Confidential enquiries into maternal deaths, 1997–1999

J. A. W. Wildsmith1, T. A. Thomas2 and G. Cooper3

1 Dundee, UK 2 Bristol, UK 3 Birmingham, UK

Editor—The triennial review of maternal mortality has, for nearly half a century, been required reading for all anaesthetists because each edition has contained reports on, and insights into, British anaesthetic practice that are relevant well beyond the obstetric unit. Your initiative in publishing both an editorial,1 and the anaesthetic chapter2 is to be commended for two reasons: it makes the key material from the report more readily available, and it provides a forum for further comment. In making such comment, I am aware that I do not practice obstetric anaesthesia currently, but sometimes the ‘outside’ view can be useful.

Thromboembolism, as in many other areas in which we work, remains an important cause of patient death. Thus, our specialty must cooperate in the delivery of appropriate prophylactic regimens although we must be aware of the complications, especially in regard to spinal and epidural block. Balancing the risks of thromboembolism and vertebral canal haematoma is never easy, but I do feel that the report has been a little simplistic in its coverage and recommendations. This is perhaps best typified by the bald statement that ‘Evidence from general and orthopaedic surgery does not point to an increased risk of spinal haematoma.’3 While exaggerated concerns about vertebral haematoma may be denying some patients optimum thromboprophylaxis, I do not believe that that this statement is justified by the evidence.4 The Scottish Intercollegiate Guideline Network has published a revised version of its recommendations on prophylaxis of thromboembolism. Detailed consideration has been given to obstetric issues (www.sign.ac.uk).

I would like to comment also on the first of those deaths described in the report as ‘due to anaesthesia’. An epidural catheter entered the subarachnoid space accidentally and, not unreasonably, was left in place during labour. Although the initial injection (bupivacaine 0.25%, 4 ml) had resulted in extensive block, exactly the same amount (bupivacaine 0.5%, 2 ml) of drug was given later (from a 20 ml syringe) to extend a block which was already partially established, so that Caesarean section could be performed. Not surprisingly, a total spinal anaesthetic developed. Having partially resuscitated the patient, the anaesthetist was then put in the invidious position of having to leave the mother to resuscitate the baby because the paediatrician had not arrived. The anaesthetist’s absence coincided with significant haemorrhage, and a downward spiral, exaggerated by an overdose of oxytocin, was established. Rarely is a patient’s death attributable to a single factor, and this was certainly the case here, but the analysis presented in the report seems to me to deflect attention from the key issues.

I agree that using a 20 ml syringe to top-up a continuous spinal block was unwise, but I know of no evidence that ‘fractions of a millilitre of bupivacaine can affect the extent of a subarachnoid anaesthetic’.2 The real problem was that an absolute overdose was administered. I would also dispute that it is necessary to invoke ‘complex reflexes’,2 to explain the cardiovascular problems. During spinal anaesthesia, as in any other situation, blood pressure and cardiac output depend on four factors: venous return (significantly influenced by both caval occlusion and haemorrhage), heart rate, myocardial contractility, and peripheral resistance. In this patient, total sympathetic block (with its adverse effects on heart rate, myocardial contractility and peripheral resistance) was complicated by severe haemorrhage, temporary absence of the anaesthetist and administration, at the request of the obstetrician, of an overdose of oxytocin, a drug with a significant vasodilator effect. No ‘complex reflexes’ were involved. This patient died because some basic errors were made by the anaesthetist, although both the paediatrician and the obstetrician must accept some responsibility.

J. A. W. Wildsmith

Dundee, UK

Editor—Thank you for the opportunity to reply to Professor Wildsmith. When reading the confidential enquiries, it must be remembered that the case vignettes allow the reader to make more interpretations than there is necessarily room to discuss in the chapters.

Professor Wildsmith’s first point is from the chapter in the report on thrombosis and thromboembolism.3 There are recommendations at the end of this chapter for thromboprophylaxis for vaginal deliveries (Annex A), for Caesarean section (Annex B), and for epidural administration in those receiving heparin (Annex C). Professor Wildsmith fails to mention these, or that the sentence previous to the one he criticizes is ‘The use of subcutaneous heparin as prophylaxis in patients with an epidural or spinal block remains contentious.’ The advice in these annexes is derived from the Royal College of Obstetricians and Gynaecologists Evidence-based Guideline,5 which refers to the editorial from Checketts and Wildsmith.4 Checketts and Wildsmith state ‘It would be most unfortunate if European patients were denied the benefits of either central nerve block or optimal thromboprophylaxis because of that [American] experience.’ Their concerns expressed in the editorial are addressed by the advice in the annexes, namely that using ‘European’ doses and timing of administration of heparin is likely to be important in reducing the risk of vertebral canal haematoma.

The second matter concerns the top-up dose required for Caesarean section after an intrathecal catheter has been used for analgesia in labour. When the catheter was first placed, bupivacaine 10 mg produced an extensive, but not total block.

Subsequently, smaller doses were used to produce pain relief in labour, but not anaesthesia. In such circumstances, deciding what is the correct dose to convert analgesia into anaesthesia for Caesarean section can be difficult. In the face of a fading analgesic block and more than 30 min since the previous dose we feel that the decision to use a 10 mg dose of bupivacaine was not unreasonable. However, by using a 20 ml syringe it is possible that a larger volume (perhaps 2.5 ml or more), and hence a larger dose was in fact given. The point was therefore made that it is sensible to use a method of administration that gives the best accuracy lest the administered volume, and thereby dose, is greater than intended.

His third point is overly simplistic. Of course, the combination of hypovolaemia and sympathetic block can cause cardiac arrest. However, such arrests are not usually refractory to resuscitation, especially when that resuscitation is instituted immediately using existing i.v. access and with a tracheal tube already in place. An additional factor must be postulated and that is the possibility of direct adverse cardiac effects of oxytocin. Oxytocin receptors are more widely distributed than is commonly realized. The presence of such receptors in the heart is often overlooked, and the possibility of dysrhythmias as a result of oxytocin administration is not widely appreciated. If Professor Wildsmith is still unsure of this potential effect we would direct him to the references at the end of our chapter as reproduced in the BJA;2 to our dismay they were not properly originated in the text of the original chapter.

T. A. Thomas1

G. Cooper2

1Bristol, UK

2Birmingham, UK

References

1 Cooper GM, Lewis G, Neilson J. Confidential Enquiries into Maternal Deaths, 1997–1999. Br J Anaesth 2002; 89: 369–72[Free Full Text]

2 Thomas TA, Cooper GM. Maternal deaths from anaesthesia. An extract from Why Mothers Die 1997–1999, The Confidential Enquiries into Maternal Deaths in the United Kingdom. Br J Anaesth 2002; 89: 499–508[Abstract/Free Full Text]

3 Drife J. Thrombosis and thromboembolism. In: Why Mothers Die 1997–1999. The Confidential Enquiries into Maternal Deaths in the United Kingdom. London: Royal College of Obstetricians & Gynaecologists, 2001; 49–69

4 Checketts MR, Wildsmith JAW. Central nerve block and thromboprophylaxis—is there a problem? Br J Anaesth 1999; 82: 164–7[Free Full Text]

5 Royal College of Obstetricians and Gynaecologists. Thromboembolic disease in pregnancy and the puerperium: acute management. Guideline No 28. London: RCOG, 2001





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