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Fetal postmortem weight loss in utero
86
CORRESPONDENCE
incontinence in the anterior pelvis (Fig. 1). Reinnervation of the myometrium following primary denervation at vaginal delivery is also asymmetrical and is frequently associated with chronic pelvic pain, menstrual disturbances and secondary dysmenorrhoea2. Each may be a consequence of the mechanics of vaginal delivery. Severe rectovaginal endometriosis frequently occurs in patients with uterine hyperstimulation following prostaglandin pessaries for induction of labour. Avulsion of uterosacral ligaments from their primary insertions into the posterior vaginal wall and rectovaginal septum not only causes significant primary damage but also disrupts the nerve bundles in the uterosacral ligaments3. Early retrograde menstruation while the injury is improving deposits endometrium, but it may be medium term reinnervation that is associated with the refractory pain. Similar reinnervation occurs in the bladder, uterus and vulva following a primary denervatory episode to account for other common sensory pelvic syndromes2. Lesser degrees of intrapartum damage may account for other patterns of parous endometriosis and their characteristic distributions. Ectopic endometrium may not account for very much of the pain in parous ‘endometriosis’.
References 1. Thalme B, Raabe N, Belfrage P. Lumbar epidural analgesia in labour: II. Effects on glucose, lactate, sodium, chloride, total protein, haematocrit and haemoglobin in maternal, fetal and neonatal blood. Acta Obstet Gynecol Scand 1974;53:113 – 119. 2. Jouppila R, Hollmen A. The effect of segmental epidural analgesia on maternal and foetal acid–base balance, lactate, serum potassium and creatinine phosphokinase during labour. Acta Anaesthesiol Scand 1976;20: 259 – 268. 3. Swanstro¨m S, Bratteby LE. Metabolic effects of regional analgesia and of asphyxia in the newborn infant during the first two hours after birth: III. Adjustment of arterial blood gases and acid – base balance. Acta Paediatr Scand 1981;70:811 – 818.
Felicity Reynolds St Thomas’ Hospital, London, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 4 3 - 8
References Fetal postmortem weight loss in utero 1. Chapron C, Fauconnier A, Dubuisson JB, Vieira M, Bonte H, VacherLaveu MC. Does deep endometriosis infiltrating the uterosacral ligaments present an asymmetric lateral distribution? Br J Obstet Gynaecol 2001;108:1021 – 1024. 2. Quinn MJ. Obstetric denervation — gynaecological reinnervation. Am J Obstet Gynecol 2002. In press. 3. Campbell RM. The anatomy and histology of the sacrouterine ligaments. Am J Obstet Gynecol 1950;59:1 – 12.
Martin Quinn Hinchingbrooke Hospital, Huntingdon, Cambridgeshire, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 4 2 - 6
Fetal and maternal lactate increase during active second stage of labour (what about the effect of maternal analgesia?) Sir, I applaud Nordstro¨m et al. (2001;108:263 – 268 [March]) for their thorough measurements of fetal and maternal lactate concentrations during the second stage of labour. They believe, however, that this is the first time such measurements have been made longitudinally. While others may not have made multiple measurements during the second stage, they have measured a rise in fetal and maternal lactate concentrations between the start and the end of the second stage of labour1,2 and a decline in the first two hours of life3. These earlier workers, moreover, compared these and many other changes (arterial blood gases, pH, base excess, glucose, glycerol, free fatty acids, electrolytes, plasma proteins etc.) in two groups of women: those receiving epidurals and those receiving so-called conventional or no analgesia (‘controls’). All reported lower lactate levels in epidural than in control mothers and their babies. Moreover, many other randomised and observational comparisons of epidural with systemic analgesia have shown a less severe metabolic acidosis at birth in babies of mothers receiving epidural analgesia (Reynolds et al., submitted to the BJOG). In the current climate of disclosing risks and benefits of various elements of obstetric intervention, is it right that women are informed of all the possible maternal complications of epidural analgesia, without disclosing the possible benefits to the baby?
