Despite advances in obstetric care and improved blood transfusion, haemorrhage is still a major cause of maternal morbidity and mortality. The Confidential Enquiry into Maternal Deaths 1997-1999 showed seven maternal deaths related directly to haemorrhage and seven other deaths where haemorrhage was a significant cause. It has been reported that death from haemorrhage occurs in 3.3 per million maternities.5 Deaths from postpartum haemorrhage (PPH) account for 17 to 40% of the maternal mortality in the developing world. For women who refuse blood transfusion, the risk of death from PPH is one in 1000, similar to that in developing countries. Morbidity is also associated with obstetric haemorrhage and studies suggest that severe, life-threatening haemorrhage may occur in 6.7 per 1000 deliveries.6,7

A recent study published in the British Journal of Obstetrics and Gynaecology, in April this year,8 suggests a severe maternal morbidity rate of 3.8 per 1000 maternities, with major obstetric haemorrhage accounting for 50% of events. It defines 13 categories of severe maternal morbidity and demonstrates that it is possible to quantify maternal morbidity on a national basis. The study also suggests that a national reporting system for maternal morbidity should be set up. This is dependent on a local risk management system being in place in every unit, as recommended in ''A First Class Service: Quality in the new NHS''.9

Congenital coagulopathies in women are not common, but are associated with obstetric haemorrhage. The most common congenital coagulopathies are von Willebrand's disease, haemophilia A, and haemophilia B (Christmas disease). von Willebrand's disease constitutes a heterogenous group of haemorrhagic disorders that are usually transmitted as autosomal dominant traits, although autosomal recessive transmission of some variant types occurs.10 The prevalence of von Willebrand's disease is at least 3 to 4 per 100,000 in the UK and due to its autosomal pattern of inheritance is the commonest congenital coagulopathy affecting women. There is an elevation in factor VIII: v WF during pregnancy or oral contraceptive use. The von Willebrand's factor acts as a carrier and stabiliser of factor VIIIc, preventing it from inactivation or catabolism. Deficiency in v WF results in defective platelet-endothelial and platelet--platelet interactions. Haemophilia A and B are X-linked recessive disorders and among carrier women only about 1 in 10 has excessive bleeding.

Cryoprecipitate has been the treatment ofchoice for severe bleeding episodes and surgical procedures in von Willebrand's disease. It was thought to be preferable to high potency factor VIII concentrates, which do not elevate ristocetin co-factors as effectively as cryoprecipitate. There is, however, considerable variability in the correction of bleeding times with cryoprecipitate and even laboratory assessment of v WF activity (ristocetin co-factor) does not predict reliably the clinical response. These patients are now generally covered in labour by an alternative to blood products, desmopressin, a synthetic analogue of anti-diuretic hormone. This treatment releases endogenous factor VIII: v WF from vascular epithelium and is used for both prophylaxis and treatment of bleeding. In the management of pregnant women it is important to establish the type and monitor haemostatic variables, especially during the third trimester.

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