By the end of this chapter you'll be able to…

  • 1Explain why uterine contraction rather than coagulation achieves postpartum haemostasis
  • 2Rank the four T's by frequency and use the contracted uterus as a discriminator
  • 3State the components of active management of the third stage
  • 4Describe the E-MOTIVE intervention and explain why it worked
  • 5Explain why visual estimation of blood loss fails and why hypotension is late
  • 6Use the shock index and explain the effect of pre-existing anaemia
  • 7Sequence the management of postpartum haemorrhage as simultaneous rather than stepwise
  • 8State the contraindications of each uterotonic and the reason for each
  • 9Justify the three-hour window for tranexamic acid
  • 10Distinguish placenta praevia from placental abruption clinically
  • 11Explain why the visible loss understates the true loss in abruption
  • 12Identify the placenta accreta spectrum risk factors and why incidence is rising
  • 13Recognise uterine rupture, inversion, amniotic fluid embolism and cord prolapse
  • 14Manage puerperal sepsis using the source control principle
  • 15Diagnose ectopic pregnancy and select expectant, medical or surgical management
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Why this chapter matters in NEET PG
Haemorrhage is the leading direct cause of maternal death in India and almost every death from it is preventable, which makes this the highest-stakes chapter in obstetrics. One physiological fact organises it: at term the uterus receives around a fifth of the cardiac output, and haemostasis after delivery is achieved mechanically by myometrial fibres occluding the spiral arteries rather than by clotting. If the uterus does not contract, no amount of clotting factor helps. That explains why atony causes 70 to 80 per cent of cases, why every first-line treatment aims at contraction, and why bimanual compression precedes drugs. The chapter also carries the most important recent trial in obstetrics, E-MOTIVE, which cut severe outcomes by around 60 per cent using drugs everyone already had.

Postpartum Hemorrhage & Obstetric Emergencies

Haemorrhage is the leading direct cause of maternal death in India, and almost every death from it is preventable.

The organising tool is that in obstetric haemorrhage the uterus is both the source and the solution. An empty, contracted uterus does not bleed.

At term the uterus receives around 600 to 800 millilitres of blood every minute, which is roughly a fifth of the cardiac output. Haemostasis after delivery is not primarily achieved by clotting. It is achieved mechanically, by the interlacing myometrial fibres contracting around the spiral arteries and occluding them, which is why they are called the living ligatures.

That single fact explains the whole subject. If the uterus does not contract, no amount of clotting factor will stop the bleeding, which is why atony causes catastrophic loss in minutes and why every first-line treatment is aimed at making the uterus contract.

It also explains the diagnostic sequence. When a woman bleeds after delivery, the questions are whether the uterus is contracted, whether it is empty, whether the tract is intact and whether the blood will clot.

1. The Four T's

The causes of postpartum haemorrhage are conventionally grouped as tone, trauma, tissue and thrombin, and the grouping is genuinely useful because it is ordered by frequency.

CauseMechanismApproximate share
ToneUterine atony70 to 80 per cent
TraumaGenital tract laceration, rupture, inversion15 to 20 per cent
TissueRetained placenta or clotUnder 10 per cent
ThrombinCoagulopathyRare as a primary cause

Atony dominates so heavily that it should be assumed until excluded, and the risk factors are anything that overstretches the uterus or exhausts it: multiple pregnancy, polyhydramnios, macrosomia, high parity, prolonged or augmented labour, chorioamnionitis and retained products.

Trauma is suggested when the uterus is well contracted and the woman is still bleeding, which is the single most useful discriminator at the bedside.

Thrombin is rarely the primary cause but is frequently a secondary one, because massive transfusion, hypothermia and consumption all produce coagulopathy, and abruption and amniotic fluid embolism cause it directly.

2. Prevention and What Changed

Active management of the third stage reduces postpartum haemorrhage substantially and is standard practice. It comprises a prophylactic uterotonic, controlled cord traction and uterine massage.

Oxytocin is the uterotonic of choice, given immediately after delivery of the baby. Heat-stable carbetocin is a useful alternative where the cold chain cannot be maintained, which matters in much of India.

The most important recent development is the E-MOTIVE trial, which changed practice by attacking detection rather than treatment.

It combined a calibrated blood-collection drape for objective early detection with an immediate bundle of uterine massage, oxytocics, tranexamic acid, intravenous fluids, examination and escalation, delivered together rather than sequentially.

The result was a roughly 60 per cent relative reduction in the composite of severe haemorrhage, laparotomy for bleeding and death from bleeding, across more than 200,000 women.

The reason it worked is instructive: the interventions were not new. What was new was measuring blood loss objectively instead of estimating it, and giving all the treatments at once rather than escalating one at a time while the woman continued to bleed.

3. Why Estimation Fails

Postpartum haemorrhage is defined as blood loss of 500 millilitres or more after vaginal delivery, or 1,000 millilitres or more after caesarean section, though any loss causing haemodynamic compromise qualifies.

Visual estimation of blood loss is unreliable and systematically underestimates large volumes, which is precisely why a calibrated drape improves outcomes.

The physiology compounds the problem. Plasma volume rises by around 40 to 50 per cent in pregnancy, so a healthy woman can lose a great deal of blood before her blood pressure falls.

Tachycardia and a narrowed pulse pressure precede hypotension, exactly as in trauma, and hypotension in an obstetric haemorrhage is a late and ominous sign.

An anaemic woman has no such reserve, which is why the same volume of blood loss kills in India that would be survived elsewhere, and why anaemia correction is part of haemorrhage prevention.

The shock index, the heart rate divided by the systolic blood pressure, is a useful bedside measure because it rises before either number alone becomes alarming.

4. Managing Postpartum Haemorrhage

Management is simultaneous rather than sequential: call for help, resuscitate, find the cause and treat it, all at once.

Resuscitation is two large-bore cannulae, blood samples including cross-match, fluid and early blood products, and a massive transfusion protocol if loss continues.

Uterine massage and bimanual compression are performed immediately while drugs are drawn up, because mechanical compression works instantly and drugs take minutes.

The uterotonics are used in sequence, and their contraindications are examined more often than their doses.

DrugMechanismCaution
OxytocinOxytocin receptor agonistHypotension with rapid bolus
ErgometrineSmooth muscle constrictionAvoid in hypertension and pre-eclampsia
CarboprostProstaglandin F2 alpha analogueAvoid in asthma
MisoprostolProstaglandin E1 analoguePyrexia, shivering; heat stable

Ergometrine in a pre-eclamptic woman and carboprost in an asthmatic are the two errors the examination tests.