Sir, Chard1 recently addressed the issue of weight loss in utero following fetal death at 24 – 32 weeks of gestation. He concluded that, although stillbirth weights were lower than live birth weights for gestation, many stillbirths may have a normal ‘true’ adjusted weight and would therefore be unlikely to be predicted by studies of fetal size alone. It is, as stated1, well recognised that stillbirth weights are lower than live birth weights at all gestations2. Furthermore, the in utero changes that occur postmortem are well reported and are due to a combination of the effects of maceration and tissue autolysis2, with resultant fetal tissue loss over a long period, as evidenced by the presence of a residual shrunken fetus at term in cases of twin pregnancies complicated by single intrauterine death in midtrimester. In order to account for at least some aspects of postmortem weight change, pathologists predominantly rely on organ weight ratios rather than actual body or organ weights to diagnose intrauterine growth restriction. Using organ weight data from live birth and stillbirth series2, organ weights are lower in stillbirths, but the brain/liver weight ratio, although marginally higher than for live births, remains within the normal range (3 – 4:1). Only when such a ratio is markedly abnormal (5 – 6:1) is the diagnosis of chronic intrauterine growth restriction due to uteroplacental insufficiency provided3, and in most of these cases, there will also be histological evidence of uteroplacental disease in the placenta. Using these criteria, only around 10% of stillbirths, most of which occur antepartum, are registered with intrauterine growth restriction as the likely cause of death3. Most cases of stillbirth therefore remain ‘unexplained’. These data, along with the conclusions of Chard1, further highlight the need for both detailed perinatal postmortem examination in all cases of stillbirth and the importance of adequate communication of the full clinical history and all relevant investigations between obstetrician and pathologist in order that improved understanding of the true aetiologies of stillbirth may be achieved.
References 1. Chard T. Does the fetus lose weight in utero following fetal death: a study in preterm infants. Br J Obstet Gynaecol 2001;108:1113 – 1115.
D RCOG 2003 Br J Obstet Gynaecol 110, pp. 83 – 93
CORRESPONDENCE 2. Wigglesworth JS, Singer DB. Textbook of Fetal and Perinatal Pathology. London, UK: Blackwell, 1998. 3. Kalousek DK. Fetal death, stillbirth and neonatal death. In: GilbertBarness E, editor. Potter’s Atlas of Fetal and Infant Pathology, 1998: 50 – 54.
N. J. Sebire Great Ormond Street Hospital for Children, London Department of Histopathology, London, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 4 5 - 1
Remote consequences of transcervical resection of the endometrium Sir, We congratulate Cooper et al. on their five-year follow up of patients following transcervical resection of the endometrium or medical treatment for menstrual problems. They conclude that transcervical resection of the endometrium ‘does not lead to an increase in the number of subsequent hysterectomies’ and recommend the procedure ‘being offered to all eligible women seeking treatment for heavy menses’1. Mean age of the transcervical resection of the endometrium group was 41 years and hysterectomy rate was 19% at five years follow up, compared with 41 years and 18%, respectively, in the medically treated group. The endometrial – myometrial interface is the site of a significant nerve plexus2. In a small series of women undergoing transcervical resection of the endometrium, we have observed nerves in the resected chippings. Furthermore, in women with severe adenomyosis, there is denervation of large areas of the uterus. Not knowing the long term consequences of the operation, are the authors confident that the transcervical resection of the endometrium group will not require hysterectomy for adenomyosis in their remaining reproductive years? Is there any difference in their management of 35and 45-year-old patients with excessive menstrual loss, or would they recommend endometrial resection to both?
References
87
to have a smaller baby, in his remarks on the article by Essen et al.1 in the same copy of the Journal. This finding should not be startling. Rush2 has pointed out that in many different cultures women deliberately reduce their intake of food in order to try to ensure a smaller baby. A big baby can mean obstructed labour and perhaps death of both baby and mother. There is often truth in folklore. In obstetrics, because of high perinatal mortality in small babies and obsessions with growth retardation, we have too long assumed that bigness in babies is necessarily good. Over the last 25 years, women in Europe and America have become heavier, with increased body mass indices. Babies have also become heavier and these two factors are probably related. While there are obviously many things which have driven up the caesarean section rate, increase in baby weight may be one of them. Although this idea does not meet with universal agreement, most studies show that bigger babies mean higher caesarean section rates3. The best single predictor of baby weight is prepregnancy maternal weight rather than weight gain in pregnancy per se. Undoubtedly, severe caloric restriction will reduce baby weight2. The factors which control baby weight are many and complex but, in countries where obesity is becoming an epidemic, we should think again about this matter. It should not be surprising that where high body mass indices are bad for maternal health they may also be harmful for the baby in the short and long term. The Somali women’s concern about having babies that are too big may not be so daft as it sounds.
