patient with a scarred uterus and no previous vaginal deliveries. It is also important that our neonatologists realise that elective section of multiple pregnancy is not without risk of atonic postpartum haemorrhage. To prevent this a high concentration oxytocin infusion is usually effective and anaesthetists can be prevailed upon to give intravenous ergometrine. New Cross Hospital, Wolverhampton WV100QP, UK 1. Samra JS,
ALAN M. SMITH
Spillance H, Mukoyoko J, Tang L, Obhrai MS. Caesarean section for the Br J Obstet Gynaecol 1986; 154: 936-39.
birth of the second twin.
SiR,—Your editorial on the delivery of the second twin was prompted by reports from two Birmingham hospitals of an increase between 1986 and 1988 in the rate of caesarean section for the birth of the second twin after vaginal delivery of the first (6-11%1 and 6’5%2). The hospitals have also reported a rise in caesarean section rate to 20%.3 Southmead Hospital, Bristol, has one of the largest maternity units in the UK. In 1988 there were 5883 deliveries, 600 caesarean sections (10-28%), and a perinatal mortality rate (PNMR)of7’8 per 1000 births. Between 1987 and 1989 there were 197 twin deliveries with no stillbirths and 3 neonatal deaths (15 -2 per 1000). There were 28 caesarean sections (14-2%), of which 4 were for the second twin, the reasons given being shoulder presentation (3) and compound presentation (1). There was no attempt at internal podalic version. D. K. James and I suggested that a rise in the rate of caesarean section is not an inevitable part of modem obstetric careWe report a low rate of caesarean section for the second twin and suggest that the Birmingham experience may not be widespread. There has been
and infiltration and were firm to the touch. 2 patients had an annular or multi-annular erythematous patch with a slightly irregular margin. 23 patients complained of itching, 5 had pain or tenderness, and 5 were symptom free. Blood samples were obtained from 9 patients for measurement of immunoglobulins. Mean IgG (1440.0 [419’1] mg/dl) and IgM (242-5 [93’7] mg/dl) concentrations were increased, but IgA, C3, C4, CHso, and CIC were normal. Skin biopsy was done in 7 patients and revealed focal or diffuse parakeratosis, microabscesses (composed of neutrophils) in the subcomeum and the upper stratum spinosum, acanthosis, intracellular and extracellular oedema, reticular degeneration, and exocytosis of the lymphoid cells in the epidermis. Moreover, swelling of the vascular endothelial cells and focal or areolar perivascular infiltration, with neutrophils, lymphoid cells, histiocytes, eosinophils, or some nuclear dust were seen in the upper and middle reticular layer of the dermis. These findings were compatible with cutaneous vasculitis. Skin samples from 2 patients showed deposition of IgG and/or IgM in the parakeratotic cells. After erythema was diagnosed the drug was withdrawn immediately and steroid creams were given. 15 patients also received oral prednisone 15-30 mg daily, the dose being dependent on the severity of the lesion and the original disease. Complete recovery occurred within 3-15 days, in all but 1 patient, who had skin necrosis at the centre of the lesion and whose course of treatment was continued for one month. Such skin reactions are often neglected. In the patients reported here the reactions seem to be attributable to the drugs because they appeared soon after injection, and sooner after a second injection in 4 patients. In addition, all but 1 patient responded to prednisone, and IgG and IgM concentrations indicated an immune response. Most of the women were obese and lesions were seen only at the injection site. The cause and pathogenesis of such reactions need to be further investigated. Department of Dermatology, Suzhov No 2 People’s Hospital, Suzhou, Ziangsu,
People’s Republic of China 1. Sanders MN, Winkelmann RK. Cutaneous reactions to vitamin Dermatol 1988; 19: 699-704.
KAI SHEN K. J
Am Acad
SIDS, surfactant, and temperature SIR,-Fleming and co-workers’ suggestion that temperature is a factor in sudden infant death syndrome (SIDS) recalls Clements" statement that "temperature has an exponentially increasing effect on the instability of the alveolar structure". Goerke and Gonzales3 showed that films of the surfactant type have a critical temperature above which they become increasingly weaker-not necessarily exponentially so, but certainly abruptly. The process has been compared to the melting point of wax. This critical temperature for the main constituent of surfactant, dipalmitoylphosphatidylcholine (DPPC) is about 45°C. The critical temperature is sensitive to changes in the fatty acid components on the DPPC. The substitution of one myristoyl chain for one of the palmitoyl chains on the DPPC molecule reduces this temperature to about 33°C, and substitution of both chains to about 29°C. The critical temperature is also reduced by inclusion of other chemical species in the film. The critical temperature for the normal lung surfactant cocktail is about 37°C, which is probably functionally important. Morley et al4 noted a disparity between the constituents of the lung lining layer in SIDS and in controls, and Gibson and McMurchies found a reduction in the disaturated form of the phosphatidylcholine component of lung surfactant in SIDS. Such defects would reduce the transition temperature, rendering the alveolar lining layer more fluid and liable to collapsed Consequently functional residual capacity (FRC) would be reduced and the rate of loss of FRC between deep breaths would increase, with smaller alveoli becoming vulnerable to closure,’ and normal respiratory control might be deranged.6 Thus if a proportion of SIDS deaths are respiratory in origin survival will be increased if air temperature is reduced and the defective surfactant made more rigid. Similarly, any manoeuvre that aids rather than hinders lung inflation will help children retain
adequate FRC, though neither measure will have any effect on those with normal surfactant. On this basis high air temperature and respiratory restriction would not be causes of cot death; their avoidance should perhaps be thought of as a precautionary measure to provide some assistance in rare cases of a respiratory disease not yet understood.
