British Journal of Obstetrics and Gynaecology July 1992, Vol. 99, pp. 625-627

CORRESPONDENCE

Prenatal microbiological risk factors associated with preterm birth Dear Sir, We found the study by McDonald et a/. (1992) interesting and a valuable contribution to our understanding of the aetiology of preterm labour. Bacterial vaginosis has been considered to be important in the aetiology of preterm labour for some time and studies conducted by Saling (1 99 1) have shown that early detection and correction of disturbances in the vaginal flora can reduce the occurrence of early preterm delivery. The two groups of micro-organisms hypothesized are interesting. The direct production of phospholipase by Gardnerella vaginalis and Ureaplasma urealyticum would result in a general increase in prostaglandin production (PGE, and PGF,,). The response to the enteropharyngeal organisms, however, would depend on the bacterial toxin composition of the particular organism. Bacterial toxins or lipoteichoic acid have been shown to act on uterine decidua to cause increased formation of cytokines (Casey et al. 1989; Romero et al. 1989). Cachetin/tumour necrosis factor-a ;TNF-a) is synthesized and secreted by human decidual cells in response to lipoteichoic acid and may also cause an increase in PGF,, production. In addition, in amnion cells in monolayer culture, TNF-a, has been shown to stimulate PGE, formation (Casey et al. 1989). Therefore, both PGF,, and PGE, may be released in response to a bacterial challenge. PGF,, is known primarily to stimulate myometrial activity, whilst the main effect of PGE, is to change the physical properties of the cervix by an alteration in its composition. Depending on the effect of the infecting organism on the decidua, varying quantities of both PGF,, and PGE, would be released. Where there is a predominance of PGF?, contractions would be stimulated, but as long as there was no change in the state of the cervix, labour would not progress (OIBh & Gee 1992). This may explain the association of U. urealyticum with preterm labour and the lack of an association with preterm delivery (Minkoff et al. 1984). However, if the release of PGE, predominates, then cervical change is possible, and in such cases little myometrial activity is required to effect delivery. Therefore, where cervical change is significant, delivery is inevitable ( O M & Gee 1992). It is with such cases that an impact will be made in the prevention of preterm delivery if correct identification of at-risk pregnancies can be made. A more comprehensive understanding of the complex biomolecular events that lead to the formation of the prostaglandins, and their relative production in response to various micro-organisms may lead to a better understanding of the pathophysiology of idiopathic preterm labour and delivery. Further studies on the infective aetiology of idiopathic preterm labour are required. Karl S. Olah Clinical Research Fellow

Harry Gee Senior Lecturer Department of Fetal Medicine Birmingham University Birmingham Maternity Hospital Edghaston Birmingham B15 2TG

References Casey M. L., Cox S. M., Beutler B., Milewich L. & McDonald P. C. (1989) Cachetin/tumor necrosis factor-A formation in human decidua. J Clin Invest 83.430436.

McDonald H. M., O’Loughlin J. A., Jolley P., Vigneswaran R., McDonald P. J. &McDonald P. J. (1992) Prenatal microbiological risk factors associated with preterm birth. Br J Ohstet Gynaecol 99, 190-196. Minkoff H., Grunebaum A. N., Schwartz R. H. et al. (1984) Risk factors for prematurity and premature rupture of membranes. A prospective study of the vaginal floral in pregnancy. Am J Ohstet Gynecol 150,965-972. Ollh K. S. &Gee H. (1992) The prevention of preterm deliverydan we afford to continue to ignore the cervix? (Commentary) Br J Ohstet Gynaecol99,278-280. Romero R., Brody T., Oyarzun E., Mazor M., King Wu Y., Hobbins J. C. & Durum S. K. (1989) Infection and labour. 111. Interleukin-I: A signal for the onset of parturition. Am J Ohstet Gynecol 160, 11 17-1 123. Saling E. (1991) Effective measures for prevention of late abortions and early premature births. J Perinat Med 19 (supplement 2), 10.

