Hypertensive Disorders
in Pregnancy
Azza Alyamani
Prof. of Obstetrics & Gynecology
Classification
Women who are pregnant and hypertensive
must be divided into :
* chronic hypertension.
* pregnancy induced hypertension (PIH)
or gestational hypertension.
those with PIH further subdivided :
* proteinuric PIH (preeclampsia)minority
* non-proteinuric PIH majority
Therefore :
women with hypertension in pregnancy are
classified as having:
1. preeclampsia (proteinuric hypertension).
2. non – proteinuric hypertension.
3. chronic hypertension:
•primary (essential) hypertension. 95%.
•secondary hypertension.5%.
..renal dis.
..adrenal dis.
..hyperthyroidism.
The aetiology and management of the three
conditions are different .
Incidence:
Worldwide , maternal mortality from hypertensive
disease accounts for :
100.000 deaths per year.
preeclampsia occurs in 5% .
non – proteinuric PIH 15%.
it accounts to 15 – 20% of maternal mortality in
the developed cuonteris.
Definition:
pregnancy induced hypertension (PIH) is :
Hypertension that occurs after 20 weeks gestation
and unrelated to other pathology.
protienuria is the excretion of 300mg or more of
protein in 24 hours urine.
hypertension and protienuria define
preeclampsia.
Preeclampsia :
* is a multisystem disorder involving the placenta ,
liver , kidneys , blood , neurological and
cardiovascular systems.
* both maternal and fetal morbidity / mortality are
more likely to occur with early – onset disease as;
placental abruption ,acute renal failure ,cerebral
Hge ,DIC and IUGR ,prematurity as delivery is
the only cure.
therefore , ANC is directed towards identifying
women with hypertension and protienuria.
* severity ranges from :
a mild disorder (transient hypertension
in the later part of the pregnancy) to
a life-threatening disorder with seizure
HELLP syndrome, fetal hypoxia, and
growth retardation.
* more severe disease: 0.5 per 1000
deliveries
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Chronic Hypertension :
is the presence of persistent hypertension of
whatever cause , before 20 weeks gestation
or
persistent hypertension beyond 6 weeks
postpartum.
sustained bl. p of 140/90 mmHg or > on two
occasions 6 hours apart is considered
hypertensive.
Aetiology
Pregnancy induced hypertension (PIH)
Preeclampsia:
is unknown , believed to be involved :
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immune maladaptation.
placental ischemia.
oxidative stress.
genetic predisposition.
Genetic Predisposition
Faulty interplay bet. invading trophoblast and decidua
Decreased bl. supply to feto-placental unit
Release of circulating factors
Endothelial cell alteration
Hypertension
Proteinuria
IUGR
Management
Screening for preeclampsia :
Risk Factors
1. +ve family history in the first –degree relative
increase the risk of PET 4 – 8 fold.
2. primiparety
3. medical disorders as :
* history of PET.
* chronic hypertension.
* diabetes.
* obesity.
* antiphospholipid syndrome.
* molar pregnancy.
* multiple pregnancy.
* hydrops fetalis.
Screening and assessment for chronic
hypertension :
Women who is found to be hypertensive before
pregnancy can be advised about :
1. weight loss.
2. restrict salt and alcohol intake.
3. change her antihypertensive agents , diuretics ,
angiotensin-converting enzyme (ACE) inhibitors
and β blockers to other alternatives.
Diagnosis
Screening tests:
to predict PET and superimposed preeclampsia
on chronic hypertension.
(1) US
it is quick ,non-invasive and inexpensive .
Uterine artery Doppler :
analysis of its waveform is an early predictor of
poor placental perfusion and development of PET ,
there is resistance circulation with notch.
Its predictive value is greater at 24 weeks or more.
Uterine art. Doppler in PET
diastolic notch
(2) Biochemical tests
in preeclampsia :
* HB , and Hematocrit concentrations.
* CBC with platelets count.
* serum uric acid .
* endothelial activation markers are increased.
* urinary excretion of Ca and microalbuminuria
in severe chronic hypertension:
* urine analysis.
* 24h urine for protein , creatinine clearance,
catecholamine metabolites and free cortisol.
* bl. Urea and electrolytes as Na & k.
* Lupus anticoagulant and anticardiolipin in APS.
* serum lipids.
in addition
(3) fundoscopy.
(4) ECG & ECHO.
(5) X ray chest.
Symptoms & Signs
hours
* Criteria of severe preeclampsia
= blood pressure : > 160 mmHg systolic or
> 110 mm Hg diastolic •
= Proteinuria: > 3 g in 24 •
= Persistent and severe cerebral or visual
disturbances (headache, blurred vision)
= Persistent and severe epigastric pain or
right upper quadrant pain.
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Pulmonary edema or cyanosis.
Oliguria ( < 500 ml urine / 24 hour).
Eclampsia ( grand mal seizures).
HELLP syndrome.
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Maternal and fetal assessment:
* the GA at which woman present with hypertension
is an important factor in establishing risk .
Late onset hypertension after 37weeks rarely result
in serious maternal or fetal complications.
