Antepartum Hemorrhage
Antepartum hemorrhage is bleeding from the genital tract from 24 weeks of gestation until delivery, most commonly caused by placenta praevia or placental abruption.
Antepartum Hemorrhage (APH)
Antepartum hemorrhage (APH) literally means bleeding before birth — from the Latin ante- (before) + partum (birth/delivery). Formally:
APH is defined as bleeding from the genital tract occurring from 24+0 weeks of gestation until delivery of the baby. [1][2]
- Why 24 weeks? Because this is the threshold of fetal viability — before 24 weeks, vaginal bleeding is classified under threatened miscarriage (< 12 weeks) or mid-trimester bleeding (12–24 weeks). The distinction matters because management pivots from pregnancy preservation to balancing maternal safety with potential fetal delivery.
- Note: Some sources use 20 weeks as the cut-off, but HKU and RCOG use 24 weeks [1].
Bleeding (haemorrhage) is one of the major causes of maternal mortality [1]. In Hong Kong, maternal mortality from hemorrhage has dramatically decreased (from 17 deaths in 1961 to approximately 0–1 per year currently), but APH remains a leading cause of maternal morbidity and perinatal mortality [1].
Bleeding can occur before the delivery of the baby (antepartum haemorrhage) or after the delivery of the baby (postpartum haemorrhage). [1]
2. Epidemiology and Risk Factors
| Parameter | Detail |
|---|---|
| Incidence | ~3–5% of pregnancies beyond 24 weeks |
| Placenta praevia incidence | ~0.3–0.5% of pregnancies at term |
| Placental abruption incidence | ~0.5–1% of pregnancies |
| Leading cause of 3rd trimester admission | Yes — APH is the #1 reason for emergency antenatal admission |
| Contribution to maternal mortality | Hemorrhage (ante- and postpartum combined) is within the top 3 direct causes of maternal death worldwide |
| Hong Kong context | Placenta praevia is relatively more common in HK due to high Caesarean section (CS) rates (~40–45% in private sector) and rising maternal age [1] |
2.2 Risk Factors
Understanding risk factors requires knowing the two major causes (placenta praevia and placental abruption) — each has distinct risk factors:
| Risk Factor | Mechanism |
|---|---|
| Previous Caesarean section | Scarred lower segment → preferential implantation on scar tissue; disrupted endometrium fails to support normal decidualization → placenta "seeks" more surface area, tends to spread over the lower segment |
| Previous surgery on uterus (myomectomy) | Same mechanism — uterine scarring [2][3] |
| Previous uterine curettage / repeated suction evacuation | Endometrial damage → abnormal implantation site [2] |
| Grand multiparity (≥ 5 births ≥ 20 weeks) | Repeated pregnancies → progressive endometrial damage and thinning → placenta migrates to lower segment [3] |
| Advanced maternal age ( > 35) | Decreased endometrial vascularity → placenta needs larger surface area → more likely to extend over os |
| Multiple pregnancy | Larger placental mass → higher probability of encroaching on the lower segment |
| Smoking | Causes relative uteroplacental hypoxia → compensatory placental enlargement → greater chance of covering os |
| IVF/ART conception | Embryo transfer technique may favour lower uterine implantation; also associated with higher rates of CS and multiple pregnancy |
| Previous placenta praevia | Recurrence risk ~4–8% |
| Risk Factor | Mechanism |
|---|---|
| Pre-eclampsia | Endothelial dysfunction and spiral artery remodeling failure → ischemia-reperfusion injury → decidual necrosis → bleeding into decidua basalis → abruption [1] |
| Chronic hypertension | Same mechanism — vascular damage to spiral arteries |
| Previous PPH / previous abruption | Underlying abnormal placentation tends to recur [2] |
| Smoking / cocaine use | Vasoconstriction → decidual ischemia and necrosis → hemorrhage into decidual-placental interface |
| Trauma (e.g. RTA, domestic violence) | Shear forces separate the inelastic placenta from the elastic uterine wall |
| Preterm premature rupture of membranes (PPROM) | Sudden decompression of the uterus → mechanical separation |
| Polyhydramnios → sudden decompression | Same mechanism as PPROM [2] |
| Thrombophilia (e.g. APLS, Factor V Leiden) | Micro-thrombosis at the uteroplacental interface → infarction → abruption |
| Short umbilical cord | Traction on placenta during fetal movement |
| Anaemia (Hb < 10 g/dL) | Reduced oxygen carrying capacity → inadequate placental perfusion → ischemic damage (also worsens outcomes) [2] |
| Abdominal trauma | Direct mechanical disruption |
3. Anatomy and Function: The Placental-Uterine Interface
To understand APH, you need to understand the architecture of where bleeding originates.
- Upper segment (fundus and body): Thick muscular wall composed of interlacing smooth muscle fibres ("living ligatures"). The upper segment of the uterus is the main contraction force → this is why the uterus contracts effectively after placental delivery (to compress the spiral arteries and stop bleeding) [3].
- Lower segment: The lower part of the uterus that develops from the isthmus during the 3rd trimester. It is:
- Thinner — fewer muscle fibres
- Less contractile — cannot effectively compress blood vessels
- Does not contract very well → hence, the blood vessels are not controlled, results in massive bleeding [3]
- This is why placenta praevia (placenta in the lower segment) bleeds so profusely — the lower segment cannot contract to compress the spiral arteries after separation.
- Anchored to the decidua basalis (modified endometrium) via cytotrophoblast columns
- Receives maternal blood supply through spiral arteries that have been remodeled by trophoblast invasion (loss of smooth muscle → low resistance, high flow system)
- At term, uterine blood flow is approximately 500–700 mL/min — this is why any disruption to the placental-uterine interface can cause catastrophic hemorrhage within minutes
- The decidua basalis is the maternal surface of the placenta
- In abruption, bleeding occurs within the decidua basalis → a retroplacental haematoma forms → separates the placenta from the uterine wall
- In praevia, the placenta is implanted over or near the internal cervical os → as the lower segment thins and stretches in the 3rd trimester, the inelastic placenta separates from the underlying uterine wall
- The cervix must dilate and efface during labor
- If a placenta overlies the internal os, any cervical change causes mechanical shearing of the placental villi from the decidua → painless, bright red bleeding (classic praevia presentation)
The placental bed is where the uterus is very vascular [3]. As a result, since this is the lower part of the uterus, does not contract very well → hence, the blood vessels are not controlled, results in massive bleeding [3].
4. Etiology (with Focus on Hong Kong)
APH is broadly classified by source:
In clinical practice, approximately 50% of APH is unclassified (no cause found despite investigation). The two major obstetric causes — placenta praevia and placental abruption — together account for about half of all identified causes.
4.1 Placenta Praevia
Definition: Placenta implanted wholly or partially in the lower uterine segment, in relation to the internal cervical os.
- Abnormal implantation site: The blastocyst implants low in the uterine cavity (reasons: prior endometrial damage, large placental surface area, random chance)
- Lower segment formation: From ~28 weeks, the isthmus of the uterus transforms into the lower segment by progressive stretching and thinning
- Shearing forces: The inelastic placenta cannot stretch with the lower segment → partial separation occurs → maternal spiral arteries at the separation site are opened → bleeding from the placental bed which is very vascular [3]
- Inability to tamponade: The lower segment has sparse muscle fibres → cannot contract to compress the torn vessels → results in massive bleeding [3]
- Provocation by cervical changes: Digital vaginal examination, sexual intercourse, or onset of labor causes further cervical dilation → further placental separation → more bleeding
Key concept: Praevia bleeding is painless because there is no uterine irritability or contractions — the blood escapes freely through the cervical os. The uterus is soft and non-tender.
Hong Kong has one of the highest CS rates in the world (overall ~30%, private sector ~45%). Each prior CS increases the risk of placenta praevia:
- 1 prior CS: RR ~1.5
- 2 prior CS: RR ~2.0
- ≥ 3 prior CS: RR ~3.0+
This also increases the risk of placenta accreta spectrum (PAS) — the feared combination of praevia + accreta.
4.2 Placental Abruption (Abruptio Placentae)
Definition: Premature separation of a normally implanted placenta from the uterine wall before delivery of the fetus.
- Decidual arterial pathology: Abnormal spiral artery remodeling (as in pre-eclampsia) → vessel wall necrosis → rupture of a decidual artery
- Retroplacental haematoma formation: Blood accumulates between the placenta and decidua basalis
- Expanding haematoma: Progressive separation → more vessels disrupted → haematoma enlarges
- Two patterns of bleeding:
- Revealed (~80%): Blood tracks down between the membranes and uterine wall → escapes through the cervix → visible vaginal bleeding
- Concealed (~20%): Blood is trapped behind the placenta → NO visible vaginal bleeding but the patient is in shock (this is the dangerous one — "the patient who looks worse than her bleeding would suggest")
- Mixed: Both revealed and concealed components
- Uterine irritability: Extravasated blood infiltrates the myometrium → acts as a powerful irritant → uterine hypertonicity, tenderness, and contractions
- Couvelaire uterus (in severe cases): Massive myometrial infiltration → the uterus appears purple/bruised at laparotomy → impaired contractility postpartum → PPH
- DIC: Release of tissue thromboplastin from the damaged placenta into the maternal circulation → activates the extrinsic coagulation pathway → disseminated intravascular coagulation [4][5]
- Fetal compromise: Placental separation reduces the functional surface area for gas exchange → fetal hypoxia → fetal distress → fetal death if > 50% separation
- Pre-eclampsia prevalence in HK: ~3–5% (similar to global)
- Smoking prevalence in HK pregnant women is low (~2%), so this is a less important risk factor locally
- However, advanced maternal age (median age of first birth in HK is ~32) increases both pre-eclampsia and abruption risk
Definition: Fetal blood vessels traverse the fetal membranes over or near the internal cervical os, unsupported by placental tissue or umbilical cord.
Pathophysiology
- "Vasa" = vessels (Latin); "praevia" = going before/in front of
- Two types:
- Type 1: Velamentous cord insertion — the umbilical vessels run through the membranes before reaching the placenta. If these vessels cross the internal os, they are vasa praevia.
- Type 2: Vessels connecting lobes of a succenturiate (accessory) or bilobed placenta cross the internal os
- When membranes rupture (spontaneously or artificially), these unsupported fetal vessels tear → fetal hemorrhage → rapid fetal exsanguination (the fetal blood volume at term is only ~250–300 mL)
- The bleeding is fetal blood, not maternal — this is the critical distinguishing feature
Clinical Pearl — Vasa Praevia
Vasa praevia has a fetal mortality rate of ~60% if undiagnosed but < 5% if diagnosed antenatally and planned CS performed before membrane rupture. Always suspect vasa praevia when there is painless vaginal bleeding at the time of amniotomy or spontaneous rupture of membranes with rapid fetal heart rate deceleration. The Apt test (or Singer test) can distinguish fetal from maternal hemoglobin — fetal hemoglobin is resistant to alkali denaturation.
- Rare but catastrophic
- Previous surgery on uterus (Caesarean section, myomectomy) is a key risk factor [2][3]
- Upper segment classical CS incisions carry a ~10% rupture risk for subsequent vaginal delivery (hence a contraindication to trial of labor after CS, or TOLAC) [3]
- Low segment C-section is not a contraindication for future vaginal delivery (rupture risk ~0.5%) [3]
- Pathophysiology: Scar tissue lacks the elasticity of normal myometrium → during labor, uterine contractions generate pressure that exceeds scar tensile strength → scar dehiscence or full-thickness rupture → hemorrhage into peritoneal cavity ± fetal expulsion
- Induced or augmented labour with oxytocin increases the risk of rupture in a scarred uterus [2]
These are generally benign and involve the cervix or vagina rather than the placenta:
| Cause | Mechanism |
|---|---|
| Cervical ectropion (erosion) | Columnar epithelium everts onto ectocervix under estrogen influence in pregnancy → fragile, bleeds on contact (post-coital) |
| Cervical polyp | Pedunculated mucosal growth → bleeds easily |
| Cervical carcinoma | Neovascularization in tumor → friable vessels → contact bleeding |
| Cervicitis (e.g., Chlamydia, gonorrhea) | Inflammation → hyperemia → bleeding |
| Vaginal varicosities | Increased pelvic blood flow in pregnancy → dilated veins → rupture |
| Trauma | E.g., post-coital trauma |
5. Classification
As above — obstetric vs. non-obstetric vs. indeterminate
| Grade | Blood Loss | Clinical Features |
|---|---|---|
| Minor / spotting | < 50 mL | Spotting, no hemodynamic changes |
| Minor | 50–1000 mL | No shock, hemodynamically stable |
| Major | 1000–2000 mL | Signs of shock (tachycardia, hypotension, pallor) |
| Massive | > 2000 mL or hemodynamic instability regardless of measured volume | Cardiovascular collapse, coagulopathy, altered consciousness |
The older 4-tier classification (Types I–IV) has been replaced by a simpler 2-tier system based on transvaginal ultrasound (TVS):
| Classification | Definition | Clinical Significance |
|---|---|---|
| Low-lying placenta | Placental edge is within 20 mm of the internal os but does NOT cover it | May still allow vaginal delivery if edge > 20 mm from os at term; close follow-up with serial TVS |
| Placenta praevia | Placenta partially or completely covers the internal os | Caesarean section is mandatory |
The old classification (Types I–IV or marginal/partial/complete) is still commonly used clinically and in some HKU teaching materials:
- Type I (marginal): Placenta in lower segment but not reaching the os
- Type II (marginal): Reaching but not covering the os
- Type III (partial): Partially covering the os
- Type IV (complete/central): Completely covering the os
| Grade | Features |
|---|---|
| Grade 0 (asymptomatic) | Diagnosed only retrospectively by finding a retroplacental clot at delivery |
| Grade 1 (mild, ~40%) | Small vaginal bleed, mild uterine tenderness, no fetal or maternal compromise |
| Grade 2 (moderate, ~45%) | Moderate vaginal bleed, uterine tenderness and hypertonicity, fetal distress present, no maternal coagulopathy |
| Grade 3 (severe, ~15%) | Severe bleed (may be concealed), uterine tetany ("board-like" rigidity), fetal death, maternal shock ± DIC |
When praevia coexists with abnormally invasive placentation:
| Type | Depth of Invasion |
|---|---|
| Accreta | Chorionic villi attached to myometrium (no intervening decidua basalis) but not invading it |
| Increta | Villi invade into myometrium |
| Percreta | Villi penetrate through the full thickness of myometrium → may invade bladder, bowel |
PAS is increasing in frequency in Hong Kong, mirroring the global trend of rising CS rates. The combination of placenta praevia + prior CS scar = highest risk for PAS.
