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Haemorrhagic Shock in APH (Antepartum Haemorrhage)

What is APH?

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Physiological Considerations in Pregnancy

• Blood volume is 40-50% increased by term - pregnant patients must lose a relatively larger volume before showing signs of hypovolaemia. This means standard shock signs appear later and may underestimate the severity of haemorrhage.
• Physiologic anaemia of pregnancy: haematocrit 32-34% at 32-34 weeks due to plasma volume expansion exceeding red cell mass expansion.
• Lower PaCO2 (30 mmHg normally) - a PaCO2 of 40 mmHg in pregnancy actually reflects hypoventilation and impending respiratory acidosis.
• Reduced bicarbonate buffering capacity - vulnerable to metabolic acidosis under stress.
• ECG changes - left axis shift, flattened T waves in lead III - do not misinterpret as pathological.
• Up to 2 litres of blood can accumulate silently in the gravid uterus with abruption, with no or minimal external bleeding.

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Classification of Haemorrhagic Shock (ATLS)

Important in pregnancy: Vital sign thresholds are less reliable. HR and BP responses are notoriously variable. A normal BP does not exclude significant haemorrhage. Use base deficit and lactate as more sensitive early markers - even before BP falls, base deficit becomes more negative as lactic acid accumulates.

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Initial Assessment: ABCDE + Obstetric Survey

Primary Survey (Simultaneous resuscitation and assessment)

• Secure and maintain airway; high-flow oxygen (15 L/min via non-rebreather mask)
• In pregnancy, risk of aspiration is higher (delayed gastric emptying) - rapid-sequence intubation if needed

• Assess ventilation and oxygenation; SpO2 monitoring
• Target SpO2 ≥95%

• Establish 2 large-bore IV cannulae (16G or larger) immediately
• Draw blood: FBC, group and crossmatch, coagulation screen (PT, aPTT, fibrinogen, FDPs), U&E, LFTs, ABG, LDH, uric acid
• Fibrinogen normal in pregnancy = 400-450 mg/dL; <300 mg/dL indicates significant coagulation factor consumption (risk of DIC)
• Insert urinary catheter and monitor hourly urine output (target ≥30 mL/h, ideally >0.5 mL/kg/h)
• Continuous cardiac monitoring + pulse oximetry

• GCS/AVPU; pupil assessment
• Altered mental status = severe shock or CNS event

• Full examination; quantify vaginal blood loss
• Keep warm - prevent hypothermia (part of the "lethal triad": hypothermia + acidosis + coagulopathy)

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Differentiation: Placenta Praevia vs. Abruption

Key rule: Never perform digital or instrumental vaginal examination until placenta praevia is excluded by ultrasound. This can precipitate catastrophic haemorrhage.

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Diagnostic Investigations

Bedside/Urgent

• Ultrasound (transabdominal ± transvaginal) - investigation of choice for placenta localisation
  • Transvaginal USS is safe and more accurate for placenta-os relationship
  • Empty bladder first to avoid false-positive praevia
  • USS has poor sensitivity for abruption (24% sensitivity, 96% specificity) - a negative USS does NOT rule out abruption
• Cardiotocography (CTG) - fetal heart rate monitoring; most sensitive indicator of placental abruption is fetal distress on CTG
  • Minimum 4 hours of monitoring recommended after any significant haemorrhage
• eFAST (in trauma settings) - evaluates for hemoperitoneum, pericardial effusion

Laboratory

• FBC (baseline haemoglobin, haematocrit, platelets)
• Coagulation: PT, aPTT, fibrinogen (key - drops early in DIC), FDPs/D-dimer
• Group and crossmatch (consider activating massive transfusion protocol early)
• Base deficit (on ABG) - early, sensitive marker of occult haemorrhage even before BP falls; normal is > -2 mEq/L
• Lactate - indicator of tissue hypoperfusion
• Kleihauer-Betke test - if Rh-negative mother (quantify fetomaternal haemorrhage)
• U&E, LFTs (exclude HELLP, pre-eclampsia-related causes)

