‘The dangerous efflux is occasioned by everything that hinders the emptied uterus from contracting … in these cases such things must be used as will assist the contractile power of the uterus and hinder the blood from flowing so fast into it and the neighboring vessels.’
Treatise on the Theory and Practice of Midwifery. London: D. Wilson, 1752, p402–404
This chapter will outline the causes and medical management of postpartum haemorrhage. Other aspects, including surgical management, are covered in separate chapters: retained placenta ( Chapter 21 ); uterine inversion ( Chapter 22 ); lower genital tract trauma ( Chapter 23 ); uterine tamponade, uterine compression sutures, pelvic vessel ligation and embolization, and obstetric hysterectomy ( Chapter 28 ).
Primary Postpartum Haemorrhage
Primary PPH is defined as bleeding from the genital tract in excess of 500 ml in the first 24 hours after delivery. In most instances this haemorrhage occurs within the first few hours of delivery. Because the diagnosis is subjective the reported incidence varies widely from 2% to 10%. Blood volume studies have shown that the normal woman loses about 500 ml at the time of spontaneous vaginal delivery, more with assisted vaginal delivery, and up to 1000 ml at caesarean section. In general, medical attendants tend to underestimate blood loss and patients overestimate it. Thus, when the attendant has estimated the blood loss to be more than 500 ml it is usually closer to 1 L, so the clinical definition is reasonable. However, it is important to remember that blood volume is related to body weight. Thus, the small, low-weight woman, particularly if she is anaemic, may tolerate poorly quite small blood losses (see Chapter 24 ).
Physiology of the Third Stage of Labour
Before discussing the causes and management of primary PPH it is necessary to understand the physiology of the third stage of labour, which lasts from delivery of the infant to delivery of the placenta. While this is the shortest of the three stages of labour it carries the greatest risk to the mother.
During pregnancy the myometrial fibres have been stretched considerably to accommodate the enlarged uterus and its contents. When the infant delivers the uterus continues to contract, leading to a dramatic shortening of these elongated fibres. The permanent shortening of the muscle fibres is achieved by retraction, a unique property of uterine muscle which, in contrast to contraction, requires no energy.
Placental separation is caused by the uterine contraction and retraction greatly reducing the site of placental implantation. The placenta is thus sheared from the uterine wall: analogous to a postage stamp stuck to the surface of an inflated balloon becoming detached when the balloon is deflated. When the placenta is completely separated from the implantation site the contractions continue its descent to the lower uterine segment, through the cervix and into the vagina.
Clinical Signs of Placenta Separation
The triad of clinical signs associated with placenta separation is as follows:
The uterus will be felt to contract and, as the placenta is sheared off the uterine wall and descends to the lower uterine segment, the uterine fundus changes from a broad and flat discoid shape to a more elevated, narrow and globular shape. This change from the discoid to globular configuration can be quite difficult to appreciate clinically except in the very thin. However, the uterus will be felt to harden as it contracts, rises in the abdomen and becomes ballotable.
A gush of blood often accompanies separation of the placenta from the uterine wall. This can be unreliable as bleeding may occur with only partial separation of the placenta and, even with complete separation of the placenta from the uterine wall, the blood may be contained behind the membranes and not be clinically apparent.
When the placenta has separated and descends to the lower uterine segment and through the cervix there is cord lengthening (8–15 cm) at the introitus. This is the most reliable sign.
The mechanism of haemostasis at the placental site is one of the physiological and anatomical marvels of nature. The muscle fibres of the myometrium are arranged in a criss-cross pattern and through this lattice-work of muscle fibres the blood vessels pass to supply the placental bed. When the uterine muscle contracts this lattice-work of fibres effectively compresses the blood vessels ( Fig 20-1 ). This myometrial architecture is sometimes appropriately referred to as the ‘living ligatures’ or ‘physiological sutures’ of the uterus.
Management of the Third Stage of Labour
After the infant has been delivered, delayed cord clamping (after 2 minutes) is advocated to allow maximum transfusion to the fetus. Then the cord is divided and the necessary cord blood samples taken. Put very light tension on the cord to ensure there are no loops free in the vagina and then place the clamp on the cord at the level of the introitus, ensuring that real cord lengthening becomes clinically apparent. One hand cradles and ‘guards the fundus’ so that the changes associated with placental separation can be appreciated or to detect an atonic enlarging uterus filling with blood. When the clinical signs of placental separation are evident, assist delivery of the placenta by controlled cord traction. The abdominal hand moves to the lower part of the uterus just above the pubic symphysis and gently applies counter-pressure, pushing the uterus upwards and backwards while the other hand exerts steady downward traction on the cord. The distance between the suprapubic hand and the sacral promontory should be such as to prevent the possibility of uterine inversion ( Fig 20-2 ).
There are two approaches, expectant and active, to the routine management of the third stage of labour:
Expectant management involves observation while awaiting the physiological changes that bring about placental separation. This usually takes 10–20 minutes and is favoured by those who prefer limited intervention in the management of labour. Some will encourage suckling immediately after delivery to stimulate physiological oxytocin release. Unfortunately, this physiologically attractive approach is not as effective at reducing PPH when compared with active pharmacological management.
