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OBSTETRIC EMERGENCIES
IN PRIMARY CARE
Dr. Chew Kah Teik
Clinical Lecturer & Specialist
Department of Obstetrics & Gynaecology
Universiti Kebangsaan Malaysia Medical Centre

Definition

Obstetrics:
A branch

of medicine that
concerns management of
women during pregnancy,
chldbirth and puerperium

Emergency:
An

sudden serious change in


a patients condition which
requires immediate medical
or surgical intervention

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Obstetric Emergencies

Miscarriage
Ectopic pregnancy
Placenta praevia
Abruptio placenta
Pre-eclampsia
Eclampsia
Cord prolapse
Shoulder dystocia
Post partum haemorrhage

Case scenario

28-year-old woman presented to you


with a short history of lower abdominal
pain and vaginal bleeding. Her period
is overdue. Summarise your approach
to diagnosis.

The

history:
the timing of onset of pain, the distribution
of pain, the occurrence of syncope and
shoulder tip pain
the timing of onset and type of bleeding
other areas including the use of
contraception, timing of last menses,
medical and surgical history, and
identification of other risk factors described
above including fertility treatments and
previous STD

The

examination:

the

general clinical state


abdominal and pelvic physical signs,
especially the cervix, uterus and adnexae
Differential
related

diagnosis:

to pregnancy
related to non-pregnant gynaecological
disorders
related to non-gynaecological disorders

Investigation:
full

blood count and grouping


clinical situation may require resuscitation
and operation without any further
investigation
if clinical situation allows further
investigation, urine pregnancy test (-hCG if
negative) and ultrasound scan

+
Early pregnancy
emergency

Presented

as acute
abdominal pain and/or
vaginal bleeding

Many

differential diagnosis
of acute abdominal pain

Require

Miscarriage
Ectopic

pregnancy

high index of
suspicious if:
Vaginal bleeding
Abdominal pain
Period of ammenorrhoea

Causes:

Miscarriage

Chromosomal

Spontaneous loss of
pregnancy before
24 weeks of
gestation

Fetal

Complete,
incomplete,
sepsis, missed,
inevitable
1st trimester or 2nd
trimester

abnormalities
abnormalities

Placenta

abnormalities

Infection
Medical

diseases

+
Miscarriage

Presentation:
Lower

abdominal pain

Vaginal

Is a leading cause
of early pregnancy
bleeding

bleeding

Fever
Purulent

vaginal discharge

Hypotension

Complications:
Haemorrhagic
shock
Sepsis

Tachycardia
Abdomen

guarding

tenderness,

+
Miscarriage

In

primary care setting,


diagnosis of miscarriage
can be difficult,
particularly when the POC
are not obvious

Definitive

diagnosis is
based on the confirmation
of passage of POC or
ultrasound findings
IUGS
Fetal echo
Endometrium thickness
Adnexal mass

+
Miscarriage

Therefore,

differential
diagnosis of early
pregnancy bleeding must
include:
Normal pregnancy
bleeding
Ectopic pregnancy

If

possible, all tissue


should be retained and
send to the receiving
hospital for HPE

+
Management
If

significant of haemorrhage, standard


protocol of resuscitation
Blood
Fluid

If

evidence of sepsis, consider antibiotics

Pain

management: analgesia

Transfer

to hospital

Ectopic
pregnancy

Is the
implantation
of a
pregnancy
outside the
endometrial
cavity

Ectopic pregnancy

The

incidence of ectopic
pregnancy in the UK is
approximately 1%

Globally,

the incidence
appears to be in increasing
trend.
More sensitive diagnostic
method
ART
Increased pelvic
inflammation disease

+
Ectopic pregnancy

Presentations:
Acute

abdomen

Lower

abdominal pain

Shock

Risk factors:
Previous ectopic
Previous tubal
surgery
IUCD
Subfertility
Smoking

Vaginal

bleeding --caution:
an ectopic pregnancy is
usually failing and so
falling progesterone levels
from the corpus luteum
can induce a withdrawal
bleed, mimicking
miscarriage

+
Ectopic pregnancy

Presentations:
Syncope
Shoulder

tip pain haemoperitoneum due to


haemorrhage from the
affected tube causes pain
and diaphragmatic irritation

Vomiting
Gastrointestinal

symptoms,
particularly diarrhoea and
dizziness, in early gestation
are important indicators of
ectopic pregnancy

Does a negative pregnancy test


exclude an ectopic pregnancy?

