Postpartum haemorrhage

• Postpartum haemorrhage (PPH) is excessive bleeding after birth. By the common definition used in most guidelines, it is 500 ml or more of blood lost from the genital tract within 24 hours of delivery; ACOG uses a quantitative definition of 1000 ml or more, or any blood loss with signs or symptoms of low blood volume, within 24 hours.
• PPH is the leading cause of maternal death worldwide and one of the leading causes of serious maternal illness even in well-resourced settings.
• Four processes cause it, remembered as the four Ts: Tone (uterine atony, about 80% of cases in the Sebghati review, about 70% in FIGO 2022), Tissue (retained placenta or clots, about 5%), Trauma (genital tract tears, uterine rupture or inversion, about 13% in the review, 15 to 20% in FIGO 2022) and Thrombin (coagulopathy, about 2%). ^[6] The split is not a mistake: the Sebghati review gives 80 / 5 / 13 / 2, whereas FIGO 2022 gives atony 70% and trauma 15 to 20%.
• It can arise in any woman, even with no risk factors, so every delivery needs a plan. Prevention rests on the third stage: active management with a prophylactic uterotonic, usually oxytocin 10 IU.
• Treatment runs in parallel: call for help, resuscitate, find the cause (the four Ts), use uterotonics, tranexamic acid, balloon tamponade and then surgery. An escalating, stepwise approach (HAEMOSTASIS) is summarised below.
• The key tranexamic acid message from WHO (2017): give 1 g intravenously within 3 hours of birth (1 g over 10 minutes), with a second 1 g dose if bleeding continues after 30 minutes. ^{[5] [4]}

By the end of this page you should be able to:

1. Define primary and secondary PPH and apply the quantitative definitions used by RCOG, ACOG, NICE and WHO.
2. Name the four Ts, their approximate proportions, and how they are distinguished at the bedside.
3. List the antenatal and intrapartum risk factors, and state the measures that reduce PPH at birth.
4. Give the correct prophylactic uterotonic and dose for vaginal and caesarean birth.
5. Diagnose PPH from blood loss, haemodynamic signs and (in massive loss) the haematocrit.
6. Run the acute management sequence: resuscitation, uterotonics with doses, tranexamic acid with its 3-hour window, balloon tamponade, and surgical steps.
7. Organise a massive transfusion using the RCOG and NICE targets for blood products and haemoglobin.
8. Recognise complications, prognosis, prevention and the special groups that change management.
9. Distinguish PPH from similar causes of heavy bleeding after birth using a feature-by-feature table.

• RCOG Green-top Guideline No. 52 (2nd edition, 2017; reviewed 2023). Primary PPH is defined as the loss of 500 ml or more of blood from the genital tract within 24 hours of birth; it can be minor (500–1000 ml) or major (more than 1000 ml), and major PPH can be moderate (1001–2000 ml) or severe (more than 2000 ml). In women of lower body mass, a smaller loss may be clinically significant. ^[1]
• ACOG Practice Bulletin No. 183 (2017; reaffirmed 2024). Maternal haemorrhage is defined as a cumulative blood loss of 1000 mL or more or blood loss accompanied by signs or symptoms of hypovolaemia within 24 hours of the birth process. ^[2]
• WHO (2012). PPH is commonly defined as a blood loss of 500 ml or more within 24 hours after birth. ^[4]
• Massive PPH refers to the loss of 30 to 40% of the woman's blood volume. ^[6]

The traditional 500 ml threshold for vaginal birth and the 1000 ml threshold sometimes used after caesarean birth are not biological switches: they are prompts to act. A woman with anaemia or low body mass can become shocked with less blood loss, so haemodynamic signs matter as much as the measured volume. ^[6]

• By volume and timing (RCOG): minor 500–1000 ml; major more than 1000 ml; moderate 1001–2000 ml; severe more than 2000 ml. ^[1]
• By cause, using the four Ts (below): Tone, Tissue, Trauma, Thrombin. ^[6]
• By the object bleeding: uterine atony (tone), retained tissue or invasive placenta (tissue), genital tract laceration or tear, uterine rupture or inversion (trauma), coagulopathy or disseminated intravascular coagulation (thrombin). ^[6]
• By origin of the bleeding: from the uterine cavity, from a placental bed site, or from the genital tract itself.