6. Clinical Features
The clinical presentation of APH depends fundamentally on the cause and severity of bleeding. The key clinical task is to distinguish between the two major causes (praevia vs. abruption), as they have opposing presentations.
| Symptom | Placenta Praevia | Placental Abruption | Pathophysiological Basis |
|---|---|---|---|
| Nature of bleeding | Painless, bright red, fresh blood | Painful, dark red blood (may be absent if concealed) | Praevia: No uterine irritability, blood flows freely out of os. Abruption: Blood irritates myometrium → contractions and pain; concealed blood is denatured → dark |
| Onset | Often unprovoked (may be during sleep) or after coitus/VE | Often sudden, may follow trauma, cocaine use, or spontaneous with pre-eclampsia | Praevia: Lower segment stretching is a passive process. Abruption: Acute vascular event (arterial rupture) |
| Recurrence | Characteristically recurrent — each episode tends to be heavier ("warning hemorrhages") | Usually a single event that is continuous | Praevia: As the lower segment continues to stretch, more separation occurs at intervals. Abruption: Ongoing arterial bleed |
| Pain | Absent | Constant, severe abdominal pain ± back pain (posterior placenta) | Praevia: No myometrial infiltration. Abruption: Blood infiltrates myometrium → irritation → tonic contraction → ischemia → pain |
| Contractions | Usually absent (unless coincidental labor) | Present — often tonic (uterus does not relax between contractions) | Blood as a potent uterine irritant → sustained myometrial contraction |
| Fetal movements | Usually normal (unless massive bleed → maternal shock → fetal hypoperfusion) | May be reduced or absent (fetal distress/death from placental insufficiency) | Abruption: Functional placental area reduced → decreased O₂ delivery to fetus |
Other Symptoms by Cause
- Vasa praevia: Sudden painless vaginal bleeding at the time of membrane rupture (spontaneous or artificial) with rapid fetal heart rate changes (sinusoidal pattern or bradycardia). The bleeding is from the fetus, not the mother — even a small amount (50–100 mL) can be lethal to the fetus.
- Uterine rupture: Acute severe abdominal pain, often during labor in a woman with a uterine scar. There may be a history of induced or augmented labour [2]. Classic symptom: "something tore" sensation → cessation of contractions → maternal shock.
- Cervical causes: Typically post-coital spotting, small volume, not associated with pain or contractions.
| Sign | Placenta Praevia | Placental Abruption | Pathophysiological Basis |
|---|---|---|---|
| General condition | Proportional to visible blood loss | Often worse than the visible blood loss would suggest (concealed component) | Concealed abruption: Large retroplacental haematoma → hypovolemia without visible bleeding |
| Vital signs | Tachycardia, hypotension if significant bleed | Tachycardia, hypotension; may be disproportionately shocked | Both → hypovolemic shock. In abruption, concealed bleed + DIC consumption worsens hemodynamics |
| Abdominal palpation — Uterine tone | Soft, non-tender, relaxed | "Woody hard" / "board-like" — tense, tender, rigid | Abruption: Extravasated blood irritates myometrium → tonic contraction. The uterus cannot be indented on palpation |
| Uterine size | Corresponds to dates | May be larger than dates (expanding retroplacental haematoma) | Concealed blood accumulates within the uterus → increasing fundal height |
| Fetal lie/presentation | Often malpresentation (breech, transverse, oblique) | Normal | Praevia: Low-lying placenta occupies the lower segment → prevents the fetal head from engaging → malpresentation |
| Fetal heart rate | Usually normal (unless maternal shock) | Often abnormal (late decelerations, bradycardia, sinusoidal pattern, absent) | Abruption: Reduced functional placental surface → fetal hypoxia → abnormal CTG |
| Presenting part | High, non-engaged head (or malpresentation) | Usually engaged (normally sited placenta) | Praevia: Placenta mechanically blocks engagement of the fetal head |
| Vaginal examination | NEVER perform digital VE until placenta praevia is excluded by USS | May show dark blood, cervical dilation | Praevia: VE can provoke catastrophic hemorrhage by further separating placenta from the os |
| Speculum examination | Blood coming from the os, cervix may look normal | Blood from the os, often mixed with clots | Both: Blood originates from above the cervix. Speculum is safe and helps exclude cervical causes |
| Signs of DIC | Rare (unless massive hemorrhage) | Common in severe abruption | Abruption: Tissue thromboplastin release → DIC → oozing from venipuncture sites, petechiae, non-clotting blood |
| Signs of pre-eclampsia | Not typically associated | May coexist (pre-eclampsia is a risk factor for abruption) [1] | Underlying mechanism: Endothelial dysfunction → both pre-eclampsia and decidual artery rupture |
NEVER Perform Digital VE in APH
This is a classic exam pitfall and an absolute clinical rule: NEVER perform a digital vaginal examination in a woman with APH until placenta praevia has been excluded by ultrasound. A digital VE through a placenta praevia can cause torrential, life-threatening hemorrhage. Speculum examination is safe and should be performed to visualize the cervix, rule out cervical causes, and assess the source of bleeding. If facilities are available, ultrasound first.
| Feature | Placenta Praevia | Placental Abruption |
|---|---|---|
| Pain | Painless | Painful (constant) |
| Blood color | Bright red | Dark red (old blood) |
| Bleeding pattern | Recurrent, provoked | Continuous, sudden onset |
| Shock vs. visible loss | Proportional | Disproportionate (worse than apparent) |
| Uterine tone | Soft, relaxed | Hard, tender ("board-like") |
| Fetal distress | Uncommon (unless massive) | Common |
| Malpresentation | Common | Uncommon |
| Coagulopathy (DIC) | Rare | Common in severe cases |
| Fetal heart | Usually reassuring | Often non-reassuring/absent |
| Digital VE | CONTRAINDICATED | Permissible (after USS excludes praevia) |
| Feature | Detail |
|---|---|
| Timing | At membrane rupture (spontaneous or ARM) |
| Blood | Small volume but fetal blood (dark red, may mix with liquor) |
| Fetal heart | Rapid deterioration — sinusoidal pattern → bradycardia → death |
| Maternal condition | Stable (bleeding is fetal, not maternal) |
| Diagnosis | Apt/Singer test (distinguishes fetal from maternal Hb); antenatal TVS with color Doppler |
| Feature | Detail |
|---|---|
| Context | Previous surgery on uterus [2][3], labor (especially induced or augmented) [2] |
| Pain | Sudden, severe, "tearing" pain → may diminish (uterus stops contracting) |
| Contractions | Cease suddenly |
| Fetal parts | May be palpable superficially ("fetus felt under the skin") if complete rupture with extrusion |
| Fetal heart | Absent or profoundly bradycardic |
| Maternal signs | Peritonism, shock, sometimes shoulder tip pain (diaphragmatic irritation from hemoperitoneum) |
| Vaginal bleeding | May be surprisingly minimal (most blood is intraperitoneal) |
| Class | Blood Loss | Heart Rate | Blood Pressure | Signs |
|---|---|---|---|---|
| I | < 750 mL (< 15%) | Normal or mild ↑ | Normal | Asymptomatic |
| II | 750–1500 mL (15–30%) | 100–120 | Narrow pulse pressure | Anxious, delayed capillary refill |
| III | 1500–2000 mL (30–40%) | > 120 | Systolic < 90 | Confused, oliguria, cold peripheries |
| IV | > 2000 mL ( > 40%) | > 140 or bradycardia | Unrecordable | Unconscious, anuria |
Remember: Pregnant women have a physiologically expanded blood volume (~40% increase, i.e., ~6–7 L at term). They can lose up to 1–1.5 L before showing signs of shock — by the time they're tachycardic, they've already lost a lot. This is why clinical signs can be deceptively reassuring early on.
Key Clinical Point
Anaemia (Haemoglobin < 10 g/dL) at onset of labour [2] is a risk factor listed for both APH complications and PPH. A woman who is already anemic tolerates blood loss very poorly — she will decompensate earlier and more severely. Always check the booking Hb and current Hb in any woman presenting with APH.
Antepartum hemorrhage is explicitly listed as a risk factor for PPH [2][3]. The mechanisms:
- Placenta praevia → atonic PPH: The placental bed in the lower segment → does not contract very well [3] → poor hemostasis after placental delivery
- Placenta praevia + accreta: Abnormal adherence means the placenta does not separate → retained placenta → massive hemorrhage
- Abruption → DIC: Release of placental materials into circulation → pro-coagulant effect [5] → consumption coagulopathy → inability to form clots → ongoing bleeding post-delivery (thrombin arm of the 4T's of PPH)
- Abruption → Couvelaire uterus: Myometrial infiltration → uterus cannot contract → uterine atony (tone arm of the 4T's)
Differential diagnosis of PPH includes the 4 T — Tone, Tissue, Trauma, Thrombin [6]
DIC in Placental Abruption
Obstetric conditions causing DIC: amniotic fluid embolism, abruptio placentae, HELLP syndrome or eclampsia or severe pre-eclampsia, septic abortion [4][5]
Mechanism:
- Damaged placenta releases tissue factor (thromboplastin) into maternal circulation
- Tissue factor activates the extrinsic pathway (Factor VII → VIIa → Factor X activation)
- Widespread thrombin generation → fibrin deposition in microvasculature → organ ischemia
- Consumption of platelets, fibrinogen, and clotting factors → bleeding diathesis
- Secondary activation of fibrinolysis → elevated D-dimer and FDPs
Laboratory findings in acute DIC [4][5]:
| Test | Finding | Reason |
|---|---|---|
| Platelets | ↓ | Consumed in microthrombi |
| PT/APTT | ↑ | Clotting factors consumed |
| Fibrinogen | ↓ | Consumed; normally elevated in pregnancy (4–6 g/L), so a "normal" level of 2 g/L is actually low |
| D-dimer | ↑↑ | Fibrinolysis of microthrombi |
| PBS | Schistocytes | RBC fragmentation through fibrin strands in microvasculature (MAHA) |
Fibrinogen in Pregnancy
Normal fibrinogen in pregnancy is 4–6 g/L (much higher than non-pregnant: 2–4 g/L). A fibrinogen level of < 2 g/L in a pregnant woman with abruption is a strong predictor of severe hemorrhage and DIC. Don't be reassured by a "normal" fibrinogen level — it's low for pregnancy.
High Yield Summary
Antepartum Hemorrhage (APH):
- Defined as bleeding from the genital tract from 24 weeks of gestation until delivery
- Two major causes: Placenta praevia (~30%) and placental abruption (~25%); ~50% are unclassified
- Placenta praevia: Painless, bright red, recurrent bleeding; soft uterus; malpresentation; high presenting part. Lower segment cannot contract → massive bleeding
- Placental abruption: Painful, dark blood (may be concealed); "woody hard" uterus; fetal distress common; DIC risk from tissue thromboplastin release
- Vasa praevia: Fetal bleeding at membrane rupture → rapid fetal death; small volume but lethal
- NEVER perform digital VE until praevia excluded by USS
- APH is a risk factor for PPH — always prepare for ongoing hemorrhage
- DIC is an important complication of abruption — check fibrinogen (low for pregnancy if < 2 g/L)
- Risk factors for praevia: prior CS, prior uterine surgery, multiparity, advanced age, IVF, smoking
- Risk factors for abruption: pre-eclampsia, hypertension, trauma, smoking, cocaine, thrombophilia, PPROM
- Placenta accreta spectrum increasingly common with rising CS rates in Hong Kong
Active Recall - Antepartum Hemorrhage
[1] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (Introduction, Definition, Risk factors sections) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (Risk factors slide, p6) [3] Lecture slides: Block C - Postpartum Haemorrhage.pdf (Risk factors p5, Summary p32) [4] Senior notes: Maksim Medicine Notes.pdf (p165, DIC section — Obstetric causes) [5] Senior notes: Ryan Ho Haemtology.pdf (p137, DIC causes — Obstetric conditions) [6] Lecture slides: PPH for teaching (20210716)v6.pdf (Summary p37)
Differential Diagnosis of Antepartum Hemorrhage
The differential diagnosis of APH is fundamentally a source-based exercise. You are asking: where is this blood coming from? The answer can be traced anatomically from above downward — placenta, uterus, cervix, vagina — and each source has a distinct mechanism, presentation, and level of danger. Let me walk you through this systematically.
When a pregnant woman > 24 weeks presents with vaginal bleeding, your thinking should follow this structure:
The 50% Rule
Approximately 50% of APH remains unexplained even after full investigation. This is important clinically — you cannot always give the patient a definitive diagnosis. But you must rule out the dangerous causes (praevia, abruption, vasa praevia, rupture) before labelling APH as "indeterminate."
The Major Differential Diagnoses
Why does it bleed? The placenta is implanted over or near the internal cervical os. As the lower segment stretches and thins from ~28 weeks onward, the inelastic placenta shears away from the underlying decidua. The placental bed is where the uterus is very vascular [3]. Since this is the lower part of the uterus, does not contract very well → hence, the blood vessels are not controlled, results in massive bleeding [3].
How to recognise it at the bedside:
- Painless bright red vaginal bleeding — classically unprovoked, often waking the patient from sleep
- Soft, non-tender uterus on palpation [7]
- Fetal head totally above brim (high presenting part) or malpresentation — because the placenta physically blocks engagement [7]
- Fetal heart rate usually normal (unless massive maternal hemorrhage → reduced uteroplacental perfusion)
- Bleeding is recurrent — each episode tends to be progressively heavier ("warning hemorrhages")
Key risk factors to spot in the clinical stem:
- Previous caesarean sections (the more CS, the higher the risk) [7]
- Multiple pregnancy, grand multiparity, advanced maternal age, prior uterine surgery [2][3]
Exam stem clues for praevia: "soft and non-tender uterus," "fetal head 5/5 above brim," "known low-lying placenta covering os," "previous 3 caesarean sections," "cephalic presentation but not engaged" [7]
Exam Pearl from Past Papers
A 38-year-old multiparous woman with three previous caesarean sections presents at 36 weeks with heavy APH. Uterus is soft and non-tender. Fetal head is totally above brim. → Most likely diagnosis: Placenta praevia [7]. The logic: multiple CS scars → high risk of praevia; soft non-tender uterus = NOT abruption; head above brim = something blocking engagement (i.e., the placenta).