* Superimposed pre eclampsia on chronic
hypertension is diagnosed by identifying proteinuria,
raised uric acid levels or failing platelets count .
chronic hypertension is associated with preeclampsia
in 20% and abruptio placenta in 2%.
* Uterine artery Doppler velocity waveforms
is used to assess risk .
* bl.pressure and urine analysis are checked
every 2 weeks.
sudden and profound rise should alert the
clinician to the possibility of PET.
* high uric acid and low platelet count
may pre –date proteinuria by some
weeks.
Management
Pre eclamptic Toxaemia
A) PET remote from term
Early onset PET is associated with :
a. placental insufficiency
resulting in IUGR and fetal death. Therefore ;
Fetal Wellbeing must be carefully considered.
1. monitoring of fetal movements.
2. serial symphesis -fundal height .
3. serial US to confirm fetal growth ,AF
volume and Umbilical A. Doppler
waveform .
b. involvement of other organ systems
resulting in increased maternal morbidity
and mortality.
1.serial platelets count
as platelets are consumed due to endothelial
activation.
Thrompocytopenia
<100.000/ml. delivery should be considered.
2.increased HB and haematocrit values indicate
hypovolaemia.
3.clotting abnormalities indicate DIC.
.
4.raised uric acid
a measure of fine renal tubular function is used
to assess severity of the disease.
raised urea and creatinine
indicate late renal involvement .
5.severe proteinuria
> 3g /24 hours urine resulting in fall of
circulating albumin and increasing the risk of
pulmonary edema.
5.HELLP syndrome
it is severe variant of PET, Haemolysis ,
Elevated Liver enzymes and Low Platelets .
PET can cause subcapsular hematoma, liver
rupture and hepatic infarction which result in
raised liver transaminases as AST indicating
hepatocellular damage and
liver involvement
and the need to consider delivery.
Delivery :
should be considered once fetal lung maturity is
likely ( at 32 weeks gestation) ,especially if either
multi-organ involvement or fetal compromise is
proved.
Corticosteroids are given to enhance fetal lung
maturity. Steroid therapy may enhance recovery
from HEELP syndrome.
Delivery before term is usually by CS .such
patients are risk of thromboembolism and should
be given prophylactic SC heparin and stockings.
Indications of termination of pregnancy
in PET :
1.
2.
3.
4.
uncontrollable hypertension.
deteriorating liver or renal function.
progressive fall in platelets.
neurological complications as cerebral Hge.
5. deteriorating fetal condition as non-reactive
CTG.
B) PET near term
Lat onset preeclampsia rarely results in
serious morbidity to mother or fetus .
Drug therapy should be considered:
a) antihypertensive
the aim is to lower the bl. pressure and
lower the risk of maternal cerebrovacular
accident without
uterine bl. flow and
compromising the fetus.
1. Labetolol
ą &β blockers .
can be given IV and orally.
safe during pregnancy.
2. Methyldopa
centrally acting agent.
very safe during pregnancy.
only given orally .
takes 24 h for its effect.
3. Nifedipine
is Ca channel blocker .
with rapid onset of action.
cause severe headache.
NB:
Diuretics ,Angiotensin-converting enzyme (ACE)
inhibitors and β-blockers are contraindicated .
b) Low dose aspirin
results in significant reduction in preeclampsia
associated fetal death and preterm delivery.
c) for prophylaxis
Ca , fish oil , antioxidants , vit. C , vit. E
Management of severe fulminating preeclampsia
and impending eclampsia :
1. IV antihypertensive
Hydralazine / labetolol
IV infusion titration rapidly against changes in
the blood pressure .
2. Anticonvulsant therapy
Magnesium Sulfate :
* it is the anticonvulsant of choice as ttt. of
eclampsia and also as prophylaxis which
reduce the risk of fits to half.
Diazepam and phenytoin can be used but
less effective .
* mode of action
= anticonvulsant.
= muscle relaxant.
=vasodilator.
reduce the intracerebral ischaemia.
* dose
2 g IV
as a loading dose then
1-2 g / h as maintenance infusion.
* toxicity is detected by :
absence of the patellar reflexes.
respiratory arrest .
may be cardiac arrest.
* antidote is:
10 ml of 10% Ca gluconate.
3. Fluid management
a Folly′s catheter should be inserted and fluid
balance recorded.
* oliguria without a rising serum urea or
creatinine is a manifestation of severe PET
and not renal failure.
however , if creatinine or potassium rises ,
haemodialysis is necessary.
* diuretics should only be given if there are
signs of pulmonary edema.
Postpartum Care
* in severe PET and eclampsia, a severe type of
of eclamptic fits occur postpartum , intensive
monitoring is required for 48 h. after delivery.
* bl. Pressure is frequently at its highest levels
3 -4 days after delivery . Therefore ,
antihypertensive therapy is need to be
continued after discharge home.
* a postnatal care visit 6 -8 w. is mandatory for
measuring bl.p , urine analysis , RFT, LFT and
predisposing factors as thrompophilia or APS
should be excluded.
* in women with severe chronic hypertension
must be carefully monitored for at least 48h
after delivery as they are at increased risk of
renal failure , pulmonary edema and
hypertensive encephalopathy.
Thank you