1177 60 mg and then 80 mg daily (with a gap of 4 days in January following a total hip replacement), in an attempt to achieve a greater reduction in growth-hormone levels than had hitherto been produced. Once again the requirement for hypotensive agents diminished, and the patient has remained normotensive on no therapy other than 80 mg bromocriptine daily for the past 6 weeks. Temporary increases in hydrocortisone were made during this period, but there was no other change in replacement therapy, which includes a maintenance dose of 50 mg hydrocortisone daily. Our studies in parkinsonism have suggested a similar effect to
using bromcriptine, whereby previously hypertensive patients became more easily controlled. These findings will be reported elsewhere. The mechanism of the hypotensive effect of bromocriptine is not understood, but further studies of its potential clinical implications in hypertension seem justified. Department of Endocrinology, University College Hospital, London WC1E 6AU
S. B. KAYE
K. M. SHAW E. J. ROSS
BROMOCRIPTINE REGIMEN FOR RESTORATION OF OVULATORY FUNCTION
SiR,—The post-partum galactorrhoea-amenorrhoea or Chiari-Frommel syndrome is often associated with raised plasma-prolactin levels. Treatment with bromocriptine reduces galactorrha:a and restores ovarian function by lowering the plasma-prolactin to normal.’ These patients, infertile by anovulation, can be successfully treated with this semisynthetic ergot alkaloid. However, during all pregnancies reported so far, the patients took bromocriptine during the earliest embryological phase. Immediate cessation of medication when pregnancy is suspected has occasionally been advised.2 We have developed a regimen with the least possible risk to the
embryo. Six patients aged 26-37 who wished
to become pregnant, selected for this study. They were all primiparas and had post-partum galactorrhoea-amenorrhoea syndrome, as indicated by raised plasma-prolactin levels of 27-68 ng/ml (normal <20). Before starting drug therapy the following examinations and tests were done: complete history, physical examination, endocrine studies, X-rays of skull and breasts, and laboratory tests on cervical mucus. All patients were treated with 2.5 mg bromocriptine/day for 2 weeks, thereafter the dose was increased to 5 mg/day. Patients were told to use mechanical contraception and to record their basal body temperature (B.B.T.). Follow-up visits were at 2-week intervals. Prolactin levels returned to normal within 4 weeks and menstruation returned in 3-7 weeks. Ovulation was confirmed by B.B.T., serum progesterone, and endometrial biopsy. After the first menstruation the patients were instructed to stop contraception and to discontinue the bromocriptine treatment as soon as the B.B.T. rose. When the temperature remained high a pregnancy test was performed, but if menstruation occurred bromocriptine treatment was started again on the first day of the next cycle, the dose being 5 mg/day until the next rise in B.B.T. Five patients became pregnant-two at the first, one at the second, and two at the third unprotected ovulation. Two healthy children have been born, and the other three pregnancies are progressing uneventfully. The sixth patient has a regular ovulatory menstrual cycle and is still trying to conceive. In man and in animals no teratological effects of bromocriptine have been reported. All the same we consider that intermittent administration of bromocriptine with discontinuation shortly after ovulation reduces the teratogenic hazard to a minimum in cases where a pregnancy is wanted. According to Horrobin,3 hyperprolactinseniia contributes to insufficiency were
1. Besser, G. M., and others Br. med.J. 1972, iii, 669. 2. Rolland, R., Schellekens, L. A., Lequin, R. M. Clin. Endocr. 1974, 3. Horrobin, D. F. Prolactin 1974; p. 56. Lancaster, 1974.
3, 155.
of luteal function. In our patients the plasma-prolactin levels about a week after conception and withdrawal of bromocriptine were still normal. Our clinical results indicate that induction of ovulation with bromocriptine in patients with the post-partum galactorrhaea-amenorrhaea syndrome is sufficient to achieve a normal pregnancy. We conclude that luteal function must have been normal. Department of Obstetrics and Gynæcology University Hospital Utrecht, H. J. T. COELINGH BENNINK Netherlands, and A. A. HASPELS Research Department Sandoz, H. SNUIVERINK Uden
RUPTURE OF UTERINE SCAR IN A PATIENT GIVEN EPIDURAL ANALGESIA
SiR,—There is always a risk of scar rupture during labour in patients previously delivered by caesarean section. Careful selection and management of these patients in whom vaginal delivery is thought to be safe, is always necessary. The case we report illustrates the risk and emphasises the need to monitor these labours very closely, especially where epidural analgesia is used. The 28-year-old patient was induced at term in view of her previous lower-segment caesarean section, done 3 years earlier for fetal distress early in labour, a live 4.37 kg female being delivered. Her postoperative recovery had been marred only by a slight fever which settled by the ninth day on a course of antibiotics. This second pregnancy had been normal. On clinical assessment the pelvis was found to be gynaecoid in shape and of good capacity. At induction the head was two-fifths above the pelvic brim. The cervix was soft, fully effaced, 3 cm dilated. Clear liquor was obtained on amniotomy. An intravenous infusion of oxytocin was started at a rate of 3.5mU/min to be increased slowly until a maximum of 24 mU/min was reached. 5 h after amniotomy labour became established and epidural analgesia using lignocaine and bupivacaine was instituted. Regular top-up doses with bupivacaine were planned at this stage. There was little change in the cervical dilatation and the head was still palpable abdominally. The epidural analgesia abolished the pain of the uterine contractions. 2 h later no untoward signs were experienced by the patient, blood-pressure, maternal pulse, and fetal heart-rate remaining normal. However, abdominal examination at this time revealed an irregular uterine outline. The cervix was found to be 5 cm dilated. The oxytocin infusion was stopped and laparotomy was arranged. On opening the abdomen the baby was found to be lying outside the uterus. It was promptly delivered but could not be resuscitated. Examination of the uterus revealed a large tear extending across the whole length of the previous lower-segment incision and beyond into the broad ligament on the right side, almost involving the uterine vessels. The tear also extended a little on the right to involve the cervix. There was no excessive bleeding. After delivery of the placenta the uterus was repaired. The bladder was slightly damaged and this was repaired, separating old adhesions. A self-retaining catheter was inserted for 10 days’ continuous drainage. The patient made an uneventful postoperative recovery, prophylactic antibiotics being given. The stillborn infant weighed 3.66 kg. The classical signs of uterine rupture after a previous caesarean section are given in most standard obstetric textbooks. They are memorised by nearly every medical student. The common symptom of abdominal pain, often central, related to the region of the scar, unassociated with the uterine contractions, and gradually becoming worse, was completely masked by the epidural analgesia. The classical sign of abdominal tenderness in the neighbourhood of the scar was similarly masked. This case reinforces the view that great vigilance is required in such labours, fetal monitoring and the continuous recording of intrauterine pressure being obligatory where epidural analgesia is used-and perhaps it should lead