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📋 ANTEPARTUM HEMORRHAGE (APH)

DC Dutta's Textbook of Obstetrics - Chapter 19

DEFINITION

  • Bleeding from or into the genital tract after 28th week but before birth of the baby (includes 1st and 2nd stage of labor)
  • 28th week = lower limit of fetal viability (arbitrary)
  • Incidence: ~3% of hospital deliveries

CAUSES OF APH

  1. Placenta Previa (~1/3)
  2. Abruptio Placentae (~1/3)
  3. Indeterminate/Unclassified (~1/3)

PART 1: PLACENTA PREVIA

DEFINITION

Placenta implanted partially or completely over the lower uterine segment (over/adjacent to internal os). Previa = "in front of" the presenting part.

INCIDENCE

  • ~1/3 of all APH cases
  • 0.5-1% of hospital deliveries
  • 80% cases in multiparous women
  • Increased risk: age >35 yrs, high birth order, multiple pregnancy

ETIOLOGY (Theories)

  1. Dropping-down theory - fertilized ovum drops and implants in lower segment; explains central placenta previa
  2. Persistence of chorionic activity in decidua capsularis - explains lesser degrees
  3. Defective decidua - chorionic villi spread wide for nourishment, encroach onto lower segment; may lead to accreta/increta/percreta
  4. Big placenta (e.g., twins) - encroaches onto lower segment

HIGH-RISK FACTORS (Box 19.1)

  • Multiparity
  • Age >35 yrs (4-fold increase)
  • Asian race
  • Infertility treatment
  • Uterine scar (LSCS, myomectomy, hysterotomy)
  • Prior curettage / prior placenta previa
  • Multiple pregnancy
  • Abnormal placenta (succenturiate lobe, big placenta)
  • Smoking (placental hypertrophy due to CO-induced hypoxemia)

PATHOLOGICAL ANATOMY

  • Placenta: large and thin, tongue-shaped extension, infarction/calcification, may be morbidly adherent
  • Umbilical cord: battledore or velamentous insertion; cord may be close to internal os (risk of vasa previa)
  • Lower uterine segment: soft, friable, increased vascularity

TYPES/DEGREES (Fig. 19.1)

TypeNameDescription
ILow-lyingPlacenta in lower segment but NOT reaching os
IIMarginalReaches margin of internal os but doesn't cover it
IIIIncomplete/Partial centralCovers os when closed, not when fully dilated
IVComplete/CentralCovers os even when fully dilated
  • Mild degree = Type I + Type II anterior
  • Major degree = Type II posterior + Type III + Type IV
  • Most common location: posterior wall

CLINICAL FEATURES

Symptoms

  • Painless, bright red vaginal bleeding - hallmark
  • Sudden onset, no precipitating cause
  • Recurrent - each bleed tends to be heavier than the last
  • First bleed usually not alarming; subsequent bleeds may be torrential
  • Most bleed before 38 weeks (earlier in major degrees)
  • Some central cases may NOT bleed until labor starts
  • No obvious trauma or hypertension as cause

Signs

  • General condition and anemia proportionate to visible blood loss
  • Uterus: size proportionate to gestation, relaxed, soft, elastic, no local tenderness
  • Malpresentation: breech, transverse lie or unstable lie (more frequent)
  • Floating head despite expected engagement - persistent head displacement (very suggestive)
  • Head cannot be pushed into pelvis
  • FHS usually present (unless major separation with exsanguination)
  • Stallworthy's sign: slowing of FHR on pressing head into pelvis, recovers on release - suggests low-lying (especially posterior) placenta
  • Vulval inspection only - note ongoing bleed, bright red blood, amount of loss
  • NEVER do vaginal examination outside OT - risk of torrential hemorrhage

DIAGNOSIS (Confirmation)

  • Painless, recurrent bleeding in 2nd half of pregnancy = placenta previa until proven otherwise
  • USG is initial and primary investigation

Placentography (USG)

  • Transabdominal USG: Simple, non-invasive, first-line
  • Transvaginal USG (TVS): More accurate for posterior placenta; safer than previously thought
    • Distance of placental edge from internal os:
      • 20 mm = vaginal delivery possible
      • <20 mm = likely to need LSCS
      • Placenta over os = LSCS mandatory
  • USG report should state exact distance from placental edge to internal os
  • Repeat USG at 32-36 weeks (placental migration occurs - many low-lying placentas move up)