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Resuscitation Protocol

Fluid Resuscitation

1. Initial: Judicious isotonic crystalloid (10-20 mL/kg) while awaiting blood products
2. Permissive hypotension strategy in uncontrolled haemorrhage - avoid aggressive crystalloid resuscitation (worsens coagulopathy, acidosis, hypothermia)
3. Blood products - preferred over crystalloid when haemorrhage is severe:

1. Fresh frozen plasma (FFP) and fresh whole blood may be needed for coagulopathy in APH
2. Cryoprecipitate for fibrinogen replacement if fibrinogen <200 mg/dL
3. Tranexamic acid (TXA) - early administration (within 3 hours of haemorrhage onset); inhibits fibrinolysis

Treating the Lethal Triad

• Hypothermia - warm IV fluids, warming blankets, warm environment
• Acidosis - adequate resuscitation, correct base deficit
• Coagulopathy - early FFP, platelets, cryoprecipitate, TXA

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Response to Initial Resuscitation

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Obstetric Management (Definitive Haemorrhage Control)

Placenta Praevia

• Obstetric consultation immediately; arrange transfer to tertiary obstetric facility
• Delivery - typically emergency Caesarean section (avoid vaginal delivery in major praevia)
• Minor praevia with stable patient - conservative management with close monitoring possible; corticosteroids for fetal lung maturity if preterm
• Avoid all digital cervical examination

Placental Abruption

• Mild (< 25% separation, stable mother + fetus): Expectant management with close monitoring; tocolytics generally not recommended (may mask symptoms)
• After 32 weeks or unstable: Delivery indicated (risk of further separation > benefit of prematurity)
• Severe abruption / DIC / fetal distress: Emergency delivery (Caesarean or expedited vaginal delivery depending on cervical status)
• Watch for DIC - coagulation factors consumed by thromboplastin released from injured placenta
• Tocolytics are contraindicated if abruption is the cause of preterm contractions

DIC Management (complicating APH)

• Correct underlying cause (deliver)
• FFP 15 mL/kg for clotting factor replacement
• Cryoprecipitate for fibrinogen <100 mg/dL
• Platelet transfusion if <50 × 10⁹/L (or <75 × 10⁹/L with ongoing haemorrhage)
• Consider recombinant Factor VIIa in refractory cases

Surgical Options for Uncontrolled Haemorrhage

• Uterine compression sutures (B-Lynch)
• Uterine artery ligation / internal iliac artery ligation
• Balloon tamponade (intrauterine)
• Interventional radiology - uterine artery embolisation (in stable patients)
• Peripartum hysterectomy - last resort for life-threatening haemorrhage

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Monitoring Targets

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Special Considerations

• Fetal monitoring: CTG must be continuous once fetal viability is established; fetal distress is the most sensitive indicator of abruption. Fetal heart rate < 110 bpm with maternal hypotension and acidosis predicts poor fetal outcome.
• Perimortem Caesarean section: If maternal cardiac arrest, perform within 4-5 minutes if fetus is viable to optimise maternal resuscitation (removes aortocaval compression).
• Aortocaval compression: Displace uterus to the left (manual or 15-degree left lateral tilt) to relieve compression on the inferior vena cava in all pregnant patients ≥20 weeks gestation.
• REBOA (Resuscitative Endovascular Balloon Occlusion of the Aorta) - emerging adjunct for haemorrhage control pending surgical intervention.

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Summary Algorithm for APH with Haemorrhagic Shock

APH Presenting with Shock
        │
        ▼
ABCDE Primary Survey + Simultaneous Resuscitation
  - O2, IV access ×2, bloods (FBC, coag, G+XM, ABG)
  - Left lateral tilt (≥20 weeks)
  - Foley catheter, monitor UO
        │
        ▼
Immediate Investigations
  - USS: localise placenta (praevia vs. abruption)
  - CTG: fetal monitoring (most sensitive for abruption)
  - NO digital VE until praevia excluded
        │
        ▼
Resuscitate: Crystalloid → PRBCs → MTP (1:1:1)
  - Treat lethal triad: warm, correct acid, correct coagulopathy
  - Tranexamic acid early
  - Anti-D for Rh-negative mothers
        │
        ├── Placenta Praevia → Emergency LSCS
        │
        └── Placental Abruption
               ├── Stable + partial (<25%) → Expectant (if <32 wks)
               └── Unstable / Severe / >32 wks → Deliver (LSCS or expedited vaginal)
                        │
                        └── DIC → FFP + Cryoprecipitate + Platelets + TXA