Tranexamic acid is given as early as possible and within three hours of onset, because it reduces death from bleeding and, as with trauma, later administration is not merely ineffective.

If bleeding continues, mechanical and surgical measures follow: intrauterine balloon tamponade, compression sutures such as the B-Lynch, stepwise devascularisation by ligating the uterine and then internal iliac arteries, and uterine artery embolisation where available.

Hysterectomy is the final step and must not be delayed too long, because the commonest contributor to death is persisting with conservative measures in a woman who is already coagulopathic.

Non-pneumatic anti-shock garments are useful for stabilising a woman during transfer in low-resource settings.

Aortic compression buys time when nothing else is available. Pressing the closed fist firmly downwards just above the umbilicus compresses the abdominal aorta against the vertebral column, reducing uterine arterial inflow, and it can be sustained by an assistant while the theatre is prepared.

Its value is that it requires no equipment and no drug, which is precisely why it belongs in the repertoire of anyone working where both may be unavailable.

5. Secondary Postpartum Haemorrhage

Secondary haemorrhage occurs between 24 hours and 12 weeks after delivery, and the two causes are retained products of conception and endometritis, often together.

Presentation is bleeding with an offensive discharge, fever, uterine tenderness and a subinvoluted uterus.

Management is antibiotics with evacuation where products are retained, and evacuation of an infected uterus carries a real risk of perforation, so it is performed carefully and after antibiotics have been started.

6. Antepartum Haemorrhage

Antepartum haemorrhage is bleeding after 24 weeks and before delivery, and two conditions dominate.

Placenta praevia is painless bleeding from a placenta lying in the lower segment. The uterus is soft and non-tender, the fetal condition is usually good, and malpresentation is common because the placenta occupies the lower segment.

Placental abruption is painful bleeding from premature separation of a normally sited placenta. The uterus is tense, tender and irritable, the fetal condition is often poor, and the visible bleeding may be far less than the actual loss because blood is concealed behind the placenta.

That concealed loss is the trap. A woman may be in profound shock with modest visible bleeding, and the degree of shock should be judged against her physiology rather than against what is on the sheet.

Vaginal examination is contraindicated in suspected placenta praevia until the placental site is known, because a digital examination can provoke torrential haemorrhage. Ultrasound is performed first.

Abruption is associated with hypertension and pre-eclampsia, trauma, smoking, cocaine use, previous abruption and sudden uterine decompression. It causes disseminated intravascular coagulation more often than any other obstetric condition, through release of thromboplastin from the damaged placenta.

Vasa praevia is rare but distinctive: painless bleeding at membrane rupture with rapid fetal deterioration, because the blood lost is fetal rather than maternal, and a fetus has very little to lose.

7. The Placenta Accreta Spectrum

Placenta accreta means abnormal adherence of the placenta to the myometrium because of a deficient decidua, and it exists on a spectrum with increta invading the myometrium and percreta penetrating the serosa.

The risk factors are previous caesarean section and placenta praevia, and the two multiply. A woman with a praevia overlying a previous caesarean scar is at very high risk, because the scar has no decidua for the placenta to stop at.

Its incidence is rising directly in proportion to caesarean section rates, which makes it a self-inflicted epidemic.

Antenatal diagnosis by ultrasound and magnetic resonance imaging is what makes the difference, because it allows delivery to be planned at a centre with blood, surgical expertise and intensive care.

Attempting to remove an accreta placenta causes catastrophic haemorrhage, so management is planned caesarean hysterectomy or leaving the placenta in situ in selected cases.

8. Other Obstetric Emergencies

Uterine rupture presents with scar tenderness, an abnormal fetal heart pattern which is often the earliest sign, cessation of contractions, loss of station and maternal collapse. It requires immediate laparotomy.

Uterine inversion follows traction on an unseparated placenta and causes profound shock, often disproportionate to the blood loss because of vagal stimulation. The uterus is replaced immediately, before the cervical ring contracts, and the placenta is removed only after replacement.

Amniotic fluid embolism is rare, unpredictable and often fatal. It presents with sudden cardiovascular collapse, hypoxia and disseminated intravascular coagulation, classically during labour or immediately after delivery. It is a diagnosis of exclusion and management is entirely supportive.

Cord prolapse is an emergency because the cord is compressed between the presenting part and the pelvis. The presenting part is elevated manually, the woman is placed knee-chest or in steep head-down tilt, the bladder may be filled, and delivery is expedited, usually by caesarean section.

Handling the cord is minimised because it causes vasospasm.

9. Puerperal Sepsis and Thromboembolism

Sepsis remains a direct cause of maternal death, and its danger lies in how well young women compensate.

Puerperal sepsis is genital tract infection at any time between the rupture of membranes and 42 days postpartum. The uterus after delivery is an ideal culture medium: a large raw placental bed, retained blood, and a cervix that is still open.

Risk factors are prolonged rupture of membranes, repeated vaginal examinations, prolonged labour, caesarean section, retained products and pre-existing anaemia.

Presentation is fever, offensive lochia, uterine tenderness, subinvolution and abdominal pain. Group A Streptococcus deserves particular fear, because it can progress from mild symptoms to fulminant septic shock within hours.

Management follows the source control principle: broad-spectrum antibiotics started immediately after cultures, and evacuation of retained products or drainage of collections, because antibiotics alone will not sterilise an undrained focus.

The obstetric trap is that the physiological tachycardia and relative hypotension of pregnancy make the early signs of sepsis look normal, so deterioration is recognised late.

Venous thromboembolism is the leading direct cause of maternal death in many high-income settings and is rising in India as caesarean rates rise.

Pregnancy is prothrombotic by design, satisfying every element of Virchow triad: clotting factors rise while protein S falls, venous stasis increases as the uterus compresses the pelvic veins, and delivery injures the vessel wall.

Risk is highest in the puerperium rather than during pregnancy, and left leg deep vein thrombosis predominates because the right common iliac artery crosses and compresses the left common iliac vein.

Low molecular weight heparin is the treatment and prophylaxis of choice, because it does not cross the placenta. Warfarin is teratogenic and is avoided, particularly in the first trimester.

10. Ectopic Pregnancy

Ectopic pregnancy is implantation outside the uterine cavity, most often in the ampulla of the fallopian tube, and it remains a cause of maternal death in early pregnancy.

Risk factors are anything damaging the tube: previous pelvic inflammatory disease, genital tuberculosis, previous ectopic pregnancy, tubal surgery, and pregnancy with an intrauterine device in place.

The classical triad is amenorrhoea, abdominal pain and vaginal bleeding, but the presentation is frequently atypical, and the crucial rule is that any woman of reproductive age with abdominal pain must have a pregnancy test.