Why does it bleed? A normally-sited placenta separates prematurely from the uterine wall due to rupture of a decidual artery → retroplacental haematoma formation → progressive separation. Blood may be revealed (tracks out through the cervix), concealed (trapped behind the placenta), or mixed.
How to recognise it at the bedside:
- Painful — constant, severe abdominal pain (blood is a potent myometrial irritant → tonic contraction → ischemic pain)
- Uterus is tender and irritable on palpation [7] — classically "woody hard" or "board-like" (tonic contraction)
- Fetal bradycardia or absent fetal heart (> 50% separation → fatal fetal hypoxia) [7]
- Patient may appear more shocked than the visible blood loss suggests (concealed component)
- Dark red blood (older, denatured blood from retroplacental collection)
Key risk factors to spot in the clinical stem:
- Chronic smoker [7]
- Hypertension / pre-eclampsia (BP 150/100 mmHg) [7]
- Previous abruption, cocaine use, trauma, thrombophilia
- Note: a previous ovarian cystectomy with a suprapubic transverse scar does NOT = uterine scar; it is not a risk factor for praevia or uterine rupture [7]
Exam stem clues for abruption: "tender and irritable uterus," "fetal bradycardia," "chronic smoker," "hypertension," "suprapubic scar from ovarian cystectomy" (indicating NO uterine surgery, hence NOT praevia or rupture) [7]
Exam Pearl — The Ovarian Cystectomy Trap
A previous laparotomy with ovarian cystectomy (suprapubic transverse scar) does NOT constitute previous uterine surgery. The scar is on the abdomen, not the uterus. This patient has no increased risk of praevia from uterine scarring or uterine rupture. If her uterus is tender and irritable, the diagnosis is placental abruption, not praevia or rupture [7].
Why does it bleed? Fetal blood vessels (from velamentous cord insertion or connecting a succenturiate lobe) traverse the membranes over the internal os, unsupported by placenta or Wharton's jelly. When membranes rupture, these fragile vessels tear → fetal hemorrhage.
How to recognise it:
- Painless vaginal bleeding occurring at the time of membrane rupture (spontaneous ROM or amniotomy)
- Small volume of bleeding (but devastating to the fetus — fetal blood volume is only ~80 mL/kg, i.e., ~250–300 mL at term)
- Rapid fetal deterioration — sinusoidal CTG pattern → bradycardia → fetal death
- Maternal haemodynamic stability — because the blood is fetal, not maternal
Key distinguishing feature from praevia:
- Praevia bleeds maternal blood from the placental bed; vasa praevia bleeds fetal blood from torn fetal vessels
- Timing: vasa praevia bleeds specifically at ROM, while praevia bleeds with cervical changes (dilation, stretching)
- The Apt test (alkaline denaturation test) can distinguish fetal from maternal hemoglobin — fetal Hb (HbF) resists alkali denaturation and stays pink, while adult Hb (HbA) denatures and turns brown/yellow
Why does it bleed? The uterine wall — usually at the site of a previous scar — gives way under the pressure of contractions. This allows hemorrhage into the peritoneal cavity and may result in fetal extrusion into the abdomen.
How to recognise it:
- Context: Previous surgery on uterus (Caesarean section, myomectomy) [2][3] — especially classical (upper segment) CS which carries ~10% rupture risk for subsequent vaginal delivery [3]
- Induced or augmented labour [2] — oxytocin increases intraluminal pressure against a weakened scar
- Acute severe abdominal pain, often with a "tearing" sensation
- Sudden cessation of contractions — the uterus has lost its wall integrity and cannot contract
- Fetal parts may be palpable superficially (if complete rupture with fetal expulsion)
- Maternal shock — often disproportionate to vaginal bleeding (most blood is intraperitoneal)
- Fetal heart absent or severely bradycardic
How to differentiate from abruption:
- Uterine rupture: cessation of contractions (uterus can't contract when ruptured)
- Abruption: increased uterine tone (tonic contraction from myometrial irritation)
- Uterine rupture: typically occurs during labor in a scarred uterus
- Abruption: can occur at any time, not necessarily during labor
These are generally benign and the bleeding is typically small volume, post-coital, and comes from a visible source on speculum examination.
| Cause | Why it bleeds | Key Clinical Features |
|---|---|---|
| Cervical ectropion | Columnar epithelium everts under estrogen influence in pregnancy → fragile, bleeds on contact | Post-coital spotting, visible red area around os on speculum |
| Cervical polyp | Pedunculated mucosal growth with fragile surface vessels | Visible polyp on speculum; painless contact bleeding |
| Cervical carcinoma | Neovascularization within the tumor; irregular friable tissue | Irregular, friable, ulcerated cervix on speculum; may have contact bleeding; consider if no smear history |
| Cervicitis | Infection (Chlamydia, gonorrhea, HSV) → inflammation → hyperemia → mucosal friability | Purulent discharge, cervical motion tenderness; bleeding with contact |
| Vaginal varicosities | Increased pelvic blood flow in pregnancy → dilated venous channels that can rupture | Visible varicosities on speculum; can bleed with minimal trauma |
| Vaginal/vulval trauma | Direct mechanical disruption of tissue | History of trauma or coitus; visible laceration |
Clinical Approach
You must perform a speculum examination (safe in APH) to visualise the cervix and rule out local causes before attributing bleeding to a placental source. A cervical carcinoma can present for the first time in pregnancy — don't miss it. However, NEVER perform a digital vaginal examination until placenta praevia has been excluded by ultrasound [1][7].
- After thorough evaluation (history, examination, USS, speculum), no cause is identified in approximately half of all APH cases
- These are often thought to be due to marginal placental separation (small separation at the placental edge) or minor decidual bleeding
- Although often self-limiting, unclassified APH is not benign — it is associated with increased risk of:
- Management: observation, serial fetal monitoring, steroids for fetal lung maturity if < 34 weeks
| Feature | Placenta Praevia | Placental Abruption | Vasa Praevia | Uterine Rupture |
|---|---|---|---|---|
| Pain | None | Severe, constant | None | Acute, tearing |
| Bleeding | Bright red, recurrent | Dark, may be concealed | Small, at ROM | Variable, often intraperitoneal |
| Blood source | Maternal | Maternal | Fetal | Maternal |
| Uterine tone | Soft | Woody hard | Normal | Loss of contour |
| Fetal heart | Usually normal | Abnormal (bradycardia, late decels) | Sinusoidal → absent | Absent or bradycardic |
| Presenting part | High / malpresentation | Normal / engaged | Normal | May be superficial |
| Shock vs. visible bleeding | Proportional | Disproportionate | Maternal stable | Disproportionate |
| Coagulopathy | Rare | Common (DIC) | No | Possible if massive |
| Key risk factor | Prior CS, placenta praevia on USS | Smoking, pre-eclampsia, cocaine | Velamentous insertion, bilobed/succenturiate placenta | Prior uterine scar + labor |
| Diagnosis | USS (TVS) | Clinical + USS | TVS with colour Doppler; Apt test | Clinical → laparotomy |
| Condition | Reason to Consider | How to Differentiate |
|---|---|---|
| "Bloody show" (labor) | Mucus plug with blood-streaked mucus as cervix effaces | Small amount, mucoid, associated with contractions; normal part of early labor |
| Cervical dilatation in preterm labor | Cervical change → rupture of small cervical vessels | Contractions present, cervical dilatation on speculum/USS, no placental cause |
| Gestational trophoblastic disease (GTD) | Very rare beyond 24 weeks (usually presents earlier) | "Snowstorm" appearance on USS, markedly elevated β-hCG, no viable fetus |
| Coagulopathy / bleeding disorder | Bleeding tendencies can cause APH without a structural cause [2] | Check platelet count, PT/aPTT, fibrinogen. History of easy bruising, family history |
| Marginal sinus rupture | Tearing of the marginal venous sinus at the placental edge | Often self-limiting; USS may show marginal collection; no retroplacental haematoma |
An important conceptual point: DIC is both a complication of APH and a contributor to ongoing APH. In placental abruption, release of placental materials into circulation → pro-coagulant effect [5] → widespread activation of the coagulation cascade → consumption of clotting factors and platelets → bleeding due to consumption coagulopathy [4].
This creates a vicious cycle:
DIC laboratory features in acute setting: ↓ platelets, ↑ PT, ↑ APTT, ↓ fibrinogen, ↑ D-dimer, schistocytes on PBS [4][5][8]
Obstetric causes of DIC include: amniotic fluid embolism, eclampsia/HELLP, placenta abruptio, septic abortion [4][5]
So when approaching the differential of APH, always ask: is the bleeding due to a structural/anatomical cause, or is there a coagulopathy making it worse (or both)?
When you see an exam question on APH, use this rapid mental algorithm:
-
Is the uterus soft or hard?
- Soft → Praevia (or local cause)
- Hard/tender → Abruption (or rupture)
-
Is there pain?
- Painless → Praevia, vasa praevia, local cause
- Painful → Abruption, rupture
-
What is the fetal condition?
- Normal → Praevia likely, local cause
- Compromised → Abruption, vasa praevia, rupture
-
What is the obstetric history?
-
When did it bleed relative to membrane rupture?
- At ROM with fetal distress → Vasa praevia
Worked Exam Examples from Past Papers
Example 1 [7]: 22-year-old nullipara, chronic smoker, 35 weeks, heavy vaginal bleeding, pulse 120, BP 150/100, uterus tender and irritable, fetal bradycardia. → Placental abruption. Why? Smoker (risk factor), hypertensive (pre-eclampsia/chronic HTN), tender irritable uterus (myometrial irritation from blood), fetal bradycardia (placental insufficiency).
Example 2 [7]: 50-year-old nullipara, 36 weeks, heavy APH, history of laparotomy with ovarian cystectomy, suprapubic transverse scar. → Placental abruption. Why? Ovarian cystectomy is NOT uterine surgery → no risk for praevia/rupture. Nullipara at 50 → likely IVF → higher risk of pre-eclampsia → abruption.
Example 3 [7]: 38-year-old multipara with 3 previous CS, 36 weeks, heavy APH, soft non-tender uterus, fetal head totally above brim. → Placenta praevia. Why? 3 CS = severe uterine scarring → high risk praevia; soft non-tender = not abruption; head above brim = placenta blocking engagement.
High Yield Summary
Differential Diagnosis of APH — Key Points:
- Two major causes: Placenta praevia (~30%) and placental abruption (~25%); ~50% remain unclassified
- Praevia = painless, bright red, recurrent, soft uterus, malpresentation, high head
- Abruption = painful, dark blood, tender/hard uterus, fetal distress, DIC risk
- Vasa praevia = fetal blood at ROM, small volume but lethal to fetus, sinusoidal CTG
- Uterine rupture = prior scar + labor, sudden pain then cessation of contractions, shock
- Local causes = cervical ectropion/polyp/carcinoma/cervicitis → diagnosed on speculum
- Never digital VE until praevia excluded by USS
- Previous ovarian cystectomy ≠ previous uterine surgery → does not increase praevia/rupture risk
- DIC is both a complication of and contributor to APH in abruption
- Abruption leads to PPH via DIC (Thrombin) and Couvelaire uterus (Tone)
Active Recall - APH Differential Diagnosis
References
[1] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (Introduction, Definition) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (Risk factors, p6) [3] Lecture slides: Block C - Postpartum Haemorrhage.pdf (Risk factors p5, Summary p32) [4] Senior notes: Maksim Medicine Notes.pdf (p165, DIC section — Obstetric causes, clinical features, lab features) [5] Senior notes: Ryan Ho Haemtology.pdf (p137–138, DIC causes, acute vs chronic DIC, laboratory features) [7] Lecture slides: OBGYN Clinical Test By Topic.pdf (p6, APH questions and answers — M27/M28 papers) [8] Senior notes: Ryan Ho Haemtology.pdf (p138, DIC evaluation and ASTH score)
Diagnosis of Antepartum Hemorrhage
APH is primarily a clinical diagnosis — you diagnose it by seeing a pregnant woman beyond 24 weeks with vaginal bleeding. The real diagnostic challenge is determining the cause of the APH, because this dictates management. There are no formal "diagnostic criteria" for APH itself (unlike, say, pre-eclampsia), but there are established diagnostic approaches for each underlying cause. Let me walk through the entire diagnostic algorithm from the moment the patient arrives.
Before diving into investigations, understand the overarching logic:
- Stabilise first, diagnose second — APH can be life-threatening. Resuscitation takes priority over diagnosis.
- History and examination give you the diagnosis in most cases — the pattern of pain, bleeding character, uterine tone, and fetal condition will point you to the cause before any investigation result returns.
- Ultrasound is the single most important investigation — it confirms or excludes placenta praevia (the diagnosis you must rule out before doing anything else).
- NEVER perform a digital vaginal examination until placenta praevia has been excluded by ultrasound [1][7] — this cannot be overemphasised. A finger through a placenta praevia can cause torrential hemorrhage.
- Speculum examination IS safe — it lets you visualise the cervix and rule out local causes (ectropion, polyp, carcinoma, cervicitis) without disturbing the placenta.