References 1. Essen B, Johnsdotter S, Houelius B, et al. Qualitative study of pregnancy and childbirth experiences in Sweden. Br J Obstet Gynaecol 2000;106:1507 – 1512. 2. Rush D. Nutrition and maternal mortality in the developing world. Am J Clin Nutr 2000;72(Suppl):2125 – 2405. 3. Parrish KM, Holt VL, Easterling TR, Connell FA, Logerfo JP. Effect of changes in maternal age parity and birth weight distribution on primary caesarean delivery rates. JAMA 1994;271:443 – 447.
W. A. Liston Simpson Memorial Maternity Pavilion, Edinburgh, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 1 3 - X
1. Cooper KG, Jack SA, Parkin DE, Grant AM. Five year follow up of women randomised to medical management or transcervical resection of the endometrium for heavy menstrual loss: clinical and quality of life outcomes. Br J Obstet Gynaecol 2001;108:1222 – 1228. 2. Krantz KE. Innervation of the human uterus. Ann NY Acad Sci 1959; 75:770 – 784.
M. J. Quinna, N. Kirka, M. C. Slackb & M. D. Harrisb a Department of Gynaecology and Pathology, Hinchingbrooke District Hospital b Department of Gynaecology and Pathology, Peterborough District Hospital PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 2 8 0 4 - 5
Somalis in Sweden: are bigger babies better? Sir, The Editor comments on the ‘startling’ finding that Somali women in Sweden reduce their food intake in pregnancy in order D RCOG 2003 Br J Obstet Gynaecol 110, pp. 83 – 93
The effectiveness of the levonorgestrel-releasing intrauterine system in menorrhagia: a systematic review Sir, Dr Stewart et al.’s comment on effectiveness of the levonorgestrel-releasing intrauterine system (LNG-IUS) in the treatment of menorrhagia based on five small randomised trials and call for comparative trials on cost effectiveness or health related quality of life. We recently reported results of a randomised trial on the quality of life and cost effectiveness of the LNG-IUS versus hysterectomy in the treatment of menorrhagia1. Of 598 women referred for menorrhagia, 236 were eligible and randomly assigned to the LNG-IUS (n ¼ 119) or hysterectomy (n ¼ 117). Menstrual blood loss was objectively measured. Health related quality of life (HRQoL) was assessed using the SF 36 health survey and the EQ-5D questionnaire. Total costs were calculated. Anxiety, depression and sexuality-related factors were also assessed.
CORRESPONDENCE
incontinence in the anterior pelvis (Fig. 1). Reinnervation of the myometrium following primary denervation at vaginal delivery is also asymmetrical and is frequently associated with chronic pelvic pain, menstrual disturbances and secondary dysmenorrhoea2. Each may be a consequence of the mechanics of vaginal delivery. Severe rectovaginal endometriosis frequently occurs in patients with uterine hyperstimulation following prostaglandin pessaries for induction of labour. Avulsion of uterosacral ligaments from their primary insertions into the posterior vaginal wall and rectovaginal septum not only causes significant primary damage but also disrupts the nerve bundles in the uterosacral ligaments3. Early retrograde menstruation while the injury is improving deposits endometrium, but it may be medium term reinnervation that is associated with the refractory pain. Similar reinnervation occurs in the bladder, uterus and vulva following a primary denervatory episode to account for other common sensory pelvic syndromes2. Lesser degrees of intrapartum damage may account for other patterns of parous endometriosis and their characteristic distributions. Ectopic endometrium may not account for very much of the pain in parous ‘endometriosis’.
References 1. Thalme B, Raabe N, Belfrage P. Lumbar epidural analgesia in labour: II. Effects on glucose, lactate, sodium, chloride, total protein, haematocrit and haemoglobin in maternal, fetal and neonatal blood. Acta Obstet Gynecol Scand 1974;53:113 – 119. 2. Jouppila R, Hollmen A. The effect of segmental epidural analgesia on maternal and foetal acid–base balance, lactate, serum potassium and creatinine phosphokinase during labour. Acta Anaesthesiol Scand 1976;20: 259 – 268. 3. Swanstro¨m S, Bratteby LE. Metabolic effects of regional analgesia and of asphyxia in the newborn infant during the first two hours after birth: III. Adjustment of arterial blood gases and acid – base balance. Acta Paediatr Scand 1981;70:811 – 818.
