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Pelvimetry and breech delivery at term
THE LANCET
COMMENTARY decisions about possible rabies exposure can be avoided. This practice will also help ensure that postexposure prophylaxis is provided to those who have probable contact with the small percentage of bats that prove to be rabid.
John G Debbie, Charles V Trimarchi New York State Department of Health, Albany, NY 12201-0509, USA 1 2 3 4
5
6
7 8
WHO. Prevention of rabies in humans. In: WHO Expert Committee on rabies: eighth report. WHO Tech Rep Ser 1992; 824: 21–26. Scatterday JE, Galton MM. Bat rabies in Florida. Vet Med 1954; 49: 133–55. Childs JE, Trimarchi CV, Krebs JW. The epidemiology of bat rabies in New York State. Epidemiol Infect 1994; 113: 501–11. Smith JS. New aspects of rabies with an emphasis on epidemiology, diagnosis, and prevention of the disease in the United States. Clin Microbiol Rev 1996; 9: 166–76. Whitby JE, Johnstone G, Parsons G, King AA, Hutson A. Ten-year survey of British bats for the existence of rabies.Vet Rec 1996; 20: 491–93. Lafon M, Herzog M, Sureau P. Human rabies vaccines induce neutralizing antibodies against the European bat rabies virus (Duvenhage). Lancet 1986; ii: 515. CDC. Human rabies - Montana and Washington, 1997. Morbid Mortal Weekly Rep 1997; 46: 770–74. Feder HM, Nelson R, Reiher HW. Bat bite? Lancet 1997; 350: 1300.
Pelvimetry and breech delivery at term See page 1799 Breech presentation at term accounts for 2–4% of all deliveries. It has been one of the most contentious areas of obstetric practice. The primary issue is the safety of vaginal breech birth for the infant. A policy of universal caesarean section is likely to increase risk of morbidity for the mother. Recent systematic analyses of published work1,2 have concluded that there is a small excess risk of mortality and serious morbidity attributable to vaginal breech birth. Both these reviews commented on the poor standard of retrospective and prospective research in this area and noted that published randomised studies show no difference in outcome between planned vaginal and planned caesarean deliveries.1 Some recent population series3,4 seem to confirm an increased risk, but others5–7 have been unable to demonstrate any short-term or longterm neurodevelopmental disadvantage to vaginal breech birth. Whatever the debate over relative risks, the absolute risks are small. In the two Scandinavian series4,7 the risk of intrapartum or early neonatal loss or both was 2·6 and 0·9 per 1000 vaginal breech deliveries. Increasingly, the view that a universal policy of caesarean section is appropriate is being challenged. Concern is focused largely on asphyxial and traumatic complications of fetopelvic disproportion. In all studies of vaginal breech birth some form of selection takes place to minimise these risks. Selection criteria generally include type of breech presentation, attitude of the fetal head, fetal size, and size of the maternal pelvis. There is agreement that both footling presentation and hyperextension of the fetal neck are contraindications to vaginal delivery,1,5 and that breech fetuses estimated to weigh over 4000 g should not undergo a trial of vaginal delivery.1,2,5 There is no such consensus on how to assess the adequacy of the maternal pelvis. The maternal pelvis can be assessed either by clinical pelvic examination or by radiological pelvimetry.
Vol 350 • December 20/27, 1997
Radiological pelvimetry plays an diminishing role in modern obstetrics because the best “pelvimeter” is the fetal head. Radiological pelvimetry is of no proven benefit in cephalic presentations. For breech presentations the overwhelming majority of reports reviewed by Cheng and Hannah1 cited X-ray pelvimetry as a selection criterion for allowing vaginal birth. However, they and others concluded that there is no good evidence to support the view that information on pelvic size by X-ray pelvimetry influences either perinatal mortality or the rate of successful vaginal delivery. Its value has not been subjected to testing in a randomised trial. Nevertheless, X-ray pelvimetry remains a common procedure. Its aim is to identify those women for whom mechanical difficulties might lead to excess mortality or morbidity due to trauma. Women not selected out in this way should have a high chance of successful and safe vaginal breech birth. The emergency caesarean section rate should fall. This effect is important because maternal morbidity is higher for emergency than for elective caesarean sections. In this issue of The Lancet, Aren van Loon and colleagues from the Netherlands have reopened the debate by reporting a randomised trial of the effect on clinical outcome of the newer but well-validated technique of magnetic-resonance (MR) pelvimetry. In this study women with breech presentations at term underwent standard MR pelvimetry. The normal pelvis was clearly defined. Results were available randomly to clinicians in charge of the cases. The availability of this information increased the elective caesarean section rate but substantially lowered the emergency caesarean section rate. 24% of women who were selected for vaginal delivery underwent emergency caesarean section in the group whose MR pelvimetry measurements were available, compared with 41% in the control group. The result was an increased vaginal breech birth rate despite more elective caesarean sections in the study arm. How MR pelvimetry increased the rate of successful vaginal delivery is not clear. MR pelvimetry may select cases accurately, but equally likely is that knowledge that the pelvis is adequate gives clinicians the confidence to allow women an attempt at vaginal breech birth, and to manage these labours without fear of borderline bony disproportion. The investigators have therefore gone some way to answer the question of the clinical efficacy of radiological pelvimetry. The debate over the safety of vaginal breech birth for the infant and the safety of the mother at caesarean section continues. The hope is that the answer to this question will come from the multinational Term Breech Trial, funded by the Canadian Medical Research Council, which started recruiting in January, 1997.
