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Database - Alliance francophone pour l'accouchement respecté (AFAR)

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Created on : 28 Oct 2004
Modified on : 01 Dec 2007

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Bibliographical entry (without author) :

Primary Postpartum Haemorrhage (PPH). 9th Postgraduate Course for Training in Reproductive Medicine and Reproductive Biology. Geneva Foundation for Medical Education and Research.

Author(s) :

J.-C. Schellenberg

Year of publication :


URL(s) :…

Résumé (français)  :

Abstract (English)  :

Primary postpartum haemorrhage is still one of the leading causes of maternal mortality. The problem has recently been reviewed (1). The risk of death from PPH in Britain is about one in one million deliveries. The risk of death from PPH in women who do not have access to blood transfusion has been estimated to approximately 1 in 1000 deliveries. Although postpartum haemorrhage is usually defined as a haemorrhage of more than 500 ml, haemorrhages of less than 1 litre are usually without major consequences (1). A pregnant non-obese woman has a blood volume of approximately 80 ml/kg body weight and signs of cardiovascular shock are usually observed after a loss of more than 15% of the circulating volume. Severe symptoms of shock are usually observed after a volume loss of 30 or more per cent of intravascular volume, i.e., of between 1.5 and 2 litres in a normal pregnant woman of 70 kilos. In a hospital setting such a degree of hypovolaemia is rare as volume replacement is instituted promptly in the case of major postpartum haemorrhage. (Note: few people die of anaemia but many die of hypovolaemia.)

Anatomy and physics of postpartum haemorrhage due to placental causes and uterine atony. As these are the most common forms of postpartum haemorrhage, it is worthwhile recalling the following facts. Postpartum haemorrhage due to other than trauma arises from the placental bed which is obviously inside the uterus. The blood supply comes from outside the uterus and traverses the myometrium. Primary haemostasis from the placental bed is due to compression of the uterine vessels as they pass through the myometrium. The degree of compression of these vessels depends on the force acting on the vessels. This force obeys the Young-Laplace relationship (F= 2T / r ), where F equals the compressive force acting on the blood vessels, T is the wall tension (generated by the uterine contraction), and r is the radius of the uterus. It is apparent that the force compressing the vessels cannot be very high if r is large. Therefore, it is essential that the radius of the uterus be made small by emptying the uterus from any blood or placental tissue and increasing the wall tension of the uterus (T) by giving ecbolics. This is the scientific basis of the initial treatment and the prevention of primary postpartum haemorrhage.

Predisposing factors. These are well known, the most important factors being previous postpartum haemorrhage, large intrauterine volume (multiple pregnancy, large baby, polyhydramnios), maternal age and obesity.

Prevention of postpartum haemorrhage. It is well accepted that active management of the third stage and routine administration of oxytocin or an ergot alkaloid, or a combination thereof, is indicated and effective. The short duration of oxytocin administered intravenously and the hypertensive effect of ergot alkaloids administered intravenously are well recognized.

Treatment of primary postpartum haemorrhage. Every obstetric unit should have a protocol for the management of postpartum haemorrhage which is well known to every member of the obstetric team. The team must be able to act as a team.

Most maternal deaths are avoidable and are due to underestimation of blood loss, inadequate volume replacement, and delay in operative intervention. Any delay in achieving haemostasis results in terminal coagulopathy (dilutional coagulaopathy and later disseminated intravascular coagulopathy due to prolonged shock). At this stage even surgery may be too late. Hence rapid and resolute action is paramount.

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Keywords :

➡ postpartum hemorrhage ; maternal age

Author of this record :

Bernard Bel — 28 Oct 2004

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