PPH is the leading cause of maternal death worldwide and is responsible for a large share of serious maternal illness even in resource-rich countries. ^[2] WHO's 2003–2009 analysis of global causes of maternal death found that haemorrhage was the leading direct cause. ^[6]

• In the United States, haemorrhage that leads to blood transfusion is the leading cause of severe maternal morbidity, closely followed by disseminated intravascular coagulation. ^[2]
• The rate of PPH in the US rose by 26% between 1994 and 2006, driven mainly by increased rates of uterine atony. ^[2]
• Maternal mortality from postpartum obstetric haemorrhage has decreased in the US since the late 1980s, accounting for slightly more than 10% of maternal deaths (about 1.7 deaths per 100,000 live births) in 2009, a fall associated with increasing rates of transfusion and peripartum hysterectomy. ^[2]
• In the UK, mortality as a direct result of haemorrhage was about 0.55 per 100,000 maternities from 2011 to 2013. ^[6]
• PPH can occur in women with no identifiable risk factors, so clinicians must be prepared for it at every delivery. ^[6]

Risk factors may be antenatal or intrapartum. Even when several are present, most affected women will not bleed, and many who bleed have none; the pattern is for anticipation, not prediction. ^{[1] [6]}

Antenatal factors ^[6]:

• age over 40 years
• high body mass index
• Asian or African ethnicity
• multiple pregnancy
• placenta praevia or suspected or proven placental abruption
• previous PPH
• grand multiparity
• anaemia
• fibroids or previous gynaecological surgery
• pre-eclampsia or hypertension
• previous caesarean sections, especially with placenta accreta or percreta
• bleeding disorders, including von Willebrand disease and thrombocytopenia
• use of anticoagulants in pregnancy

Intrapartum factors ^[6]:

• caesarean birth (especially repeat or emergency)
• instrumental delivery (forceps or ventouse)
• prolonged labour (more than 12 hours) or prolonged third stage
• induction of labour
• a baby weighing more than 4 kg
• retained placenta or membranes
• perineal or upper genital tract trauma
• fever in labour
• general anaesthesia during delivery

Antenatal anaemia is worth singling out. Treating anaemia before birth (iron, plus blood products where indicated) reduces the morbidity of PPH and the need for transfusion. ^[1]

PPH is ultimately a haemostasis problem. After delivery the myometrium must contract and retract. Its fibres shorten and thicken, and this mechanical compression pinches shut the uterine arteries and the placental bed spiral arteries. When the uterus is soft (atonic), that compression fails and bleeding continues. ^[6]

• Uterine atony (Tone). The placenta separates by the shearing forces of uterine contraction; a flaccid uterus cannot expel the placenta nor close the vessels at the placental bed. Active management of the third stage (prophylactic uterotonic, controlled cord traction, uterine palpation) has been shown to reduce the risk of blood loss above 500 ml, largely through uterotonics. ^[6]
• Retained tissue (Tissue). Retained placenta, membranes or clots keep the myometrium from clamping down on the placental site. Invasive placenta (accreta, increta, percreta) is a special case in which the placenta does not separate at all. ^[6]
• Trauma (Trauma). Lacerations, uterine rupture and inversion all leave vessels open and bleeding. Upper vaginal and cervical tears are often high and hidden. ^[6]
• Coagulopathy (Thrombin). Congenital or acquired clotting disorders (factor VIII or IX deficiency, von Willebrand disease) or acquired consumptive coagulopathy (for example after abruption or amniotic fluid embolism) allow bleeding from otherwise minor sites. ^[6]
• Massive haemorrhage itself generates a coagulopathy: clotting factors are consumed and diluted, core temperature and blood pH fall, and acidosis impairs clot function. This "washout" is why massive transfusion protocols use matched red cells, plasma and platelets together, and why keeping the patient warm matters. ^[6]

PPH may be obvious, with visible heavy bleeding, or concealed, pooling in the tissues or abdomen (for example after uterine rupture or inversion, or behind a tamponade effect). The diagnosis rests on measured or estimated loss plus haemodynamic signs. ^[6]

Symptoms and signs include:

