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Rate of caesarean section and pregnancy outcome in women lawyers
RESEARCH LETTERS
aCL, have similar inhibitory activity towards trophoblast proliferation. This finding suggests that 2-glycoprotein-I contains the critical antigenic determinant upon which aCL exert their pathogenic activity. These findings have significant implications for understanding of the pathogenesis of aCL-mediated fetal loss. During implantation, villous cytotropholast cells are protected from maternal antibodies, first by the trophectoderm and then by syncytiotrophoblast. Therefore, villous cytotrophoblast cells would be unaffected by maternal aCL through early pregnancy. However, extravillous trophoblasts that invade maternal vessels (endovascular trophoblast) must proliferate in the presence of maternal blood. Thus, in a woman with aCL, proliferation of endovascular trophoblast cells would be inhibited, which would decrease the number and extent of vessels undergoing the essential physiological changes of pregnancy. This finding is consistent with a report that aCL inhibit outgrowth from mouse blastocysts.5 These proposed aetiopathogenic events would allow the development of the villous placenta, with inadequate implantation limiting the success of the pregnancy in aCL-positive women, leading to the obstetric complications associated with aCL. Our results raise a caveat about the use of heparin anticoagulant therapy for women who have aCL and recurrent fetal loss. Although heparin may have other effects in pregnancy, the aim of this treatment is to prevent thrombosis in the uteroplacental circulation. Heparin has, however, potentially significant side-effects and, if aCL disrupt pregnancy by a non-thrombotic mechanism, as our results suggest, the basis for use of heparin therapy (especially if the only clinical manifestation of aCL is recurrent first-trimester miscarriage) must be questioned. This research was funded by grants from the Auckland Research Medical Foundation, Health Research Council of New Zealand, and the Wellcome Trust. 1
2
3
4 5
Harris EN, Gharavi AE , Boey ML, et al. Aanticardiolipin antibodies: detection by radioimmunoassay and association with thrombosis in systemic lupus erythematosus. Lancet 1983; ii: 1211–14. Matsuura E, Igarashi Y, Yasuda T, Triplett DA, Koike T. Anticardiolipin antibodies recognise 2 glycoprotein 1 structure altered by interacting with an oxygen modified solid phase surface. J Exp Med 1994; 179: 457-62. Brosens I, Robertson WB, Dixon HG. The physiological response of the vessels of the placental bed to normal pregnancy. J Pathol Bacteriol 1967; 93: 569–79. Chamley LW, Allen JL, Johnson PM. Synthesis of 2 glycoprotein I by the human placenta. Placenta 1997; 18: 403–10. Sthoeger ZM, Mozes E, Tartakovsky B. Anti-cardiolipin antibodies induce pregnancy failure by impairing embryonic implantation. Proc Natl Acad Sci (USA) 1993; 90: 6464–67.
Departments of Obstetrics and Gynaecology (L Chamley; e-mail [email protected]), Pharmacology, and Clinical Pharmacology, University of Auckland, National Women’s Hospital, Epsom, Auckland, New Zealand; and Department of Immunology, University of Liverpool Medical School, Liverpool, UK
Rate of caesarean section and pregnancy outcome in women lawyers Marcia Persaud, Michael Geary, Jean Wilshin, Peter C Hindmarsh, Charles H Rodeck
£235 million was paid out by the UK National Health Service (NHS) in legal fees in 1997. The Health Secretary has accused lawyers of milking the health service for money needed to treat patients. Many of the larger claims are in Obstetrics and Gynaecology,1 and 70% of the money spent on medical litigation is spent on those specialties.2 There is a
1038
Lawyers (n=62)
Doctors (n=52)
Controls (n=62)
Induction of labour
13 (21%)
11 (21·1%)
10 (16·1%)
Mode of delivery Normal vaginal delivery Forceps Ventouse
45 (72·6%) 2 (3·2%) 10 (16·1%)
29 (55·8%) 1 (1·9%) 6 (11·5%)
35 (56·5%) 2 (3·2%) 8 (12·9)
5 (8·0%) 3 (4·8%) 2 (3·2%)
16 (30·8%) 10 (19·2%) 6 (11·6%)
17 (27·4%) 8 (12·9%) 9 (14·5%)
Caesarean section Total Elective Emergency
Induction of labour and mode of delivery in lawyers, doctors, and controls
suggestion that health carers may intervene in childbirth earlier and more frequently because of this rising trend of litigation. The UK government publication Changing Childbirth,3 has resulted in more informed choice and greater involvement of patients in their care, which may have some influence on rates of obstetric intervention and caesarean section. Obstetric management and mode of delivery may be influenced by a woman’s professional status. A study has suggested that the rate of caesarean section was no different among women who were doctors and those who were not, but there was a trend towards increased elective section for maternal requests in doctors.4 Although health carers should treat all pregnant women in the same way, there is suspicion that carers are wary of women lawyers, and may subconsciously change their usual management of labour and delivery for