Clinical Confirmation (Double Setup Examination)

  • Done in OT under anesthesia with everything ready for LSCS
  • Cervix examined with finger - if placenta felt, CS is done
  • Only if CS is NOT planned (Type I, II anterior with fetal head well below the placenta)

DIFFERENTIAL DIAGNOSIS (Table 19.1)

FeaturePlacenta PreviaAbruptio Placentae
PainPainlessPainful
Blood colorBright redDark
UterusSoft, relaxedTense, tender ("woody")
MalpresentationCommonUncommon
FHSUsually presentMay be absent
ShockProportionate to blood lossOften disproportionate
RecurrenceYes (repeated)No
  • Local cervical lesions (polyp, carcinoma) - differentiated by speculum exam
  • Circumvallate placenta - slight bleeding, confirmed after placental inspection

COMPLICATIONS

Maternal

During Pregnancy:
  • APH with varying degrees of shock (inevitable)
  • Co-existent placental abruption (~10%)
  • Malpresentation, unstable lie
  • Premature labor (spontaneous or induced)
During Labor:
  • Early rupture of membranes
  • Cord prolapse (abnormal cord attachment)
  • Slow cervical dilatation
  • Intrapartum hemorrhage
  • Increased operative interference (LSCS, hysterectomy)
Postpartum:
  • PPH due to: imperfect lower segment retraction, large placental surface area with atonic uterus, pre-existing anemia
  • Morbidly adherent placenta (accreta/increta/percreta) - 15% association; 10-15% risk with 1 prior CS, ~60% with 3+ prior CS
  • Retained placenta, manual removal hazards
  • Cervical and lower segment trauma
During Puerperium:
  • Sepsis (increased operative interference + placental site near vagina + anemia)

Fetal

  • Prematurity (most common cause of fetal loss)
  • IUGR
  • Congenital malformations (increased)
  • Fetal asphyxia from placental separation
  • Fetal anemia from fetal blood loss
  • Perinatal mortality: ~10% (major degrees)

MANAGEMENT

On Admission (Immediate)

  1. IV access (wide bore), IV fluids
  2. Blood grouping, cross-matching; Hb, hematocrit
  3. Urine for protein
  4. Do NOT do vaginal examination
  5. USG to confirm diagnosis and placental location
  6. Blood transfusion if required
  7. Assess fetal well-being (CTG, USG)

Subsequent Management

A. Expectant Management (Conservative)

Suitable when:
  • Hb >10 g%, hematocrit >30%
  • <37 weeks gestation
  • No active bleeding
  • Fetal well-being assured
Conduct:
  1. Bedrest (bathroom/toilet privileges)
  2. Hb estimation, blood grouping, urine protein
  3. Vulval pad inspection periodically; USG every 2-3 weeks
  4. Hematinics; cross-matched blood transfusion if anemic
  5. Speculum (Cusco's) exam 2-3 days after bleeding stops (to exclude local causes)
  6. Tocolysis (MgSO4) if bleeding + uterine contractions
  7. Cervical cerclage - NOT helpful (RCOG 2005)
  8. Rh immunoglobulin to all Rh-negative unsensitized women
  9. Betamethasone if <34 weeks (for fetal lung maturity)
Hospital vs Home: Hospital is ideal; home allowed if patient compliant, lives close to hospital, 24-hr transport available
Duration: Continue up to 37 weeks
Terminate expectant if:
  • Recurrent brisk, continuing hemorrhage
  • Fetal death
  • Congenital malformation of fetus

B. Active/Definitive Management (Delivery)

Indications:
  1. Bleeding at or after 37 weeks
  2. Patient in labor
  3. Exsanguinated state on admission
  4. Continuing moderate-degree bleeding
  5. Non-reassuring fetal cardiac status / dead fetus / known fetal malformation
Method:
  • Cesarean section for all with sonographic evidence of major placenta previa (Type II posterior, III, IV) or clinical signs
  • Vaginal delivery may be considered for Type I and Type II anterior with engaged fetal head and facilities for immediate LSCS