Felicity Reynolds St Thomas’ Hospital, London, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 4 3 - 8
References Fetal postmortem weight loss in utero 1. Chapron C, Fauconnier A, Dubuisson JB, Vieira M, Bonte H, VacherLaveu MC. Does deep endometriosis infiltrating the uterosacral ligaments present an asymmetric lateral distribution? Br J Obstet Gynaecol 2001;108:1021 – 1024. 2. Quinn MJ. Obstetric denervation — gynaecological reinnervation. Am J Obstet Gynecol 2002. In press. 3. Campbell RM. The anatomy and histology of the sacrouterine ligaments. Am J Obstet Gynecol 1950;59:1 – 12.
Martin Quinn Hinchingbrooke Hospital, Huntingdon, Cambridgeshire, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 4 2 - 6
Fetal and maternal lactate increase during active second stage of labour (what about the effect of maternal analgesia?) Sir, I applaud Nordstro¨m et al. (2001;108:263 – 268 [March]) for their thorough measurements of fetal and maternal lactate concentrations during the second stage of labour. They believe, however, that this is the first time such measurements have been made longitudinally. While others may not have made multiple measurements during the second stage, they have measured a rise in fetal and maternal lactate concentrations between the start and the end of the second stage of labour1,2 and a decline in the first two hours of life3. These earlier workers, moreover, compared these and many other changes (arterial blood gases, pH, base excess, glucose, glycerol, free fatty acids, electrolytes, plasma proteins etc.) in two groups of women: those receiving epidurals and those receiving so-called conventional or no analgesia (‘controls’). All reported lower lactate levels in epidural than in control mothers and their babies. Moreover, many other randomised and observational comparisons of epidural with systemic analgesia have shown a less severe metabolic acidosis at birth in babies of mothers receiving epidural analgesia (Reynolds et al., submitted to the BJOG). In the current climate of disclosing risks and benefits of various elements of obstetric intervention, is it right that women are informed of all the possible maternal complications of epidural analgesia, without disclosing the possible benefits to the baby?
Sir, Chard1 recently addressed the issue of weight loss in utero following fetal death at 24 – 32 weeks of gestation. He concluded that, although stillbirth weights were lower than live birth weights for gestation, many stillbirths may have a normal ‘true’ adjusted weight and would therefore be unlikely to be predicted by studies of fetal size alone. It is, as stated1, well recognised that stillbirth weights are lower than live birth weights at all gestations2. Furthermore, the in utero changes that occur postmortem are well reported and are due to a combination of the effects of maceration and tissue autolysis2, with resultant fetal tissue loss over a long period, as evidenced by the presence of a residual shrunken fetus at term in cases of twin pregnancies complicated by single intrauterine death in midtrimester. In order to account for at least some aspects of postmortem weight change, pathologists predominantly rely on organ weight ratios rather than actual body or organ weights to diagnose intrauterine growth restriction. Using organ weight data from live birth and stillbirth series2, organ weights are lower in stillbirths, but the brain/liver weight ratio, although marginally higher than for live births, remains within the normal range (3 – 4:1). Only when such a ratio is markedly abnormal (5 – 6:1) is the diagnosis of chronic intrauterine growth restriction due to uteroplacental insufficiency provided3, and in most of these cases, there will also be histological evidence of uteroplacental disease in the placenta. Using these criteria, only around 10% of stillbirths, most of which occur antepartum, are registered with intrauterine growth restriction as the likely cause of death3. Most cases of stillbirth therefore remain ‘unexplained’. These data, along with the conclusions of Chard1, further highlight the need for both detailed perinatal postmortem examination in all cases of stillbirth and the importance of adequate communication of the full clinical history and all relevant investigations between obstetrician and pathologist in order that improved understanding of the true aetiologies of stillbirth may be achieved.
References 1. Chard T. Does the fetus lose weight in utero following fetal death: a study in preterm infants. Br J Obstet Gynaecol 2001;108:1113 – 1115.
D RCOG 2003 Br J Obstet Gynaecol 110, pp. 83 – 93
CORRESPONDENCE 2. Wigglesworth JS, Singer DB. Textbook of Fetal and Perinatal Pathology. London, UK: Blackwell, 1998. 3. Kalousek DK. Fetal death, stillbirth and neonatal death. In: GilbertBarness E, editor. Potter’s Atlas of Fetal and Infant Pathology, 1998: 50 – 54.