Diagnosis uses transvaginal ultrasound with serum human chorionic gonadotropin. In a normal early pregnancy the level roughly doubles every 48 hours, and a suboptimal rise suggests an abnormal pregnancy.

An empty uterus with a level above the discriminatory zone suggests ectopic pregnancy, because an intrauterine pregnancy should be visible at that level.

Management is expectant in selected resolving cases, medical with methotrexate where the woman is stable with a small unruptured ectopic and a low hormone level, and surgical where she is unstable, the ectopic is large or ruptured, or medical treatment fails.

A ruptured ectopic causing haemodynamic instability is a surgical emergency, and resuscitation and surgery proceed together.

11. Worked Examples

Example 1. A woman bleeds heavily after a prolonged augmented labour with twins. The uterus is soft and boggy.

Tone accounts for 70 to 80 per cent of postpartum haemorrhage, and every risk factor here points to it: twins overdistended the uterus, and prolonged augmented labour exhausted it.

Bimanual compression and massage begin immediately while uterotonics are prepared, because mechanical compression acts instantly. Oxytocin is first line, tranexamic acid is given within three hours, and resuscitation runs in parallel. A soft boggy uterus is the definition of atony.

Example 2. A pre-eclamptic woman has postpartum haemorrhage. Oxytocin has failed and a colleague suggests ergometrine.

Ergometrine causes generalised smooth muscle constriction including vascular smooth muscle, so it raises blood pressure and is contraindicated in hypertension and pre-eclampsia, where it risks stroke.

Carboprost is the appropriate second-line agent unless she is asthmatic, and misoprostol is an alternative. Mechanical measures continue throughout, and tranexamic acid is given if not already.

Example 3. A woman at 32 weeks with pre-eclampsia has continuous abdominal pain and a tense tender uterus, with only modest vaginal bleeding but a pulse of 130 and a systolic pressure of 88.

This is placental abruption, and the modest visible bleeding is the trap. Blood is concealed behind the placenta, so the visible loss bears no relation to the actual loss, and her tachycardia and hypotension indicate substantial haemorrhage.

Resuscitation with blood, delivery, and anticipation of disseminated intravascular coagulation are required, since abruption causes it more often than any other obstetric condition through thromboplastin release. Pre-eclampsia is a recognised risk factor.

Summary

  • The uterus is both source and solution; an empty contracted uterus does not bleed.
  • Myometrial fibres are the living ligatures occluding the spiral arteries.
  • The uterus receives about a fifth of cardiac output at term.
  • Tone causes 70 to 80 per cent of postpartum haemorrhage.
  • A contracted uterus with continued bleeding means trauma.
  • Active management uses a uterotonic, cord traction and massage.
  • Heat-stable carbetocin is useful where the cold chain fails.
  • The E-MOTIVE bundle cut severe outcomes by around 60 per cent.
  • It worked by objective detection and simultaneous rather than sequential treatment.
  • Visual estimation systematically underestimates large blood loss.
  • Plasma volume rises 40 to 50 per cent, so hypotension is late.
  • Tachycardia and narrowed pulse pressure precede hypotension.
  • An anaemic woman has no reserve, so the same loss kills.
  • Massage and bimanual compression act instantly; drugs take minutes.
  • Ergometrine is contraindicated in hypertension and pre-eclampsia.
  • Carboprost is contraindicated in asthma.
  • Tranexamic acid is given within three hours of onset.
  • Escalate to balloon, compression sutures, devascularisation, embolisation.
  • Delayed hysterectomy in a coagulopathic woman is a common contributor to death.
  • Secondary haemorrhage is retained products or endometritis, often both.
  • Praevia is painless with a soft uterus; abruption is painful with a tense uterus.
  • In abruption the visible loss understates the actual loss.
  • No vaginal examination in suspected praevia until the placental site is known.
  • Abruption causes disseminated intravascular coagulation through thromboplastin release.
  • Vasa praevia bleeds fetal blood, so the fetus deteriorates rapidly.
  • Accreta risk multiplies with previous caesarean plus praevia.
  • Accreta incidence rises with the caesarean rate.
  • Antenatal diagnosis of accreta is what allows planned safe delivery.
  • Uterine rupture often shows fetal heart changes first.
  • Inversion causes shock out of proportion to loss; replace before removing the placenta.
  • Amniotic fluid embolism is a diagnosis of exclusion, managed supportively.
  • In cord prolapse elevate the presenting part and minimise cord handling.
  • Puerperal sepsis spans membrane rupture to 42 days postpartum.
  • Group A Streptococcus can progress to septic shock within hours.
  • Antibiotics will not sterilise retained products; evacuation is needed.
  • Pregnancy satisfies every element of Virchow triad.
  • Thromboembolic risk is highest in the puerperium, and the left leg predominates.
  • Low molecular weight heparin does not cross the placenta; warfarin is teratogenic.
  • Any woman of reproductive age with abdominal pain needs a pregnancy test.
  • An empty uterus above the discriminatory zone suggests ectopic pregnancy.
  • Methotrexate suits a stable small unruptured ectopic with a low hormone level.

Key formulas & results

Everything to memorise for the exam hall, in one card. Screenshot this for revision.