The implications of introducing the symphysealfundal height-measurement. A prospective randomized controlled trial Dear Sir, There is a serious weakness in most of the research on symphysisfundus height measurements and the paper by Lindhard et al. (1990) illustrates this very well. How can you test a method’s validity if it is not given the opportunity to show its full potential? In this paper only three S-F measurements were taken during the whole pregnancy and in 21% only one or two. With so few measurements it is not worth doing it at all! The Oxford Clinical Trial Data Base Editor’s conclusion regarding this paper was ‘It would seem unwise to abandon the use of symphysis fundal height measurement unless a much larger trial likewise suggests that it is unhelpful’. Galbraith et al. (1979) commented ‘The clinical prediction of IUGR in . . . low risk patients is heavily dependent on the serial measurement of fundal height in order to demonstrate plateauing or static fetal growth’. At this hospital SF measurements have been used on every pregnant woman at every antenatal visit since 1976. Our original method was rather rough but, since 1981, we have used the method described by Westin (1977). Since 1984, the method has also been used nationally in all government antenatal clinics. Perinatal mortality covering about 8000 deliveries at Ramotswa has fallen to a record low level of 18/1000 at a time when the perinatal mortality rate at most district hospitals in Africa is at least 30/1000 and often as much as 60/1000. What is most noteworthy about these figures is that since 1981, the stillbirth and neonatal death rate had been consistently low although the figure elsewhere is in the region of 2.5 to 3. Of the only two stillbirths which occurred after admission to hospital last year, both showed clear failure of fetal growth on their flat S-F graphs. The problem was not whether the graph indicated fekd growth impairment or not but when was the best moment to intervene? Both babies died inutero suddenly and unexpectedly, and we clearly waited far too long. Those who have never used the graph regularly in woman after woman throughout pregnancy are not in any position to make useful comments on its value, even after elegant research and apparently significant statistics. None of the doctors who have worked here and who

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626 c O R R E s PON D E N C E have used the graph over the years would ever go back to the blind guesswork of pre-SF days. One of the commonest objections to using the graph is that it will increase interference and the caesarean section rate. Our section rate for many years was 5% and has never gone above lo%! But the graph has many other uses; the early diagnosis of twins, the detection of polyhydramnios, the usefulness in estimating fatal size in breech and cephalo-pelvic disproportion and the indication of fetal abnormality as in anencephaly when S-F height measurement and dates seem to be inconsistent. Also, the estimation of gestation when dates are not known or are clearly wrong, these problems are our daily bread and butter. What seems most to deter Western obstetricians from using the SF graph is the ready availability of high-tech methods for assessing fetal well-being. It must be remembered that most of the world’s women are not looked after by obstetric teams with all the latest aids to hand, but are, if they are lucky, looked after by general doctors and midwives, who may have little or no interest or experience in obstetrics. If these doctors come out to Africa thinking that without high-tech machines there is nothing they can do to assess pregnant women, how can we ever reduce the appalling statistics? They need every assistance in making the best of a bad job and for experts to argue about what are significant statistics while babies are dying in thousands is contributing nothing to solving Third World problems. Western centres of excellence have as great a responsibility to mothers in the Third World as they have to their own patients. Failure to use the partogram is another example. The partogram is still not being used everywhere in the Third World because of the ‘we can take it or leave it’ attitude of obstetricians in the West. The Third World will only follow if they lead. What you have to do is imagine yourself in a rural centre with only your eyes, ears and hands to help you and see what you make of your patient’s condition then! We desperately need you to give the lead. Please don’t let us down. Ian Kennedy Bamalete Lutheran Hospital Box 6 Ramotswa Botswana

References Galbraith R. S., Karchmar E. J., Piercy W. N. & Low J. A. (1979) The clinical prediction of IUGR. Am J Obsret Gynecol 133, 286. Lindhard A., Nielsen F? V., Mouritsen L. A,, Zachariassen A,, Serensen H. U. & Rosenfl H. (1990) The implications of introducing the symphyseal-fundal height measurement. A prospective randomized controlled trial. Br J Obstet GynaecoE97, 675480. Westin B. (1977) Gravidogram and fetal growth. Acta Obstet Gynecol Scand 56,273-282.