Initial Assessment (Before Any Investigation)
| Question | What you're looking for | Why it matters |
|---|---|---|
| Character of bleeding — Colour? Amount? Clots? | Bright red = fresh arterial/venous bleeding (praevia); Dark = older denatured blood (abruption) | Blood trapped behind placenta oxidises → dark colour |
| Pain — Present? Character? Constant vs. intermittent? | Painless → praevia; Constant severe pain → abruption; Acute tearing pain → rupture | Pain in abruption = blood infiltrating myometrium → irritation → tonic contraction → ischemia |
| Provocation — Post-coital? Post-VE? Spontaneous? | Post-coital = cervical cause or praevia; Spontaneous = praevia or abruption | Coital trauma disrupts fragile cervical ectropion or provokes separation in praevia |
| Timing relative to ROM | Bleeding AT membrane rupture = vasa praevia | Fetal vessels over os tear when membranes rupture |
| Recurrence | Recurrent episodes → praevia (warning hemorrhages); Single event → abruption | Progressive lower segment stretching causes intermittent praevia separation |
| Fetal movements | Reduced/absent → fetal compromise (abruption) | Placental separation → reduced gas exchange → fetal hypoxia |
| Risk factors | Previous CS, myomectomy → praevia/rupture; Smoking, pre-eclampsia → abruption [2][7] | Uterine scarring = praevia + PAS risk; Vascular disease = abruption risk |
| Known placental localisation | Was the anomaly scan at 20 weeks reassuring? Was placenta low-lying? | Most praevia diagnosed antenatally at the 20-week morphology scan; if "low-lying" at 20 weeks, serial TVS should follow |
| Bleeding tendencies | Inherited or acquired coagulopathy? | May cause APH without a structural cause [2] |
| Anaemia (Haemoglobin < 10 g/dL) | Baseline Hb? | Anaemic patients decompensate earlier [2] |
Performed before any vaginal assessment. Key findings:
| Component | What to assess | Interpretation |
|---|---|---|
| Inspection | Scars? Distension? | Scars from previous CS or myomectomy suggest risk of praevia/rupture vs. ovarian cystectomy scar (no uterine risk) [7] |
| Symphysial-fundal height (SFH) | Measure with tape (ulnar border of left hand to locate fundus) [9] | Larger than dates → polyhydramnios, multiple pregnancy, macrosomia, concealed abruption (expanding haematoma increases uterine size). Smaller → IUGR, oligohydramnios [9] |
| Uterine tone | Soft? Tense? "Woody hard"? | Soft = praevia or normal; Hard/tense/tender = abruption (myometrial irritation); Loss of uterine contour = rupture |
| Tenderness | Localised? Generalised? | Abruption = localised tenderness over haematoma site; Rupture = generalised peritonism |
| Fetal lie and presentation | Longitudinal/transverse/oblique? Cephalic/breech? | Malpresentation or high head (5/5 above brim) = praevia (placenta blocking engagement) [7] |
| Engagement | How many fifths palpable above brim? | 5/5 above = completely unengaged (praevia). A normally engaged head makes praevia very unlikely |
SFH interpretation [9]: Usually number of weeks ≈ cm (from 20–36 weeks). Large SFH — wrong dates, polyhydramnios, multiple pregnancy, macrosomia. Small SFH — IUGR, wrong dates, oligohydramnios, intrauterine death, transverse lie.
- Performed after ultrasound confirms no praevia, or if USS is unavailable, speculum can be done first (it does not disturb the placenta)
- Visualise: cervical os (open? closed?), cervical surface (ectropion? polyp? carcinoma?), source of bleeding (from os vs. cervical surface)
- Take swabs if cervicitis suspected (Chlamydia/gonorrhea NAAT)
- If cervical carcinoma suspected → biopsy (colposcopy-guided if possible)
Investigation Modalities
1. Ultrasound — The Cornerstone Investigation
Ultrasound is the first-line investigation in APH. It answers the critical question: where is the placenta?
| Aspect | Detail |
|---|---|
| Role | Initial screening to localise placenta; assess fetal viability, presentation, amniotic fluid volume |
| Sensitivity for praevia | ~95% — good for detecting a posterior placenta praevia but can overcall anterior low-lying placenta due to full bladder artefact |
| Limitation | Cannot precisely measure the placental edge-to-os distance when the placenta is posterior or when there is a presenting part obscuring the lower segment |
| Key findings | Placenta overlying or near the internal os; retroplacental haematoma (hypoechoic/mixed echogenicity collection); fetal presentation; AFI |
| Aspect | Detail |
|---|---|
| Role | Gold standard for diagnosing placenta praevia and measuring the precise distance from placental edge to internal os |
| Safety | TVS is SAFE in placenta praevia — the probe is placed in the vagina (not through the cervix). It does NOT touch the placenta. This is different from a digital VE which can disrupt the placenta |
| Precision | Can measure placental edge-to-os distance to within 5 mm |
| Key measurements | Placental edge ≥ 20 mm from os → low-lying but vaginal delivery may be possible; Placental edge < 20 mm from os or covering os → placenta praevia (CS mandatory) |
| Colour Doppler | Essential for diagnosing vasa praevia (fetal vessels seen traversing membranes over the os) and placenta accreta spectrum (abnormal lacunae, loss of retroplacental clear zone, bladder wall invasion) |
TVS is Safe in Praevia
Students often confuse transvaginal ultrasound with digital vaginal examination. TVS is completely safe — the ultrasound probe goes into the vagina but does not pass through the cervical os or touch the placenta. It is the gold standard for measuring placental edge-to-os distance. Digital VE is the dangerous one — your finger goes through the cervix and can separate the placenta.
| Diagnosis | USS Findings |
|---|---|
| Placenta praevia | Placenta covering or within 20 mm of the internal os on TVS. May be anterior (higher risk of PAS if prior CS scar), posterior, or lateral |
| Low-lying placenta | Placental edge within 20 mm of os but not covering it. ~90% of "low-lying" placentas at 20 weeks will "migrate" upward by term (differential growth of lower segment draws the placenta away) |
| Placental abruption | Retroplacental hapoechoic or mixed-echogenicity collection (haematoma). However, USS sensitivity for abruption is only ~25–50% — a normal USS does NOT exclude abruption. Abruption is primarily a clinical diagnosis |
| Placenta accreta spectrum | Irregular lacunae ("Swiss cheese" appearance), loss of the retroplacental clear zone (hypoechoic zone between placenta and myometrium), thinning or interruption of the hyperechoic uterine serosa-bladder interface, colour Doppler showing abnormal vascularity crossing the myometrium-placenta interface |
| Vasa praevia | Colour Doppler showing fetal vessels traversing the membranes over or near the internal os. Best seen on TVS with colour flow mapping |
USS Cannot Exclude Abruption
A common exam mistake: assuming that a normal ultrasound rules out abruption. USS sensitivity for detecting retroplacental haematoma is only 25–50%. Fresh blood can be isoechoic with the placenta and therefore invisible. Placental abruption is a CLINICAL diagnosis based on painful bleeding + tender/hard uterus + fetal distress. USS supports but does not exclude.
- At the 20-week anomaly scan, approximately 5–10% of women have a low-lying placenta
- By term, ~90% of these will have "migrated" — not because the placenta physically moves, but because the lower segment grows differentially, drawing the placental edge away from the os
- Serial TVS is performed at 32 weeks and again at 36 weeks if the placenta remains low
- If the placenta still covers or is within 20 mm of the os at 36 weeks → plan elective CS at 37–38 weeks (praevia) or await further migration (low-lying)
| Aspect | Detail |
|---|---|
| Role | Continuous electronic fetal heart rate monitoring — assesses fetal well-being |
| Normal CTG | Baseline 110–160 bpm, presence of accelerations, absence of decelerations, moderate variability (5–25 bpm) |
| Abnormal patterns in APH | |
| — Fetal bradycardia | Sustained FHR < 110 bpm → acute fetal hypoxia (seen in severe abruption with massive placental separation) [7] |
| — Late decelerations | FHR dips occurring after the peak of contraction → uteroplacental insufficiency (abruption) |
| — Sinusoidal pattern | Smooth, sine-wave-like undulation without accelerations → fetal anaemia (vasa praevia — the fetus is bleeding out, or severe abruption with massive feto-maternal hemorrhage) |
| — Absent variability | Loss of the normal beat-to-beat variation → severe fetal compromise |
| — Tachycardia | FHR > 160 bpm → early compensatory response to hypoxia, maternal fever, or dehydration |
Cardiotocography shows fetal bradycardia is a key exam finding pointing toward placental abruption in the context of a tender, irritable uterus [7].
These serve two purposes: (a) assess the severity of maternal blood loss, and (b) detect coagulopathy (especially DIC in abruption).
| Test | What it tells you | Key findings / interpretation |
|---|---|---|
| CBC (FBC) | Hemoglobin, hematocrit, platelet count | ↓ Hb suggests significant blood loss (but Hb takes time to drop — may be falsely reassuring acutely due to hemoconcentration). Anaemia Hb < 10 g/dL worsens prognosis [2]. ↓ Platelets → suggests DIC (consumption) |
| Blood group and crossmatch | ABO/Rh type; crossmatch blood for transfusion | Essential — have at least 4 units crossmatched and available for major APH. Check Rh status for anti-D prophylaxis if Rh-negative |
| Coagulation screen (PT, aPTT, fibrinogen) | Assess for DIC | ↑ PT, ↑ aPTT, ↓ fibrinogen → DIC [4][5]. Remember: Normal pregnancy fibrinogen is 4–6 g/L. A level of < 2 g/L is alarming. Lab features of acute DIC: ↓ platelet, ↑ PT, ↑ APTT, ↓ fibrinogen, ↑ D-dimer, schistocytes on PBS [4][5] |
| D-dimer | Fibrin degradation products | ↑ D-dimer in DIC [4][5]. Note: D-dimer is physiologically elevated in pregnancy, so interpretation requires clinical context |
| Peripheral blood smear (PBS) | Microangiopathic hemolytic anemia (MAHA) | Schistocytes (fragmented RBCs) → blood forced through fibrin meshwork in microvasculature → MAHA (seen in DIC, TTP/HUS, HELLP) [4][5] |
| Renal function (RFT) | Urea, creatinine, electrolytes | Assess for acute kidney injury from hypovolemia or DIC-related renal microthrombosis |
| Liver function (LFT) | AST, ALT, bilirubin, albumin | Screen for HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets) — which can coexist with abruption in the context of pre-eclampsia |
| Urate | Serum uric acid | Elevated in pre-eclampsia (reduced renal urate clearance from endothelial dysfunction); useful if abruption coexists with pre-eclampsia |
| Kleihauer-Betke test | Quantifies fetal cells in maternal circulation | Used in Rh-negative mothers to calculate the dose of anti-D immunoglobulin needed. Also useful in suspected feto-maternal hemorrhage (FMH) — seen in abruption, trauma |
| Apt test (Singer test) | Distinguishes fetal from maternal hemoglobin | Fetal Hb (HbF) resists alkali denaturation (stays pink in NaOH). Maternal Hb (HbA) denatures (turns brown/yellow). Used when vasa praevia is suspected — the bleeding is fetal blood |
| Urinalysis | Protein, glucose | Proteinuria ≥ 2+ → pre-eclampsia (which is a risk factor for abruption) [10]. Also check urine output (oliguria suggests significant hypovolemia or renal involvement) |
Interpreting Coagulation in APH — A Practical Framework
| Parameter | Normal in Pregnancy | Mild APH | Severe APH with DIC |
|---|---|---|---|
| Platelets | 150–400 × 10⁹/L | Normal | ↓↓ (< 100, sometimes < 50) |
| PT | Normal (11–13s) | Normal | ↑ (> 1.5× control) |
| aPTT | Normal (25–35s) | Normal | ↑ |
| Fibrinogen | 4–6 g/L | Normal | ↓↓ (< 2 g/L = critical) |
| D-dimer | Mildly ↑ (physiological) | Mild ↑ | ↑↑↑ |
- Hypertension (BP 150/100 mmHg) in the context of APH points toward pre-eclampsia as the underlying cause of abruption [7]
- Pre-eclampsia diagnostic criteria: new-onset hypertension after 20 weeks + proteinuria ≥ 300 mg/day OR end-organ damage (kidneys, liver, neuro, haematological) OR uteroplacental dysfunction [10]
- Serial BP monitoring is essential as pre-eclampsia can evolve rapidly
| Aspect | Detail |
|---|---|
| Role | Second-line investigation, primarily for placenta accreta spectrum (PAS) when USS findings are equivocal |
| Advantages | Superior soft-tissue contrast; can visualise the depth of placental invasion (accreta vs. increta vs. percreta), especially posterior placenta and parametrial involvement |
| Limitations | Not available emergently; expensive; patient must be stable enough to lie still |
| Key findings in PAS | Dark T2 intraplacental bands, uterine bulging, focal myometrial thinning or disruption, bladder wall irregularity |
| Investigation | Role |
|---|---|
| Biophysical Profile (BPP) | USS-based assessment of fetal breathing, movements, tone, and amniotic fluid + CTG. Used if ongoing monitoring is needed (e.g., conservative management of minor praevia) |
| Doppler velocimetry | Umbilical artery Doppler → assess placental resistance. Absent or reversed end-diastolic flow = severe placental insufficiency → consider delivery |
| Middle cerebral artery (MCA) Doppler | Peak systolic velocity (PSV) → non-invasive assessment of fetal anemia. Elevated MCA-PSV suggests fetal anemia (feto-maternal hemorrhage from abruption, or fetal bleeding from vasa praevia) |
Diagnostic Criteria for Specific Causes of APH
While APH itself has no formal diagnostic criteria, the major underlying causes do:
| Category | TVS Finding | Clinical Implication |
|---|---|---|
| Placenta praevia | Placenta partially or completely covers the internal cervical os | Caesarean section mandatory; delivery at 37–38 weeks (earlier if bleeding) |
| Low-lying placenta | Placental edge within 20 mm of internal os but not covering it | Serial TVS at 32 and 36 weeks; vaginal delivery may be possible if edge > 20 mm from os at term |
| Normally sited placenta | Placental edge > 20 mm from internal os | Praevia excluded; look for other causes of APH |
There are no formal diagnostic criteria for abruption. It is a clinical diagnosis supported (but not excluded) by investigations:
| Component | Findings |
|---|---|
| Clinical | Painful vaginal bleeding + tender/hard uterus + fetal distress = clinical triad of abruption |
| USS | Retroplacental haematoma (sensitivity only 25–50%; absence does NOT exclude) |
| Laboratory | Coagulopathy (↓ platelets, ↑ PT/aPTT, ↓ fibrinogen, ↑ D-dimer) supports the diagnosis and indicates severity |
| Retrospective | Definitive diagnosis at delivery → retroplacental clot adherent to the placental surface |
The key teaching point: Abruption is diagnosed clinically, not by ultrasound. If the clinical picture fits (painful bleeding, hard tender uterus, fetal distress), treat as abruption regardless of USS findings.