The organising tool
IN OBSTETRIC HAEMORRHAGE THE UTERUS IS BOTH THE SOURCE AND THE SOLUTION. AN EMPTY, CONTRACTED UTERUS DOES NOT BLEED. At term the uterus receives 600 TO 800 mL PER MINUTE, roughly A FIFTH OF CARDIAC OUTPUT. HAEMOSTASIS AFTER DELIVERY IS ACHIEVED MECHANICALLY, by INTERLACING MYOMETRIAL FIBRES CONTRACTING AROUND THE SPIRAL ARTERIES - THE LIVING LIGATURES.
IF THE UTERUS DOES NOT CONTRACT, NO AMOUNT OF CLOTTING FACTOR WILL STOP THE BLEEDING, which is why ATONY CAUSES CATASTROPHIC LOSS IN MINUTES and why EVERY FIRST-LINE TREATMENT IS AIMED AT MAKING THE UTERUS CONTRACT. The diagnostic sequence follows: IS IT CONTRACTED, IS IT EMPTY, IS THE TRACT INTACT, WILL THE BLOOD CLOT.
The four T's
TONE (UTERINE ATONY) 70 TO 80 PER CENT. TRAUMA (LACERATION, RUPTURE, INVERSION) 15 TO 20 PER CENT. TISSUE (RETAINED PLACENTA OR CLOT) UNDER 10 PER CENT. THROMBIN (COAGULOPATHY) RARE AS A PRIMARY CAUSE.
ATONY DOMINATES SO HEAVILY THAT IT SHOULD BE ASSUMED UNTIL EXCLUDED. TRAUMA IS SUGGESTED WHEN THE UTERUS IS WELL CONTRACTED AND THE WOMAN IS STILL BLEEDING, WHICH IS THE SINGLE MOST USEFUL DISCRIMINATOR AT THE BEDSIDE. THROMBIN is FREQUENTLY A SECONDARY CAUSE, because MASSIVE TRANSFUSION, HYPOTHERMIA and CONSUMPTION all produce coagulopathy.
Risk factors for atony
ANYTHING THAT OVERSTRETCHES THE UTERUS OR EXHAUSTS IT: MULTIPLE PREGNANCY, POLYHYDRAMNIOS, MACROSOMIA, HIGH PARITY, PROLONGED OR AUGMENTED LABOUR, CHORIOAMNIONITIS, RETAINED PRODUCTS.
THE LIST IS DEDUCIBLE RATHER THAN MEMORISABLE ONCE THE MECHANISM IS CLEAR: a muscle that has been OVERSTRETCHED or WORKED TO EXHAUSTION contracts poorly, and INFECTION IMPAIRS CONTRACTILITY DIRECTLY.
Active management and prevention
ACTIVE MANAGEMENT OF THE THIRD STAGE: a PROPHYLACTIC UTEROTONIC, CONTROLLED CORD TRACTION and UTERINE MASSAGE. OXYTOCIN is the uterotonic of choice, given IMMEDIATELY AFTER DELIVERY OF THE BABY. HEAT-STABLE CARBETOCIN is a useful alternative WHERE THE COLD CHAIN CANNOT BE MAINTAINED.
THE CARBETOCIN POINT MATTERS IN MUCH OF INDIA, because oxytocin degrades without refrigeration and a degraded uterotonic is worse than none, since it creates false reassurance.
The E-MOTIVE trial
Combined a CALIBRATED BLOOD-COLLECTION DRAPE for OBJECTIVE EARLY DETECTION with an IMMEDIATE BUNDLE of UTERINE MASSAGE, OXYTOCICS, TRANEXAMIC ACID, INTRAVENOUS FLUIDS, EXAMINATION and ESCALATION, DELIVERED TOGETHER RATHER THAN SEQUENTIALLY. Result: ROUGHLY 60 PER CENT RELATIVE REDUCTION in the composite of SEVERE HAEMORRHAGE, LAPAROTOMY FOR BLEEDING and DEATH FROM BLEEDING, across MORE THAN 200,000 WOMEN.
THE REASON IT WORKED IS INSTRUCTIVE: THE INTERVENTIONS WERE NOT NEW. What was new was MEASURING BLOOD LOSS OBJECTIVELY INSTEAD OF ESTIMATING IT, and GIVING ALL THE TREATMENTS AT ONCE RATHER THAN ESCALATING ONE AT A TIME WHILE THE WOMAN CONTINUED TO BLEED. This is the most important recent development in the subject.
Defining and detecting haemorrhage
BLOOD LOSS OF 500 mL OR MORE AFTER VAGINAL DELIVERY, or 1,000 mL OR MORE AFTER CAESAREAN, though ANY LOSS CAUSING HAEMODYNAMIC COMPROMISE QUALIFIES. VISUAL ESTIMATION IS UNRELIABLE AND SYSTEMATICALLY UNDERESTIMATES LARGE VOLUMES.
THAT UNDERESTIMATION IS PRECISELY WHY A CALIBRATED DRAPE IMPROVES OUTCOMES - the intervention corrects a measurement failure rather than a knowledge failure. The functional definition matters more than the number, because a woman with a haemoglobin of 6 can be compromised by 400 mL.
Why hypotension is late
PLASMA VOLUME RISES BY 40 TO 50 PER CENT IN PREGNANCY, so a healthy woman CAN LOSE A GREAT DEAL OF BLOOD BEFORE HER BLOOD PRESSURE FALLS. TACHYCARDIA AND A NARROWED PULSE PRESSURE PRECEDE HYPOTENSION. The SHOCK INDEX is HEART RATE DIVIDED BY SYSTOLIC BLOOD PRESSURE.
HYPOTENSION IN AN OBSTETRIC HAEMORRHAGE IS A LATE AND OMINOUS SIGN, exactly as in trauma. THE SHOCK INDEX IS USEFUL BECAUSE IT RISES BEFORE EITHER NUMBER ALONE BECOMES ALARMING. AN ANAEMIC WOMAN HAS NO SUCH RESERVE, WHICH IS WHY THE SAME VOLUME OF BLOOD LOSS KILLS IN INDIA THAT WOULD BE SURVIVED ELSEWHERE.
Managing haemorrhage
SIMULTANEOUS RATHER THAN SEQUENTIAL: CALL FOR HELP, RESUSCITATE, FIND THE CAUSE AND TREAT IT, ALL AT ONCE. TWO LARGE-BORE CANNULAE, SAMPLES INCLUDING CROSS-MATCH, FLUID AND EARLY BLOOD PRODUCTS, MASSIVE TRANSFUSION PROTOCOL if loss continues. UTERINE MASSAGE AND BIMANUAL COMPRESSION IMMEDIATELY.
MASSAGE AND COMPRESSION ARE PERFORMED WHILE DRUGS ARE DRAWN UP, BECAUSE MECHANICAL COMPRESSION WORKS INSTANTLY AND DRUGS TAKE MINUTES. The sequential mindset - try one drug, wait, try the next - is exactly what E-MOTIVE showed to be harmful.
The uterotonics and their contraindications
OXYTOCIN: oxytocin receptor agonist; HYPOTENSION WITH RAPID BOLUS. ERGOMETRINE: smooth muscle constriction; AVOID IN HYPERTENSION AND PRE-ECLAMPSIA. CARBOPROST: prostaglandin F2 alpha analogue; AVOID IN ASTHMA. MISOPROSTOL: prostaglandin E1 analogue; PYREXIA and SHIVERING, but HEAT STABLE.
ERGOMETRINE IN A PRE-ECLAMPTIC WOMAN AND CARBOPROST IN AN ASTHMATIC ARE THE TWO ERRORS THE EXAMINATION TESTS. THE CONTRAINDICATIONS ARE EXAMINED MORE OFTEN THAN THE DOSES. Ergometrine constricts vascular as well as uterine smooth muscle, so it raises blood pressure and risks stroke; carboprost is a bronchoconstrictor.
Escalation
TRANEXAMIC ACID as early as possible and WITHIN THREE HOURS OF ONSET. Then INTRAUTERINE BALLOON TAMPONADE, COMPRESSION SUTURES such as the B-LYNCH, STEPWISE DEVASCULARISATION ligating the UTERINE then INTERNAL ILIAC arteries, and UTERINE ARTERY EMBOLISATION where available. HYSTERECTOMY is the final step.
HYSTERECTOMY MUST NOT BE DELAYED TOO LONG, BECAUSE THE COMMONEST CONTRIBUTOR TO DEATH IS PERSISTING WITH CONSERVATIVE MEASURES IN A WOMAN WHO IS ALREADY COAGULOPATHIC. NON-PNEUMATIC ANTI-SHOCK GARMENTS are useful for STABILISING A WOMAN DURING TRANSFER in low-resource settings. The tranexamic acid window mirrors that in trauma.
Secondary postpartum haemorrhage
BETWEEN 24 HOURS AND 12 WEEKS AFTER DELIVERY. Two causes: RETAINED PRODUCTS OF CONCEPTION and ENDOMETRITIS, OFTEN TOGETHER. Presentation: BLEEDING with OFFENSIVE DISCHARGE, FEVER, UTERINE TENDERNESS and a SUBINVOLUTED UTERUS.