S A Walkinshaw Fetal Centre, Liverpool Women’s Hospital, Liverpool LA 7SS, UK 1 2
3 4 5
Cheng M, Hannah M. Breech delivery at term: a critical review of the literature. Obstet Gynecol 1993; 82: 605–18. Spellicy Gifford D, Morton SC, Fiske M, Kahn K. A meta-analysis of infant outcomes after breech delivery. Obstet Gynecol 1995; 85: 1047–54. Thorpe-Beeston JG, Banfield PJ, Saunders NJ. Outcome of breech delivery at term. BMJ 1992; 305: 746–47. Krebs L, Langhoff-Roos J, Weber T. Breech at term—mode of delivery? Acta Obstet Gynaecol Scand 1995; 74: 702–04. Schiff E, Friedman SA, Mashiach S, Hart O, Barkai G, Sibai BM. Maternal and neonatal outcome of 846 singleton breech deliveries:
1791
THE LANCET
COMMENTARY
6
7
seven year experience at a single centre. Am J Obstet Gynecol 1996; 175: 18–23. Danielian PJ, Wang J, Hall MH. Long term outcome by method of delivery in breech presentation at term: population based follow up. BMJ 1996; 312: 1451–53. Lindqvist A, Norden-Lindeberg S, Hanson U. Perinatal mortality and route of delivery in term breech presentations. Br J Obstet Gynaecol 1997; 104: 1288–91.
Understanding human parturition
dehydroepiandrosterone sulphate (DHEAS), which the fetal liver can convert to precursors of placental oestrogens; ● the placenta cannot convert oestrogen to progesterone, and instead uses maternal and fetal androgens; and ● maternal cortisol easily crosses the placenta, exposing the fetus to high basal levels, which prevents fetal cortisol from triggering labour. One hypothesis6 is that, at term, raised concentrations of oestriol stimulate placental 11β-hydroxysteroid dehydrogenase, which converts cortisol to inactive cortisone and thus lowers exposure of the fetus to maternal cortisol (figure, A). Negative feedback to the fetal pituitary releases fetal corticotropin, which stimulates fetal adrenal DHEAS production. This increases placental oestriol output, which, in turn, not only creates a positive feedback loop but also increases oxytocin, prostaglandins and gap junctions, leading to uterine contractions and cervical dilatation. Experiments in human trophoblasts done by J A Majzoub’s group3 provide another model, whereby cortisol blockade of progesterone serves to initiate parturition (figure, B). At term, massive fetal adrenal cortisol output not only induces fetal lung maturity but also competes with progesterone for glucocorticoidreceptor binding, thereby blocking progesterone inhibition of the placental corticotropin-releasinghormone (CRH) gene. This paradoxically increases placental CRH, which augments fetal corticotropin production. Raised fetal corticotropin stimulates fetal adrenal cortisol and DHEAS production. DHEAS serves as the substrate for placental oestrogen synthesis, which then initiates the events culminating in labour and delivery.3 The pathogenesis of dysfunctional labour (affecting 3–8% of parturient women) has been even less investigated than has normal parturition. Uterine oestrogen-receptor and progesterone-receptor levels during dysfunctional labour are not known but, compared with patients in normal labour, those with dysfunctional labour have lower myometrial oxytocin-
