9th Postgraduate Course for Training in Reproductive Medicine and Reproductive Biology

 Primary Postpartum Haemorrhage (PPH)

J.-C. Schellenberg
Department of Obstetrics and Gynecology, Geneva University Hospital

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.

The key steps are as follows.

(1) Placenta - where?

Establish whether the placenta is delivered.

(2) Shock?

Establish the mother's cardiovascular status (pulse, and if immediately available, blood pressure)

(3) Source of bleeding?

Palpate the abdomen to establish whether haemorrhage is likely to come from the placental bed or the lower genital tract.

(4) Help

Call for help.

These four steps take less than one minute.

(5) Remove placenta

If the placenta has not been removed from the uterus and the patient's cardiovascular condition is worrying, remove the placenta. Do not wait for the anaesthetist because if you wait the patient may be dead by the time the anaesthetist arrives. In less acute cases or where the placenta has been delivered, insert a wide gauge intravenous cannula and infuse colloid and crystalloid solutions and red blood cells if available. As soon as anaesthesia is available deliver the placenta, check the uterine cavity and the lower genital tract. Meanwhile, unless bleeding is major, proceed with the following steps.

(6) Make uterus contract - treat hypovolaemia

Manually stimulate the uterus to contract, give further injections of ergometrine or Syntometrine, intravenously if deemed necessary. Start continuous infusion of oxytocin (30 units in 500 ml saline).

(7) Bimanual compression - uterine artery stretch

Bimanual compression of the uterus prevents an increase in the radius of the uterus due to bleeding in the uterus and atony. Simultaneously, the uterus is pushed cephalad, which puts the uterine arteries under tension and reduces blood flow to the uterus. Catheterise bladder.

(8) If bleeding persists and the uterus is not firmly contracted (indicating that at least part of the bleeding is due to uterine atony rather than trauma) administer the prostaglandin drug that is part of the hospital's routine.

To my knowledge, all the uterocontracting prostaglandins currently available have been used successfully in the treatment of uterine atony (2-17). The success rate for cases refractory to oxytocin and the ergot alkaloids seems to be situated between 80-90% for all prostaglandins used. The analogues (15-methyl-...PGF2a = carboprost = Prostin /15MR = HemabateR etc., 16, 16-dimethyl..PGE1 methylester = gemeprost = CervagemR etc., sulprostone = NaladorR etc., and misoprostol = CytotecR) seem to have less side effects than the natural prostaglandins (PGF2a et PGE2). Various routes of administration ro have been described, even for the same drug (intrauterine, intramyometrial, transabdominal and intracervical, transvaginal, intravenous, intramuscular, vaginal and rectal). The most interesting drug seems to be misoprostol which is cheap and does not require storage at a low temperature. Rectal administration ((5 tables of 200 m g = 1 g) is efficient in cases refractory to oxytocin and ergometrine (16). After administration of misoprostol (400 m g rectally) given prophylactically the duration of the 3d stage and blood loss were similar to that after syntometrine (1 ampoule) but the incidence of diastolic hypertension was lower (18). This is in keeping with reports on the prophylactic use of carboprost vaginally or rectally (19). Direct intramyometrial injection of prostaglandins may act faster but carries the risk of intravenous injection which may lead to several cardiovascular side effects including cardiac arrest (20-23)

(9) Uterine packing

Packing using gauze, gauze placed within a plastic bag, or using inflatable tubes (e.g., Sengstaken-Blakemore), accompanied by temporary external compression of the uterus has been recommended. It may be particularly useful in cases of placenta praevia accreta (24,25).

(10) Aortic compression

Transabdominal compression of the aorta against the promontorium is done in preparation for laparotomy if required. In all cases the uterus must be closely supervised i.e., a midwife must be with the patient with her hand on the patient's uterus and ensuring that the uterus does not relax and fill with blood.

(11) Treat anaemia, coagulopathy, thrombocytopenia

(12) Operative procedures

Operative procedures are required in cases of refractory uterine atony and in cases of pathological placentation (the worst cases being those of placenta previa accreta/increta). Hysterectomy and ligation of the internal iliac arteries are well known procedures but not necessarily the best, particularly not in the case of placenta praevia. Hysterectomy may not be necessary while ligation of the internal iliac arteries may be ineffective (65% success rate in one report (26)), particularly in cases of uterine atony and placenta praevia where the already rich collateral circulation is particularly well developed. If internal iliac artery ligation is carried out the artery should be ligated quite distally from its origin from the common illiac arteries as the uterine arteries originate from distal branches of the internal iliac. This is technically difficult.

Better alternatives.

I. Bilateral mass ligation of the uterine arteries. This has been used in cases of bleeding during Caesarean sections (n=265 over 30 years (27)). Sutures including 2-3 cm of myometrium are placed 2-3 cm below the uterine incision.

II. Stepwise uterine devascularisation. This consists of (1) unilateral and, if required (2) bilateral uterine vessel ligation, followed by (3) low bilateral uterine vessel ligation after mobilisation of the bladder, and (4) unilateral or bilateral ovarian vessel ligation (28) Both techniques allow revascularisation of the ligated vessels with subsequent normal uterine function.

III. Uterine compression sutures. A technique used in cases of uterine atony has been described by B-Lynch (29,30). A similar method has been used also ( 31)

IV. Arterial embolisation. This effective technique is often impractical for primary massive haemorrhage for organisational reasons. It should be considered in cases of protracted primary PHH and in cases of secondary PPH (32-34). A highly skilled invasive radiologist is required.


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