Cesarean Section for Placenta Previa - Key Points

  • Adequate blood (4-6 units) cross-matched and ready
  • Incision away from placenta (do NOT incise through placenta)
  • Deliver baby first without placental separation if possible
  • Placenta accreta suspected: leave placenta in situ if no bleeding; close uterus; consider hysterectomy if bleeding
  • Conservative methods to control hemorrhage: B-Lynch suture, isthmic cervical apposition suture, uterine/internal iliac artery ligation, uterine artery embolization (UAE)
  • Multidisciplinary team (urologists, pelvic surgeons, transfusion specialists) essential
  • Check baby's Hb at birth; arrange transfusion if needed

PART 2: ABRUPTIO PLACENTAE

(Syn: Accidental Hemorrhage, Premature Separation of Normally Situated Placenta)

DEFINITION

Premature separation of a normally situated placenta causing APH.

VARIETIES

TypeDescription
RevealedBlood tracks down between membranes and decidua, exits via cervix - most common
ConcealedBlood collects behind placenta or between membranes/decidua; presenting part prevents escape; may cause Couvelaire uterus
MixedBoth revealed and concealed components
Couvelaire uterusBlood percolates through myometrial layers to serosa; uterus appears bruised/purple

USG Localization of Hemorrhage

  • Retroplacental - between placenta and myometrium (worst prognosis; 50% fetal mortality)
  • Subchorionic - between placenta and membranes (10% fetal mortality)
  • Preplancental/Subamniotic - between placenta and amniotic fluid

ETIOLOGY

Exact cause unknown. Contributing factors:
  • Pre-eclampsia/hypertension - most common association (in 45% cases)
  • Trauma (direct blow, external version)
  • Sudden decompression of uterus (ROM in polyhydramnios, delivery of first twin)
  • Short umbilical cord
  • Folic acid deficiency
  • Uterine anomaly or fibroid
  • Smoking, cocaine use
  • Thrombophilias (antiphospholipid syndrome, Factor V Leiden)
  • Previous abruption (10x recurrence risk)

PATHOPHYSIOLOGY

  • Decidual arterial spasm → vascular congestion → rupture → retroplacental hematoma
  • Hematoma expands → further placental separation
  • Couvelaire uterus: blood extravasation between muscle fibers → bruised, tense uterus
  • DIC: release of tissue thromboplastin → consumptive coagulopathy → hypofibrinogenemia (<150 mg/dL), elevated FDP and D-dimer

CLINICAL GRADING

GradeFrequencyFeatures
0-Asymptomatic; found on placental inspection post-delivery
140%Slight vaginal bleeding; minimal/absent uterine tenderness; BP and fibrinogen normal; good FHS
245%Mild-moderate bleeding; uterine tenderness always present; pulse ↑, BP maintained; fibrinogen may fall; fetal distress or death possible
315%Moderate-severe or concealed bleeding; marked uterine tenderness; pronounced shock; fetal death is the rule; coagulation defect/anuria may occur

CLINICAL FEATURES

Symptoms

  • Painful, dark red vaginal bleeding (contrast to placenta previa)
  • Abdominal pain - sudden onset, constant, severe
  • History of precipitating cause often present

Signs

  • Uterus: tense, hard, "woody" or board-like, very tender - hallmark
  • Fundal height may be MORE than expected (concealed blood)
  • Fetal parts difficult to feel
  • FHS may be absent (especially Grade 3)
  • Shock may be disproportionate to visible blood loss (concealed hemorrhage)
  • Pre-eclampsia signs may coexist

INVESTIGATIONS

  • Hb, hematocrit
  • Coagulation profile: fibrinogen level, FDP, prothrombin time, APTT, platelets
  • ABO/Rh grouping
  • Urine for protein
  • USG: confirms retroplacental hematoma (may miss acute bleed)

COMPLICATIONS

Maternal

  • Hemorrhagic shock (often out of proportion to visible loss)
  • DIC (consumptive coagulopathy) - fibrinogen <150 mg/dL
  • Acute renal failure/cortical necrosis (from severe hypotension + DIC)
  • Postpartum hemorrhage (Couvelaire uterus, atony)
  • Sepsis
  • Sheehan's syndrome

Fetal

  • Fetal distress
  • IUGR
  • Prematurity
  • Fetal death (especially Grade 3; retroplacental hematoma has 50% mortality)