Despite remarkable advances in the science and technology of reproduction, the signals initiating human parturition remain elusive. Scientists had initially been thrown off the scent by the relative simplicity of the hormonal regulation of sheep parturition. In sheep fetal cortisol triggers parturition by inducing placental enzymatic activities that enable progesterone (P4) conversion to oestradiol (E2).1 The resultant rise in E2/P4 ratio stimulates myometrial oxytocin receptors, gap junctions, prostaglandin production, and maternal pituitary oxytocin synthesis and release, events leading directly to labour and delivery.1 In human parturition the enigma is that these same pathways are activated at term despite raised circulating progesterone and an unaltered E2/P4 ratio. Also, our “trigger happy” search for a stimulus similar to fetal cortisol in the sheep has been somewhat frustrating, starting with oxytocin in the early 1900s, and going on to prostaglandins, growth factors, cytokines, nitric oxide withdrawal, endothelins, gap-junction formation, and, most recently, placental cortisol-releasing factor.2 The progesterone-withdrawal theory remains the leading hypothesis. Placental progesterone acts locally to suppress uterine contractility. This local block diminishes at term despite raised maternal serum progesterone. Although exogenous progesterone does not delay human labour in human beings as it does in sheep, antiprogestagens induce human uterine contractility and cervical ripening.3 Progesterone inhibits human myometrial contractions,4 and decreases gap-junction formation.5 An uncoupling of progesterone action has been proposed, to account for the start of parturition in the presence of high circulating progesterone levels. Possible uncoupling mechanisms include local Theories on human parturition metabolism, sequestration by Cortisol (active) A B a binding protein, decreased Placental 11β-HSD Oestriol progesterone receptor (PR) Fetal number or affinity, formation adrenal Cortisone (inactive) of an antiprogestagen, or inhibition by an endogenous antiprogestagen (ie, Maternal cortisol transforming growth factor , in the fetus Positive cortisol).6 The numbers of feedback Negative feedback on human decidual and established pituitary gland released myometrial oestrogen and progesterone receptors fall Fetal corticotropin release with advancing gestation and are undetectable at term.7-11 DHEAS Models of the human parturition cascade developed Progesterone Oxytocin synthesis, Progesterone production, from insight into differences uncoupling Uterine oxytocin receptors, + between sheep and human mechanism Number and size of gap junctions beings. Unlike sheep, in human beings: Labour and delivery ● the fetal adrenal produces 1792
Fetal lung maturation
Cortisol
Blocking inhibitory effect of progesterone on the placental CRH gene
Placental CRH
Fetal corticotropin
Fetal adrenal DHEAS Oestrogen Fetal Maternal/placental
Vol 350 • December 20/27, 1997
COMMENTARY decisions about possible rabies exposure can be avoided. This practice will also help ensure that postexposure prophylaxis is provided to those who have probable contact with the small percentage of bats that prove to be rabid.
John G Debbie, Charles V Trimarchi New York State Department of Health, Albany, NY 12201-0509, USA 1 2 3 4
5
6
7 8
WHO. Prevention of rabies in humans. In: WHO Expert Committee on rabies: eighth report. WHO Tech Rep Ser 1992; 824: 21–26. Scatterday JE, Galton MM. Bat rabies in Florida. Vet Med 1954; 49: 133–55. Childs JE, Trimarchi CV, Krebs JW. The epidemiology of bat rabies in New York State. Epidemiol Infect 1994; 113: 501–11. Smith JS. New aspects of rabies with an emphasis on epidemiology, diagnosis, and prevention of the disease in the United States. Clin Microbiol Rev 1996; 9: 166–76. Whitby JE, Johnstone G, Parsons G, King AA, Hutson A. Ten-year survey of British bats for the existence of rabies.Vet Rec 1996; 20: 491–93. Lafon M, Herzog M, Sureau P. Human rabies vaccines induce neutralizing antibodies against the European bat rabies virus (Duvenhage). Lancet 1986; ii: 515. CDC. Human rabies - Montana and Washington, 1997. Morbid Mortal Weekly Rep 1997; 46: 770–74. Feder HM, Nelson R, Reiher HW. Bat bite? Lancet 1997; 350: 1300.