• heavy vaginal bleeding, often a steady flow, or sudden gushes
• soft, "boggy" uterus that does not become firm
• a fall in blood pressure and rise in pulse rate; tachycardia is an early sign, and hypotension a late one
• restlessness, anxiety, pallor, breathlessness, sweating, thirst
• cold extremities and a low core temperature
• raised respiratory rate; in severe loss, oliguria or anuria
• a full bladder, which worsens atony
• an obstetric shock index (pulse divided by systolic blood pressure) above 1, which signals significant blood loss and a higher chance of needing transfusion ^[6]

• Estimate blood loss quantitatively where possible: weigh swabs, drapes and under-pads (1 g equals 1 ml), use calibrated collection drapes, and record the time of onset. Visual estimation alone is inaccurate. ^[1]
• Palpate the uterus for tone and position of the fundus; if it is soft, massage it and expel clots.
• Examine the perineum, vagina and cervix systematically for tears.
• Check that the placenta is complete; inspect for missing cotyledons or membranes.
• Check blood pressure, pulse, respiratory rate, oxygen saturation and temperature repeatedly.
• Empty the bladder with a catheter; a distended bladder stops the uterus contracting.
• Check the coagulation screen, platelets and haemoglobin early in major loss.
• Look for the four Ts one by one: Tone (is the uterus firm?), Tissue (is anything retained, is the placenta complete?), Trauma (where is the tear, is the uterus intact?), Thrombin (is the blood clotting, is the fibrinogen low?).

The obstetric shock index is the pulse rate divided by the systolic blood pressure. In pregnancy a higher resting pulse and lower systolic pressure than outside pregnancy mean that the usual adult thresholds do not apply. A value above 1 is associated with a greater likelihood of needing transfusion after PPH, so it is a useful bedside check when measured blood loss seems modest. ^[6]

The fundamental diagnosis is clinical, based on measured blood loss and haemodynamic status. Tests quantify the problem and guide transfusion.

ACOG's cumulative-quantity definition (1000 ml or more, or loss with symptoms) is intended to match the loss that actually requires intervention and avoids classing every 500 ml bleed as a PPH. ^[2] There is no single best definition in practice; both are widely used and the clinical context decides. ^{[4] [6]}

The question splits in two. Clinically, PPH must be told apart from other causes of heavy bleeding and shock after birth. At the bedside, once a bleed is recognised, the four Ts separate the cause.

Uterine atony is the most common cause, so assume atony first but always check the other Ts, because giving uterotonics alone will not fix a tear or retained placenta. ^[6]

Management follows a stepwise, escalating plan. Use the local PPH algorithm (HAEMOSTASIS is one published version) and practise it in simulation before it is needed. ^{[4] [6]}

• Active management of the third stage of labour (prophylactic uterotonic, controlled cord traction, uterine examination) reduces the risk of blood loss above 500 ml compared with expectant management, mainly through uterotonics. ^[6]
• Prophylactic uterotonics are offered to all women because uterine atony is unpredictable and most affected women have no risk factors. ^{[1] [4]}
• Uterine massage is of no benefit for prophylaxis once a prophylactic uterotonic has been given; sustained massage only causes discomfort. ^{[1] [4]}
• Controlled cord traction is optional when skilled attendants are available and contraindicated when not; early cord clamping is generally avoided because of neonatal iron stores. ^[4]
• Postpartum abdominal palpation of uterine tone is recommended for all women to detect atony early. ^[4]
• Antenatal anaemia: investigate and treat (iron, with haematology input as needed) so there is less buffer lost at birth. ^[1]
• Women with known risk factors should deliver where a blood bank is on site, with early written plan for the third stage. ^[1]
• For women with a bleeding disorder, active management of the third stage is recommended and intramuscular uterotonics should be avoided; plan with a haematologist. ^[3]

Choice of prophylactic uterotonic ^{[1] [4]}:

