Management of Uterine Atony

Curriculum

This page comes under the auspices of curriculum items such as "Risk factors, recognition and management of massive obstetric haemorrhage including... the use of uterotonics and point of care coagulation tests... [and] causes such as genital tract trauma, uterine atony etc."

Examiner feedback

This topic is a core component of MOH management, on which there have been two CRQs in recent times.

The February 2023 paper was answered well (71.9%), but candidates performed less well in the March 2026 paper (where half of the available marks were on generic MOH management).

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Postpartum haemorrhage (PPH) is the leading cause of maternal death worldwide, and most PPH deaths are preventable
Uterine atony is failure of the uterus to contract adequately after delivery and is the commonest cause of PPH, responsible for up to 80% of cases
Over half of cases occur in patients with no identifiable risk factors, so vigilance is required at every delivery
Management centres on prophylactic oxytocin or carbetocin for all, early escalation to second-line uterotonics and early tranexamic acid once PPH occurs

Uterine atony complicates approximately 1 in 20 births, and around 6% of primary Caesarean deliveries
The incidence of PPH is rising worldwide in both high and low resource settings, largely attributed to an increase in uterine atony
Atony is also the leading cause of obstetric massive transfusion

Physiology

Uterine blood flow at term is approximately 700ml/min, of which about 80% perfuses the placenta
The spiral arteries of the placental bed lack the muscular wall needed to vasospasm in response to injury

A healthy patient can therefore exsanguinate within minutes if placental bed bleeding does not stop

Haemostasis after placental delivery relies on:

Strong, sustained myometrial contraction which mechanically compresses the bleeding vessels
Local clotting within the vessels, driven by platelets, clotting factors, tissue factor and plasminogen activator inhibitor type 1

Uterine smooth muscle has limited intracellular calcium stores and relies on calcium influx from the extracellular fluid to contract

Diagnosis

Atony is diagnosed when the uterus fails to become firm to palpation after delivery of the placenta
Tone may be quantified on a 0-10 scale (0 = flaccid; 10 = firmly contracted), which is feasible during Caesarean delivery
Blood loss may be concealed: over 1L can accumulate within a flaccid uterus, so early recognition of poor tone is critical

Uterine overdistension	Impaired contractility: patient factors	Impaired contractility: labour and delivery
Multiple gestation	Previous PPH due to atony	Induction or augmentation with prolonged oxytocin infusion
Fetal macrosomia	Anaemia	Chorioamnionitis
Bulky fibroids	Nulliparity or high parity	Arrested labour or arrest of descent
Polyhydramnios	Diabetes mellitus	Tocolytics: magnesium, calcium channel blockers, β-agonists
	Hypertensive disorders	Uterine rupture
	IVF pregnancy
	Asian, Pacific Islander or Hispanic ethnicity

Previous PPH is one of the strongest risk factors, increasing the risk of atony 4-6 fold, and should be specifically asked about in all multiparous patients

A family history (e.g. a sister with atonic PPH) also increases risk, suggesting a genetic component

Antenatal anaemia is important as it is modifiable with iron replacement before delivery

As well as reducing reserve, anaemia may increase nitric oxide production, which relaxes the uterus

Prolonged exogenous oxytocin causes oxytocin receptor desensitisation (see prophylaxis below)

Risk prediction performs poorly in practice:

More than half of atony cases at primary Caesarean delivery occur in patients without risk factors
In one validation study only 22% of PPH cases came from the "high risk" group, and only 7.3% of high risk patients went on to have a PPH

All patients should receive uterotonic prophylaxis with oxytocin or carbetocin after vaginal or Caesarean delivery
See also: oxytocin pharmacology

Pharmacology

Peptide agonist at oxytocin receptors on uterine smooth muscle; cheap and widely available
Low dose infusions (as for induction of labour) cause rhythmic contractions; higher doses after delivery cause firm, tetanic contraction
IV: onset 30-60s with a half-life of only 3-5mins, hence the need for an infusion to maintain effect
IM: onset 3-7mins with clinical effect lasting about 1hr
Denatured by heat, so requires a cold chain

Dosing principles

IV is superior to IM, but 10IU IM is acceptable without IV access and is recommended by the RCOG for vaginal births
IV boluses should not exceed 5IU

The ED₉₀ at elective Caesarean in oxytocin-naïve patients is less than 1IU, including in obese patients
Higher risk patients (e.g. intrapartum Caesarean after prolonged oxytocin, multiple gestation, macrosomia) may need more, but still no more than 5IU
Larger boluses add side-effects with little or no additional benefit

A small bolus followed by an infusion is probably superior to a bolus alone
Higher dose infusions produce more adverse effects than lower dose infusions

Adverse effects

Vascular smooth muscle relaxation causes dose-dependent flushing, ↓ SVR and compensatory tachycardia
Rapid, high dose boluses can cause severe hypotension, chest pain, cardiovascular collapse and cardiac arrest, particularly when combined with the sympathectomy of neuraxial anaesthesia
Nausea and vomiting

Oxytocin desensitisation

Prolonged exposure to exogenous oxytocin during labour leads to internalisation of oxytocin receptors from the myometrial cell surface
Higher oxytocin doses and/or second-line uterotonics are then required to achieve adequate tone; early use of second-line agents should be considered

Long-acting synthetic oxytocin analogue
Onset within 2mins of an IV bolus with a half-life of around 40mins, so no maintenance infusion is needed
Heat stable formulation which does not require a cold chain
At least non-inferior to oxytocin for PPH prophylaxis, with some analyses suggesting superiority