MANAGEMENT IS ANTIBIOTICS WITH EVACUATION WHERE PRODUCTS ARE RETAINED, and EVACUATION OF AN INFECTED UTERUS CARRIES A REAL RISK OF PERFORATION, so it is performed CAREFULLY AND AFTER ANTIBIOTICS HAVE BEEN STARTED. The soft infected uterus is easily perforated by a curette.
Praevia against abruption
PLACENTA PRAEVIA: PAINLESS bleeding, placenta in the LOWER SEGMENT, uterus SOFT AND NON-TENDER, fetal condition USUALLY GOOD, MALPRESENTATION COMMON. PLACENTAL ABRUPTION: PAINFUL bleeding from PREMATURE SEPARATION of a NORMALLY SITED placenta, uterus TENSE, TENDER AND IRRITABLE, fetal condition OFTEN POOR, VISIBLE BLEEDING MAY BE FAR LESS THAN ACTUAL LOSS.
THE CONCEALED LOSS IS THE TRAP: A WOMAN MAY BE IN PROFOUND SHOCK WITH MODEST VISIBLE BLEEDING, and the degree of shock SHOULD BE JUDGED AGAINST HER PHYSIOLOGY RATHER THAN AGAINST WHAT IS ON THE SHEET. VAGINAL EXAMINATION IS CONTRAINDICATED IN SUSPECTED PRAEVIA UNTIL THE PLACENTAL SITE IS KNOWN, because a digital examination CAN PROVOKE TORRENTIAL HAEMORRHAGE.
Abruption specifics
Associated with HYPERTENSION AND PRE-ECLAMPSIA, TRAUMA, SMOKING, COCAINE USE, PREVIOUS ABRUPTION and SUDDEN UTERINE DECOMPRESSION. It causes DISSEMINATED INTRAVASCULAR COAGULATION MORE OFTEN THAN ANY OTHER OBSTETRIC CONDITION, through RELEASE OF THROMBOPLASTIN FROM THE DAMAGED PLACENTA.
VASA PRAEVIA is rare but distinctive: PAINLESS BLEEDING AT MEMBRANE RUPTURE with RAPID FETAL DETERIORATION, because THE BLOOD LOST IS FETAL RATHER THAN MATERNAL, AND A FETUS HAS VERY LITTLE TO LOSE. That is the discriminating logic rather than the bleeding pattern.
Placenta accreta spectrum
ABNORMAL ADHERENCE OF THE PLACENTA TO THE MYOMETRIUM because of a DEFICIENT DECIDUA. ACCRETA adheres, INCRETA INVADES THE MYOMETRIUM, PERCRETA PENETRATES THE SEROSA. RISK FACTORS: PREVIOUS CAESAREAN SECTION and PLACENTA PRAEVIA, AND THE TWO MULTIPLY.
A WOMAN WITH A PRAEVIA OVERLYING A PREVIOUS CAESAREAN SCAR IS AT VERY HIGH RISK, BECAUSE THE SCAR HAS NO DECIDUA FOR THE PLACENTA TO STOP AT. ITS INCIDENCE IS RISING DIRECTLY IN PROPORTION TO CAESAREAN SECTION RATES, WHICH MAKES IT A SELF-INFLICTED EPIDEMIC. ATTEMPTING TO REMOVE AN ACCRETA PLACENTA CAUSES CATASTROPHIC HAEMORRHAGE, so management is PLANNED CAESAREAN HYSTERECTOMY or LEAVING THE PLACENTA IN SITU in selected cases. ANTENATAL DIAGNOSIS IS WHAT MAKES THE DIFFERENCE.
Rupture, inversion, embolism and prolapse
UTERINE RUPTURE: SCAR TENDERNESS, ABNORMAL FETAL HEART PATTERN OFTEN EARLIEST, CESSATION OF CONTRACTIONS, LOSS OF STATION, MATERNAL COLLAPSE - IMMEDIATE LAPAROTOMY. UTERINE INVERSION: follows TRACTION ON AN UNSEPARATED PLACENTA, PROFOUND SHOCK OFTEN DISPROPORTIONATE TO BLOOD LOSS because of VAGAL STIMULATION. AMNIOTIC FLUID EMBOLISM: SUDDEN COLLAPSE, HYPOXIA and DISSEMINATED INTRAVASCULAR COAGULATION. CORD PROLAPSE: cord COMPRESSED BETWEEN PRESENTING PART AND PELVIS.
IN INVERSION, REPLACE THE UTERUS IMMEDIATELY BEFORE THE CERVICAL RING CONTRACTS, AND REMOVE THE PLACENTA ONLY AFTER REPLACEMENT. AMNIOTIC FLUID EMBOLISM IS A DIAGNOSIS OF EXCLUSION AND MANAGEMENT IS ENTIRELY SUPPORTIVE. IN CORD PROLAPSE, ELEVATE THE PRESENTING PART, POSITION KNEE-CHEST OR HEAD-DOWN, CONSIDER FILLING THE BLADDER, AND EXPEDITE DELIVERY - MINIMISE HANDLING THE CORD BECAUSE IT CAUSES VASOSPASM.
Puerperal sepsis
GENITAL TRACT INFECTION AT ANY TIME BETWEEN RUPTURE OF MEMBRANES AND 42 DAYS POSTPARTUM. The postpartum uterus is an IDEAL CULTURE MEDIUM: a LARGE RAW PLACENTAL BED, RETAINED BLOOD, and a CERVIX STILL OPEN. Risk factors: PROLONGED RUPTURE, REPEATED VAGINAL EXAMINATIONS, PROLONGED LABOUR, CAESAREAN SECTION, RETAINED PRODUCTS, ANAEMIA.
GROUP A STREPTOCOCCUS DESERVES PARTICULAR FEAR, BECAUSE IT CAN PROGRESS FROM MILD SYMPTOMS TO FULMINANT SEPTIC SHOCK WITHIN HOURS. Management follows SOURCE CONTROL: BROAD-SPECTRUM ANTIBIOTICS AFTER CULTURES, plus EVACUATION OF RETAINED PRODUCTS OR DRAINAGE, because ANTIBIOTICS ALONE WILL NOT STERILISE AN UNDRAINED FOCUS. THE OBSTETRIC TRAP IS THAT PHYSIOLOGICAL TACHYCARDIA AND RELATIVE HYPOTENSION MAKE EARLY SEPSIS LOOK NORMAL.
Venous thromboembolism
PREGNANCY IS PROTHROMBOTIC BY DESIGN, satisfying EVERY ELEMENT OF VIRCHOW TRIAD: CLOTTING FACTORS RISE WHILE PROTEIN S FALLS, VENOUS STASIS INCREASES as the uterus compresses the pelvic veins, and DELIVERY INJURES THE VESSEL WALL. RISK IS HIGHEST IN THE PUERPERIUM. LEFT LEG DEEP VEIN THROMBOSIS PREDOMINATES.
THE LEFT-SIDED PREDOMINANCE OCCURS BECAUSE THE RIGHT COMMON ILIAC ARTERY CROSSES AND COMPRESSES THE LEFT COMMON ILIAC VEIN. LOW MOLECULAR WEIGHT HEPARIN IS THE TREATMENT AND PROPHYLAXIS OF CHOICE BECAUSE IT DOES NOT CROSS THE PLACENTA. WARFARIN IS TERATOGENIC AND IS AVOIDED, particularly in the FIRST TRIMESTER.
Ectopic pregnancy
IMPLANTATION OUTSIDE THE UTERINE CAVITY, most often in the AMPULLA of the fallopian tube. Risk factors are ANYTHING DAMAGING THE TUBE: PREVIOUS PELVIC INFLAMMATORY DISEASE, GENITAL TUBERCULOSIS, PREVIOUS ECTOPIC, TUBAL SURGERY, PREGNANCY WITH AN INTRAUTERINE DEVICE IN PLACE. Classical triad: AMENORRHOEA, ABDOMINAL PAIN, VAGINAL BLEEDING.
THE PRESENTATION IS FREQUENTLY ATYPICAL, AND THE CRUCIAL RULE IS THAT ANY WOMAN OF REPRODUCTIVE AGE WITH ABDOMINAL PAIN MUST HAVE A PREGNANCY TEST. In a normal early pregnancy the CHORIONIC GONADOTROPIN ROUGHLY DOUBLES EVERY 48 HOURS, and a SUBOPTIMAL RISE SUGGESTS AN ABNORMAL PREGNANCY. AN EMPTY UTERUS WITH A LEVEL ABOVE THE DISCRIMINATORY ZONE SUGGESTS ECTOPIC PREGNANCY, because AN INTRAUTERINE PREGNANCY SHOULD BE VISIBLE AT THAT LEVEL.
Treating ectopic pregnancy
EXPECTANT in SELECTED RESOLVING CASES. MEDICAL with METHOTREXATE where the woman is STABLE with a SMALL UNRUPTURED ECTOPIC and a LOW HORMONE LEVEL. SURGICAL where she is UNSTABLE, the ectopic is LARGE OR RUPTURED, or MEDICAL TREATMENT FAILS.
A RUPTURED ECTOPIC CAUSING HAEMODYNAMIC INSTABILITY IS A SURGICAL EMERGENCY, AND RESUSCITATION AND SURGERY PROCEED TOGETHER rather than in sequence - the same principle as in trauma laparotomy.
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Traps NEET PG sets — and how to dodge them