+Tubal rupture has been reported with a


negative urinary and sometimes even a
negative serum pregnancy test. This is
extremely rare. A negative test normally
excludes a 'clinically significant' ectopic
pregnancy due to insufficient functioning
trophoblast.

+
Ectopic pregnancy
Ultrasound
investigations
Is the single most
useful diagnostic
tool
To detect an IUGS
or identify
features of
ectopic
pregnancy

An

intrauterine gestation
sac is highly specific (99%)
for exclusion of an ectopic
pregnancy

Errors

may be due to a
pseudosac or heterotopic
pregnancy

Transvaginal

scanning can
identify most intrauterine
pregnancies from when
the hCG level reaches
1000 iu/l (the
discriminatory level)

Ectopic Pregnancy: ultrasound features

Free peritoneal fluid


A complex or homogenous adnexal
mass
An adnexal gestation sac with or
with out fetal pole
A tubal ring sign

+
Ectopic pregnancy

In

early viable intrauterine


pregnancies, the level of
serum doubles (rises by
66% or more) approximately
every two days

In

Beta hCG:
Level do not tell
us the location of
a pregnancy

failing intrauterine and


continuing ectopic
pregnancy, the doubling
time for -hCG is usually
longer

Plateauing

levels of serial hCG measurements indicate


that further assessment is
necessary

+
Ectopic pregnancy

Levels

below 20 suggest a
failing pregnancy,
irrespective of location

Levels

Progesterone:
May improve
diagnostic
accuracy if used
in combination
with -hCG

from 20 to 60 are
associated with a high risk
of ectopic pregnancy in
the face of -hCG levels
above 25 iu/l

Levels

>60 suggest a
progressing pregnancy,
most of which will be
intrauterine

+
Management
Stable
History
Examination
Ultrasound

scan
Refer hospital

Unstable
Call

for help
Check airway
Oxygen
IV line
Fluid resuscitation
Blood
Refer hospital

+
Case scenario

A 19 year old single school drop-out in her


first pregnancy complained of severe
abdominal pain after being punched in the
stomach by her boyfriend.
She was pale and tachycardic. The uterus
was about 28 weeks size, tender and hard.
No fetal heart activity was detected.
What is the diagnosis?

+
Antepartum
haemorrhage

Complicates 2 -5% of
all pregnancy
It is defined as
bleeding of the
genital tract,
occurring from 24
weeks of gestation
until birth

Causes:
Placenta

praevia (20%)

Abruptio

placenta (#)%)

Vasa

paevia

Uterine

rupture

Cervical
Trauma

lesion

+
Placenta Praevia

Is a placenta that is
partially or wholly
implanted into the
lower uterine
segment

Bleeding occurs when


uterine contractions dilate
the cervix, thereby applying
the shearing forces to the
placental attachment in the
lower uterine segment

+
Placenta praevia

About 3% of
pregnancies are
praevia
Symptomatic
placenta praevia
occurs in between
0.4 and 0.8% of
pregnancies

Risk factors:
Increased

maternal age

Increase

parity

Previous

Caesarean

section
Previous

uterine surgery

Increased

placenta
Smoking

surface area of

+
Placenta praevia

Presentation:
Painless

vaginal bleeding

Vaginal

bleeding usually
bright red

Shock
Soft,

non-tender uterus

+
Management
If

profuse bleeding, resuscitation and refer to


nearest hospital for delivery regardless the
gestational age of the fetus

If

stable, admit to hospital for expectant


management

+
Abruptio placenta

It

is often an unanticipated
emergency, although a small
bleed can suddenly evolve
into a major abruption

Therefore,

vigilance is

essential

It is defined as the
premature
separation of the
normally sited
placenta from the
uterus

Bleeding

begins in the
decidua basalis and leads to
separation of the placenta
from its attachment to the
uterine wall

This

separation can be partial


and self-limiting or can extend
until there is fetal hypoxia
and, ultimately, demise