Platelets in pregnancy induced hypertension Dear Sir, With great interest we read the important article by Louden et al. (1991) in which they demonstrated a decreased platelet reactivity in women with pre-eclampsia. In the context of platelet activation in preeclampsia, the authors interpreted their observations as reflecting platelet exhaustion. This cross-sectional study performed with the most appropriate methods is very impressing, however, to our estimation the interpretation of changes associated with platelets in pregnancy hypertension need to be explained. At recent knowledge platelet-activating factor (PAF) has an important role in the female genital tract during human reproduction, including ovulation, fertilization, implantation, embryo development and initiation of parturition (Harper 1989). An increased consumption of platelets, resulting in a mild, transient thrombocytopenia in the mother

was observed as a first maternal response to pregnancy (O’Neill ef al. 1985). Most investigators agree that low grade chronic intravascular coagulation within the utero-placental circulation is part of the physiological response of all women to pregnancy (Letsky 1991). Wallenburg (1987) has suggested that activated platelets are involved in the pathogenesis of pre-eclampsia. The reports indicate, that there are many problems in the view of consideration and explanation associated with platelets in pregnancy. We therefore propose the following schematic explanation. The controlled activation of platelets is required in physiological pregnancy because of implantation, placental development, maintenance of placental blood flow, induction of labour, etc. In pregnancy-induced hypertension and pre-eclampsia there is a controlled hyperactivation of platelets (controlled by other regulatory mechanisms and by therapy). This hyperactivation of platelets, at least in part, may be physiological and contributes to the maintenance of placental blood supply, but has some pathophysiological consequences (e.g. high blood pressure, increased coagulability). In HELLP syndrome there is an uncontrolled hyperactivation of platelets with concomitant haemolysis, elevated liver enzymes and low platelet count. Using our terminology, the results of Louden et al. (1991) can be explained as the low reactivity of platelets is the consequence of their hyperfunction in pre-eclampsia, furthermore platelet exhaustion is the well documented sign of their hyperfunction. Jozsef Bodis Hans-Rudolf Tinneberg Attila Torok Volker Hanf University Women’s Hospital of Tiihingen W-7400 Tiibingen 1 Schleichstrasse 4 Germany

References Harper M. J. K. (1989) Platelet-activating factor: a paracrine factor in preimplantation stages of reproduction. Biol Reprod 40,907-912. Letsky E. A. (1991) Mechanisms of coagulation and the changes induced by pregnancy. Current Obstet Gynaecol 1,203-209. Louden K. A., Broughton Pipkin F., Heptinstall S., Fox S. C., Mitchell J. R. A. & Symonds E. M. (1991) Platelet reactivity and serum thromboxane B, production in whole blood in gestational hypertension and pre-eclampsia. Brd Obstet Gynaecol98, 1239-1244. O’Neill C., Gidley-Baird A. A., Pike J. L., Porter R. N., Sinosich M. J. & Saunders D. M. (1985) Maternal blood platelet physiology as a means of monitoring pre- and postimplantation embryo viability following in vitro fertilization. J I n Vitro Fertil Embryo Trans 2, 87-93. Wallenburg H. C. S., Dekker G. A., Markovitz J. W, & Rotmans P. (1986) Low-dose aspirin prevents pregnancy-induced hypertension and pre-eclampsia in angiotensin-sensitive primigravidae. Lancet i, 1-3.

Transvaginal sonography for fetal measurement in early pregnancy Dear Sir, I read the report by Kustermann ef al. (1992) with considerable interest as I have also been collecting data in the first trimester of pregnancy relating fetal size to gestational age. However, there are errors in the regression equations given in their report in Figs. 4 and 5. Inspection of the scatter plots shows that both equations should be simple linear rather than quadratic equations (the regression variables have been squared in error in both cases). Having taken this into account my data are similar to Kustermann’s data as they show that

The implications of introducing the symphyseal-fundal height-measurement. A prospective randomized controlled trial.

British Journal of Obstetrics and Gynaecology July 1992, Vol. 99, pp. 625-627 CORRESPONDENCE Prenatal microbiological risk factors associated with p...
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