• Vaginal birth without risk factors: oxytocin 10 IU by intramuscular injection. A higher dose is unlikely to add benefit. ^[1]
• Caesarean section: oxytocin 5 IU by slow intravenous injection. ^[1]
• Women at increased risk of haemorrhage: ergometrine-oxytocin may be used in women without hypertension, as it reduces minor PPH; a combination of preventive measures may be better than oxytocin alone. ^[1]
• RCOG, 2017: clinicians should consider intravenous tranexamic acid 0.5 to 1.0 g, in addition to oxytocin, at caesarean section in women at increased risk of PPH. ^[1]
• FIGO 2022: tranexamic acid is used to treat diagnosed PPH, and prophylactic use is not recommended because the evidence is limited.
• WHO, 2012: oxytocin 10 IU IV or IM is the uterotonic of choice; where oxytocin is unavailable, use other injectable uterotonics, or oral misoprostol (600 micrograms) by trained workers. ^[4]
• WHO, 2012: oxytocin 10 IU IV or IM is the uterotonic of choice, including at caesarean section. ^[4] This differs from RCOG's recommendation of oxytocin 5 IU by slow intravenous injection at caesarean section, so follow the guideline your service uses.
• Sustained uterine massage is not recommended for prevention once prophylactic oxytocin has been given. ^[4]

NICE NG235 (2023) sets out a clear "call for help, in/out, uterus" approach for obstetric-led care. ^[3]

Call and organise:

• Make the call if blood loss is 500 ml or more; make a major haemorrhage call at 1000 ml or more or with continuing bleeding or clinical shock.
• Summon senior midwives, an obstetrician and an anaesthetist; alert the haematologist.
• Arrange transfer to obstetric-led care and delegate specific roles (team leader, scribe, runner).
• Review the whole picture every 15 minutes and record estimated blood loss and temperature every 15 minutes. ^[3]

Resuscitate (In / Out):

• Assess airway and breathing; high-flow oxygen (15 L/min aiming for oxygen saturation 94 to 98%); keep the woman warm. ^[3]
• Set up two points of IV access (14 to 16 G), give 2 litres of warmed balanced crystalloid (such as Hartmann's) initially, and continue as needed to a total of up to 3.5 L of warmed clear fluid; avoid hydroxyethyl starch; do not use vasopressors as a substitute for volume. ^{[1] [3] [4]}
• RCOG: position flat, keep warm, high concentration oxygen via face mask, rapid warmed infusion with no special blood filters, and, if no haemostatic results are available after 4 units of red blood cells, give fresh frozen plasma at 12 to 15 ml/kg. ^[1]
• RCOG (major loss): transfuse blood as soon as possible if clinically required; compatible red cells as soon as available; group O RhD-negative K-negative units in emergencies, switching to group-specific blood as soon as possible. ^[1]

Assess and correct the cause (Uterus):

• Empty the bladder by catheter and leave it in place.
• Check the four Ts: Tone, Tissue, Trauma, Thrombin.
• Rub up a contraction; perform bimanual uterine compression and massage; check that the placenta is complete and that there is no genital tract trauma. ^[3]

First-line drugs for a PPH (administer according to the NICE table, taking account of what was given for the third stage; do not repeat ergometrine or carbetocin) ^[3]:

• Oxytocin 5 units slow IV, or 10 units IM
• Ergometrine 0.5 mg IM ^[3]
• Combined oxytocin and ergometrine (5 units / 0.5 mg) IM ^[3]
• Tranexamic acid 1 g IV (over 10 minutes), repeated if needed after at least 30 minutes
• Misoprostol 800 micrograms sublingual or rectal ^[3]
• Oxytocin infusion 40 units in 500 ml over 4 hours
• Carboprost 250 micrograms IM, repeated at intervals of 15 minutes or more, maximum 8 doses ^[3]
• Carbetocin 100 micrograms slow IV ^[3]

These drugs should be given in combination or in sequence. Uterotonics and tranexamic acid can be given together because they work by different mechanisms. ^{[1] [3]}

• Oxytocin is the first uterotonic for both prevention and treatment and has fewer side effects than the ergot alkaloids. ^[6]
• Ergometrine (ergot alkaloid) causes strong upper and lower uterine segment contraction; it is contraindicated in hypertension, severe cardiac disease and eclampsia. ^[6]
• Misoprostol is less effective than oxytocin against PPH but usable when nothing else is available; 800 micrograms sublingually or rectally, and 600 micrograms orally by prevention routes. ^{[3] [4] [6]}
• Carboprost is a 15-methyl prostaglandin F2 alpha analogue; it is used for atonic PPH (caution with asthma). ^[6]
• Carbetocin, a long-acting oxytocin analogue, is used in some services (100 micrograms slow IV in the NICE table). ^[3]
• Prophylactic options where oxytocin is unavailable (WHO): other injectable uterotonics or oral misoprostol (600 micrograms). ^[4]