| Setting | Diagnostic Method |
|---|---|
| Antenatal (ideal) | TVS with colour Doppler at 20 weeks and again in 3rd trimester → fetal vessels seen traversing membranes over the internal os |
| Acute presentation | Bleeding at ROM + acute fetal distress + stable mother → Apt test to confirm fetal blood → emergency CS |
| Screening indication | Velamentous cord insertion, bilobed/succenturiate placenta, IVF conception, low-lying placenta → all warrant colour Doppler screening for vasa praevia |
| Priority | Investigation | Purpose |
|---|---|---|
| Immediate | CBC, coagulation screen (PT/aPTT/fibrinogen), group & crossmatch | Assess blood loss severity, detect DIC, prepare for transfusion |
| Immediate | CTG | Fetal well-being assessment |
| Urgent | Transabdominal USS → TVS if needed | Localise placenta, detect retroplacental haematoma, assess fetal condition |
| Urgent | Speculum examination (after praevia excluded or if USS unavailable) | Visualise cervix, rule out local causes |
| As indicated | Kleihauer-Betke test | Rh-negative mothers (anti-D dosing); suspected FMH |
| As indicated | Apt test | Suspected vasa praevia (distinguish fetal vs. maternal blood) |
| As indicated | D-dimer, PBS, LFT, RFT | DIC workup, HELLP screen, renal assessment |
| As indicated | Urinalysis | Screen for proteinuria (pre-eclampsia) |
| As indicated | MRI | Equivocal USS for PAS |
| As indicated | MCA Doppler | Suspected fetal anemia |
High Yield Summary
Diagnosis of APH — Key Points:
- APH is a clinical diagnosis — the cause is determined primarily by history and examination pattern
- Ultrasound (TVS = gold standard) confirms/excludes placenta praevia and measures edge-to-os distance (< 20 mm or covering = praevia; within 20 mm = low-lying)
- TVS is SAFE in praevia — do not confuse with digital VE which is CONTRAINDICATED
- USS sensitivity for abruption is only 25–50% — a normal USS does NOT exclude abruption; it is a clinical diagnosis (painful bleeding + hard tender uterus + fetal distress)
- Speculum examination is safe and essential to rule out local cervical/vaginal causes
- CTG is essential for fetal assessment — fetal bradycardia in context of tender uterus → abruption [7]
- Coagulation screen is critical — look for DIC (↓ fibrinogen < 2 g/L in pregnancy is alarming; ↓ platelets, ↑ PT/aPTT, ↑ D-dimer)
- Kleihauer-Betke for Rh-negative mothers; Apt test to distinguish fetal from maternal blood in suspected vasa praevia
- Placental migration: ~90% of low-lying placentas at 20 weeks resolve by term; serial TVS at 32 and 36 weeks
- Pre-eclampsia screening (BP + urinalysis) important when abruption suspected — they often coexist [7][10]
Active Recall - APH Diagnosis and Investigation
References
[1] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (Introduction, Definition) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (Risk factors, p6) [4] Senior notes: Maksim Medicine Notes.pdf (p165, DIC section — laboratory features, clinical features) [5] Senior notes: Ryan Ho Haemtology.pdf (p137–138, DIC causes, laboratory features) [7] Lecture slides: OBGYN Clinical Test By Topic.pdf (p6, APH questions — clinical features pointing to diagnosis) [9] Senior notes: Ryan Ho Fundamentals.pdf (p191, Obstetric examination, SFH measurement and interpretation) [10] Lecture slides: Block C - Hypertension and Pregnancy (CFB WCS in 2023_24).pdf (p15, p25, pre-eclampsia diagnostic criteria and management)
Management of Antepartum Hemorrhage
Management of APH follows the same universal principles as any major hemorrhage — but with the unique obstetric dimension of having two patients (mother and fetus). Every decision balances maternal safety against fetal maturity and well-being. Let me build this from first principles.
Similar to the management of heavy bleeding elsewhere, the principles are to replace the blood loss to reverse or prevent shock while efforts are made to identify and stop the source of bleeding [1][11].
The management framework mirrors what the lecture slides describe for PPH — 4 major principles [1][11]:
- Communication with all relevant professionals
- Resuscitation
- Monitoring and investigation
- Arresting the bleeding
These same principles apply to APH. The key difference is that in APH, you have an additional decision: deliver now vs. conservative management — which depends on the severity of bleeding, the cause, gestational age, and fetal condition.
This is an obstetric emergency. You need a team:
| Team Member | Role |
|---|---|
| Senior obstetrician | Decision-making on mode and timing of delivery |
| Anaesthetist | Airway management, IV access, blood products, possible emergency GA for CS |
| Midwife | Monitoring, IV fluid administration, catheterisation |
| Haematologist / blood bank | Crossmatch, massive transfusion protocol (MTP) activation |
| Neonatologist | Standby for preterm or compromised neonate |
| Porter | Blood product transport, patient transfer to theatre |
Communication with all relevant professionals is listed as the first principle — not resuscitation. Why? Because in obstetric emergencies, outcomes depend on team coordination. A single doctor cannot manage APH alone [1][11].
Step 2: Resuscitation
This follows the standard approach to hypovolemic shock [12]:
- Ensure patent airway
- Position: left lateral tilt (15–30°) or manual uterine displacement to the left — this relieves aortocaval compression by the gravid uterus
- Why? After ~20 weeks, the uterus compresses the IVC in the supine position → reduced venous return → reduced cardiac output → worsening hypotension. Tilting left shifts the uterus off the IVC.
- High flow O₂ via face mask with reservoir bag (15 L/min) [12]
- Why? Maximise maternal oxygen delivery → maximise oxygen delivery to the fetus via the placenta. The fetus is entirely dependent on maternal pO₂.
| Action | Detail | Rationale |
|---|---|---|
| Large bore IV access | 14/16G at antecubital vein — ideally two lines [12] | Large bore allows rapid fluid infusion (flow rate ∝ r⁴/length by Poiseuille's law → short, wide cannulae give fastest flow) |
| Bloods | CBC, RFT, clotting, type & screen/crossmatch [12] | Baseline Hb, detect DIC, prepare blood products |
| Rapid fluid challenge | 500–1000 mL crystalloid over 5–10 min [12] | Volume replacement to maintain an effective circulation [1][11] |
| Reassess BP/P every 5 min | Repeat fluid bolus if not responding [12] | Titrate resuscitation to clinical response |
| Foley catheter | Monitor urine output (target > 0.5 mL/kg/hr) [12] | Urine output is the best bedside indicator of end-organ perfusion |
| Blood transfusion | Crossmatch 4–6 units packed RBCs; use O-negative if emergency and crossmatch unavailable | Red cell replacement (oxygen carriage) [1][11] |
Massive Transfusion Protocol (MTP)
Activate when estimated blood loss > 2 L or clinical signs of Class III/IV shock:
| Component | Ratio | Purpose |
|---|---|---|
| Packed RBCs | 6 units | Oxygen carrying capacity |
| FFP | 4 units (target 1:1 or 1:1.5 ratio with pRBC) | Replace clotting factors — FFP contains all soluble plasma proteins and clotting factors [13] |
| Cryoprecipitate | 10 units (if fibrinogen < 2 g/L) | Concentrated fibrinogen (1 adult dose typically raises fibrinogen by 1 g/L) + Factor VIII + vWF [13] |
| Platelets | 1 pool (if platelet count < 50 × 10⁹/L with active bleeding) | Replace consumed platelets |
| Tranexamic acid | 1 g IV slowly | Antifibrinolytic — inhibits plasmin → reduces clot breakdown → reduces ongoing hemorrhage |
Blood components replacement (platelet and FFP) to correct coagulation defect [1][11]
Fibrinogen Target in Obstetric Hemorrhage
In obstetric hemorrhage, the fibrinogen target is > 2 g/L (higher than the non-obstetric target of > 1 g/L). This is because pregnancy normally raises fibrinogen to 4–6 g/L, and a level below 2 g/L in pregnancy is a strong predictor of progression to massive hemorrhage. Cryoprecipitate is indicated for documented fibrinogen deficiency [13].
- Assess GCS — altered consciousness indicates severe hypovolemic shock (Class III/IV)
- Check blood glucose
- Quantify blood loss (weigh swabs, measure in kidney dishes)
- Check for concealed bleeding (palpate uterus — a tense, enlarging uterus suggests concealed abruption)
This should be monitored with blood pressure, pulse rate, urine output, central venous pressure, laboratory haematology tests [1][11].
| Parameter | Frequency | Target |
|---|---|---|
| Blood pressure | Every 5–15 min (depending on severity) | Systolic > 90 mmHg |
| Heart rate | Continuous or every 5 min | < 100 bpm |
| Urine output | Hourly via indwelling catheter | > 0.5 mL/kg/hr (i.e., > 30 mL/hr) |
| CTG | Continuous | Normal baseline 110–160, presence of accelerations, no decelerations |
| Repeat bloods | Every 1–4 hours depending on severity | Hb stable, fibrinogen > 2 g/L, platelets > 50, PT/aPTT normalising |
| CVP | If persistent shock or cardiac disease history [12] | Guides fluid administration — avoid over-resuscitation |
| Blood loss | Ongoing quantification | Objective measurement (weighing) over visual estimation |
Step 4: Arresting the Bleeding — Cause-Specific Management
This is where APH management diverges based on the underlying cause. The fundamental decision is always: deliver now or manage conservatively?
4A. Management of Placenta Praevia
The decision hinges on three factors: severity of bleeding, gestational age, and maternal/fetal stability.
| Component | Detail | Rationale |
|---|---|---|
| Admission | Inpatient observation (many centres keep praevia patients hospitalised from the first significant bleed until delivery) | Unpredictable, potentially massive rebleeding — need immediate access to theatre and blood bank |
| Bed rest | Activity restriction, avoid coitus and digital VE | Minimise provocation of further separation |
| IV access | Maintained at all times | Rapid volume replacement if sudden rebleed |
| Blood available | Crossmatched blood kept on standby (at least 2–4 units) | Praevia can rebleed massively without warning |
| Corticosteroids | If < 34+6 weeks: Betamethasone 12 mg IM × 2 doses, 24 hours apart (or Dexamethasone 6 mg IM × 4 doses, 12 hours apart) | Accelerates fetal lung maturity (stimulates surfactant production by Type II pneumocytes). Takes 24–48 hours for full effect. Given because premature delivery may become necessary at any time |
| Anti-D immunoglobulin | If mother is Rh-negative | APH causes feto-maternal hemorrhage (FMH) → fetal Rh-positive RBCs enter maternal circulation → maternal anti-D antibody production → haemolytic disease of the fetus/newborn (HDFN) in subsequent pregnancies. Anti-D neutralises the fetal RBCs before maternal immune sensitisation occurs |
| Kleihauer-Betke test | Quantify FMH to calculate anti-D dose | Standard dose (250–500 IU) covers up to 4 mL fetal RBCs. Larger FMH requires additional doses |
| Serial USS | TVS at 32 and 36 weeks | Monitor for placental migration; assess for PAS (accreta spectrum) |
| Iron supplementation | Oral or IV iron | Optimise Hb to tolerate further blood loss. Anaemia (Hb < 10 g/dL) worsens outcomes [2] |
| Fetal monitoring | Serial CTG, growth scans | Ensure fetal well-being |
| Scenario | Action | Reasoning |
|---|---|---|
| Major APH with haemodynamic instability | Emergency CS regardless of gestation | Maternal life always takes priority over fetal maturity |
| Praevia persisting at 36 weeks, asymptomatic | Planned elective CS at 37+0 to 37+6 weeks (RCOG 2018) | Balances fetal maturity against risk of emergency bleed before term |
| Praevia + suspected PAS (accreta) | Planned CS at 35–36+6 weeks in a tertiary centre with multidisciplinary team | PAS carries risk of catastrophic hemorrhage requiring hysterectomy; earlier delivery reduces risk of emergency presentation |
| Low-lying placenta (edge 11–20 mm from os) | Consider vaginal delivery with caution; senior obstetrician present | Edge > 20 mm from os at term → low risk of significant hemorrhage during vaginal delivery |
Exam Pearl — Emergency CS for Praevia
A 40-year-old G2P0 at 37 weeks with known placenta praevia covering os, first episode of profuse vaginal bleeding, pulse 108, BP 100/60, soft non-tender uterus, head 5/5 above brim, profuse bleeding from os on speculum → the most appropriate management is emergency Caesarean section [7]. Conservative management is inappropriate when there is active profuse bleeding with haemodynamic compromise. Digital vaginal examination is absolutely contraindicated [7].
4B. Management of Placental Abruption
| Component | Detail | Rationale |
|---|---|---|
| Admission | Inpatient monitoring | Risk of progression; concealed bleeding may not be clinically apparent initially |
| Corticosteroids | If < 34+6 weeks | Same as praevia — anticipating possible preterm delivery |
| Anti-D | If Rh-negative | Abruption causes significant FMH |
| Coagulation monitoring | Serial CBC, fibrinogen, PT/aPTT, D-dimer every 4–6 hours | Detect evolving DIC early — fibrinogen < 2 g/L is a red flag |
| CTG | Continuous initially, then 4–6 hourly if stable | Detect fetal deterioration early |
| USS | Assess retroplacental haematoma size, fetal growth | Monitor for progression; remember USS may be normal even in significant abruption |
| Tocolysis | Generally avoided — controversial | Tocolytics (e.g., nifedipine, atosiban) may be considered if preterm contractions are present and the abruption is mild. BUT: tocolysis masks the clinical sign of uterine hypertonicity and may delay recognition of worsening abruption. Most obstetricians avoid tocolysis in abruption |
| Scenario | Mode | Reasoning |
|---|---|---|
| Severe abruption with fetal distress (fetal alive) | Emergency CS | Time-critical — every minute of delay worsens fetal outcome |
| Severe abruption with fetal death | Vaginal delivery (aim for delivery within 4–6 hours) | No fetal indication for CS; vaginal delivery is safer for the mother when there is DIC (avoids surgical bleeding in a coagulopathic patient). Amniotomy ± oxytocin augmentation |
| Moderate abruption at term (> 37 weeks), stable | Amniotomy + vaginal delivery if cephalic and favourable cervix; CS if not | At term, no benefit to prolonging pregnancy. Amniotomy reduces intrauterine pressure, may slow further separation, and allows labour to progress |
| Mild abruption, preterm, stable | Conservative — defer delivery, optimise fetal maturity | Risk of prematurity outweighs risk of rebleeding if small abruption, stable mother and fetus |
Key concept — Why vaginal delivery in fetal death? If the fetus has died, there is no fetal urgency for CS. A woman with DIC is at extreme risk during surgery — she will bleed from every incision site because she cannot form clots. Vaginal delivery minimises tissue trauma. Moreover, the abruption itself often triggers intense uterine contractions that facilitate rapid vaginal delivery.
