Pelvic pain—are we any nearer the answer?
Training with Richard Beard at St Mary’s Hospital in Paddington (London, UK) in the 1970s and 1980s meant seeing lots of women with pelvic pain because it was for him a major research challenge. One simple rule of thumb I developed was that all women with undiagnosed pelvic pain deserve a laparoscopy, but that if it was negative, further operative intervention should be avoided whenever possible—unless it was intended to be a definitive treatment such as oophorectomy with hysterectomy (Beard et al. Br J Obstet Gynaecol 1991;98:988–92). Some women referred from elsewhere had had multiple laparoscopies with serious surgical complications from inadvertent bowel puncture, bleeding and infection. Primum, non nocere. Richard’s primary hypothesis was of ‘pelvic congestion’ (Foong et al. BJOG 2002;109:867–73), demonstrated by pelvic venograms and treated with drugs such as ergometrine (Reginald et al. Lancet 1987;2:351–353), or by estrogen suppression using progestogens (Reginald et al. Br J Obstet Gynaecol 1989;96:1148–52). Psychotherapy appeared only to be of value in conjunction with progestogens (Farquhar et al. Br J Obstet Gynaecol 1989;96:1153–62). Various sociopathic explanations such as previous sexual abuse were explored, but there were no definitive findings (Fry et al. J Psychosom Res 1997;42:1–15). So the search for an effective treatment short of oophorectomy and hysterectomy goes on. As recently as September this year, the results of the LUNA randomised controlled trial showed that laparoscopic uterosacral nerve ablation fails to improve pain, dysmenorrhoea, dyspareunia, or quality of life, compared with laparoscopy alone (Daniels et al. JAMA 2009;302:955–61). As many as one in seven women experience pelvic pain and yet it remains as much of a medical challenge today as it was 25 years ago. Accordingly, we are pleased to publish in this month’s issue a detailed exploration of the topic by Patwardhan et al. (page 1551). Their primary hypothesis is that the condition is caused by visceral hyperalgesia (cf. the irritable bowel syndrome). They suggest testing for effectiveness a new range of drugs not typically used in gynaecology—opioid agonists, serotonin receptor antagonists, mast cell inhibitors and immune modulators, among others. So anyone looking to continue the tradition of research into pelvic pain should read this article carefully. Pelvic pain is likely to provide many more higher degrees for researchers in the years to come.
Depression in pregnancy and outcome for the child
At any given time, as many as one in eight women will be troubled by depression, and for women, the lifetime risk of an episode is 20%. Although pregnancy may be protective, many women still face the dilemma of whether to take antidepressant drugs while they are pregnant. A particular concern is whether the drugs cross the placenta, influence the developing brain, and have permanent effects on the baby. Some studies published in BJOG have been reassuring (Maschi et al. BJOG 2008;115:283–9) whereas others have suggested almost a 10% risk of developmental delay (Deave et al. BJOG 2008;115:1043–51). In this month’s BJOG, Ververs et al. (page 1568) report a study of over 38 000 children (using data from an insurance company in the Netherlands) and found a relative risk of 5.6 (95% CI 1.8–17.4) of cardiac interventions such as surgery or catheterisation. Another recent study has shown an increase in the incidence of congenital heart disease in infants whose mothers took serotonin reuptake inhibitors prenatally (Oberlander et al. Res B Dev Reprod Toxicol 2008;83:68–76). Ververs et al. go so far as to suggest that continuing antidepressant use in pregnancy justifies detailed fetal echocardiography screening. The usual conclusion applies: further research is needed.
How likely is a recurrence of pre-eclampsia in the next pregnancy?
Most obstetricians will have been asked this question many times, and the answer remains unclear. One of the most influential studies was reported by Sibai et al. in 1991 (Sibai et al. Am J Obstet Gynecol 1991;165:1408–12). Of 169 women with severe pre-eclampsia in the second trimester who had another pregnancy, 65% had a recurrence of pre-eclampsia, 32% in the second trimester. Yet my own experience has been that the recurrence rate is less than this. My rule of thumb (I have lots of these) has been to advise women that in most cases if the pre-eclampsia did recur, it would on average start about 4 weeks later in gestation in a subsequent pregnancy. Perhaps the key to the high rate that Sibai et al. observed was that 35% of their patients had chronic hypertension; 67% if their pre-eclampsia recurred in the second trimester. So what is the risk in women with ‘pure’ pre-eclampsia (cases without diagnosed underlying chronic hypertension at the time of the index pregnancy)? On page 1578, McDonald et al. report on their study of over 188 000 women without chronic hypertension. Of these, 1954 had severe pre-eclampsia in the index pregnancy (1.1%). Pre-eclampsia recurred in the next pregnancy in fewer than 20%, and was severe in only 6.8%. As expected, the incidence was higher in older mothers and those with renal disease. When women have severe pre-eclampsia in their first pregnancy, they deserve close monitoring in their next pregnancy, but they can be reassured that most likely the outcome will be favourable.