+
Abruptio placenta

Blood

is seen at the vagina


as it tracks down the uterus
between the membranes
and the uterine wall

If

there is a large pressure


generated in the uterus,
the blood can extend into
the myometrium
(Couvelaire uterus)

This

uterus becomes
weakened and can rupture
with increased intrauterine
pressure during
contractions

+
Abruptio placenta

The diagnosis
should be
considered in any
pregnant women
with abdominal
pain, even without
evidence of vaginal
bleeding

Presentation:
Painful
Dark

vaginal bleeding

blood

Abdominal

pain
commonly constant pain

Uterine

tenderness fetal
distress or IUD

Evidence
Shock

of DIVC

Abruptio placenta

Abruptio placenta

+
Abruptio placenta: classification
Class 0

Class 0 is asymptomatic

Diagnosis is made retrospectively by finding an organised


blood clot or a depressed area on a delivered placenta

Class 1

Mild or no vaginal bleeding with no maternal or fetal


compromise

Class 2

Moderate or no vaginal bleeding with possible maternal


evidence of blood loss (tachycardia/mild hypotension but no
clinical coagulopathy)

Fetal distress

Class 3

Severe or no vaginal bleeding with maternal compromise


(tachycardia, hypotension and coagulopathy)

Tense, tender uterus, 'woody hard'

Intrauterine fetal death

Hypovolaemic

Abruptio placenta

Coagulopathy

shock
secondary to haemorrhage
disseminated
intravascular coagulation
(DIC)

Acute

Maternal
complications

renal failure

Couvelaire
Postpartum

uterus
haemorrhage

Ischemic

necrosis of distal
organs (adrenal, pituitary)

Fetomaternal

haemorrhage

+
Abruptio placenta

Intrauterine
Hypoxi

death

a and its sequelae

Anaemia
Fetal

growth restriction
(FGR) if chronic

Risks

Fetal complications

of preterm birth

+
Management of an APH

+
Resuscitation
Resuscitation should follow the standard A
(airway), B (breathing), C (circulation) approach
high-flow

oxygen (1015 l/min) and left lateral tilt


bag and mask if necessary
large bore intravenous access preferably two
14-gauge cannulae
IV fluids
Up

to 2 l crystalloid
Up to 12 l colloid until blood arrives
Consider

CVP
Indwelling bladder catheter

Pre-eclampsia
Gestational hypertension of at least
140/90 mmHg on two separate
occasions 4 hours apart
accompanied by significant proteinuria
of at least 300 mg in a 24-hour
collection of urine, arising de novo
after the 20th week of gestation in a
previously normotensive woman and
resolving completely by the 6th
postpartum week

result

from a combination
of impaired trophoblast
differentiation and
invasion during the first
trimester

Pre-eclampsia

complicating 28%
of pregnancies

resulting in the failure of


trophoblast cells to destroy
the muscularis layer of the
spiral arterioles resulting
in the development of a
poorly perfused placenta

Pre-eclampsia

Risk factors:
Primigravida
Advanced

maternal age

Previous

history of preeclampsia

Obesity
Diabetes

mellitus

Pre-existing
APS

hypertension

+
Pre-eclampsia:
prediction

There is still no
clinically useful
screening test to
predict preeclampsia

Angiogenic factors
vascular endothelial
growth factor (VEGF)
placental growth factor
(PlGF)
soluble endoglin (sEng)
and sFlt-1
have been shown to be
altered in pregnancy
the use as predictive
tests has been
disappointing

+
Pre-eclampsia:
prediction

Uterine artery Doppler


velocimetry
Increased impedance in
the uterine arteries is an
early radiographic
feature of pre-eclampsia

+
Pre-eclampsia:
prevention

Aspirin
Anticoagulation
Calcium
Antioxidant

Low-dose

aspirin has been


shown to prevent the
development of preeclampsia in woman at
moderate-to-high risk of
pre-eclampsia by
approximately 1015%

Advise

women at high risk


of pre-eclampsia to take
75 mg of aspirin daily from
12 weeks until the birth of
the baby