them. We determined the rate of caesarean section and pregnancy outcome in lawyers at University College London Hospitals, who were taking part in a study of fetal growth. These were compared with the 52 doctors previously reported,4 and also to a control group of women matched to the lawyers for age, parity, and socioeconomic status. Mean maternal age was 33 years (range 26–40); 43% were nulliparous and all were from socioeconomic group 1. Only one lawyer smoked during pregnancy. There were no sociodemographic differences between the three groups. Induction of labour and mode of delivery is shown in the table. Labour was induced in 21% of lawyers; five lawyers (8%) had a caesarean section, three elective. None of the sections were done for maternal request. Caesarean-section rate was lower in the lawyer group than in the other two groups, and than the overall rate at the hospital for 1997 (24·6%). The normal vaginal delivery rate was 73%, and 19% had instrumental delivery. There was no significant difference in pregnancy outcome. No lawyer had a preterm delivery, there were no perinatal deaths, and only one baby (1·6%) was transferred to the neonatal unit. A much larger number of lawyers would be needed to make statistically valid comparisons with the general population. However, our study suggests that lawyers are treated no differently to other women, and, if anything, they have a lower rate of caesarean section and a very low incidence of adverse pregnancy outcome, suggesting that health professionals do not vary their management of labour and delivery for lawyers. 1
2 3 4
Sloan FA, Whetten-Goldstein K, Stout EM, Entman SS, Hickson GB. No-fault system of compensation for obstetric injury: winners and losers. Obstet Gynecol 1998; 91: 437–43. Sanderson IM. Clinical Risk: a review of its present function. Clinical Risk 1998; 4: 37–43. Department of Health. Changing Childbirth: report of the Expert Maternity Group. 1993. Geary M, Wilshin J, Persaud M, Hindmarsh PC, Rodeck CH. Do doctors have an increased rate of Caesarean section. Lancet 1998; 351: 1177.
Departments of Obstetrics and Gynaecology (M Persaud), and Paediatric Endocrinology, University College London, London WC1E 6AU, UK.
THE LANCET • Vol 352 • September 26, 1998
aCL, have similar inhibitory activity towards trophoblast proliferation. This finding suggests that 2-glycoprotein-I contains the critical antigenic determinant upon which aCL exert their pathogenic activity. These findings have significant implications for understanding of the pathogenesis of aCL-mediated fetal loss. During implantation, villous cytotropholast cells are protected from maternal antibodies, first by the trophectoderm and then by syncytiotrophoblast. Therefore, villous cytotrophoblast cells would be unaffected by maternal aCL through early pregnancy. However, extravillous trophoblasts that invade maternal vessels (endovascular trophoblast) must proliferate in the presence of maternal blood. Thus, in a woman with aCL, proliferation of endovascular trophoblast cells would be inhibited, which would decrease the number and extent of vessels undergoing the essential physiological changes of pregnancy. This finding is consistent with a report that aCL inhibit outgrowth from mouse blastocysts.5 These proposed aetiopathogenic events would allow the development of the villous placenta, with inadequate implantation limiting the success of the pregnancy in aCL-positive women, leading to the obstetric complications associated with aCL. Our results raise a caveat about the use of heparin anticoagulant therapy for women who have aCL and recurrent fetal loss. Although heparin may have other effects in pregnancy, the aim of this treatment is to prevent thrombosis in the uteroplacental circulation. Heparin has, however, potentially significant side-effects and, if aCL disrupt pregnancy by a non-thrombotic mechanism, as our results suggest, the basis for use of heparin therapy (especially if the only clinical manifestation of aCL is recurrent first-trimester miscarriage) must be questioned. This research was funded by grants from the Auckland Research Medical Foundation, Health Research Council of New Zealand, and the Wellcome Trust. 1
2
3
4 5
Harris EN, Gharavi AE , Boey ML, et al. Aanticardiolipin antibodies: detection by radioimmunoassay and association with thrombosis in systemic lupus erythematosus. Lancet 1983; ii: 1211–14. Matsuura E, Igarashi Y, Yasuda T, Triplett DA, Koike T. Anticardiolipin antibodies recognise 2 glycoprotein 1 structure altered by interacting with an oxygen modified solid phase surface. J Exp Med 1994; 179: 457-62. Brosens I, Robertson WB, Dixon HG. The physiological response of the vessels of the placental bed to normal pregnancy. J Pathol Bacteriol 1967; 93: 569–79. Chamley LW, Allen JL, Johnson PM. Synthesis of 2 glycoprotein I by the human placenta. Placenta 1997; 18: 403–10. Sthoeger ZM, Mozes E, Tartakovsky B. Anti-cardiolipin antibodies induce pregnancy failure by impairing embryonic implantation. Proc Natl Acad Sci (USA) 1993; 90: 6464–67.