WHO (2017) updated its recommendation after the WOMAN trial: early use of intravenous tranexamic acid within 3 hours of birth, in addition to standard care, for clinically diagnosed PPH after vaginal birth or caesarean section. ^[5]

• Dose: a fixed dose of 1 g (100 mg/mL) IV at 1 mL per minute, that is 1 g over 10 minutes (rapid bolus can drop the blood pressure transiently), with a second dose of 1 g IV if bleeding continues after 30 minutes or restarts within 24 hours of completing the first dose. ^[5]
• Window: start as soon as possible after onset of bleeding and within 3 hours of birth; TXA given more than 3 hours after birth does not reduce bleeding death and may cause harm. The benefit falls by about 10% for each 15-minute delay. ^[5]
• Use in all PPH: give tranexamic acid in all cases of PPH, regardless of whether bleeding is due to genital tract trauma or another cause. ^[5]
• Should not be used in a clear contraindication to antifibrinolytic therapy (known thromboembolic event in pregnancy, history of coagulopathy, active intravascular clotting, hypersensitivity). ^[5]
• Route: intravenous only; research into other routes is a priority. ^[5]
• It should be given with, and not delayed by, uterotonics. ^{[3] [5]}

Non-pharmacological temporising measures include uterine massage, bimanual uterine compression and external aortic compression until care arrives. ^{[4] [6]}

• Intrauterine balloon tamponade is recommended when uterotonics fail or are unavailable, and before moving to surgical options. ^{[1] [4]}
• Fill with about 300 to 400 mL of sterile saline or water, creating counter-pressure at the placental bed. ^[6]
• The tamponade test (whether the balloon stops the bleeding) has a high positive predictive value: if bleeding stops, further radical surgery is usually unnecessary; if not, escalate. ^[6]
• Uterine packing is not recommended for atonic PPH after vaginal birth. ^[4]
• The non-pneumatic anti-shock garment can be used as a temporising measure where transfer to higher care is needed. ^[4]

If bleeding continues despite uterotonics and conservative measures, escalate to surgery without further delay. ^{[4] [6]}

1. Examination under anaesthesia: ensure the uterus is empty and repair any trauma. ^[3]
2. Compression sutures: B-Lynch brace suture and its modern modifications appose the anterior and posterior uterine walls to compress the bleeding placental site, while keeping the uterine vessels open. ^[6]
3. Artery ligation: systematic pelvic devascularisation, ligating the uterine arteries, the tubal branches of the ovarian arteries, the internal iliac arteries, or a quadruple ligation if bleeding persists. ^[6]
4. Interventional radiology: uterine artery embolisation in haemodynamically stable women; a two-centre UK series reported an 89.4% success rate, and published rates vary by case mix and selection. ^[6]
5. Hysterectomy (subtotal or total): the life-saving last resort, to be decided by the most senior obstetrician and never delayed in haemodynamic instability. ^{[1] [6]}
6. Placenta accreta spectrum: the Triple-P procedure (perioperative localisation, delivery of the baby above the placenta, pelvic devascularisation and myometrial excision with reconstruction) is an alternative to hysterectomy, but needs specialist resources (including prophylactic internal iliac occlusion balloons) and is not universally available. ^[6]

Each step should be tried in order, with senior review at every escalation, and with continuous communication to the woman and her partner. ^{[1] [6]}

• There are firm criteria as such: the decision to transfuse is based on clinical and haematological assessment. ^[1]
• PPH protocols include emergency group O, RhD-negative and K-negative units with immediate issue, switching to group-specific blood as soon as possible. ^[1]
• Aim for haemoglobin above 90 g/L, correcting coagulopathy according to the local major haemorrhage protocol. ^[3]
• After 4 units of red cells, give fresh frozen plasma at 12 to 15 ml/kg until haemostatic tests are available. ^[1]
• A fixed 1:1:1 ratio of packed red cells, fresh frozen plasma and platelets (mimicking whole blood) is used in massive transfusion protocols. ^[2]
• Cell salvage should be considered in PPH associated with caesarean or vaginal delivery. ^[1]
• Fibrinogen targets are set by the local protocol; RCOG guidance gives cryoprecipitate when fibrinogen falls below about 2 g/L, while transfusion guidance commonly aims to keep levels above about 1.5 g/L. ^[1]
• Keep the woman warm, use rapid warmed infusion and avoid unnecessary delay: restoring both volume and oxygen-carrying capacity together limits the washout phenomenon. ^{[1] [6]}