N. J. Sebire Great Ormond Street Hospital for Children, London Department of Histopathology, London, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 4 5 - 1
Remote consequences of transcervical resection of the endometrium Sir, We congratulate Cooper et al. on their five-year follow up of patients following transcervical resection of the endometrium or medical treatment for menstrual problems. They conclude that transcervical resection of the endometrium ‘does not lead to an increase in the number of subsequent hysterectomies’ and recommend the procedure ‘being offered to all eligible women seeking treatment for heavy menses’1. Mean age of the transcervical resection of the endometrium group was 41 years and hysterectomy rate was 19% at five years follow up, compared with 41 years and 18%, respectively, in the medically treated group. The endometrial – myometrial interface is the site of a significant nerve plexus2. In a small series of women undergoing transcervical resection of the endometrium, we have observed nerves in the resected chippings. Furthermore, in women with severe adenomyosis, there is denervation of large areas of the uterus. Not knowing the long term consequences of the operation, are the authors confident that the transcervical resection of the endometrium group will not require hysterectomy for adenomyosis in their remaining reproductive years? Is there any difference in their management of 35and 45-year-old patients with excessive menstrual loss, or would they recommend endometrial resection to both?
References
87
to have a smaller baby, in his remarks on the article by Essen et al.1 in the same copy of the Journal. This finding should not be startling. Rush2 has pointed out that in many different cultures women deliberately reduce their intake of food in order to try to ensure a smaller baby. A big baby can mean obstructed labour and perhaps death of both baby and mother. There is often truth in folklore. In obstetrics, because of high perinatal mortality in small babies and obsessions with growth retardation, we have too long assumed that bigness in babies is necessarily good. Over the last 25 years, women in Europe and America have become heavier, with increased body mass indices. Babies have also become heavier and these two factors are probably related. While there are obviously many things which have driven up the caesarean section rate, increase in baby weight may be one of them. Although this idea does not meet with universal agreement, most studies show that bigger babies mean higher caesarean section rates3. The best single predictor of baby weight is prepregnancy maternal weight rather than weight gain in pregnancy per se. Undoubtedly, severe caloric restriction will reduce baby weight2. The factors which control baby weight are many and complex but, in countries where obesity is becoming an epidemic, we should think again about this matter. It should not be surprising that where high body mass indices are bad for maternal health they may also be harmful for the baby in the short and long term. The Somali women’s concern about having babies that are too big may not be so daft as it sounds.
References 1. Essen B, Johnsdotter S, Houelius B, et al. Qualitative study of pregnancy and childbirth experiences in Sweden. Br J Obstet Gynaecol 2000;106:1507 – 1512. 2. Rush D. Nutrition and maternal mortality in the developing world. Am J Clin Nutr 2000;72(Suppl):2125 – 2405. 3. Parrish KM, Holt VL, Easterling TR, Connell FA, Logerfo JP. Effect of changes in maternal age parity and birth weight distribution on primary caesarean delivery rates. JAMA 1994;271:443 – 447.
W. A. Liston Simpson Memorial Maternity Pavilion, Edinburgh, UK PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 1 8 1 3 - X
1. Cooper KG, Jack SA, Parkin DE, Grant AM. Five year follow up of women randomised to medical management or transcervical resection of the endometrium for heavy menstrual loss: clinical and quality of life outcomes. Br J Obstet Gynaecol 2001;108:1222 – 1228. 2. Krantz KE. Innervation of the human uterus. Ann NY Acad Sci 1959; 75:770 – 784.
M. J. Quinna, N. Kirka, M. C. Slackb & M. D. Harrisb a Department of Gynaecology and Pathology, Hinchingbrooke District Hospital b Department of Gynaecology and Pathology, Peterborough District Hospital PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 2 8 0 4 - 5
Somalis in Sweden: are bigger babies better? Sir, The Editor comments on the ‘startling’ finding that Somali women in Sweden reduce their food intake in pregnancy in order D RCOG 2003 Br J Obstet Gynaecol 110, pp. 83 – 93
The effectiveness of the levonorgestrel-releasing intrauterine system in menorrhagia: a systematic review Sir, Dr Stewart et al.’s comment on effectiveness of the levonorgestrel-releasing intrauterine system (LNG-IUS) in the treatment of menorrhagia based on five small randomised trials and call for comparative trials on cost effectiveness or health related quality of life. We recently reported results of a randomised trial on the quality of life and cost effectiveness of the LNG-IUS versus hysterectomy in the treatment of menorrhagia1. Of 598 women referred for menorrhagia, 236 were eligible and randomly assigned to the LNG-IUS (n ¼ 119) or hysterectomy (n ¼ 117). Menstrual blood loss was objectively measured. Health related quality of life (HRQoL) was assessed using the SF 36 health survey and the EQ-5D questionnaire. Total costs were calculated. Anxiety, depression and sexuality-related factors were also assessed.