Departments of Obstetrics and Gynaecology (L Chamley; e-mail [email protected]), Pharmacology, and Clinical Pharmacology, University of Auckland, National Women’s Hospital, Epsom, Auckland, New Zealand; and Department of Immunology, University of Liverpool Medical School, Liverpool, UK
Rate of caesarean section and pregnancy outcome in women lawyers Marcia Persaud, Michael Geary, Jean Wilshin, Peter C Hindmarsh, Charles H Rodeck
£235 million was paid out by the UK National Health Service (NHS) in legal fees in 1997. The Health Secretary has accused lawyers of milking the health service for money needed to treat patients. Many of the larger claims are in Obstetrics and Gynaecology,1 and 70% of the money spent on medical litigation is spent on those specialties.2 There is a
1038
Lawyers (n=62)
Doctors (n=52)
Controls (n=62)
Induction of labour
13 (21%)
11 (21·1%)
10 (16·1%)
Mode of delivery Normal vaginal delivery Forceps Ventouse
45 (72·6%) 2 (3·2%) 10 (16·1%)
29 (55·8%) 1 (1·9%) 6 (11·5%)
35 (56·5%) 2 (3·2%) 8 (12·9)
5 (8·0%) 3 (4·8%) 2 (3·2%)
16 (30·8%) 10 (19·2%) 6 (11·6%)
17 (27·4%) 8 (12·9%) 9 (14·5%)
Caesarean section Total Elective Emergency
Induction of labour and mode of delivery in lawyers, doctors, and controls
suggestion that health carers may intervene in childbirth earlier and more frequently because of this rising trend of litigation. The UK government publication Changing Childbirth,3 has resulted in more informed choice and greater involvement of patients in their care, which may have some influence on rates of obstetric intervention and caesarean section. Obstetric management and mode of delivery may be influenced by a woman’s professional status. A study has suggested that the rate of caesarean section was no different among women who were doctors and those who were not, but there was a trend towards increased elective section for maternal requests in doctors.4 Although health carers should treat all pregnant women in the same way, there is suspicion that carers are wary of women lawyers, and may subconsciously change their usual management of labour and delivery for them. We determined the rate of caesarean section and pregnancy outcome in lawyers at University College London Hospitals, who were taking part in a study of fetal growth. These were compared with the 52 doctors previously reported,4 and also to a control group of women matched to the lawyers for age, parity, and socioeconomic status. Mean maternal age was 33 years (range 26–40); 43% were nulliparous and all were from socioeconomic group 1. Only one lawyer smoked during pregnancy. There were no sociodemographic differences between the three groups. Induction of labour and mode of delivery is shown in the table. Labour was induced in 21% of lawyers; five lawyers (8%) had a caesarean section, three elective. None of the sections were done for maternal request. Caesarean-section rate was lower in the lawyer group than in the other two groups, and than the overall rate at the hospital for 1997 (24·6%). The normal vaginal delivery rate was 73%, and 19% had instrumental delivery. There was no significant difference in pregnancy outcome. No lawyer had a preterm delivery, there were no perinatal deaths, and only one baby (1·6%) was transferred to the neonatal unit. A much larger number of lawyers would be needed to make statistically valid comparisons with the general population. However, our study suggests that lawyers are treated no differently to other women, and, if anything, they have a lower rate of caesarean section and a very low incidence of adverse pregnancy outcome, suggesting that health professionals do not vary their management of labour and delivery for lawyers. 1
2 3 4
Sloan FA, Whetten-Goldstein K, Stout EM, Entman SS, Hickson GB. No-fault system of compensation for obstetric injury: winners and losers. Obstet Gynecol 1998; 91: 437–43. Sanderson IM. Clinical Risk: a review of its present function. Clinical Risk 1998; 4: 37–43. Department of Health. Changing Childbirth: report of the Expert Maternity Group. 1993. Geary M, Wilshin J, Persaud M, Hindmarsh PC, Rodeck CH. Do doctors have an increased rate of Caesarean section. Lancet 1998; 351: 1177.
Departments of Obstetrics and Gynaecology (M Persaud), and Paediatric Endocrinology, University College London, London WC1E 6AU, UK.
THE LANCET • Vol 352 • September 26, 1998