+
Pre-eclampsia:
prevention

Aspirin
Anticoagulation
Calcium
Antioxidant

Women

at high risk are


those with any of the
following:
hypertensive disease
during a previous
pregnancy
chronic kidney disease
autoimmune disease,
such as systemic lupus
erythematosis or
antiphospholipid
syndrome
type 1 or type 2 diabetes
chronic hypertension

+
Pre-eclampsia:
prevention

Aspirin
Anticoagulation
Calcium
Antioxidant

The

use of anti-coagulants,
such as low-molecularweight heparin or
unfractionated heparin,
are not recommended for
reducing the risk of preeclampsia in either the
general population or in
those with a previous
history of pre-eclampsia

+
Pre-eclampsia:
prevention

Aspirin
Anticoagulation
Calcium
Antioxidant

Routine

calcium
supplementation for
healthy, nulliparous women
is not recommended in the
prevention of pre-eclampsia

There

may be some benefit


in calcium supplementation
in some high-risk
populations with a lowcalcium diet

+
Pre-eclampsia:
prevention

Aspirin
Anticoagulation
Calcium
Antioxidant

No

benefit has been


demonstrated with the use
of antioxidants, such as
vitamin C and E

Pre-eclampsia

Occurrence

of one or more
convulsions, not
attributable to other
cerebral conditions in a
patient with pre-eclampsia

May

Eclampsia
Severe preeclampsia

occur as part of the


initial presentation of preeclampsia:
38% of fits occur
antenatally
18% occur intrapartum
the remaining 44% occur
postpartum, usually in
the first 2448 hours

Pre-eclampsia

Eclampsia
Severe

hypertension SBP >160


mmHg or DBP >110 mmHg with at
least proteinuria of + or 1g on
semiquantitative assessment

Moderate

hypertension SBP >140


mmHg or DBP >90 mmHg with at
least proteinuria ++ or 3g on a
semiquantitative assessment

Eclampsia
Severe preeclampsia

Any of:
severe headache and visual
disturbance
epigastric pain
clonus
papilloedema
liver tenderness
platelets <100 x 109/l
alanine amino transferase >50 iu/l
creatinine >100 mmol/l

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

Blood should be sent for:


serum electrolytes (Na,
K, urea, creatinine, urate)
liver function tests
(albumin, ALT)
full blood count(Hb,
WCC, platelets)
clotting (PT, APTT)

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

BP

and pulse measured every 15


minutes until stabilised then half
hourly

indwelling

catheter inserted urine


output measured hourly whenever IV
fluids are given. All urine tested for
protein

O2

saturation measured continuously


and charted with BP. If saturation
<95%, then medical review is
essential

fluid

balance should be monitored


very carefully. Detailed input and
output recordings should be charted
hourly

respiratory
fetal

rate measured hourly

wellbeing should be assessed


carefully CTG, possibly growth
scan, liquor assessment and
umbilical artery Doppler

+
Pre-eclampsia:
Management

Aim

to reduce blood
pressure to <160/105
(MAP <125 mmHg)

This

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

necessitates the
constant attendance of
medical staff

BP

may drop suddenly

Treatment

should be
titrated gradually

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

First agent of choice labetalol


Initial 200 mg can be given orally
(prior to, or in the absence of, IV
access)
If no response in 30 minutes, a
second oral dose can be given
If there is no initial response to oral
therapy or it is not tolerated,
proceed to give a bolus of 50 mg by
IV, over at leastfive minutes,
repeated to a maximum of 200 mg
at 10 minute intervals
Following this, or as treatment for
moderate hypertension, a labetalol
infusion should be commenced; 5
mg/ml at 4 ml/hour via syringe pump
infusion rate doubled every 30
minutes to a maximum of 32 ml (160
mg)/hour until BP has dropped and is
stabilised at an acceptable level
Contraindication severe asthma,
caution in cardiac disease

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

Second agent of choice


hydralazine

Bolus infusion is 1020 mg


over 1020 minutes,
measuring BP every 5 min

May be followed by an infusion


of 40 mg of hydralzine in 40
ml normal saline, which should
run at 15 ml/hr (15 mg/hr)