an
Royal Postgraduate Medical School, Institute of Obstetrics and Gynaecology, Queen Charlotte’s Hospital for Women,
D. G. TALBERT
London W6 OXG, UK
1.
2
Fleming PJ, Gilbert R, Azaz Y, et al. Interaction between bedding and sleeping position m the sudden infant death syndrome: a population based case-control study. Br Med J 1990; 301: 85-89. Clements JA. The alveolar lining layer In: de Reuck AVS, Porter R, eds. Ciba Foundation symposium proceedings: development of the lung. London: Churchill,
1967: 203-37. 3. Goerke J, Gonzales
J. Temperature dependence of dipalimtoyl phosphatidylcholine monolayer stability. J Appl Physiol 1981, 51: 1108-14. 4. Morley CJ, Hill CM, Brown BD, Barson AJ, Davies JA. Surfactant abnormalities in babies dying from sudden infant death syndrome. Lancet 1982; i: 1320-23. 5. Gibson RA, McMurchie EJ. Changes in lung surfactant lipids associated with sudden infant death syndrome. Aust Paediatr J 1986; 22 (suppl 1): 77-80. 6. Southall DP, Talbert DG. Sudden atelectasis apnea braking syndrome. In Hollinger MA, ed. Current topics in pulmonary pharmocology. New York: Elsevier, 1987 210-81
Birth of second twin SiR,—Your Aug 4 editorial reminds obstetricians of the contribution that twin pregnancy makes to perinatal morbidity and mortality statistics. We are all too well aware that a brain-damaged second twin may be a greater family tragedy than a stillbirth. On occasion such damage may occur before labour, especially if this takes place after the 38th week, but a traumatic delivery can cause irreversible damage. Skilled delivery can and does save life, as shown by the report from the Birmingham Matemity Hospital But such delivery may tax the obstetrician’s and anaesthetist’s skill. Internal version and breech extraction may be very satisfying but in the grand multigravida may be fraught with the hazards of uterine rupture, catastrophic haemorrhage, hysterectomy, and ureteric injury. A more recent problem is the management of the second twin lying transversely in a secundigravida with a previous caesarean section scar. Uterine rupture can follow when external version has failed to correct a transverse lie and internal version is done. It is therefore worth considering elective section for twin pregnancy in a patient with a scarred uterus and no previous vaginal deliveries. It is also important that our neonatologists realise that elective section of multiple pregnancy is not without risk of atonic postpartum haemorrhage. To prevent this a high concentration oxytocin infusion is usually effective and anaesthetists can be prevailed upon to give intravenous ergometrine. New Cross Hospital, Wolverhampton WV100QP, UK 1. Samra JS,
ALAN M. SMITH
Spillance H, Mukoyoko J, Tang L, Obhrai MS. Caesarean section for the Br J Obstet Gynaecol 1986; 154: 936-39.
birth of the second twin.
SiR,—Your editorial on the delivery of the second twin was prompted by reports from two Birmingham hospitals of an increase between 1986 and 1988 in the rate of caesarean section for the birth of the second twin after vaginal delivery of the first (6-11%1 and 6’5%2). The hospitals have also reported a rise in caesarean section rate to 20%.3 Southmead Hospital, Bristol, has one of the largest maternity units in the UK. In 1988 there were 5883 deliveries, 600 caesarean sections (10-28%), and a perinatal mortality rate (PNMR)of7’8 per 1000 births. Between 1987 and 1989 there were 197 twin deliveries with no stillbirths and 3 neonatal deaths (15 -2 per 1000). There were 28 caesarean sections (14-2%), of which 4 were for the second twin, the reasons given being shoulder presentation (3) and compound presentation (1). There was no attempt at internal podalic version. D. K. James and I suggested that a rise in the rate of caesarean section is not an inevitable part of modem obstetric careWe report a low rate of caesarean section for the second twin and suggest that the Birmingham experience may not be widespread. There has been