Antepartum Haemorrhage

Kerrie Bailey

Objectives

Definition

Epidemiology

Aetiology

Pathophysiology

Treatment

Complications

Summary

Definition

Antepartum haemorrhage (APH) is defined as bleeding from or in to the

genital tract, occurring from 24+0 weeks of pregnancy and prior to the
birth of the baby

Epidemiology

It affects 3-5% of all pregnancies

Up to 20% of very preterm babies are born in association with APH,

which explains the association between APH and cerebral palsy.

Aetiology

Obstetric

Placenta
Maternal blood

Bloody show

Placental abruption

Placenta previa

Fetal blood

Vasa previa

Uterus
Uterine rupture

Nonobstetric

Bleeding from the lower genital tract

Cervical bleeding -cervicitis,cervical neoplasm,cervical polyp
Bleeding from the vagina itself - trauma, neoplasm

Bleeding that may be confused with vaginal bleeding

GI bleed-haemorrhoids,inflammatory bowel disease
Urinary tractbleed -UTI

Spotting staining, streaking or blood spotting noted on underwear or

sanitary protection

Minor haemorrhage blood loss less than 50 ml that has settled

Major haemorrhage blood loss of 501000 ml, with no signs of clinical

shock

Massive haemorrhage blood loss greater than 1000 ml and/or signs of

clinical shock

Assessment
History
Examination
Investigations

 NB Treatment varies based on

Amount of blood loss
Fetal state; stable vs unstable
Gestational age
Maternal state; stable vs unstable

Placental abruption

Premature separation of a normally implanted placenta prior to delivery

Most common pathological cause of APH (1-2%)

Incidence highest in age groups <20 & >35

Classification

Extent of separation - partial vs complete

Location of separation - marginal vs central

Clincal Class 0 to 3

Couvelaire Uterus

Couvelaire Uterus

Utero-Placental Apoplexy

Assoc. with servere form of placental separation with widespread

extravasation of blood into uterine musculature and below the serous
coat of the uterus

May lead to uterine tetany, shock and fetal death

Complications;

Clotting defects

Renal failure

Pathophysiology

Underlying cause maternal vessels tearing away from thedecidua

basalis, not the fetal vessels separation of uterine wall and placenta

Due to 3Ss;

Sudden stretch of Uterus eg Trauma

Structural abnormalities eg Spiral arteries

Smoking; drugs eg Tobacco and cocaine

Pathophysiology

Risk Factors

Trauma- MVA, Abuse

Infection - Chorioamnionitis

Maternal hypertension - Most common cause of abruption, occurring in approximately 44% of all cases

Drugs - Cigarette smoking, Alcohol consumption, Cocaine use

Short umbilical cord

Sudden decompression of the uterus (eg, PROM, delivery of first twin)

Retroplacental fibromyoma

Retroplacental bleeding from needle puncture (ie, postamniocentesis)

Idiopathic (probable abnormalities of uterine blood vessels and decidua) [4]

Previous placental abruption

Prolonged rupture of membranes (24 h or longer)

Maternal age 35 years or older

Maternal age younger than 20 years

Male fetal sex

Low socioeconomic status

Elevated second trimester maternal serum alpha-fetoprotein (associated with up to a 10-fold increased risk of abruption)

Subchorionic hematoma[6]

Presentation

Painful vaginal bleed

Uterine tenderness

Contractions

shock/anemia out of proportion to apparent blood loss

fetal distress, fetal demise (15% present with demise), bloody

amniotic fluid (fetal presentation typically normal)

coagulopathy

Complications

Fetal complications:

perinatal mortality 25-60%

Prematurity

intrauterine hypoxia

Maternal complications:

<1% maternal mortality,

DIC (in 20% of abruptions),

acute renal failure, anemia,

hemorrhagic shock,

pituitary necrosis (Sheehan syndrome),

amniotic fluid embolus

Investigations

Blood workup

CBC

GXM

PT/PTT

Fibrinogen study, FDP

BUN and creatinine

Kleihauer-Betke test

Imaging

U/S Retroplacental clot, haemorrhage

Management

Assess ABC O2 for hypotensive pts

Large bore IV access x 2 (16G )

CBC, GXM, PT, PTT

IV fluid resuscitation

CTG for fetal assessment +/- uterine activity

Ultrasound for placental localization and fetal assessment

blood products on hand (red cells, platelets, cryoprecipitate) because of DIC risk

Rhogam if Rh negative

mild abruption
GA <37 wk: use serial Hct to assess concealed bleeding, deliver when fetus is mature or
when hemorrhage dictates
GA 37 wk: stabilize and deliver

moderate to severe abruption

hydrate and restore blood loss and correct coagulation defect if present
vaginal delivery if no contraindication and no evidence of fetal or maternal distress OR
fetal demise

C/S if live fetus and fetal or maternal distress develops with fluid/blood
replacement, labor fails to progress or if vaginal delivery otherwise contraindicated

Placenta Previa

Exists when the placenta is inserted wholly or in part into the lower segment
of the uterus