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• ROSEN's Emergency Medicine, 9e - Haemorrhagic Shock, Placenta Previa, Placental Abruption
• Schwartz's Principles of Surgery, 11e - Signs & Symptoms of Hemorrhagic Shock (Table 7-4); Damage Control Resuscitation
• Creasy & Resnik's Maternal-Fetal Medicine - Effect of Pregnancy on Haemostasis
• Textbook of Family Medicine, 9e - Abruptio Placentae

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APH: Complete Notes Based on Learning Outcomes

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LO 1 - Definition of Antepartum Haemorrhage

• Incidence: affects approximately 3-5% of pregnancies
• It is a major cause of maternal and perinatal morbidity and mortality worldwide
• Bleeding may be revealed (external, visible) or concealed (blood pools behind placenta - may have NO visible bleeding but severe maternal compromise)

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LO 2 - Causes, Clinical Features, and Complications of APH

Causes (in order of clinical importance)

Key rule: Do NOT perform a digital or speculum pelvic examination to assess vaginal bleeding in APH until transvaginal ultrasound has confirmed the location of the placenta. Mechanical disruption of the placenta by speculum or digital examination may precipitate catastrophic haemorrhage.

General Clinical Features of APH

• Vaginal bleeding after 24 weeks (may be bright red or dark)
• May be painless (praevia) or painful (abruption)
• Uterine tenderness, contractions
• Signs of maternal shock: tachycardia, hypotension, pallor, diaphoresis
• Fetal distress on CTG

Complications

• Haemorrhagic shock
• DIC (especially with abruption)
• Renal failure (from ischaemia)
• Pituitary necrosis (Sheehan's syndrome) from prolonged hypotension
• Peripartum hysterectomy
• Death

• Fetal distress, hypoxia, acidosis
• Intrauterine death (fetal mortality ~15% with abruption overall; 100% with severe complete abruption if not immediately delivered)
• Prematurity and its sequelae
• Growth restriction

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LO 3 - Initial Management Approach to APH

Step 1 - Immediate Stabilisation (Simultaneous Assessment + Resuscitation)

• Establish 2 large-bore IV cannulae (16G or larger) immediately
• IV fluid resuscitation: crystalloid initially (10-20 mL/kg); then blood products if haemodynamically unstable
• Left lateral tilt (≥20 weeks) - prevents aortocaval compression by gravid uterus
• Insert urinary catheter; monitor urine output (target ≥30 mL/h)
• Continuous maternal cardiac monitoring + pulse oximetry

Step 2 - Investigations

Step 3 - Urgent Obstetric Consultation

• Arrange immediate obstetric review and/or transfer to tertiary facility with obstetric + neonatal services
• If Rh-negative and not yet received prophylaxis at 28 weeks: anti-D immunoglobulin 300 μg

Step 4 - Blood Transfusion / Massive Transfusion Protocol (if needed)

• PRBCs for significant blood loss; if massive haemorrhage: activate MTP with 1:1:1 ratio (PRBCs : FFP : Platelets)
• FFP and cryoprecipitate for DIC
• Tranexamic acid (TXA) early - inhibits fibrinolysis
• O-negative blood until type-specific available

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LO 4 - Abruptio Placentae: Clinical Features, Investigations & Management

Definition

Pathophysiology

Risk Factors

• Hypertension and pre-eclampsia (40-50% of cases)
• Abdominal trauma (motor vehicle accidents, intimate partner violence)
• Cocaine use
• Smoking
• Advanced maternal age (>35) or young age (<20)
• High parity (≥3)
• Prior abruption
• Chorioamnionitis, oligohydramnios
• Thrombophilia

Types

Grades of Severity

Clinical Features (the classic triad)

1. Painful vaginal bleeding - dark blood (70% of patients)
2. Uterine tenderness with "woody hard" or tetanic uterus (in severe cases)
3. Fetal distress on CTG (most sensitive indicator)