These are the exact option-traps and misreads that cost marks under negative marking.

WATCH OUT
Reaching for drugs before performing bimanual compression
Mechanical compression works instantly while uterotonics take minutes to act. Massage and bimanual compression are started immediately, by whoever is present, while drugs are being drawn up by someone else.
WATCH OUT
Escalating uterotonics one at a time while the woman continues to bleed
The E-MOTIVE trial showed that delivering the whole bundle together, rather than sequentially, reduced severe outcomes by around 60 per cent. Massage, uterotonics, tranexamic acid, fluids, examination and escalation happen simultaneously.
WATCH OUT
Relying on visual estimation of blood loss
Estimation systematically underestimates large volumes, which is why a calibrated collection drape improved outcomes so substantially. Objective measurement is the intervention, not better guessing.
WATCH OUT
Waiting for hypotension before treating obstetric haemorrhage aggressively
Plasma volume rises 40 to 50 per cent in pregnancy, so blood pressure is maintained until a large volume has been lost. Tachycardia and a narrowed pulse pressure come first, and hypotension is a late and ominous sign.
WATCH OUT
Giving ergometrine to a pre-eclamptic woman
Ergometrine constricts vascular as well as uterine smooth muscle, raising blood pressure further in a woman already at risk of intracerebral haemorrhage. Carboprost or misoprostol is used instead.
WATCH OUT
Giving carboprost to an asthmatic
Carboprost is a prostaglandin F2 alpha analogue and a potent bronchoconstrictor, capable of precipitating severe bronchospasm. Misoprostol, a prostaglandin E1 analogue, does not carry the same risk.
WATCH OUT
Delaying hysterectomy while trying further conservative measures
The commonest contributor to death from postpartum haemorrhage is persistence with conservative measures in a woman who has already become coagulopathic. Hysterectomy is a last step but must not become a late one.
WATCH OUT
Performing a vaginal examination in suspected placenta praevia
A digital examination can dislodge the placenta from the lower segment and provoke torrential haemorrhage. Ultrasound establishes the placental site first, and this is why bleeding after 24 weeks is scanned before it is examined.
WATCH OUT
Judging abruption severity by the visible blood loss
In abruption much of the blood is concealed behind the placenta, so a woman can be profoundly shocked with modest external bleeding. Severity is judged by her physiology, and a tense tender uterus with tachycardia signals major loss.
WATCH OUT
Forgetting that abruption causes disseminated intravascular coagulation
Thromboplastin released from the damaged placenta activates the coagulation cascade, making abruption the commonest obstetric cause of disseminated intravascular coagulation. Coagulation studies and blood products are anticipated rather than awaited.
WATCH OUT
Attempting to remove an adherent placenta at caesarean section
In placenta accreta there is no cleavage plane, and attempting removal tears the myometrium and causes catastrophic haemorrhage. Where accreta is suspected antenatally, delivery is planned with caesarean hysterectomy or leaving the placenta in situ.
WATCH OUT
Removing the placenta before replacing an inverted uterus
Replacement becomes progressively harder as the cervical ring contracts, and removing the placenta first adds bleeding from the placental bed while the uterus is still inverted. The uterus is replaced immediately, then the placenta removed.
WATCH OUT
Handling the cord repeatedly in cord prolapse
Manipulation and exposure cause vasospasm in the umbilical vessels, worsening the very hypoxia being treated. The presenting part is elevated to relieve compression, the woman is positioned head-down, and handling is minimised.
WATCH OUT
Treating puerperal sepsis with antibiotics alone when products are retained
Retained products are an undrained focus that antibiotics cannot sterilise, exactly as with an abscess. Evacuation is required, performed carefully after antibiotics are started because the infected uterus perforates easily.
WATCH OUT
Excluding ectopic pregnancy because the woman denies missed periods
The classical triad is frequently absent, and bleeding from an ectopic is often mistaken for a period. Any woman of reproductive age with abdominal pain requires a pregnancy test before any other reasoning proceeds.