An abnormal placentation near or covering the internal cervical os

Classification

Complete - complete coverage of the cervical os by the placenta

Marginal - leading edge of the placenta is less than 2 cm from the internal os

Aetiology/Risk factors

Advancing maternal age (>35 y)

Infertility treatment

Multiparity (5% in grand multiparous patients)

Multiple gestation

Short interpregnancy interval

Previous uterine surgery, uterine insult or injury

Previous cesarean delivery,including first subsequent pregnancy following a cesarean delivery [1]

Previous or recurrent abortions

Previous placenta previa (4-8%)

Nonwhite ethnicity

Low socioeconomic status

Smoking

Cocaine use

Presentaion

PAINLESS bright red vaginal bleeding (recurrent), may be minimized and

cease spontaneously, but can become catastrophic

mean onset of bleeding is 30 wk GA, but onset depends on degree of

previa

physical exam

uterus soft and non-tender

presenting fetal part high or displaced

FHR usually normal

shock/anemia correspond to degree of apparent blood loss

NB: Avoid performing a vaginal exam on suspected placenta previa

Investigations

Imaging

Ultrasound transvaginal > transabdominal

Blood workup

CBC

PT/PTT

GXM

Fibrinogen

Amniocentesis

Treatment
General

goal: keep pregnancy intrauterine until the risk of delivery < risk of
continuing pregnancy

stabilize and monitor

maternal stabilization: large bore IV with hydration, O2 for hypotensive

patients

maternal monitoring: vitals, urine output, blood loss, blood work (CBC,
PT/ PTT, platelets, fibrinogen, FDP, group and cross match)

electronic fetal monitoring (CTG)

Specific
U/S assessment: when fetal and maternal condition permit,
determine fetal viability, gestational age, and placental
status/position
Rhogam if mother is Rh negative

Kleihauer-Betke test to determine extent of fetomaternal transfusion

so that appropriate dose of Rhogam can be given

GA <37 wk and minimal bleeding: expectant management

admit to hospital

limited physical activity, no douches, enemas, or sexual intercourse

consider corticosteroids for fetal lung maturity
delivery when fetus is mature or hemorrhage dictates

GA 37 wk, profuse bleeding, or L/S ratio is >2:1 deliver by C/S

Vasa Previa

Unprotected fetal vessels pass over the cervical os

Due to:

a velamentous insertion of the umbilical cord

joining an accessory (succenturiate) placental lobe to the main disk of the

placenta

Occurs 1 in 5000 births

Pathophysiology

It is thought

Early placenta previa atrophy of placenta tissue surrounding the vessels

over the cervix the placenta grows preferentially toward the upper portion
of the uterus unprotected vessels running over the cervix and in the lower
uterine segment

Rupture of fetal vessels fetal exanguination fetal death

Types

Type 1 - velamentous insertion with vessels running over the cervix.

Type 2 - unprotected vessels run between lobes of a bilobed or succenturiate

lobed placenta

Type 3 - a portion of the placenta overlying the cervix undergoes atrophy

Risk factors

Multiple gestation

Accessory lobes

Velamentous insertions of umbilical cord

IVF pregnancies

Presentaion

Usually seen as a triad

Painless vaginal bleed

Fetal distress

Membrane rupture

Investigations

Apt test (NaOH mixed with the blood) can be done immediately to
determine if the source of bleeding is fetal (supernatant turns pink) or
maternal (supernatant turns yellow)

Wright stain on blood smear and look for nucleated red blood cells (in
cord, not maternal blood)

Management

Emergency C-Section

Administer 10-20cc/kg bolus to newborn if found to be in shock after

delivery

Uterine Rupture

A potentially catastrophic event duringchildbirthby which the integrity

of themyometrialwall is breached

0.5-0.8% incidence, up to 12% with classical incision

Classificaition

Complete - contents of the uterus may spill into the peritoneal cavity or
thebroad ligament

Incomplete peritoneum is intact

Dehiscence - limited to a scar dehiscence, it does not disrupt the overlying

visceral peritoneum and it does not result in clinically significant bleeding
from the edges of the pre-existing uterine scar

Risk Factors

Uterine scarring (i.e. previous uterine surgeries including Cesarean,

perforation with D&C)

Excessive uterine stimulation (i.e. protracted labor, oxytocin)

Uterine trauma (i.e. operative equipment, ECV)

Multiparity

Uterine abnormalities

Presentation

prolonged fetal bradycardia most common presentation

acute onset abdominal pain

hyper or hypotonic uterine contractions

vaginal bleed

Chest pain

Maternal shock

Cessation of uterine contractions

Palpable fetal parts through abdomen

Investigation

Transvaginal U/S evaluate uterine wall

MRI- confirm possible placenta abruption

Management

Goal stabilize mother and deliver fetus

Fetal Cesarean section

Maternal

Conservative repair

Hysterectomy

Summary

APH may herald diagnosis with significant morbidity/mortality

Determining diagnosis is important as treatment is dependent on cause

Avoid vaginal exam when placental location is unknown