MANAGEMENT

On Admission

  1. IV access (wide bore); Ringer's solution; arrange blood transfusion
  2. Bloods: Hb, hematocrit, coagulation profile (fibrinogen, FDP, PT, APTT, platelets), ABO/Rh, urine protein
  3. Close maternal and fetal monitoring (Flowchart 19.3)

Management Options

(a) Immediate delivery (b) Manage complications (shock, DIC) (c) Expectant management (rare - only mild/Grade 1 cases)

Definitive Treatment (Delivery)

If patient is in labor:
  • Amniotomy (low rupture of membranes) - accelerates labor, increases uterine tone
  • Advantages: initiates myometrial contraction, expedites delivery, better compression of spiral arteries, reduces thromboplastin entry → reduces DIC/renal cortical necrosis risk
  • Oxytocin drip to accelerate if needed
  • Vaginal delivery favored if: limited abruption, reassuring FHR, facilities for continuous electronic monitoring, prospect of early vaginal delivery, or dead fetus
If patient NOT in labor:
  • Continuing bleeding or >Grade 1:
    • (A) Induction of labor by amniotomy + oxytocin; delivery usually in 4-6 hours
    • (B) Cesarean section if:
      • Severe abruption with live fetus
      • Unfavorable cervix (amniotomy not possible)
      • Vaginal delivery not imminent despite amniotomy
      • Amniotomy failed to control bleeding or stop process
      • Adverse features: fetal distress, falling fibrinogen, oliguria
    • Note: Regional anesthesia generally avoided with significant coagulopathy (use general anesthesia)

Managing Complications

A. Hemorrhagic Shock
  • Volume replacement based on volume deficit
  • Fresh blood, packed cells, FFP, platelets as needed
B. DIC
  • Target fibrinogen >150 mg/dL
  • 1 unit (500 mL) fresh blood contains 0.5 g fibrinogen, raises level by ~12.5 mg/dL
  • Platelet count increases by 10,000-15,000/mm³ per unit
  • Deliver to arrest pathological process
  • Details - see coagulopathy chapter
C. Fetomaternal Hemorrhage
  • Common with traumatic abruption
  • 300 mg anti-D immunoglobulin to all Rh-negative women
  • Fetal-to-maternal bleed usually <15 mL

PART 3: INDETERMINATE BLEEDING

  • Cause not clearly understood
  • Diagnosis by exclusion (rule out placenta previa, abruption, local causes)
Possible causes:
  • Vasa previa - most important
  • Marginal sinus hemorrhage
  • Circumvallate placenta
  • Marked decidual reaction on endocervix
  • Excessive show

VASA PREVIA

Definition

Unsupported umbilical vessels (in velamentous placenta) lie below the presenting part and run across the cervical os. Torn spontaneously or at membrane rupture.

Diagnosis

  • Color-flow Doppler TVS: antenatal diagnosis
  • Detection of nucleated RBCs (Singer's alkali denaturation test) or fetal Hb (Apt test) in vaginal blood - diagnostic
  • Associated with fetal distress (tachycardia, sinusoidal FHR pattern)

Fetal Prognosis

  • Fetal mortality ~50% (fetal exsanguination - fetal vessels bleed)

Management

  • Antenatal admission at 28-32 weeks for confirmed vasa previa
  • Expectant management (for fetal lung maturity) - similar to placenta previa
  • Antenatal corticosteroids given
  • Bleeding vasa previaCategory-1 emergency LSCS immediately
  • Intrapartum diagnosis → expeditious delivery
  • Confirmed vasa previa at term (≥37 wks) → elective LSCS before labor onset
  • Neonatal blood transfusion may be needed

KEY COMPARISON: PLACENTA PREVIA vs ABRUPTIO PLACENTAE

FeaturePlacenta PreviaAbruptio Placentae
BleedingPainless, bright red, recurrentPainful, dark red, may be concealed
UterusSoft, relaxed, non-tenderTense, tender, board-like
ShockProportionate to visible lossDisproportionate
MalpresentationCommonUncommon
FHSUsually presentMay be absent
CoagulopathyRareCommon (DIC)
USGPlacenta over/near osRetroplacental clot
Vaginal examFORBIDDEN outside OTAvoided
Definitive RxUsually LSCSAmniotomy preferred if in labor

Source: DC Dutta's Textbook of Obstetrics (9th Edition), Chapter 19 - Antepartum Hemorrhage
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