Active management entails giving an oxytocic drug during or just after delivery of the infant in order to consistently cause the uterine contractions that lead to placental separation and haemostasis. Active management of the third stage of labour has evolved over the past half century and several randomized controlled trials have shown that it effectively reduces blood loss, need for therapeutic doses of oxytocic drugs, PPH and blood transfusion by 50–70% when compared with expectant management. The evidence and experience with active management is such that this has become the standard of care. Expectant management is only followed at the express and informed request of the woman.
The choice of oxytocic for routine active management is usually between the cheaper injectable drugs, oxytocin and ergometrine, or a combination of both in the compound Syntometrine®. Of these, oxytocin is the cheapest, has the fewest side effects and does not cause retained placenta. It is, however, shorter-acting (15–30 minutes). Ergometrine is effective but has more side effects (see below), has a longer duration of action (60–120 minutes) and a slightly higher risk of causing retained placenta. Thus, oxytocin is the drug of first choice and is given as a dose of either 5 units intravenously or 10 units by intramuscular injection with delivery of the anterior shoulder or as soon thereafter as feasible.
‘The uniform operation of the ergot to restrain uterine haemorrhage … has frequently been prescribed, a little previous to the birth of the child, or immediately after, to the patients who have been accustomed to flow immoderately, at such times, and it has always proved an effectual preventive.’
A Dissertation on the Natural History and Medical Effects of Secale Cornutum or Ergot. Andover: Flagg & Gould, 1813, p14
‘In patients liable to haemorrhage, immediately after delivery … ergot may be given as a preventive a few minutes before the termination of the labour.’
Observations on the secale cornutum or ergot, with directions for its use in parturition. Med Rec 1822; 5:90
The risk of atonic postpartum haemorrhage is greatest in the hour following delivery. However, the woman is susceptible to atonic haemorrhage over the next 2–3 hours. Thus, if oxytocin has been used for active management its short duration of action may necessitate the addition of oxytocin to the intravenous infusion for the next 2–3 hours. If ergometrine or Syntometrine® have been used the longer duration of action will usually suffice. In women with risk factors for more prolonged postpartum uterine atony (e.g. multiple pregnancy) longer-acting oxytocic drugs such as a prolonged oxytocin infusion and, in selected cases, prostaglandins or carbetocin may be necessary for adequate prophylaxis.
It is important to know the characteristics and side effects of the available oxytocic drugs, each of which has application in a variety of clinical circumstances ( Table 20-1 ).
|Drug||Dose and Route||Duration of Action||Adverse Effects||Contraindication|
|Oxytocin||5 units IV |
10 units IM
20 units in
500 ml infusion
|15–30 minutes||Insignificant hypotension and flushing. Water intoxication in high doses (> 200 units)||None|
|Ergometrine||0.2–0.25 mg IV or IM||1–2 hours||Nausea, vomiting, hypertension, vasospasm||Pre-eclampsia/hypertension, cardiovascular disease|
|Syntometrine® (5 units oxytocin, 0.5 mg ergometrine) 15-methyl PGF 2α||1 ampoule IM||1–2 hours||Nausea, vomiting, hypertension, vasospasm||Pre-eclampsia/hypertension, cardiovascular disease|
|0.25 mg IM or IMM |
0.25 mg in 500 ml infusion
|4–6 hours||Vomiting, diarrhoea, flushing, shivering, vasospasm, bronchospasm||Cardiovascular disease, asthma|
|Misoprostol||600 µg oral, sublingual |
800–1000 µg, sublingual or rectal
|1–2 hours||Nausea, diarrhoea, shivering, pyrexia||None|
|Carbetocin||100 µg IM or IV||1–2 hours||Flushing||None|
Oxytocin is the cheapest and safest of the injectable oxytocic drugs. It induces the rapid onset of strong rhythmic uterine contractions which last for 15–30 minutes. The effect is mainly on the upper uterine segment. Oxytocin also produces a transient vascular smooth muscle relaxant effect which may lead to a mild, brief reduction in blood pressure because of the reduced total peripheral resistance. This hypotension is mild and clinically insignificant except in cases of cardiovascular instability. The dose is 5 units intravenously by slow intravenous bolus, 10 units intramuscularly or 20 units in 500 ml crystalloid by intravenous infusion.
Ergometrine was the first of the injectable oxytocics and has been in use for 75 years. It produces prolonged uterine contractions involving the upper and lower uterine segments with a duration of 60–120 minutes. Ergometrine produces contraction of smooth muscle throughout the body and this is particularly relevant in the vascular tree. Peripheral vasoconstriction, which in the normal woman is not clinically significant, can produce a severe rise in blood pressure in the hypertensive or pre-eclamptic woman. In such cases it is contraindicated. Ergometrine can also induce coronary artery spasm which is also of no significance in the healthy woman, but has been incriminated in very rare cases of myocardial infarction in susceptible women. Ergometrine-induced vasospasm is responsive to glyceryl trinitrate.
Because of its prolonged effect, ergometrine causes a slight increase in uterine entrapment of the separated placenta. Compared with oxytocin this amounts to about an additional 1 in 200 cases requiring manual removal. Nausea and/or vomiting occur in 20–25% of women who receive ergometrine. The dose of ergometrine is 0.2–0.25 mg by intramuscular injection. Because of the vasopressor effect it is better not given intravenously, although if the indication is urgent it can be given as a slow intravenous bolus of 0.2 mg. The higher dose of 0.5 mg should not be given initially as the side-effect profile is increased, without a concomitant improvement in the uterotonic effect.