Exam-pattern practice

PYQ-style questions with full solutions. Work through them as a readiness check — mark yourself honestly and get your gap report at the end.

Readiness check

Are you exam-ready for "Postpartum Hemorrhage & Obstetric Emergencies"?

9 problems from this chapter. Try each one, reveal the worked solution, mark yourself honestly — get your gap report at the end.

9 questions~6 min

5-minute revision

The whole chapter, distilled. Read this the night before the exam.

  • The uterus is both source and solution; an empty contracted uterus does not bleed.
  • Myometrial fibres are the living ligatures occluding the spiral arteries.
  • The uterus takes about a fifth of cardiac output at term.
  • Tone causes 70 to 80 per cent of postpartum haemorrhage.
  • A contracted uterus with continued bleeding means trauma.
  • Atony risk factors are overstretch, exhaustion and infection.
  • Active management is uterotonic, cord traction and massage.
  • Heat-stable carbetocin matters where the cold chain fails.
  • E-MOTIVE cut severe outcomes by around 60 per cent.
  • It worked by objective detection and simultaneous treatment.
  • Visual estimation underestimates large blood loss.
  • Plasma volume rises 40 to 50 per cent, so hypotension is late.
  • Tachycardia and narrowed pulse pressure precede hypotension.
  • The shock index rises before either number alone.
  • An anaemic woman has no reserve.
  • Massage and bimanual compression act instantly; drugs take minutes.
  • Ergometrine is contraindicated in hypertension and pre-eclampsia.
  • Carboprost is contraindicated in asthma.
  • Misoprostol is heat stable and causes pyrexia and shivering.
  • Tranexamic acid is given within three hours of onset.
  • Escalate to balloon, B-Lynch, devascularisation, embolisation.
  • Delayed hysterectomy in a coagulopathic woman contributes to death.
  • Anti-shock garments help stabilise during transfer.
  • Secondary haemorrhage is retained products or endometritis.
  • The infected uterus perforates easily at evacuation.
  • Praevia is painless with a soft uterus; abruption painful with a tense uterus.
  • In abruption the visible loss understates the true loss.
  • No vaginal examination in suspected praevia before ultrasound.
  • Abruption is the commonest obstetric cause of disseminated intravascular coagulation.
  • Vasa praevia loses fetal blood, so the fetus deteriorates fast.
  • Accreta risk multiplies with previous caesarean plus praevia.
  • Accreta incidence rises with the caesarean rate.
  • Antenatal diagnosis of accreta allows planned safe delivery.
  • Uterine rupture often shows fetal heart changes first.
  • Inversion gives shock out of proportion to loss.
  • Replace an inverted uterus before removing the placenta.
  • Amniotic fluid embolism is a diagnosis of exclusion, managed supportively.
  • In cord prolapse elevate the presenting part and minimise cord handling.
  • Puerperal sepsis spans membrane rupture to 42 days.
  • Group A Streptococcus can progress to shock within hours.
  • Antibiotics will not sterilise retained products; evacuate.
  • Pregnancy satisfies every element of Virchow triad.
  • Thrombotic risk peaks in the puerperium; the left leg predominates.
  • Low molecular weight heparin does not cross the placenta; warfarin is teratogenic.
  • Any woman of reproductive age with abdominal pain needs a pregnancy test.
  • Chorionic gonadotropin roughly doubles every 48 hours in normal pregnancy.
  • An empty uterus above the discriminatory zone suggests ectopic pregnancy.
  • Methotrexate suits a stable small unruptured ectopic with a low hormone level.

NEET PG question blueprint

How this topic is asked, tier by tier — so you can prep to the pattern.

Typical weightage: Each NEET PG question is worth +4/-1; postpartum haemorrhage and obstetric emergencies contribute 6-7 questions per attempt and overlap with Anaesthesia, Surgery and PSM

Question styleMarks eachTypical countWhat it tests
Causes and prevention4~1The four T's and their frequencies, atony risk factors, active management, carbetocin and the E-MOTIVE bundle
Recognition and physiology4~1Definitions, why estimation fails, the plasma volume effect, the shock index and the role of pre-existing anaemia
Uterotonics and management4~2Simultaneous management, the uterotonic contraindications, tranexamic acid timing, and the surgical escalation ladder including accreta
Antepartum haemorrhage4~1Praevia against abruption, concealed loss, the ban on vaginal examination, disseminated intravascular coagulation and vasa praevia
Other emergencies4~1Uterine rupture and inversion, amniotic fluid embolism, cord prolapse, puerperal sepsis and thromboembolism
Ectopic pregnancy4~1Risk factors, the discriminatory zone and doubling time, and the choice between expectant, medical and surgical management
Prep strategy
  • First pass: fix the mechanical basis of haemostasis and the four T's with their frequencies, since together they make the management sequence deducible.
  • Second pass: memorise the uterotonic contraindications and the praevia against abruption table, which generate direct questions every year.
  • Final pass: drill the emergencies where the correct action is counterintuitive - replacing the uterus before removing the placenta, not examining a suspected praevia, minimising cord handling, and not delaying hysterectomy.