Pelvimetry and breech delivery at term See page 1799 Breech presentation at term accounts for 2–4% of all deliveries. It has been one of the most contentious areas of obstetric practice. The primary issue is the safety of vaginal breech birth for the infant. A policy of universal caesarean section is likely to increase risk of morbidity for the mother. Recent systematic analyses of published work1,2 have concluded that there is a small excess risk of mortality and serious morbidity attributable to vaginal breech birth. Both these reviews commented on the poor standard of retrospective and prospective research in this area and noted that published randomised studies show no difference in outcome between planned vaginal and planned caesarean deliveries.1 Some recent population series3,4 seem to confirm an increased risk, but others5–7 have been unable to demonstrate any short-term or longterm neurodevelopmental disadvantage to vaginal breech birth. Whatever the debate over relative risks, the absolute risks are small. In the two Scandinavian series4,7 the risk of intrapartum or early neonatal loss or both was 2·6 and 0·9 per 1000 vaginal breech deliveries. Increasingly, the view that a universal policy of caesarean section is appropriate is being challenged. Concern is focused largely on asphyxial and traumatic complications of fetopelvic disproportion. In all studies of vaginal breech birth some form of selection takes place to minimise these risks. Selection criteria generally include type of breech presentation, attitude of the fetal head, fetal size, and size of the maternal pelvis. There is agreement that both footling presentation and hyperextension of the fetal neck are contraindications to vaginal delivery,1,5 and that breech fetuses estimated to weigh over 4000 g should not undergo a trial of vaginal delivery.1,2,5 There is no such consensus on how to assess the adequacy of the maternal pelvis. The maternal pelvis can be assessed either by clinical pelvic examination or by radiological pelvimetry.
Vol 350 • December 20/27, 1997
Radiological pelvimetry plays an diminishing role in modern obstetrics because the best “pelvimeter” is the fetal head. Radiological pelvimetry is of no proven benefit in cephalic presentations. For breech presentations the overwhelming majority of reports reviewed by Cheng and Hannah1 cited X-ray pelvimetry as a selection criterion for allowing vaginal birth. However, they and others concluded that there is no good evidence to support the view that information on pelvic size by X-ray pelvimetry influences either perinatal mortality or the rate of successful vaginal delivery. Its value has not been subjected to testing in a randomised trial. Nevertheless, X-ray pelvimetry remains a common procedure. Its aim is to identify those women for whom mechanical difficulties might lead to excess mortality or morbidity due to trauma. Women not selected out in this way should have a high chance of successful and safe vaginal breech birth. The emergency caesarean section rate should fall. This effect is important because maternal morbidity is higher for emergency than for elective caesarean sections. In this issue of The Lancet, Aren van Loon and colleagues from the Netherlands have reopened the debate by reporting a randomised trial of the effect on clinical outcome of the newer but well-validated technique of magnetic-resonance (MR) pelvimetry. In this study women with breech presentations at term underwent standard MR pelvimetry. The normal pelvis was clearly defined. Results were available randomly to clinicians in charge of the cases. The availability of this information increased the elective caesarean section rate but substantially lowered the emergency caesarean section rate. 24% of women who were selected for vaginal delivery underwent emergency caesarean section in the group whose MR pelvimetry measurements were available, compared with 41% in the control group. The result was an increased vaginal breech birth rate despite more elective caesarean sections in the study arm. How MR pelvimetry increased the rate of successful vaginal delivery is not clear. MR pelvimetry may select cases accurately, but equally likely is that knowledge that the pelvis is adequate gives clinicians the confidence to allow women an attempt at vaginal breech birth, and to manage these labours without fear of borderline bony disproportion. The investigators have therefore gone some way to answer the question of the clinical efficacy of radiological pelvimetry. The debate over the safety of vaginal breech birth for the infant and the safety of the mother at caesarean section continues. The hope is that the answer to this question will come from the multinational Term Breech Trial, funded by the Canadian Medical Research Council, which started recruiting in January, 1997.
S A Walkinshaw Fetal Centre, Liverpool Women’s Hospital, Liverpool LA 7SS, UK 1 2
3 4 5
Cheng M, Hannah M. Breech delivery at term: a critical review of the literature. Obstet Gynecol 1993; 82: 605–18. Spellicy Gifford D, Morton SC, Fiske M, Kahn K. A meta-analysis of infant outcomes after breech delivery. Obstet Gynecol 1995; 85: 1047–54. Thorpe-Beeston JG, Banfield PJ, Saunders NJ. Outcome of breech delivery at term. BMJ 1992; 305: 746–47. Krebs L, Langhoff-Roos J, Weber T. Breech at term—mode of delivery? Acta Obstet Gynaecol Scand 1995; 74: 702–04. Schiff E, Friedman SA, Mashiach S, Hart O, Barkai G, Sibai BM. Maternal and neonatal outcome of 846 singleton breech deliveries:
1791
THE LANCET
COMMENTARY
6
7
seven year experience at a single centre. Am J Obstet Gynecol 1996; 175: 18–23. Danielian PJ, Wang J, Hall MH. Long term outcome by method of delivery in breech presentation at term: population based follow up. BMJ 1996; 312: 1451–53. Lindqvist A, Norden-Lindeberg S, Hanson U. Perinatal mortality and route of delivery in term breech presentations. Br J Obstet Gynaecol 1997; 104: 1288–91.
