PRE-ECLAMPSIA

BY
DR OJULE J D
Department of Obstetrics and Gynaecology,
UPTH
 INTRODUCTION / PREAMBLE
 Hypertensive dx occurs in approximately 12-22%
of pregnancies. It is the most common medical
disorder of Pregnancy.

 Incidence as high as 21.6 – 26.2% of all

deliveries in hospital based studies in Nigeria.
 In UPTH incidence is 14.5%

 Responsible for 17.6% of maternal deaths in the

USA
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  70-129 maternal death / 100,000
maternities in the developing countries.
 Most common cause of maternal
mortality in UPTH
 Clinical course of pre-eclampsia is
progressive characterised by continuous
deterioration.

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  It varies from mild to severe disease, to
eclampsia.
 Aetiology is still largely unknown, with but
though to be a mulifactorial interplay play of
genetic, hormonal and environmental factors.
 Trials on prevention have also been largely
disappointing and mainstay of RX have been
integrated ANC and access to monitoring
services.
 Mgt is ideally collaborative – the obstetrician
the physician, laboratory scientists, Physician,
Radiologist and the Neonatologist.
 Definitive RX is delivery of baby / placenta.

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 Definition of terms
 Hypertension
 Systemic Bp ≥ 140/90 mmHg on ≥ 2 occasions
at least 4-6 hours apart
 Increase SBp ≥ 30 mmHg, D Bp ≥ 1 5 mmHg
over booking BP
 Single DBP ≥ 110 mmHg
 Mean arterial pressure MAP ≥ 20 mmHg over
the booking value.
 Mean arterial pressure ≥ 105 mmHg.
 MAP = Diastolic Bp + (1/3 pulse pressure)
 Pulse pressure = systolic Bp – Diastolic BP)

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  Proteinuria
 ≥ 300mg of protein in a 24 hr urine sample
 ≥1g/L (clean catch / catheter urine on 2 or more
occasions) = 2 + proteinuria.
 Severe proteinuria = 5g/L 24 hrs urine sample
 Chronic Hypertension
 Persistent elevation in blood pressure of 140/90
mmHg or greater before 20 weeks of gestation
or persistent hypertension beyond 6 weeks post
partum.
 Essential –cause unknown

 Secondary- Cushings dx, phaechromocytoma.

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  PIH
 Hypertension and or proteinuria developing after
20 weeks of presenting, during labour or the
puerperuim in previously normotensive
nonprotenuric woman subdivided into
 PIH (without proteinuria) – gestational hypertension
 Pregnancy induced protenuria – (without
hypertension)
 Pregnancy induced – proteinuric - hypertension

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 PRE-ECLAMPSIA

 Occurrence of hypertension with proteinuria

in a pregnant woman after 20 weeks of
gestation.

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 AETIOPATHOGENSIS OF PRE-
ECLAMPSIA
 Now thought to be a multifactorial interplay of genetic,
hormonal, immunological, and environmental factors
which leads to
 Release of factor X from the placenta which causes
 Relative lack of trophoblastic invasion of the spiral arterial
walls during placentation which - to uteroplacenta
insusfficiency – placenta ischemia and hypoxia.
 Activation of neutrophils and production of reactive 02 Spp
and lipid peroxidase - acute atherosis (aggregates of fibrin,
platelets and lipophages – partially or completely blocking the
arterioles.

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  The damaged endothetial cells lead to
 Reduce PGI2 production – vasodilator and
antiplatelet aggregator
 Increased platelet activation – increased
TXA2 (vasoconstrictor/vasospasm
 Increased sensitivity to vasoactive
substances – vasospasm
 Increased leaky capillaries – fluid retention

 Increase TPR

 Decrease plasma vol. expansion

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  Microangiopathic haemolysis
 Glomerular endotheliosis – proteinuria,
decreased uric acid, GFR, reduced renal blood
flow.
 Focal cerebral Spasm – abn. Electrical activity
 Focal parenchymal necrosis –increase LFT ,
hepatic capsule distension.
 These changes can progress to cause
decompensation of one or more systems.
 The maternal response to these changes modify
the way the dx manifest, the severity of signs and
symptoms and the outcome for mother and child.
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 Risk factors

Genetic
 Women whose mothers had pre-eclampsia
have a 20-25% risk
 In women with a sister with a history of pre-
eclampsia risk may be as high as 35-40%

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 Obstetric risk factors
 Primiparity
 Multiple gestation
 Primipaternity/Pregnancy for a new consort
 Previous pre-eclampsia
 Hydrops with a large placenta
 Hydatidiform mole

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 Medical risk factors
 Pre-existing hypertension
 Renal disease
 Diabetes(pre-existing or gestational)
 Antiphospholipid syndrome
 Connective tissue diseases

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 Classification
 Mild pre-eclampsia- asymptomatic

 Severe pre-eclampsia/ imminent eclampsia

-Proteinuria>2g in 24 hours/ 2-4+
-Bp>160/110mmHg

-Cerebral manifestations;
headache
dizziness
drowsiness
tinnitus
- visual disturbances

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 Severe Pre-eclampsia/imminent
eclampsia
 Visual disturbances
 Diplopia
 blurred vision
 scotomata
 Gastrointestinal
 Nausea
 Vomitting
 Haematemesis
 Epigastric pain/Tenderness
 Renal
 Oliguria
 Haematuria
 Haemaoglobinuria
 Anuria

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  Cardiovascular
 Oedema
 Severe hypertension

 Respiratory
 Cyanosis
 Pulmonary oedema

 Foetal
 IUGR

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 INVESTIGATIONS

 FBC + Platelets
 Serum E/U/Cr
 Uric acid (≥ 6mg/dl)
 FBS
 LFT – AST, ALT, LDH (1000iu/L)
 Clotting profile
 Urinalysis
 USS

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 Predictive Test
 Roll-over test
 + roll over test -≥ 20mmHg increase in DBp
when measured 5 minutes afer gravida is rolled
from the lat. To supine position between 28-32
weeks gestation.
 Not sufficiently reliable, sensitive and specific.

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  Angiotensin II test
 A normal pregnant patient requires mean
angiotensin II dose of 13.5 – 14.9 ng/kg/min to
increase DBp by 20 mmHg.
 Normotensive primigravidae destined to develop
PE respond at < 8ng/kg/min as early as 28 – 32
weeks. 90% of these patients will subsequently
develop PE.

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 COMPLICATIONS
 FOETAL
 Oligohydramnios
 IUGR
 Prematurity
 IUFD

 MATERNAL
 Eclampsia
 CVD
 Cortical blindness
 HELLP syndrome
 Hepatic rupture
 Renal failure
 Pulmonary oedema
 Maternal death

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 Thank
you
for

Listening

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