• Severe anaemia and exhaustion in the postnatal period.
• Hypovolaemic shock, multi-organ failure, acute renal failure and adult respiratory distress syndrome. ^[2]
• Disseminated intravascular coagulation and the consumptive coagulopathy of massive haemorrhage. ^{[2] [6]}
• Loss of fertility after peripartum hysterectomy, and pituitary necrosis (Sheehan syndrome) from severe hypotension. ^[2]
• Infection after retained products, transfusion or surgery.
• Psychological morbidity, including post-traumatic stress, is common after a major PPH; a debrief with access to counselling is part of care.
• Thrombosis is a risk after massive haemorrhage and transfusion, so prophylaxis should follow the local protocol once bleeding is controlled.

Most episodes settle with first-line measures and a blood transfusion. Maternal mortality from postpartum haemorrhage in well-resourced settings is now low (about 1.7 per 100,000 live births in the US in 2009), but morbidity remains high. ^[2] Where PPH persists, outcomes depend on the speed of escalation: blood loss above 1500 ml should be formally reviewed in the unit so systems can be improved. ^[1]

• Screen all women for risk factors at booking and at every contact, using the lists above.
• Identify and treat anaemia (see the prevention section). ^[1]
• Plan the third stage before birth for women at increased risk: place of delivery, blood available, anaesthetist aware, and documented escalation plan. ^[1]
• Active management of the third stage for all women, with a prophylactic uterotonic (oxytocin 10 IU IM for vaginal births, oxytocin 5 IU slow IV at caesarean section, with extra measures for high-risk women). ^{[1] [4]}
• Risk-factor reassessment at delivery, because new intrapartum factors emerge; do not downgrade plans when labour lengthens or instrumentation becomes likely.
• Drills and standardised bundles (policies, guidelines and algorithms) improve teamwork and outcomes; simulation of PPH is recommended for all maternity staff. ^{[2] [4]}
• Tranexamic acid is used to treat PPH (1 g IV within 3 hours), as above. RCOG considers prophylactic use (0.5 to 1.0 g IV at caesarean section in at-risk women), but FIGO 2022 does not recommend prophylactic use because the evidence is limited; it is not part of routine prevention in low-risk women. ^{[5] [1]}

• Adolescents and young mothers. Teenagers are more prone to anaemia and may present late; they need access to transfusion, monitoring and postnatal follow-up, and the same stepwise escalation.
• Women of older age. Age over 40 is a risk factor; caesarean and instrumental births are more common; plan delivery in a consultant-led unit. ^[6]
• Women with bleeding disorders (von Willebrand disease, haemophilia carriers, immune thrombocytopenia, platelet disorders under 100 times 10^9/L). Active management of the third stage is recommended; intramuscular uterotonics are avoided, and individualised care is planned with a senior haematologist, including measurement of blood loss and haematological monitoring. ^[3]
• Women taking anticoagulants. Their care requires haematology input; the RCOG PPH guideline does not cover specific management for women on therapeutic anticoagulation. ^[1]
• Women with a hypertensive disorder. Ergometrine is contraindicated, so select alternatives such as oxytocin, misoprostol or carboprost. ^[6]
• Women giving birth outside an obstetric unit. Start first-line measures and transfer promptly; uterotonics and tranexamic acid should be given before transfer where possible. ^[3]
• Multiple pregnancy. Uterine atony is more likely, and uterine over-distension contributes; plan active management and early access to uterotonics. ^[6]
• Women declining blood transfusion. Specialist protocols exist; the RCOG guideline does not itself cover the management of haemorrhage in women who refuse transfusion. ^[1]

Related MedGrasp topics (plain text, pending verified links): antepartum haemorrhage; placenta praevia, accreta and vasa praevia; HELLP syndrome and eclampsia; disseminated intravascular coagulation; von Willebrand disease; haemophilia; coagulation screening tests; obstetric analgesia and anaesthesia; neonatal resuscitation.