Understanding human parturition
dehydroepiandrosterone sulphate (DHEAS), which the fetal liver can convert to precursors of placental oestrogens; ● the placenta cannot convert oestrogen to progesterone, and instead uses maternal and fetal androgens; and ● maternal cortisol easily crosses the placenta, exposing the fetus to high basal levels, which prevents fetal cortisol from triggering labour. One hypothesis6 is that, at term, raised concentrations of oestriol stimulate placental 11β-hydroxysteroid dehydrogenase, which converts cortisol to inactive cortisone and thus lowers exposure of the fetus to maternal cortisol (figure, A). Negative feedback to the fetal pituitary releases fetal corticotropin, which stimulates fetal adrenal DHEAS production. This increases placental oestriol output, which, in turn, not only creates a positive feedback loop but also increases oxytocin, prostaglandins and gap junctions, leading to uterine contractions and cervical dilatation. Experiments in human trophoblasts done by J A Majzoub’s group3 provide another model, whereby cortisol blockade of progesterone serves to initiate parturition (figure, B). At term, massive fetal adrenal cortisol output not only induces fetal lung maturity but also competes with progesterone for glucocorticoidreceptor binding, thereby blocking progesterone inhibition of the placental corticotropin-releasinghormone (CRH) gene. This paradoxically increases placental CRH, which augments fetal corticotropin production. Raised fetal corticotropin stimulates fetal adrenal cortisol and DHEAS production. DHEAS serves as the substrate for placental oestrogen synthesis, which then initiates the events culminating in labour and delivery.3 The pathogenesis of dysfunctional labour (affecting 3–8% of parturient women) has been even less investigated than has normal parturition. Uterine oestrogen-receptor and progesterone-receptor levels during dysfunctional labour are not known but, compared with patients in normal labour, those with dysfunctional labour have lower myometrial oxytocin-
Despite remarkable advances in the science and technology of reproduction, the signals initiating human parturition remain elusive. Scientists had initially been thrown off the scent by the relative simplicity of the hormonal regulation of sheep parturition. In sheep fetal cortisol triggers parturition by inducing placental enzymatic activities that enable progesterone (P4) conversion to oestradiol (E2).1 The resultant rise in E2/P4 ratio stimulates myometrial oxytocin receptors, gap junctions, prostaglandin production, and maternal pituitary oxytocin synthesis and release, events leading directly to labour and delivery.1 In human parturition the enigma is that these same pathways are activated at term despite raised circulating progesterone and an unaltered E2/P4 ratio. Also, our “trigger happy” search for a stimulus similar to fetal cortisol in the sheep has been somewhat frustrating, starting with oxytocin in the early 1900s, and going on to prostaglandins, growth factors, cytokines, nitric oxide withdrawal, endothelins, gap-junction formation, and, most recently, placental cortisol-releasing factor.2 The progesterone-withdrawal theory remains the leading hypothesis. Placental progesterone acts locally to suppress uterine contractility. This local block diminishes at term despite raised maternal serum progesterone. Although exogenous progesterone does not delay human labour in human beings as it does in sheep, antiprogestagens induce human uterine contractility and cervical ripening.3 Progesterone inhibits human myometrial contractions,4 and decreases gap-junction formation.5 An uncoupling of progesterone action has been proposed, to account for the start of parturition in the presence of high circulating progesterone levels. Possible uncoupling mechanisms include local Theories on human parturition metabolism, sequestration by Cortisol (active) A B a binding protein, decreased Placental 11β-HSD Oestriol progesterone receptor (PR) Fetal number or affinity, formation adrenal Cortisone (inactive) of an antiprogestagen, or inhibition by an endogenous antiprogestagen (ie, Maternal cortisol transforming growth factor , in the fetus Positive cortisol).6 The numbers of feedback Negative feedback on human decidual and established pituitary gland released myometrial oestrogen and progesterone receptors fall Fetal corticotropin release with advancing gestation and are undetectable at term.7-11 DHEAS Models of the human parturition cascade developed Progesterone Oxytocin synthesis, Progesterone production, from insight into differences uncoupling Uterine oxytocin receptors, + between sheep and human mechanism Number and size of gap junctions beings. Unlike sheep, in human beings: Labour and delivery ● the fetal adrenal produces 1792
Fetal lung maturation
Cortisol
Blocking inhibitory effect of progesterone on the placental CRH gene
Placental CRH
Fetal corticotropin
Fetal adrenal DHEAS Oestrogen Fetal Maternal/placental
Vol 350 • December 20/27, 1997