Antepartum hemorrhage is bleeding from the genital tract from 24 weeks of gestation until delivery, most commonly caused by placenta praevia or placental abruption.

Exam domain	One-glance essentials
Definition / diagnosis	*APH is genital-tract bleeding from 24 weeks of gestation until delivery* ^[1]^[2] Major causes are placenta praevia, placental abruption, vasa praevia, uterine rupture, and local genital-tract lesions ^[1]
Epidemiology / risks	Praevia risk rises with previous Caesarean or uterine surgery, placenta praevia, multiparity, multiple pregnancy, and smoking ^[1]^[2] Abruption is associated with hypertension or pre-eclampsia, previous abruption, trauma, smoking or cocaine, and sudden uterine decompression ^[1]
Core mechanism	Praevia places placenta over or near the os; abruption separates a normally sited placenta, causing bleeding, uterine irritability, and fetal hypoxia ^[1] Vasa praevia rupture causes fetal, not maternal, blood loss and can rapidly exsanguinate the fetus ^[1]^[2]
Clinical picture	*Praevia: painless bright bleeding with a soft uterus; abruption: painful bleeding with a tender, tense uterus and shock that may exceed visible loss* ^[1]^[2] Bleeding at membrane rupture with fetal bradycardia suggests vasa praevia ^[1]
Investigations	Assess maternal ABCs and fetal status; obtain CBC, coagulation profile including fibrinogen, group and crossmatch, CTG, and ultrasound placental localisation ^[1]^[2] Ultrasound cannot exclude abruption; diagnosis remains clinical ^[1]
Management	*Call the multidisciplinary obstetric haemorrhage team, resuscitate the mother, monitor the fetus, and control the source* ^[1]^[2] Timing and mode of delivery depend on cause, bleeding severity, maternal or fetal compromise, gestation, and placental location ^[1]
Complications	Maternal complications include shock, DIC, renal injury, massive transfusion, hysterectomy, and death ^[1]^[2] Fetal complications include hypoxia, anaemia, growth restriction, prematurity, stillbirth, and neonatal death ^[1]
Prevention / follow-up	Identify placenta praevia or accreta risk antenatally, optimise anaemia, stop smoking, and plan delivery where blood products and senior teams are available ^[1]^[2] Give anti-D to eligible unsensitised RhD-negative patients according to local protocol ^[1]
Exam traps	*Never perform a digital vaginal examination until placenta praevia has been excluded* ^[1]^[2] A reassuring ultrasound does not rule out abruption, and visible bleeding can markedly underestimate concealed loss ^[1]

References

^[1] Lecture slides: Block C - Obstetric Emergency Notes to Students.pdf (APH causes, assessment and management) ^[2] Lecture slides: GCBC-OG-Obs emergency_Notes to students_Sep2024.pdf (pp. 3–7 — obstetric haemorrhage and placenta accreta)

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]

Clinical Pearl

APH complicates approximately 3–5% of all pregnancies. Although many cases are mild and self-limiting, APH is a risk factor for postpartum hemorrhage (PPH) — always be prepared for ongoing bleeding after delivery in a woman who has had APH ^[2]^[3].

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

Exam High Yield

Antepartum hemorrhage is itself a risk factor for postpartum hemorrhage ^[2]^[3]. Always plan for the possibility of PPH when managing APH. The mechanism: APH indicates abnormal placentation or coagulopathy — both predispose to continued bleeding after delivery.

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]
- This is the obstetric cause par excellence of acute DIC
- Obstetric causes of DIC include amniotic fluid embolism, eclampsia/HELLP, placenta abruptio ^[4]
- Release of placental materials into circulation → pro-coagulant effect ^[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:
- Preterm delivery
- Low birth weight
- Adverse perinatal outcomes
- Postpartum hemorrhage ^[2]^[3]
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?
- Prior CS / uterine surgery → Praevia or rupture (depending on uterine tone and pain)
- Prior ovarian/non-uterine surgery → NOT a risk for praevia/rupture ^[7]
- Smoker / hypertension → Abruption ^[7]
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).

Antepartum Hemorrhage

1. Definition

2. Epidemiology and Risk Factors

2.1 Epidemiology

2.2 Risk Factors

Risk Factors for Placenta Praevia

Risk Factors for Placental Abruption

3. Anatomy and Function: The Placental-Uterine Interface

3.1 The Uterus

3.2 The Placenta

3.3 The Decidua

3.4 The Cervix

4. Etiology (with Focus on Hong Kong)

4.1 Placenta Praevia

Pathophysiology

Relevance to Hong Kong

4.2 Placental Abruption (Abruptio Placentae)

Pathophysiology

Hong Kong Relevance

4.3 Vasa Praevia

4.4 Uterine Rupture

4.5 Local (Non-Obstetric) Causes

5. Classification

5.1 By Cause

5.2 By Severity

5.3 Classification of Placenta Praevia (Updated — RCOG / ISUOG 2019)

5.4 Classification of Placental Abruption

5.5 Placenta Accreta Spectrum (PAS)

6. Clinical Features

6.1 Symptoms

6.2 Signs

6.3 Comparison Table: Praevia vs. Abruption

6.4 Vasa Praevia — Specific Features

6.5 Uterine Rupture — Specific Features

6.6 Clinical Signs of Hypovolemic Shock in APH

7. Link to Postpartum Hemorrhage

8. Coagulopathy in APH

Active Recall - Antepartum Hemorrhage

References

Conceptual Framework

The Major Differential Diagnoses

1. Placenta Praevia (~30% of diagnosed APH)

2. Placental Abruption (~25% of diagnosed APH)

3. Vasa Praevia (Rare, ~1:2500 but lethal if missed)

4. Uterine Rupture (Rare but catastrophic)

5. Local (Non-Obstetric) Cervical and Vaginal Causes

6. Indeterminate / Unclassified APH (~50%)

Systematic Comparison of Major Differentials

Less Common Differentials to Consider

DIC as a Complication Mimicking a "Cause" of Bleeding

Approach to Narrowing the Differential

Active Recall - APH Differential Diagnosis

Principles of Diagnostic Approach

Diagnostic Algorithm

Initial Assessment (Before Any Investigation)

A. History — What to Ask and Why

B. Abdominal Examination

C. Speculum Examination (Safe — Do This, Not Digital VE)

Investigation Modalities

1. Ultrasound — The Cornerstone Investigation

a. Transabdominal Ultrasound (TAS)

b. Transvaginal Ultrasound (TVS)

c. USS Findings in Specific Diagnoses

d. Placental Migration / Serial USS

2. Cardiotocography (CTG) — Fetal Assessment

3. Laboratory Investigations

4. Blood Pressure Monitoring

5. MRI (Adjunct)

6. Fetal Assessment Beyond CTG

Diagnostic Criteria for Specific Causes of APH

Placenta Praevia — Diagnostic Criteria (RCOG / ISUOG)

Placental Abruption — Diagnostic Approach

Vasa Praevia — Diagnostic Approach

Summary: Investigations Ordered in APH

Active Recall - APH Diagnosis and Investigation

Overarching Principles

Master Management Algorithm

Step 1: Communication — Call for Help

Step 2: Resuscitation

A — Airway