Dosing

Licensed dose is 100μg IV or IM
Dose-finding studies at elective Caesarean suggest much lower doses are effective: 20μg was non-inferior to 100μg, and the ED₉₀ is around 15μg
As with oxytocin, requirements are higher at intrapartum Caesarean delivery

Guidelines

NICE considers routine carbetocin cost-effective for Caesarean but not vaginal delivery
The WHO considers it an acceptable first-line agent where the lack of a cold chain makes costs comparable with oxytocin

Adverse effects

Similar to oxytocin: flushing, hypotension and compensatory tachycardia
Its long half-life means the drug cannot be "withdrawn" if poorly tolerated, unlike an oxytocin infusion

Combination uterotonics

Combinations such as oxytocin with ergometrine, misoprostol or carboprost have been studied as prophylaxis in high-risk patients
Overall these offer modest reductions in blood loss at best, at the cost of more side-effects (particularly nausea and vomiting)
Prophylactic ergometrine with oxytocin may benefit patients at intrapartum Caesarean delivery, provided a low dose oxytocin protocol is used and there are no contraindications to ergometrine

Calcium

Uterine smooth muscle depends on extracellular calcium influx to contract
Lower serum calcium before transfusion is associated with more severe PPH
Calcium chloride 1g IV over 10mins after cord clamping reduced atonic blood loss at intrapartum Caesarean delivery in a small single-centre trial
Rapid infusion may cause bradycardia, pain and nausea; extravasation causes tissue injury
Larger trials are needed before routine use can be recommended

First-line treatment of atony is further oxytocin, escalating the bolus and infusion as above
If atony persists, second-line agents act via mechanisms independent of the oxytocin receptor and so remain effective after desensitisation

Ergometrine

Ergot alkaloid (methylergometrine is a closely related derivative used in the USA); see also ergometrine pharmacology
Binds α-adrenergic, 5HT and dopamine receptors; direct action at myometrial α-receptors causes calcium influx and contraction
Given IM (500μg in UK practice) with onset in 2-5mins and a long half-life of around 3hrs
Slow IV administration is used in some centres for faster onset, but this causes more profound hypertension and coronary vasospasm
Combined with oxytocin 5IU as syntometrine for IM use
Requires refrigeration

Ergometrine: adverse effects and contraindications

Potent vasoconstriction: hypertension and coronary vasospasm
Relatively contraindicated in hypertension, pre-eclampsia, coronary artery disease and Raynaud's phenomenon
Headache, abdominal pain, nausea and vomiting are more common than with oxytocin
Repeat doses should not be given more often than every 2-4hrs due to cumulative hypertensive effects

Carboprost

Synthetic PGF_2α analogue (Haemabate) acting on prostaglandin F receptors on myometrium; see also prostaglandin analogue pharmacology
250μg IM, repeated every 15mins if needed up to a maximum of 8 doses (2mg); may also be given intramyometrially
Onset 2-5mins, peak effect at 30mins and half-life around 3hrs
Requires refrigeration and is more costly than ergometrine

Carboprost: adverse effects and contraindications

Contracts smooth muscle elsewhere in the body:

GI: nausea, vomiting and profound diarrhoea; an antiemetic ± antidiarrhoeal is often co-administered
Bronchial: bronchospasm, which may be severe and life-threatening; contraindicated in asthma
Pulmonary vascular: vasospasm, so avoid in parenchymal lung disease and pulmonary hypertension

Misoprostol

Synthetic PGE₁ analogue given as tablets; cheap, heat stable and requires no needles or skilled staff
400-800μg, preferably buccal or sublingual (onset 10-20mins); the rectal route is slower and vaginal dosing is impractical in active bleeding
Half-life 20-40mins
Inferior to oxytocin for prophylaxis and adds no benefit to oxytocin in treatment
Its role is limited to settings where injectable uterotonics are unavailable or contraindicated

Misoprostol: adverse effects

Shivering and fever, often within 20mins; shivering may interfere with non-invasive BP measurement during haemorrhage
Nausea, vomiting and diarrhoea
No absolute contraindications

Not a uterotonic, but an important adjunct in the management of PPH
Antifibrinolytic: binds plasminogen and prevents its interaction with fibrin, preventing clot breakdown
1g IV, repeated after 30mins if bleeding continues

Treatment of PPH

The WOMAN trial (>20,000 women with PPH) showed TXA reduced death from bleeding from 1.9% to 1.5%

The benefit was greater when given within 3hrs of delivery
Criticisms include a high NNT (~250) and uncertain benefit in high resource settings

Early TXA in established PPH is supported by the evidence

Prophylaxis

Large trials of prophylactic TXA at vaginal and Caesarean delivery have shown little or no clinically significant benefit (e.g. no reduction in transfusion or death)
Routine prophylaxis is therefore not recommended, but may be considered in very high-risk cases such as Caesarean hysterectomy for suspected placenta accreta spectrum

Risks

No increased risk of thromboembolism has been demonstrated in the obstetric trials
Inadvertent intrathecal or epidural injection is catastrophic, causing seizures, arrhythmias and death; in one case series 20 of 21 cases were life-threatening and 10 were fatal
The risk is heightened in busy obstetric theatres where neuraxial drugs and TXA may be drawn up at the same time, so systems to prevent drug errors are essential

Haemorrhage care bundles combine evidence-based drug therapy with standardised systems of care, using a stage-based approach to PPH and treatment algorithms for atony
Their implementation has been associated with reductions in maternal morbidity and mortality, as well as in ethnic disparities in PPH outcomes
Freely available examples include the AIM obstetric haemorrhage bundle and the CMQCC obstetric haemorrhage toolkit