Treat underlying cause: most important [5]. In abruption, the definitive treatment of DIC is delivery — removing the source of tissue thromboplastin.
| Component | Indication | Detail |
|---|---|---|
| FFP | PT/aPTT > 1.5× control with active bleeding [13] | Replaces all consumed clotting factors. Dose: 12–15 mL/kg |
| Cryoprecipitate | Fibrinogen < 2 g/L (obstetric threshold) | Dose: 10 units for adults — raises fibrinogen by ~1 g/L [13] |
| Platelets | Platelet < 50 × 10⁹/L with active bleeding or need for invasive procedures [5] | Or < 20 × 10⁹/L in the presence of sepsis [5] |
| Tranexamic acid | Adjunct in major hemorrhage | 1 g IV over 10 min; can repeat after 30 min. WHO recommends giving within 3 hours of onset of bleeding |
| Avoid heparin | Acute obstetric DIC | Heparin is used in chronic (compensated) DIC to prevent thrombosis, but in acute DIC with active bleeding, it worsens hemorrhage |
| Good circulation and good urine output should be maintained to help clear the fibrin degradation products which cause further DIC [1] | Maintain UO > 0.5 mL/kg/hr | FDPs themselves are anticoagulant — they interfere with fibrin polymerisation and platelet function. Renal clearance removes them |
| Setting | Management |
|---|---|
| Antenatal diagnosis (asymptomatic) | Admit at 30–32 weeks; planned elective CS at 35–36 weeks (before risk of spontaneous membrane rupture). Corticosteroids for fetal lung maturity. Avoid amniotomy. |
| Acute presentation (bleeding at ROM) | Emergency CS — immediate delivery. Neonatal resuscitation team on standby for severely anaemic neonate requiring transfusion |
| Key: Outcome depends entirely on antenatal diagnosis | If diagnosed antenatally and delivered by planned CS: fetal survival > 95%. If undiagnosed and presents at ROM: fetal mortality ~60% |
| Action | Detail |
|---|---|
| Emergency laparotomy | Immediate — this is a surgical emergency |
| Deliver the fetus | Often already partially or fully extruded into the peritoneal cavity |
| Repair or hysterectomy | If the tear is small and clean → uterine repair (preserves fertility). If extensive, necrotic, or uncontrollable bleeding → subtotal or total hysterectomy |
| Massive transfusion | Expect significant blood loss (often several litres in the peritoneal cavity) |
| Neonatal resuscitation | Fetus almost always severely compromised |
| Cause | Management |
|---|---|
| Cervical ectropion | Reassurance — no treatment needed in pregnancy. Usually resolves postpartum. Avoid cauterisation during pregnancy (risk of bleeding from the vascular cervix) |
| Cervical polyp | Usually left alone during pregnancy (polypectomy risks bleeding). Remove postpartum if persistent |
| Cervical carcinoma | Multidisciplinary management: staging, fetal maturity assessment. If early stage and preterm → may delay treatment until after delivery. If advanced or at/near term → deliver then treat |
| Cervicitis | Treat underlying infection (e.g., azithromycin for Chlamydia, ceftriaxone for gonorrhea) |
| Vaginal varicosities | Compression, elevation, avoid prolonged standing. Rarely require intervention |
| Component | Detail |
|---|---|
| Admission | At least 48 hours observation |
| Steroids | If < 34+6 weeks — potential for preterm delivery |
| Anti-D | If Rh-negative |
| Fetal monitoring | Serial CTG, growth scans |
| Delivery planning | Usually at term (37–39 weeks) via normal obstetric indications |
| Counsel about PPH risk | APH is a risk factor for PPH [2][3] — ensure active management of the third stage of labor |
These drugs are primarily used for PPH management (uterine atony) but are relevant to APH when atony complicates delivery:
| Drug | Route/Dose | Mechanism | Contraindications |
|---|---|---|---|
| Syntometrine | 1 mL IMI (ergometrine 0.5 mg + oxytocin 5 units) [1][14] | Dual action: oxytocin causes rhythmic uterine contractions; ergometrine causes sustained tonic contraction | Hypertension, heart disease [14] — ergometrine is a vasoconstrictor that raises BP (can precipitate hypertensive crisis or coronary spasm) |
| Syntocinon (oxytocin) | 5 units IVI after delivery; then infusion 40 units in 500 mL NS over 4 hours (prophylaxis) [14]; 10 units IVI + infusion 10 units/hr (treatment) [14] | Binds oxytocin receptors on myometrium → ↑ intracellular Ca²⁺ → rhythmic uterine contraction | Relatively safe; avoid rapid bolus > 5 IU (can cause hypotension, water retention at high doses due to ADH-like effect) |
| Carbetocin | 100 μg IV bolus [14] | Long-acting oxytocin analogue (half-life ~40 min vs. ~3 min for oxytocin) → prolonged uterine contraction | For Caesarean section with high risk for PPH [14]; single dose only |
| Carboprost (15-methyl PGF₂α) | 250 μg IMI, can repeat every 15 min, up to 2 mg (8 doses) [14] | Prostaglandin F₂α analogue → potent myometrial contraction via smooth muscle stimulation | Asthma (causes bronchospasm — PGF₂α constricts bronchial smooth muscle); use with caution in hepatic/renal/cardiac disease |
| Misoprostol (PGE₁ analogue) | 800–1000 μg per rectal or sublingual [14] | Prostaglandin E₁ → stimulates myometrial contraction | Few absolute contraindications; causes fever, diarrhoea (prostaglandin side effects). Advantage: does not require refrigeration, can be given rectally/sublingually without IV access |
| Tranexamic acid | 1 g IV over 10 min (can repeat × 1 after 30 min) | Lysine analogue → binds plasminogen → inhibits plasmin-mediated fibrinolysis → stabilises existing clots | Active thromboembolic disease; use within 3 hours of bleeding onset for maximum benefit (WOMAN trial) |
Why is Syntometrine contraindicated in hypertension?
Syntometrine contains ergometrine — an ergot alkaloid that causes sustained vasoconstriction by acting on α-adrenergic and serotonin receptors in vascular smooth muscle. In a woman with pre-eclampsia or hypertension, this can precipitate a hypertensive crisis, stroke, or myocardial ischemia. Use oxytocin instead if Syntometrine is contraindicated (hypertension, heart disease) [14].
If the APH continues despite medical management and delivery, surgical options escalate. This parallels the PPH surgical algorithm — these include tension, pressure, balloon, medication, embolization and surgery [1][11]:
| Intervention | Mechanism | When to use |
|---|---|---|
| Uterine massage | Mechanical stimulation of myometrium → contraction → compression of spiral arteries | First-line for uterine atony post-delivery |
| Bimanual uterine compression | One hand on the abdomen, one hand as a fist in the vagina → compresses uterus between both hands → tamponades the bleeding while awaiting other measures | Temporising measure — buys time |
| Intrauterine balloon tamponade | Bakri balloon or Sengstaken-Blakemore tube inserted into uterine cavity → inflated with 300–500 mL saline → exerts direct pressure on the placental bed | If atony persists despite uterotonics. Particularly useful in praevia (lower segment bleeding). "Tamponade test" — if bleeding stops after inflation, the balloon is sufficient |
| Uterine compression sutures | B-Lynch suture: compresses the uterus mechanically by "sandwiching" anterior and posterior walls together | At laparotomy if balloon tamponade fails. Preserves fertility |
| Uterine artery ligation | Surgical ligation of uterine arteries → reduces pulsatile blood flow to the uterus | Stepwise devascularisation at laparotomy |
| Internal iliac artery ligation | Bilateral ligation → converts pulsatile arterial flow to low-pressure venous flow in the pelvis | Technically demanding; reduces pelvic blood flow by ~50% |
| Uterine artery embolization (UAE) | Interventional radiology: selective catheterisation of uterine arteries → injection of embolic agents (Gelfoam, PVA particles) → occludes blood supply [15] | Post-partum haemorrhage or arteriovenous malformation [15]. Requires haemodynamic stability and access to interventional radiology suite. Advantage: preserves uterus |
| Hysterectomy | Subtotal (supracervical) or total abdominal hysterectomy → definitive. Removes the source of bleeding entirely | Last resort — when all other measures fail, or in PAS (placenta accreta/percreta) where the placenta cannot be separated. Life-saving procedure |
Laparotomy is required in exceptional circumstances when the source of bleeding cannot be identified or to stop the bleeding [1][11]
This is the most dangerous variant of placenta praevia and warrants specific management:
| Principle | Detail |
|---|---|
| Antenatal planning | Multidisciplinary team conference: senior obstetrician, urologist (if bladder invasion suspected), interventional radiologist, anaesthetist, haematologist, blood bank, neonatologist |
| Timing | Planned CS at 35–36+6 weeks (RCOG / FIGO) — earlier than uncomplicated praevia because the risk of emergency hemorrhage increases after 36 weeks |
| Surgical approach | CS hysterectomy — the placenta is left in situ (NOT removed manually, as this would cause catastrophic hemorrhage from the raw myometrial surface). The uterus is removed with the placenta still attached |
| Blood products | Have at least 6 units pRBC crossmatched, FFP, cryoprecipitate, and platelets available. Cell salvage should be set up |
| UAE | Prophylactic uterine artery balloon catheter placement pre-operatively (by interventional radiology) → inflate during surgery to reduce blood loss |
| Conservative (uterine-sparing) approach | In selected cases where the patient strongly desires fertility preservation: leave the placenta in situ, close the uterus, monitor with serial USS and β-hCG for gradual placental resorption. High risk of secondary hemorrhage and infection |
| Indication | Dose | Timing |
|---|---|---|
| Any APH in an Rh-negative mother | Minimum 250 IU (before 20 weeks) or 500 IU (after 20 weeks) | Within 72 hours of the bleeding episode |
| Quantify FMH with Kleihauer-Betke test | Additional doses if FMH > 4 mL fetal cells | Calculated based on Kleihauer result |
| Repeat if further episodes of APH | Each new bleed may cause additional FMH | Within 72 hours of each new episode |
Why anti-D? An Rh-negative mother exposed to Rh-positive fetal blood (via placental separation in APH) will mount an immune response producing anti-D antibodies. In future pregnancies, these antibodies cross the placenta and destroy fetal Rh-positive RBCs → haemolytic disease of the fetus and newborn (HDFN). Anti-D immunoglobulin is a passive immunisation — it binds and clears fetal RBCs from the maternal circulation before the maternal immune system can mount a primary response.
| Parameter | Detail |
|---|---|
| Indication | Any APH at 24+0 to 34+6 weeks where preterm delivery is considered possible within the next 7 days |
| Drug | Betamethasone 12 mg IM × 2 doses, 24 hours apart (preferred) OR Dexamethasone 6 mg IM × 4 doses, 12 hours apart |
| Mechanism | Crosses the placenta → induces fetal Type II pneumocyte maturation → increases surfactant production → reduces severity of respiratory distress syndrome (RDS), intraventricular hemorrhage (IVH), and necrotising enterocolitis (NEC) |
| Time to effect | Optimal benefit at 24–48 hours; some benefit even if delivered within hours of first dose |
| Repeat courses | Generally a single course is given. A "rescue" course may be considered if > 2 weeks since the first course and delivery is again anticipated |
| Not indicated | If > 34+6 weeks (minimal benefit; fetal lungs are usually mature) or if delivery is imminent and cannot be delayed |
| Situation | Recommendation | Rationale |
|---|---|---|
| Placenta praevia with preterm contractions | May consider short-term tocolysis (nifedipine or atosiban) to allow steroid completion | Buying 48 hours for steroids can significantly reduce neonatal morbidity |
| Placental abruption | Generally AVOID tocolysis | Tocolysis masks uterine hypertonicity (a key clinical sign of worsening abruption) and may delay recognition of deterioration. Moreover, abruption is driven by decidual artery rupture, not contractions — stopping contractions does not treat the cause |
| Active hemorrhage of any cause | AVOID tocolysis | Tocolysis relaxes the uterus → reduced tamponade effect → may worsen bleeding |
High Yield Summary
Management of APH — Key Points:
- 4 principles: Communication, Resuscitation, Monitoring, Arresting the bleeding [1][11]
- Resuscitation: Left lateral tilt, high flow O₂, 2× large bore IV, rapid crystalloid, crossmatch blood, Foley catheter
- Placenta praevia: Conservative if minor and preterm (admit, steroids, anti-D, serial USS); emergency CS if major bleed or > 37 weeks; planned CS at 37–38 weeks if asymptomatic praevia at 36 weeks
- Abruption: Deliver if maternal/fetal compromise; CS if fetal alive + distress; vaginal delivery if fetal death (avoid surgery in DIC); treat DIC with FFP + cryoprecipitate
- Vasa praevia: Emergency CS immediately if acute; planned CS at 35–36 weeks if diagnosed antenatally
- Uterine rupture: Emergency laparotomy → repair or hysterectomy
- Syntometrine contraindicated in hypertension and heart disease — use oxytocin instead [14]
- Carboprost contraindicated in asthma (bronchospasm from PGF₂α)
- Anti-D for all Rh-negative mothers with APH within 72 hours; Kleihauer to quantify FMH
- Steroids for fetal lung maturity at 24–34+6 weeks
- Surgical escalation: balloon tamponade → compression sutures → artery ligation → UAE → hysterectomy (last resort)
- PAS (accreta): Planned CS hysterectomy at 35–36 weeks, multidisciplinary, leave placenta in situ
Active Recall - APH Management
References
[1] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (p5, p7 — Management principles, blood replacement, oxytocic agents) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (p6 — Risk factors including APH, anaemia) [3] Lecture slides: Block C - Postpartum Haemorrhage.pdf (p5, p32 — Risk factors, summary) [5] Senior notes: Ryan Ho Haemtology.pdf (p138 — DIC management, platelet/FFP/cryoprecipitate indications) [7] Lecture slides: OBGYN Clinical Test By Topic.pdf (p6, p11 — APH and PPH clinical questions) [11] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf (p5, p7 — Management principles, oxytocic agents) [12] Senior notes: Ryan Ho Critical Care.pdf (p21 — Hypovolemic shock management) [13] Senior notes: Ryan Ho Haemtology.pdf (p144 — FFP, cryoprecipitate, PCC indications and dosing) [14] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (p7 — Appendix I, oxytocic agents dosage and contraindications) [15] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p85 — Uterine artery embolization indications)
Complications of Antepartum Hemorrhage
Complications of APH affect both mother and fetus/neonate. Understanding them requires tracing the pathophysiology from the initial hemorrhagic insult through to its downstream consequences. Every complication can be explained from first principles — hemorrhage reduces perfusion, coagulopathy amplifies bleeding, and prematurity results from early delivery forced by the emergency.
