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Rapid Responses: Rapid Responses published:
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Why fetal blood sampling?
- Philip Steer (22 April 1999)
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Use of prostaglandins to induce labour in women with a CS scar
- T G Nash (29 April 1999)
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Why and when was the section?
- H S Gohar (3 May 1999)
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What was the purpose of publishing this paper?
- Nikolai Manassiev (12 May 1999)
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An avoidable disaster
- Philip Watters (12 May 1999)
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Mechanics of Uterine Rupture
- Ronnie Falcao (7 June 1999)
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New evidence of risks of misoprostol induction with vaginal birth after caesarean
- Marsden Wagner (13 August 1999)
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Philip Steer, Head of Maternal Fetal Medicine Imperial College School of Medicine
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This paper is an interesting and useful review of the use of prostaglandins for induction of labour in the presence of a uterine scar. However, I am concerned that the response to a complicated fetal tachycardia in the presence of a uterine scar was to prepare for fetal blood sampling. The first sign of scar rupture can be a fetal heart rate abnormality, and in this situation, a normal fetal pH does not mean that the labour should be allowed to continue. Following a similar case in which a delay in delivery associated with fetal blood sampling was regarded as indefensible by independent review, I have recommended immediate delivery if the fetal heart rate becomes abnormal in the presence of a uterine scar. I would be interested in other views on this. |
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T G Nash
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Dear Sir When I started to read the paper by Vause and Macintosh1 I immediately thought of your leader "Learning from history?"2. Before I reached the end of the first paragraph I knew there was a disaster waiting to happen and this proved to be correct. The paper should be a lesson to those in training how not to manage a labour, regardless of whether the woman has a scarred uterus or not, and will do nothing to further the debate on whether prostaglandins should be used to induce labour in women with a caesarean scar. The same care should be taken of a woman in labour after a previous caesarean section, whether the onset is spontaneous or induced by prostaglandins . During my apprenticeship I was taught that a "trial of scar" should only be allowed if there were no other unfavourable factors present. I would suggest that the need for induction because the woman is 10 days post term might be considered such a risk factor. The other dictum I learnt was the if a "trial of scar" is allowed progress should be straight forward and the woman delivered, or about to deliver, 6-8 hours from the onset of labour. This was clearly not the case and moreover additional unfavourable factors developed. This baby should not have been lost and no amount of evidence based medicine will bring it back. I submit that the outcome would not have been so disastrous if the art of obstetrics had been taught properly and more credence given to the experience of their seniors than the wonder of evidence based medicine. I am appalled that neither the authors nor, apparently, those attending the perinatal meeting considered that the ruptured uterus resulted from inappropriate use of oxytocin. The dangers of this drug have been known for so long that they must now be part of history. Yours faithfully T.G.Nash 1 Vause S, Macintosh M. Use of prostaglandins to induce labour in women with a caesarean section scar BMJ 1999;318:1056-8 2 Editor's Choice Learning from history? BMJ 1999;318 |
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H S Gohar, Specialist Obstetricians and Gynaecologist Cairo - Egypt
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I read with interest your review about the use of prostaglandin to induce labour in women with a caesarean section scar. The need for guidelines based on RCTs is intense. However I would like to mention two factors that may influence the decision and/or course of induction of labour after caesaren section. An important factor is whether the woman has laboured before or not as this will influence the response of the cervix to the uterine contractions. The other factor is the indication for the caesarean section i.e. if it was done due to failure of progress, which may indicate a degree of feto-pelvic disproportion or due to another reason e.g. fetal distress. This could have been the case in Mrs. B's situation i.e. she has not gone through labour in her first delivery and the inefficient contractions that lead to augmentation by syntocinon could have been due to some degree of feto-pelvic disproportion. Yours sincerely H S Gohar MRCOG Specialist Obstetrician & Gynaecologist |
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Nikolai Manassiev
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Sir After reading the article published in the BMJ (1), I was not clear why the authors have submitted it for publishing. It could not have been to inform us about the possibility of uterine rupture after induction of labour in women with prior Caesarean section because this is common knowledge. If it was in order to make the readers aware how to do literature search and to use the evidence when faced with a particular case, then the readers should be aware that they should read far and wide, otherwise they may be over four years late. The method for gathering evidence and its usefulness and applicability to the individual case have already been demonstrated (2,3). Perhaps the moral of the publication is that any physician undertaking a potentially lethal procedure should do his/her literature search before going ahead. Of course, the latter is something that we are taught in medical school, so I am left bewildered. Would the authors of the publication care to help? Dr Nikolai Manassiev Yardley Birmingham References 1 Vause S, Macintosh M. Use of prostaglandins to induce labour in women with a caesarean section scar. Evidence based case report. BMJ 1888; 318:1056-8 2 Guyatt G, Sackett D, Cook D. Users' Guides to the Medical Literature. II. How to use an article about therapy or prevention. A. Are the results of the study valid? JAMA 1993; 270: 2598-2601 3 Guyatt G, Sackett D, Cook D. Users' Guides to the Medical Literature. II. How to use an article about therapy or prevention. B. What were the rsults and will they help me in caring for my patients? JAMA 1994; 271: 59-63 |