Exam-hall strategy

Battle-tested tips from mentors and toppers for this topic under the sectional clock.

  1. Establish whether the uterus is contracted before choosing any treatment.
  2. Scan the history for pre-eclampsia or asthma, which exclude specific uterotonics.
  3. For antepartum bleeding, use pain and uterine tone to separate praevia from abruption.
  4. Calculate the pulse pressure before reading the systolic value.
  5. Treat options involving observation or delay as wrong in this chapter.
  6. Remember that tranexamic acid has a three-hour window, as in trauma.
  7. With NEET PG's +4/-1 marking, the four T's, uterotonic contraindications and the praevia-abruption table are high-certainty recall worth securing quickly.
  8. Under the 5-group, 42-minute time-bound format, these vignettes are long but formulaic; extract uterine tone and the planted comorbidity on the first read, since a closed group cannot be reopened.

Beyond the exam

Where this skill shows up in the job you're competing for — and in life.

The first two minutes of a haemorrhage

Putting a hand on the uterus and compressing while calling for help, before any drug is drawn up, is the single action that buys time in the period when women actually die.

Using a calibrated drape

Replacing visual estimation with objective measurement changes the moment at which the team recognises haemorrhage, which is what the E-MOTIVE trial showed translates into survival.

Planning delivery for suspected accreta

Diagnosing accreta antenatally allows a scheduled operation with blood cross-matched and senior staff present, instead of an emergency in the middle of the night with a placenta that will not separate.

The pregnancy test in the emergency department

Testing every woman of reproductive age with abdominal pain is the rule that catches the ectopic pregnancies presenting as gastroenteritis or renal colic.

Where else this topic is tested

Prepare once, score in every exam that asks it.

FMGE / NExTVery high overlap — the four T's, uterotonics, antepartum haemorrhage and ectopic pregnancy are examined at identical depth and weighted heavily
USMLE Step 2 CKHigh overlap — haemorrhage management, accreta and ectopic pregnancy are shared, with anaemia as a modifier far less emphasised
MS Obstetrics and Gynaecology entranceFoundational — assumed working knowledge, with compression suture technique, interventional radiology and obstetric critical care examined far more deeply

Questions aspirants ask

Pulled from the Q&A community and mentor sessions.

Because the volumes involved are far beyond what clotting can handle in the time available. At term the uterine arteries deliver 600 to 800 millilitres a minute into the placental bed, which is roughly a fifth of the cardiac output, and after the placenta separates that flow is pouring into an open surface the size of a dinner plate. A clot forming at that rate of flow would be washed away as fast as it formed, and a woman would exsanguinate in three or four minutes waiting for coagulation to catch up. The solution is mechanical. The myometrium is arranged as interlacing figure-of-eight fibres, and the spiral arteries run between them. When the myometrium contracts, those fibres shorten and kink the vessels closed, occluding them physically. Only once flow has stopped can clot form in the stationary blood behind the occlusion and make the haemostasis permanent. This is why a woman with perfectly normal coagulation dies of atony, and why bimanual compression, which simply supplies the compression the uterus is failing to generate, works instantly.

Because the bleeding is happening in a closed space with a narrow exit. In abruption the placenta separates from the decidua and blood collects in the plane between them, behind the placenta. For that blood to appear at the vulva it must dissect all the way to the placental edge, strip the membranes off the uterine wall, and then pass through the cervix. Much of it does not. It stays retroplacental, and it also infiltrates the myometrium, which is what produces the tense, tender, woody uterus and the continuous pain that distinguishes abruption from praevia. A concealed abruption can therefore involve litres of blood with almost nothing visible. Two consequences follow. First, the amount on the pad tells you nothing, and the assessment must rest on the pulse, the pulse pressure, the shock index and the uterine findings. Second, the retroplacental blood is in prolonged contact with damaged decidua, which releases thromboplastin, and this is why abruption is the leading obstetric cause of disseminated intravascular coagulation.

Because the drugs were never the limiting factor. The trial ran in hospitals that already stocked oxytocin, tranexamic acid and intravenous fluids, and where staff already knew how to use them. The two problems it fixed were both about process. The first was detection: clinicians estimate blood loss visually and systematically underestimate it, so a woman who had lost a litre was often recorded as having lost 400 millilitres, and the response began late. A calibrated collection drape removes the guesswork, and the trigger for action becomes a measurement rather than an impression. The second was sequencing. Conventional practice escalates stepwise, giving one uterotonic, reassessing after some minutes, then giving another, and the woman bleeds throughout every interval. The bundle gives massage, uterotonics, tranexamic acid and fluids together the moment the threshold is crossed, with examination and escalation built in. Compressing that timeline is what produced roughly a 60 per cent relative reduction in severe outcomes. The broader lesson is that in time-critical emergencies, how quickly you recognise and how completely you respond can matter more than what is in the cupboard.

Because its principal cause is an operation performed for other reasons, and the operation is being done more often. Accreta requires a deficient decidua basalis, so that the trophoblast has nothing to stop at and implants directly into myometrium. A caesarean scar is exactly such a defect: fibrous tissue with no decidua. The consequence is arithmetic. As caesarean rates rise, the population of women with uterine scars rises, and accreta incidence rises behind it with a delay of one pregnancy. The risk compounds in two ways: it increases with each additional caesarean, and it multiplies when the next placenta happens to be a praevia, because a praevia implants in the lower segment, which is precisely where the scar is. Each caesarean therefore raises the risk for the pregnancy after it, and the woman who has three previous caesareans and now has a praevia is in a very high-risk category. This is one of the strongest arguments for keeping first caesarean rates appropriate, since the harm falls not on that pregnancy but on subsequent ones.

Ask three questions in order. First, is the uterus contracted? If the stem describes a soft or boggy uterus, the answer is atony and involves compression and uterotonics. If it says the uterus is well contracted and she is still bleeding, the answer is trauma, and the action is to examine the genital tract. Second, what has been planted in the history that forbids a drug? Pre-eclampsia or hypertension rules out ergometrine, asthma rules out carboprost, and those two exclusions generate a question almost every year. Third, if the bleeding is antepartum, is there pain? Painless with a soft uterus is praevia and forbids vaginal examination; painful with a tense uterus is abruption, and the visible loss is unreliable. Two further habits: whenever the stem gives a pulse and a blood pressure, calculate the pulse pressure before reading the systolic value, because narrowing appears first. And treat any option that involves waiting, observing or reassessing in an hour as wrong, since the defining feature of this chapter is that everything happens simultaneously.
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