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

Magnesium

sulfate is THE
drug of choice

Loading

dose then infusion


for 24 hours or until 24
hours after delivery:
loading 4 g IV >over 5
10 minutes
maintenance 4 g IV
over 4 hours (1 g/hour)

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

Clinical

review should occur


every 4 hours:
continuous pulse
oximetry (alert
anaesthetist if O2
saturation <95%)
hourly urine output
hourly respiratory rate
reflexes (4 hourly)

Cessation

or reduction of
magnesium therapy if:
reflex absent
respiratory rate is
<12/minute

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

Adverse

effects of
magnesium sulfate toxicity
include:
motor paralysis
absent reflexes
respiratory depression
cardiac arrhythmia

Note

that 97% of MgSO4 is


excreted in the urine
oliguria (<80 ml/24 hours)
can lead to toxicity.
Therefore, in the presence of
oilguria, MgSO4 should be
reduced/withheld

Antidote

10 ml 10%
calcium gluconate slowly

+
Pre-eclampsia:
Management

Careful

fluid balance is
aimed at avoiding fluid
overload

Total

input should be limited


to 80 ml/hour (approximately
1 ml/kg/hour)

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

If

oxytocin is used, it should


be at high concentration and
the volume of fluid included
in total input

Oliguria

should not
precipitate any specific
intervention, except to
encourage early delivery

+
Pre-eclampsia:
Management

Basic investigation
Monitoring
Anti-hypertensive
Anti-convulsant
Fluid management
Delivery

Delivery

should be well
planned, on the best day,
in the best place, by the
best route and with the
best support team

Once

stabilised and in the


absence of eclampsia, a
decision can be taken
regarding aiming to
prolong pregnancy to
improve fetal outcome

Delivery

is not necessarily
by caesarean section

Case scenario

A Gravida 4 Para 3 at 38 weeks gestation


has been refusing hospital admission for
unstable lie. She is being under your care in
BTS
While waiting to be seen in your clinic, she
has leaking- flooding
Will you attend to this patient urgently?

Cord Prolapse

It

occurs after the


membranes have
ruptured, when the
umbilical cord slips down
in front of the presenting
part of the fetus and
protrudes into the vagina

Rare

obstetric emergency

Associated

with high
perinatal mortality

Cord Prolapse

Can

be overt or occult

Overt

cord prolapse can be diagnosed


either by seeing the cord presenting
from the vagina, or un- expectedly
palpated during a vaginal
examination

Occult

cord prolapsed can occur


anytime during labour; it can be
suspected with bradycardia,
prolonged decelerations, and/or
variable decelerations with CTG

Abnormal

FHR pattern following ROM


may be the first indication of cord
prolapse

Occult

cord prolapse cannot be


diagnosed definitively until the time
of cesarean section or unless the
umbilical cord is seen in front of
presenting part during an ultrasound

Cord Prolapse

Risk factors:
Unengaged presenting
part
Malpresentation
Unstable lie
Polyhydramnios
Prematurity
Grand multiparity ( >5)
Breech presentation
PPROM
ARM

Cord Prolapse

Special considerations
Pressure

of the presenting
part on the cord may
restrict umbilical cord blood
flow resulting in acute fetal
heart rate changes, which,
if persistent hypoxia leads
to asphyxia

The

principle of pre-hospital
management is to monitor
the
cord for pulsations and use
maternal positioning to
prevent compression

+
Management
If

cord prolapse is suspected, perform a


vaginal examination to determine
Cervical length / effacement / dilatation
Station of presenting part
If the cord is palpated, determine if
pulsations are present (without
unnecessary manipulation of the cord)

+
Management
If

cord prolapse is confirmed (cord


palpated), call for help
Position pt head down with hips
elevated (in knee-chest, modified Sims,
or Trendelenburg)
Keep gloved hand in vagina (or insert
gloved hand into vagina if not already
performing digital vaginal exam) and
exert upward pressure on the fetal
presenting part to stop compression of
the cord
Keep hand in position until delivery

+
Management
Do

not attempt to replace cord above the


presenting part (touching the cord may cause
vasospasm)

If

require transfer to another hospital:


Filling bladder with 500 700 mL normal
saline to elevate fetal head from pelvic brim
tocolysis

Case scenario

A Gravida 3 Para 2 at 38 weeks of gestation


with uncontrolled GDM presented in labour
with fully dilated os- pending delivery.
What problems would anticipate in this
labour?