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Philip Watters, VMO Obst&Gynae...Royal Hobart,Calvary,St Helens and St Joh's Hospitals,Hobart,Tasmania,Australia
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I would like to add my support to the comments made by Mr Nash. Part of the art of obstetrics is in treating labouring mothers as real people and therefore treating them gently. Why oxytocin in addition to amniotomy? This I believe was the fundamental error. If you push ANY labouR too hard you are asking for trouble,let alone a "trial of scar". I commend the unit for their bravery in hanging out the "dirty washing" but I hope the perinatal death was listed as "avoidable" in the record. Philip Watters FRANZCOG.FRCOG. |
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Ronnie Falcao, Independent Licensed Midwife Domiciliary Care - Mountain View, CA USA
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It is imperative to consider two distinct causes of uterine rupture: 1) Strong uterine forces in an obstructed labor and 2) A benign dehiscence of a uterine scar which is converted into a catastrophic uterine rupture by the pressure of the fetal head on the dehiscence. In the case of a trial of scar, it is significantly more likely that a rupture will be caused by the second case rather than the first. Practitioners who provide care for women with uterine scars would do well to read: Uterine rupture after previous cesarean delivery: maternal and fetal consequences. Leung AS, Leung EK, Paul RH Am J Obstet Gynecol 1993 Oct;169(4):945-950 This article discusses the sequence of mechanical events which occurs as a benign dehiscence becomes compromised by pressure of the fetal head, typically consequent to a change in the relative position of the maternal pelvis and the fetal head. Two things to note about this tragic case: 1) Early decelerations were being observed in conjunction with almost complete dilation - the baby's head was well down in the pelvis. A head that is engaged in the pelvis cannot come through a dehiscence and thus convert it to a rupture. What happened to change this situation? 2) Scalp sampling was being undertaken. A most crucial piece of information missing from this brief is what was happening with the mother's position. Was she being moved so as to facilitate scalp sampling? It seems likely that some movement of the mother and baby was taking place, and I submit that it was this movement rather than the use of prostaglandins or oxytocics which precipitated the uterine rupture. Movement of the mother into position for examination or other procedures often causes a shift in the baby's position and sometimes can bring the head out of the pelvis. The article states, "Hypertonic uterine activity is more common with prostaglandin than with other methods of induction,2 and it has been suggested that this may also increase the risk of scar rupture." However, there is no mention of hypertonus or hyperstimulation in this case, which is another missing piece of information that would be useful. Rather than guessing as to what caused the uterine rupture, why not look at the larger picture of how to prevent it? Leung et al. help us to see that much can be done to prevent uterine rupture through intelligent positioning of the mother and fetus. In particular, upright positions force the fetal head to remain in the pelvis where it belongs, rather than bursting through weakened scar tissue or a dehiscence and further rupturing the uterus as the fetal head and body are extruded into the maternal abdomen. Even if a tearing of the dehiscence were caused by a fetal shoulder, an upright maternal position trapping the fetal head in the pelvis will prevent the extrusion of the baby's body into the abdominal cavity, which is the key event leading to the placental abruption that compromises fetal well being in these cases. Regardless of whether or not artificial substances are being used to drive the trial of labor, protecting the vulnerable scar area through thoughtful positioning of the mother and baby can only reduce the incidence of tragic ruptures. In addition, it seems only prudent to combine EFM for monitoring the fetal heart rate with auscultation or some form of direct care which brings a heightened awareness of the fetal position and the precise location of the fetal heart, which are early indicators of gross fetal movement preceding or accompanying uterine rupture. Had the occurrence of a rupture-in-progress been suspected before the prolonged deceleration in the fetal heart rate and fresh vaginal bleeding, the fetus could have been bound in place to prevent the continuation of the rupture and the ultimate placental abruption leading to fetal demise. It is folly to ignore the mechanics of uterine rupture while playing numbers games with all the different ways to induce or augment labor. |
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Marsden Wagner, Retired from WHO
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Sirs, Two papers published in the American Journal of Obstetrics and Gynecologists in June 1999 report alarming rates of uterine rupture after misoprostol induction when there has been a previous cesarean section. The uterine rupture rate for patients attempting vaginal birth after cesarean was 5.6% in one paper (1)---a 28 fold increase over those who did not have misoprostol induction for their vaginal birth after cesarean (VBAC). In the second paper (2) the rate of uterine rupture after misoprostol induction with VBAC was 3.7% --still markedly higher than the 0.2% reported rate of uterine rupture with a VBAC but no induction. In these two papers, of 170 women given misoprostol for induction with VBAC, eight women ruptured their uterus and two women lost their baby. Perhaps it is time to call a moratorium on misoprostol induction with VBAC. 1. Plaut M, Schwartz M, Lubarsky S "Uterine rupture associated with the use of misoprostol in the gravid patient with a previous cesarean section" Am J Obstet Gynecol vol 180, number 6, part 1, 1535-1542 June 1999 2. Blanchette H, Nayak S, Erasmus S "Comparison of the safety and efficacy of intravaginal misoprostol (prostaglandin E1) with those of dinoprostone (prostaglandin E2) for cervical ripening and induction of labor in a community hospital" Am J Obstet Gynecol vol 180, number 6, part 1, 1543-1550 June 1999 |
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