A. Maternal Complications
Bleeding (haemorrhage) is one of the major causes of maternal mortality [1][11]. Primary postpartum haemorrhage is often torrential and can cause shock and death within a short period of time [1][11].
Why does APH cause shock so quickly?
- Uterine blood flow at term is ~500–700 mL/min — the placental bed is among the most richly perfused vascular beds in the body
- The placental bed is where the uterus is very vascular [3]. Any disruption to this interface opens high-flow maternal spiral arteries
- In placenta praevia, the lower part of the uterus does not contract very well → hence, the blood vessels are not controlled, results in massive bleeding [3]
- Although pregnant women have expanded blood volume (~40% increase, to ~6–7 L), they can decompensate rapidly once compensatory mechanisms are exhausted — and young, healthy women maintain normal vital signs until they have lost 30–40% of their blood volume, after which collapse is sudden
Pathophysiology of hypovolemic shock:
- Blood loss → ↓ circulating volume → ↓ venous return → ↓ preload
- ↓ Preload → ↓ stroke volume → ↓ cardiac output (Frank-Starling mechanism)
- Sympathetic activation → tachycardia + peripheral vasoconstriction (cold extremities, pallor, delayed capillary refill) → attempts to maintain MAP
- If blood loss continues → sympathetic compensation overwhelmed → ↓ MAP → ↓ end-organ perfusion → organ ischemia → multi-organ failure → death
Aortocaval compression worsens shock in the supine position — the gravid uterus compresses the IVC → further reduces venous return → compounds hypovolemia. This is why left lateral uterine displacement or left lateral tilt is essential during resuscitation [16].
This is the most feared hematological complication of APH, particularly placental abruption.
Whatever the initial cause of bleeding, the patient can develop blood coagulation defects after heavy bleeding, and this causes more bleeding. Furthermore, there are some pregnancy complications which are associated with disseminated intravascular coagulation and can be the cause of postpartum haemorrhage. [1][11]
Mechanism (from first principles):
- Damaged placenta releases tissue factor (thromboplastin) into maternal circulation
- Tissue factor activates Factor VII → extrinsic pathway activation
- Massive thrombin generation → widespread fibrin deposition in microvasculature
- Consumption of platelets, fibrinogen, Factor V, Factor VIII → consumption coagulopathy → inability to form clots → bleeding diathesis
- Secondary fibrinolysis (plasmin activation) → fibrin degradation products (FDPs) and D-dimer ↑↑ → FDPs themselves are anticoagulant (they interfere with fibrin polymerisation and platelet function) → worsening bleeding
- RBCs forced through fibrin strands in microvasculature → mechanical fragmentation → schistocytes on PBS → microangiopathic haemolytic anaemia (MAHA) [4][5]
- Microvascular thrombosis → end-organ ischemia → renal cortical necrosis, hepatic dysfunction, ARDS
Vicious cycle: Bleeding → tissue damage → more thromboplastin release → more DIC → more bleeding → death if not interrupted by treating the cause (delivery) and replacing consumed components.
| Lab Finding | Mechanism |
|---|---|
| ↓ Platelets | Consumed in microthrombi [4][5] |
| ↑ PT, ↑ aPTT | Clotting factors consumed [4][5] |
| ↓ Fibrinogen | Consumed; "normal" for pregnancy is 4–6 g/L so < 2 g/L is critically low [4][5] |
| ↑ D-dimer | Fibrinolysis of microthrombi [4][5] |
| Schistocytes on PBS | RBC fragmentation through fibrin meshwork (MAHA) [4][5] |
Antepartum hemorrhage is explicitly listed as a risk factor for postpartum hemorrhage [2].
APH leads to PPH through multiple mechanisms — and the 4 T's framework of PPH causes maps directly onto APH pathophysiology:
| 4 T's of PPH | How APH causes this |
|---|---|
| Tone (uterine atony) | Couvelaire uterus in severe abruption: blood infiltrates the myometrium → disrupts contractile function → uterus cannot contract after delivery. Also, placenta praevia: lower segment does not contract very well [3] — the placental bed in the lower segment has sparse muscle fibres |
| Tissue (retained placenta) | Placenta accreta spectrum (PAS): especially when praevia coexists with prior CS scar → chorionic villi adhere to/invade myometrium without intervening decidua basalis → placenta does not separate → massive hemorrhage at attempted removal. Placenta accreta: abnormal implantation where the placenta invades into the myometrium. Part or whole of the placenta cannot be separated from the uterus [1][11] |
| Trauma | Emergency CS for APH may cause surgical trauma; rupture of the body of the uterus can complicate delivery [1][11] |
| Thrombin (coagulopathy) | DIC from abruption → consumption coagulopathy → unable to form clots → ongoing hemorrhage post-delivery [1][11] |
Whatever the initial cause of bleeding, the patient can develop blood coagulation defects after heavy bleeding, and this causes more bleeding [1][11]. This is the critical teaching point — APH begets PPH through a self-perpetuating cycle of hemorrhage and coagulopathy.
| Organ | Complication | Mechanism |
|---|---|---|
| Kidneys | Acute kidney injury (AKI) → may progress to acute tubular necrosis (ATN) or renal cortical necrosis | Hypovolemia → ↓ renal perfusion → tubular ischemia. In DIC, fibrin deposition in glomerular capillaries causes cortical necrosis (irreversible, unlike ATN). Clinical: oliguria → anuria → rising creatinine and urea |
| Pituitary | Sheehan syndrome (postpartum hypopituitarism) | The anterior pituitary is physiologically enlarged in pregnancy (lactotroph hyperplasia for prolactin production) but its blood supply does not increase proportionately → vulnerable to ischemia. Severe hemorrhagic shock → anterior pituitary infarction → panhypopituitarism. Classic presentation: failure of lactation (↓ prolactin), then gradual loss of other pituitary hormones (TSH, ACTH, FSH/LH, GH) |
| Lungs | ARDS (Acute Respiratory Distress Syndrome) | Massive transfusion → transfusion-related acute lung injury (TRALI). DIC → pulmonary microvascular thrombosis. Systemic inflammatory response from shock → capillary leak → non-cardiogenic pulmonary edema |
| Liver | Hepatic ischemia / HELLP syndrome | Reduced hepatic perfusion → centrilobular necrosis → elevated transaminases. If pre-eclampsia coexists → HELLP (Haemolysis, Elevated Liver enzymes, Low Platelets) |
| Heart | Myocardial ischemia | Severe anemia + tachycardia → increased myocardial oxygen demand with reduced oxygen supply → subendocardial ischemia (especially in women with pre-existing cardiac disease) |
| Brain | Cerebral hypoperfusion → watershed infarcts | Prolonged hypotension → ischemia in vulnerable watershed zones between major cerebral artery territories |
Sheehan Syndrome — A Delayed Complication
Sheehan syndrome may present weeks to months after the hemorrhagic event. The earliest sign is usually failure to lactate (agalactia) because prolactin-producing lactotrophs are the first to be affected. Later features include amenorrhea (↓ FSH/LH), hypothyroidism (↓ TSH), adrenal insufficiency (↓ ACTH — potentially life-threatening), and growth hormone deficiency. Always ask a woman who had massive obstetric hemorrhage about breastfeeding ability at follow-up.
Emergency delivery for APH often requires emergency general anaesthesia (GA), which carries unique risks in pregnancy [16]:
| Complication | Mechanism |
|---|---|
| Difficult intubation | Difficult intubation is 8 times more common than normal patients — due to weight gain and oedema, pre-existing obstetric disease e.g. pre-eclampsia [16] |
| Aspiration (Mendelson's syndrome) | Delayed gastric emptying and relaxed LES due to progesterone → risk of aspiration even with fasting [16]. Aspiration of acidic gastric contents → chemical pneumonitis → ARDS. Prevented by RSI and antacids (30 mL sodium citrate + H₂RA/PPI) [16] |
| Rapid desaturation during intubation | Increased oxygen demand by 20% and reduced oxygen reserve (FRC drop 20%): less apnea time allowed [16]. Pregnant women desaturate much faster during apnea than non-pregnant patients |
| Aortocaval compression | Supine hypotension syndrome: reduced by left lateral uterine displacement [16]. Placenta bed has no autoregulation to compensate for drop in BP [16] — any drop in maternal BP directly reduces uteroplacental perfusion |
The key teaching point: Placenta bed has no autoregulation to compensate for drop in BP [16]. This means even brief maternal hypotension (e.g., during anaesthetic induction) can cause acute fetal hypoxia. This is fundamentally different from the cerebral or renal circulations, which have autoregulatory mechanisms to maintain perfusion across a range of MAP.
Massive transfusion: transfusion of > 10 units (or 1–2× blood volume) [17]. Indication: severe trauma, ruptured AAA, obstetric complications [17].
| Complication | Mechanism |
|---|---|
| Hypothermia | Stored blood is cold (4°C) → rapid infusion of multiple units drops core temperature → hypothermia impairs coagulation (enzyme reactions are temperature-dependent) → worsens bleeding |
| Dilutional coagulopathy | Packed RBCs contain no clotting factors or platelets → dilution of existing factors → coagulopathy. Mitigated by empirical transfusion of packed cells:FFP:PLT = 1:1:1 [17] |
| Hyperkalemia | Stored RBCs leak K⁺ (the Na⁺/K⁺-ATPase stops working in storage) → ↑ serum K⁺ → risk of cardiac arrhythmia |
| Citrate toxicity → Hypocalcaemia | Citrate is the anticoagulant in blood bags → chelates ionised Ca²⁺ → hypocalcaemia → muscle cramps, tetany, QT prolongation, cardiac dysfunction. The liver normally metabolises citrate, but in massive transfusion the liver is overwhelmed |
| Metabolic alkalosis | Citrate is metabolised to bicarbonate → metabolic alkalosis (paradoxically, after initial lactic acidosis from shock resolves) |
| ABO incompatibility (1/6000) | Clerical error → haemolytic transfusion reaction → DIC, renal failure, death [17] |
| ARDS (< 1/10,000) | TRALI: donor antibodies react with recipient leukocytes → pulmonary capillary leak → non-cardiogenic pulmonary oedema [17] |
- APH causes feto-maternal hemorrhage (FMH) — fetal RBCs cross into maternal circulation through the disrupted placental-decidual interface
- If the mother is Rh-negative and the fetus is Rh-positive, maternal exposure to Rh(D) antigen stimulates anti-D IgG antibody production
- In subsequent pregnancies, these IgG anti-D antibodies cross the placenta → bind fetal Rh-positive RBCs → haemolysis → haemolytic disease of the fetus and newborn (HDFN) — ranging from mild neonatal jaundice to fatal hydrops fetalis
- Prevention: Anti-D immunoglobulin within 72 hours of any sensitising event (including APH); Kleihauer-Betke test to quantify FMH and calculate additional anti-D dose
- Emergency peripartum hysterectomy may be required for uncontrollable hemorrhage, particularly in placenta accreta spectrum (PAS)
- This is a definitive, life-saving procedure but results in permanent loss of fertility — psychologically devastating for many women
- In Hong Kong, where family sizes are typically small and fertility is highly valued, this is an important counselling point
| Condition | Mechanism |
|---|---|
| Post-traumatic stress disorder (PTSD) | Acute life-threatening hemorrhagic event → intrusive flashbacks, hyperarousal, avoidance behaviours |
| Postnatal depression | Traumatic delivery, emergency surgery, NICU admission of preterm baby, loss of fertility from hysterectomy → complex grief and depression |
| Anxiety about future pregnancies | Fear of recurrence — especially relevant in abruption (recurrence risk 5–17%) and praevia (recurrence 4–8%) |
| Bonding difficulties | Maternal-infant separation if baby in NICU; maternal illness/ICU admission |
B. Fetal and Neonatal Complications
Mechanism:
- Placental separation (abruption) or maternal hypovolemia (any cause) → reduced functional placental surface area for gas exchange → fetal hypoxia
- In abruption: > 50% separation is typically incompatible with fetal survival
- In praevia: fetal death is less common unless maternal hemorrhage is massive (the placenta itself may still be well-perfused if only the lower edge has separated)
- In vasa praevia: fetal blood loss → fetal exsanguination (fetal blood volume is only ~250–300 mL at term — even 50–100 mL loss can be lethal)
CTG findings indicating fetal compromise:
- Late decelerations → uteroplacental insufficiency
- Prolonged bradycardia → acute hypoxia
- Sinusoidal pattern → fetal anaemia (vasa praevia, massive FMH)
- Loss of variability → advanced hypoxic injury to autonomic nervous system
This is the most common fetal complication of APH. Many women with APH require emergency delivery before term — either because of massive hemorrhage necessitating immediate CS, or because of fetal distress.
| Complication of Prematurity | Mechanism |
|---|---|
| Respiratory distress syndrome (RDS) | Immature Type II pneumocytes → insufficient surfactant → alveolar collapse → impaired gas exchange. Prevented/mitigated by antenatal corticosteroids |
| Intraventricular hemorrhage (IVH) | Fragile germinal matrix capillaries in preterm brain → susceptible to rupture with changes in cerebral blood flow (e.g., birth asphyxia, resuscitation) |
| Necrotising enterocolitis (NEC) | Immature intestinal barrier + ischemia-reperfusion injury → bacterial translocation → intestinal necrosis |
| Retinopathy of prematurity (ROP) | Immature retinal vasculature → abnormal neovascularisation in response to supplemental oxygen |
| Bronchopulmonary dysplasia (BPD) | Chronic lung injury from prolonged ventilation and oxygen therapy in preterm lungs |
| Sepsis | Immature immune system → susceptibility to nosocomial infections in NICU |
| Hypothermia | High surface area-to-volume ratio + immature thermoregulation → rapid heat loss |
| Feeding difficulties | Immature suck-swallow coordination → requires tube feeding |
- Chronic or recurrent abruption → chronic uteroplacental insufficiency → reduced nutrient and oxygen supply to fetus → growth restriction
- Also seen in praevia with repeated bleeds (chronic relative placental insufficiency)
- IUGR fetuses are at higher risk during delivery and have higher perinatal morbidity and mortality
| Cause | Mechanism |
|---|---|
| Vasa praevia | Direct fetal blood loss through torn fetal vessels |
| Massive feto-maternal hemorrhage | Abruption disrupts placental integrity → fetal RBCs enter maternal circulation → fetal anaemia |
| Chronic abruption | Ongoing low-grade FMH → gradual fetal anaemia |
Detection: Middle cerebral artery (MCA) Doppler — elevated peak systolic velocity (PSV > 1.5 MoM) indicates fetal anaemia (low viscosity blood flows faster).