Heart disease in pregnancy
Because of the success of cardiac surgery, growing numbers of women with repaired congenital heart disease are presenting to obstetricians for pregnancy care. One of the most difficult dilemmas is how to advise women with mechanical heart valves requiring anticoagulation. Warfarin is safer for the mother but because it crosses the placenta, it can cause embryopathy. It also anticoagulates the fetus, resulting in an increased risk of fetal brain haemorrhage with death or neurological dysfunction. On the other hand, although low-molecular-weight heparin does not cross the placenta, it is less efficient at preventing thrombosis of the valve. On page 1585, McLintock et al. report on the outcome of 47 pregnancies in women with mechanical heart valves. In 34, anticoagulation was primarily with enoxaparin, and in 13 it was with warfarin. There were seven cases of valve thrombosis, five associated with enoxaparin, and four perinatal deaths, three associated with warfarin. This substantial addition to previous data confirms the starkness of the dilemma facing the mother, who must be carefully counselled. I agree with the recent American College of Chest Physicians’ guidelines that the woman’s preference should be the deciding factor, as the overriding concern for many women is to avoid harm to their unborn child.
It is difficult to carry out randomised controlled trials in relation to uncommon disorders. Although congenital cardiac disease in pregnant women is now relatively common, there are many syndromes requiring different care, and so management remains largely based on case series. One of the priorities of preconception care is thorough evaluation to see if improvements in cardiac status can be made before pregnancy. On page 1593, Yap et al. report a series of 188 pregnancies in women with atrial septal defect. In 55 the defect had been repaired before pregnancy, and in 133 it remained open. Although the risk of cardiac complications was comparable, pregnancies in women with an unrepaired lesion were more likely to be associated with fetal loss (adjusted odds ratio 5.55) or small-for-gestational-age babies (adjusted odds ratio 1.95). In contrast, the neonatal outcome from pregnancies in women with a repaired lesion was not significantly different from the general population. These findings emphasise the importance of all women with congenital heart disease being assessed in a combined clinic with an obstetrician and cardiologist as soon as they are of an age when they might be contemplating pregnancy (certainly not later than 16 years old).
This month’s BJOG contains two stimulating hypotheses for further investigation. Gordon Smith on page 1613 has re-evaluated the well-known concept that older mothers are more likely to need instrumental delivery. He makes a good case for the hypothesis that it is actually length of time from the menarche (endocrine age) rather than length of time from their own birth (chronological age) that influences uterine function and the progress of labour. To further stimulate your brain cells, editor Anthony Odibo has added to it a series of ‘Journal Club’ questions to structure discussion of this fascinating hypothesis. Another intriguing hypothesis is the suggestion by Jordan et al. on page 1622 that routine administration of oxytocics at delivery to prevent postpartum haemorrhage reduces the likelihood of successful breastfeeding. Because theirs was an observational study, the potential for confounding was great and so we commissioned several mini-commentaries to discuss the significance of the finding.
What happens in China?
Despite a large proportion of the world’s population living in China, information about many basic aspects of their health and health care is scarce. In this issue we publish a paper which looks at the profile of the various forms of polycystic ovary syndrome (PCOS) in a large-scale Chinese population (H Zhang, page 1633). The authors conclude that there are significant racial differences, resulting in a lower metabolic risk associated with PCOS in the Chinese. XJ Zhang et al. (page 1640) have investigated current contraceptive choices and report that in a large population of rural married women in Anhui Province, sterilisation remains the most common choice (43.6%) followed by the intrauterine device (41.1%).
All our patients should be treated with dignity, respect and the best possible care, irrespective of colour, creed or nationality. But giving the best possible care does involve recognising the differences that exist between individuals, and giving treatment that is appropriate. Some of those differences are systematic between genetically distinct groups. There are a number of examples in this month’s issue of such differences, for example in the paper by H Zhang already described above. Another is in the paper by Mittal et al. (page 1671), who report that the high incidence of the IFN-γ + 874 AA genotype in the north Indian population may account for some of their increased risk of cervical cancer. This genotype is an example of a single nucleotide polymorphism (SNP, pronounced ‘snip’). Not sure what these are? Read Harley and Narod’s commentary (page 1556) for a wonderfully clear explanation. On page 1678, Alexander et al. report that in a multicentre London (UK) audit from January 2006 to June 2008, 68 of 74 children identified as having vitamin D deficiency had pigmented skin (46 were South Asian). Over half were severely deficient. They recommend that women with dark skins living in northern latitudes should routinely have their vitamin D status checked. All our patients should be given equal status; this often means treating them differently.