• Nausea, vomiting, back pain may be present
• Up to 10% have only occult bleeding with NO external haemorrhage
• Up to 2 litres of blood can be sequestered in the gravid uterus
• Uterine contractions are often 1-2 minutes apart with high baseline pressure

Investigations

Management

• 2 large-bore IVs, bloods, maternal stabilisation
• Continuous CTG monitoring
• Emergency obstetric consultation
• Anti-D if Rh-negative

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LO 5 - Placenta Praevia: Clinical Features, Investigations & Management

Definition

Types (Classification)

Placental migration: Up to 90% of placentae diagnosed as praevia on 2nd trimester USS resolve by term as the lower uterine segment elongates. Central previa (20% of cases) is less likely to migrate and carries highest haemorrhage risk.

Risk Factors

• Previous Caesarean section (most important - risk increases with number of prior sections)
• Multiple uterine surgeries
• Advanced maternal age
• Multiparity
• Multiple gestation
• Tobacco / cocaine use
• Prior placenta praevia
• Assisted reproductive technology
• Prior miscarriage or induced abortion

Clinical Features

• Painless, bright-red, fresh vaginal bleeding - hallmark; this is the key differentiator from abruption
• Typically begins at 27-32 weeks (average first bleed)
• Initial bleeding is often self-limited, then recurs
• Women with central praevia bleed earlier and more severely
• Soft, non-tender uterus
• Fetal malpresentation common (transverse or breech) - floating, unengaged presenting part
• ~20% have some uterine irritability, but this is minor

Investigations

Management

• 2 large-bore IVs; fluid/blood resuscitation; obstetric consultation
• Continuous CTG monitoring
• Baseline fibrinogen (normal in pregnancy = 400-450 mg/dL)
• Do NOT perform speculum or digital examination until placental position confirmed
• Anti-D if Rh-negative

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LO 6 - Indeterminate APH, Local Causes, and Vasa Praevia

Indeterminate APH

• Accounts for approximately 50% of all APH cases
• No placenta praevia on USS, no clinical/ultrasound features of abruption
• Includes small subclinical marginal abruptions, decidual bleeding
• Management: treat empirically as significant APH until cause found; close monitoring; CTG
• Many resolve spontaneously but carry residual risk of preterm labour and fetal growth restriction

Local Causes of APH

These causes can only be assessed AFTER placenta praevia has been excluded by ultrasound. Only then should a careful speculum examination be done.

Vasa Praevia

• Velamentous cord insertion
• Placenta praevia
• Bilobed or succenturiate lobe placenta
• In vitro fertilisation (IVF)
• Multiple gestation

• Classic triad: Painless bleeding + rupture of membranes + acute fetal distress / sudden fetal bradycardia
• Blood is fetal in origin - very small volumes (100-200 mL) can cause fetal shock
• Pulsatile vessels may be palpated before the presenting part on digital examination (if done)
• Fetal heart rate may be sinusoidal or show deep, late decelerations
• Fetal mortality: 33-100% if not diagnosed/managed before rupture

• Colour Doppler USS - can identify aberrant vessels at the internal os early in pregnancy (primary screening tool)
• At time of acute bleeding: Apt test / Kleihauer test on vaginal blood - confirms fetal haemoglobin (fetal origin)
• CTG: fetal distress is rapid and severe
• Often a retrospective diagnosis after emergency LSCS for fetal distress

• Emergency LSCS is the treatment - there is NO time for conservative management once bleeding starts
• Antenatal diagnosis by Doppler USS allows planned elective LSCS before 36-37 weeks (before membrane rupture)
• If diagnosed antenatally: close monitoring, hospital admission near term, avoid artificial rupture of membranes
• Fetal mortality dramatically reduced with antenatal diagnosis and planned delivery

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Quick Comparison: The Three Major Causes of APH

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• Tintinalli's Emergency Medicine, 9e - Abruptio Placentae, Placenta Praevia, Vasa Praevia (pp. 674-676)
• ROSEN's Emergency Medicine, 9e - Abruptio Placentae, Placenta Praevia
• Textbook of Family Medicine, 9e - Abruptio Placentae, Placenta Praevia, Vasa Praevia
• Creasy & Resnik's Maternal-Fetal Medicine - Haemostasis in Pregnancy