+
Shoulder
dystocia

It is associated with
serious complications for
both the mother and baby
Perinatal morbidity
includes asphyxia, birth
trauma such as brachial
plexus injury and fractured
clavicles, and permanent
neurological damage

In

shoulder dystocia,
disproportion occurs
between the bisacromial
diameter of the fetus and
the antero-posterior
diameter of the pelvic
inlet, resulting in
impaction of the anterior
shoulder of the fetus
behind the symphysis
pubis

+
Shoulder

It

is usually becomes
obvious after the fetal
head emerges and retracts
up against the perineum,
failing to undergo external
rotation (turtle sign)

dystocia

It is confirmed when the


standard delivery
manoeuvres (downward
traction) fail to deliver the
fetus and the head to body
delivery interval is
prolonged 60 seconds.

+
Shoulder
dystocia

Risk factors:
Prolonges second stage
Assisted delivery
Maternal diabetes with or
without macrosomia
Previous shoulder
dystocia
A large fetus > 4.5 kg
(macrosomia)
History of a large foetus
Maternal obesity
Multiparity

Post-partum Haemorrhage

The most common form of major


obstetric haemorrhage
Primary PPH: loss of 500mls or more
of blood from the genital tract withi
24 hours of delivery
Secondary PPH: excessive bleeding
from the birth canal between 24
hours to 12 weeks postnatally

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Primary PPH

Causes:
Uterine

atony (79-90%)
Retained placenta /
cotyledons
Trauma :
Uterine rupture
Broad ligament
haematoma
Cervical tears
Vaginal tears / haematoma
Vulval tears / haematoma

Primary PPH

Active

management of the
third stage of labour lower
reduces the risk of PPH

Prophylaxis

Most cases of PPH


have no identifiable
risk factors

oxytocin
should be offered routinely
the management of the
third stage of labour in all
women as they reduce the
risk of PPH by about 60%

+
Primary PPH: risk
factors

Tone
Tissue
Trauma
Thrombin

Etiology

Risk factors

Uterus over
distension

Multiple
pregnancy
Macrosomia
Polyhydramnios
Fetal
abnormalities

Uterine muscle
fatigue

Prolonged
labour esp
oxytocin use
High parity
Previous
history of PPH

Uterine
infection/
chorioamnionit
is

Prolonged
rupture of
membrane
Fever

Uterine
distortion /
abnormality

Fibroid uterus
Placenta
praevia

+
Primary PPH: risk

Etiology

Risk factors

Retained
placenta /
membranes

Tone
Tissue
Trauma
Thrombin

Incomplete
placenta at
delivery esp<
24 weeks
Previous
uterine
surgery

Abnormal
placenta

Abnormal
placenta on
ultrasoundaccessory /
succinturiate
lobe

factors

+
Primary PPH: risk
factors

Tone
Tissue
Trauma
Thrombin

Etiology

Risk factors

Cervical/vagina
l/perineal
tears

Precipitiousl
abour
Episiotomy
Operative
delivery

Extended tear
at caesarean
section

Malposition
Fetal
manipulation
Deep
engagement

Uterine rupture

Previous
uterine
surgery

Uterine
inversion

High parity
Fundal
placenta
Excessive
cord traction

+
Primary PPH: risk
factors

Tone
Tissue
Trauma
Thrombin

Etiology

Risk factors

Pre-existing
clotting
abnormality
eg.
Haemophilia/vonW
ille-brand
disease

History of
coagulopathy
/ liver
disease

Acquired in
pregnancy
Immune
thrombocytopaeni
cpurpura (ITP)
Preeclampsia
with
thrombocytopaeni
a (HELLP)
DIC from PET,
IUD, abruption,
sepsis

Bruising
Elevated BP
Proteinuria
Fetal demise
Antepartum
haemorrhage

+
Management

+
Conclusion
Primary

prevention

Identify

problems

Prompt

actions

Seek

help and immediate but safe transfer to


hospital

Frequent,
Written

regular obstetrics drills and training

protocol and guidelines

THANK YOU