Obstetric complications — including antepartum haemorrhage, preterm labour and low birth weight, fetal hypoxia or asphyxia — are identified as distal environmental risk factors for schizophrenia (2× risk) [18].
Mechanism: Perinatal hypoxia-ischemia → subtle damage to developing brain → disruption of normal neurodevelopment → predisposition to psychotic disorders decades later. This is part of the neurodevelopmental hypothesis of schizophrenia — early insults (genetic + environmental) alter brain maturation, with clinical manifestation in adolescence/early adulthood.
Other neurodevelopmental consequences of perinatal hypoxia:
- Cerebral palsy — hypoxic-ischemic encephalopathy at birth → motor cortex and white matter damage
- Learning difficulties — frontal lobe and hippocampal vulnerability to hypoxia
- Epilepsy — cortical scarring from ischemic injury → epileptogenic foci
APH and Schizophrenia — An Exam Connection
Antepartum haemorrhage is listed as a distal risk factor (prenatal, perinatal) for schizophrenia with approximately 2× risk [18]. The mechanism is fetal hypoxia causing subtle brain injury during critical periods of neurodevelopment. This is a cross-specialty link that may appear in psychiatry or obstetrics exams.
- Perinatal mortality rate in APH is approximately 10–15% overall (higher in severe abruption, approaching 30–50%)
- Causes: birth asphyxia, extreme prematurity, fetal exsanguination (vasa praevia)
- Even with modern neonatal intensive care, very preterm infants born in the context of APH have high morbidity and mortality
| Cause of APH | Specific Complications |
|---|---|
| Placenta praevia | PPH (atonic lower segment); PAS (accreta/increta/percreta) → CS hysterectomy; malpresentation requiring CS; preterm delivery; recurrence in future pregnancies |
| Placental abruption | DIC (most important); Couvelaire uterus → PPH; renal cortical necrosis; Sheehan syndrome; IUFD; IUGR (if chronic); recurrence risk 5–17% |
| Vasa praevia | Fetal exsanguination → fetal death (~60% if undiagnosed); fetal anaemia requiring neonatal transfusion |
| Uterine rupture | Maternal hemorrhagic shock; fetal death from extrusion; hysterectomy; bladder injury; peritonitis if contamination |
| PAS | Massive intraoperative hemorrhage; need for CS hysterectomy; bladder/bowel injury (percreta invading adjacent organs); ICU admission; massive transfusion complications |
| System | Maternal Complication | Fetal/Neonatal Complication |
|---|---|---|
| Haematological | DIC, dilutional coagulopathy, transfusion reactions | Fetal anaemia, neonatal anaemia |
| Cardiovascular | Hypovolemic shock, cardiac arrest | Fetal hypoxia, bradycardia |
| Renal | AKI, renal cortical necrosis | — |
| Endocrine | Sheehan syndrome | — |
| Respiratory | ARDS, aspiration pneumonitis (Mendelson's) | RDS (prematurity) |
| Neurological | Watershed cerebral infarcts | Cerebral palsy, IVH, neurodevelopmental delay, schizophrenia risk |
| Reproductive | Hysterectomy, Rh isoimmunisation, recurrence risk | — |
| Psychological | PTSD, postnatal depression | Bonding difficulties |
| Mortality | Maternal death | IUFD, neonatal death |
High Yield Summary
Complications of APH — Key Points:
- Maternal death: Haemorrhage is one of the major causes of maternal mortality [1][11]
- DIC: Most important haematological complication; especially with abruption; the patient can develop blood coagulation defects after heavy bleeding, and this causes more bleeding [1][11]
- PPH: APH is a risk factor for PPH [2] — via uterine atony (Couvelaire/lower segment), retained placenta (PAS), trauma (CS), and coagulopathy (DIC)
- Sheehan syndrome: Anterior pituitary infarction from severe hemorrhagic shock → failure to lactate, then panhypopituitarism (delayed presentation)
- AKI/Renal cortical necrosis: Hypovolemia + DIC → renal ischemia (cortical necrosis is irreversible)
- ARDS: From massive transfusion (TRALI), DIC, or aspiration
- Anaesthetic risks in pregnancy: Difficult intubation 8× more common; aspiration risk from delayed gastric emptying; rapid desaturation from ↓FRC; aortocaval compression [16]
- Massive transfusion complications: Hypothermia, dilutional coagulopathy, hyperkalemia, citrate toxicity (hypocalcaemia) [17]
- Fetal: Hypoxia → IUFD; prematurity (most common fetal complication); IUGR; fetal anaemia
- Long-term: APH is a distal risk factor for schizophrenia (2× risk) via fetal hypoxia affecting neurodevelopment [18]
- Rh isoimmunisation: FMH in Rh-negative mothers → anti-D production → HDFN in future pregnancies; prevented by anti-D immunoglobulin
Active Recall - APH Complications
References
[1] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (p3 — Introduction, maternal mortality; p4 — coagulation defects after heavy bleeding; p7 — placenta accreta definition) [2] Lecture slides: PPH for teaching (20210716)v6.pdf (p6 — APH as risk factor for PPH) [3] Lecture slides: Block C - Postpartum Haemorrhage.pdf (p5 — lower segment cannot contract, massive bleeding) [4] Senior notes: Maksim Medicine Notes.pdf (p165 — DIC aetiology, lab features) [5] Senior notes: Ryan Ho Haemtology.pdf (p137–138 — DIC causes, clinical features, laboratory features) [11] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf (p3 — maternal mortality; p4 — coagulation defects; p7 — placenta accreta) [16] Senior notes: Maksim Surgery Notes.pdf (p298 — Obstetric anaesthesia complications, aortocaval compression, Mendelson's, difficult intubation, placental bed autoregulation) [17] Senior notes: Ryan Ho Critical Care.pdf (p20 — Massive transfusion definition, complications, 1:1:1 ratio) [18] Senior notes: Ryan Ho Psychiatry.pdf (p135 — Distal risk factors for schizophrenia including APH, obstetric complications)
High Yield Summary
Definition: Antepartum hemorrhage (APH) is bleeding from the genital tract from 24+0 weeks of gestation until delivery. It is an obstetric emergency because maternal haemorrhage, fetal hypoxia, and preterm delivery can all occur rapidly.
Big causes: Placenta praevia, placental abruption, vasa praevia, uterine rupture, local cervical/vaginal causes, and indeterminate APH. About half of APH remains unexplained after assessment, but dangerous causes must be excluded first.
Placenta praevia: Placenta implanted in the lower segment near or over the internal os. Presents with painless, bright red, recurrent bleeding, soft non-tender uterus, high presenting part or malpresentation, and usually normal fetal heart unless bleeding is massive. Risk factors include previous Caesarean section, uterine surgery/curettage, grand multiparity, age > 35, multiple pregnancy, IVF, and smoking.
Placental abruption: Premature separation of a normally sited placenta. Presents with painful dark bleeding, tender/irritable "woody hard" uterus, fetal distress, shock disproportionate to visible blood loss if concealed, and high DIC risk. Risk factors include pre-eclampsia, chronic hypertension, previous abruption, smoking/cocaine, trauma, PPROM, polyhydramnios decompression, thrombophilia, and anaemia.
Vasa praevia: Fetal vessels cross near the internal os. Bleeding occurs at membrane rupture, maternal condition may remain stable, but fetal bradycardia/sinusoidal CTG can develop quickly because the blood loss is fetal.
High Yield Summary
Differential diagnosis of APH:
- Praevia: Painless bright red bleeding, soft uterus, high head/malpresentation, prior CS.
- Abruption: Painful bleeding, hard tender uterus, fetal distress, DIC risk, hypertension/smoking.
- Vasa praevia: Bleeding at ROM, fetal blood, rapid fetal compromise, stable mother.
- Uterine rupture: Previous uterine scar plus labour, sudden tearing pain, cessation of contractions, shock, fetal parts may be palpable.
- Local causes: Cervical ectropion, polyp, carcinoma, cervicitis, vaginal varicosities, trauma. Usually small-volume or contact bleeding and identified on speculum.
- Indeterminate APH: No cause found despite assessment; still associated with preterm birth, low birth weight, PPH, and adverse perinatal outcomes.
Do not miss: Previous ovarian cystectomy is not previous uterine surgery and does not increase praevia or rupture risk. Never perform digital vaginal examination until placenta praevia has been excluded by ultrasound.
High Yield Summary
Initial diagnostic approach: Stabilise first, diagnose second. Assess ABCDE, maternal observations, fetal status, bleeding amount, pain, uterine tone, presentation, and risk factors.
Safe examination sequence:
- Abdominal examination first: uterine tenderness/tone, lie, presentation, engagement, scars, SFH.
- Ultrasound to localise placenta.
- Speculum examination to inspect cervix/vagina and source of bleeding.
- Digital vaginal examination only after praevia is excluded.
Key investigations:
- CBC, coagulation screen, fibrinogen, group and crossmatch: Assess blood loss and DIC risk.
- CTG: Fetal wellbeing; bradycardia suggests severe abruption, sinusoidal pattern suggests fetal anaemia.
- USS/TVS: Localise placenta. TVS is safe and is gold standard for praevia edge-to-os distance.
- Colour Doppler: Vasa praevia and placenta accreta spectrum.
- Kleihauer-Betke: Rh-negative mothers and suspected fetomaternal haemorrhage.
- Apt test: Suspected vasa praevia to distinguish fetal from maternal blood.
- LFT/RFT/urinalysis: Screen for pre-eclampsia/HELLP and shock-related organ dysfunction.
Ultrasound trap: USS cannot exclude abruption. Abruption is a clinical diagnosis supported by painful bleeding, hard/tender uterus, fetal compromise, and coagulopathy.
High Yield Summary
Management principles: APH management follows four priorities: communication, resuscitation, monitoring/investigation, and arresting bleeding. Mother comes first; fetal outcome depends on maternal oxygenation and circulation.
Immediate actions: Call senior obstetrician, anaesthetist, midwife, haematologist/blood bank, and neonatologist. Left lateral tilt, high-flow oxygen, 2 large-bore IV lines, CBC/RFT/coagulation/crossmatch, crystalloid while arranging blood, Foley catheter, continuous CTG, quantify blood loss, and activate massive transfusion if needed.
Placenta praevia:
- Minor bleeding and preterm/stable: Admit, maintain IV access, crossmatched blood available, avoid digital VE/coitus, steroids if < 34+6 weeks, anti-D if Rh-negative, serial TVS, and plan CS if praevia persists.
- Major bleeding, maternal compromise, fetal compromise, or term: Deliver by Caesarean section.
Placental abruption:
- Mild, preterm, stable mother/fetus: Admit, close monitoring, steroids, anti-D if Rh-negative, serial coagulation and CTG.
- Fetal distress with fetus alive: Emergency CS.
- Fetal death: Prefer vaginal delivery if possible, especially if DIC, because CS increases maternal bleeding risk.
Vasa praevia: Antenatal diagnosis requires planned CS before membrane rupture; acute bleeding at ROM requires immediate emergency CS and neonatal resuscitation.
Uterine rupture: Immediate laparotomy, delivery, repair or hysterectomy, massive transfusion, and neonatal resuscitation.
High Yield Summary
DIC in APH: Especially associated with abruption. Placental tissue factor activates coagulation -> consumption of platelets, fibrinogen, and clotting factors -> bleeding worsens. Labs: low platelets, prolonged PT/APTT, low fibrinogen, high D-dimer, schistocytes.
Blood product priorities: Packed RBCs for oxygen carriage, FFP for clotting factors, cryoprecipitate if fibrinogen < 2 g/L, platelets if < 50 x 10^9/L with active bleeding or procedure, and tranexamic acid early in major haemorrhage.
Maternal complications: Hypovolaemic shock, maternal death, DIC, PPH, AKI/ATN/cortical necrosis, Sheehan syndrome, ARDS/TRALI, hepatic ischaemia or HELLP overlap, myocardial/cerebral hypoperfusion, Rh isoimmunisation, hysterectomy/loss of fertility, anaesthetic complications, and psychological morbidity.
Fetal/neonatal complications: Fetal hypoxia/asphyxia, IUFD, prematurity, IUGR, fetal anaemia, neonatal death, and long-term neurodevelopmental effects after hypoxic injury.
PPH link: APH is a major PPH risk factor. Mechanisms map to the 4 T's: tone (Couvelaire uterus/lower segment bleeding), tissue (accreta), trauma (CS/rupture), and thrombin (DIC).
Obstetric History
A systematic record of a woman's past pregnancies, deliveries, and their outcomes, typically summarized using the gravida-para (GTPAL) system to guide current obstetric care.
Postpartum Hemorrhage
Postpartum hemorrhage is excessive blood loss after delivery, defined as more than 500 mL after vaginal or caesarean delivery, or symptoms and signs of shock regardless of measured loss.