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Hypertensive Disorders in Pregnancy:
Hypertension - one of the most common medical complications of pregnancy. It complicates 5-7 % of all
pregnancies.
» Along with hemorrhage, complications of hypertensive disorders are a leading cause of
maternal death (~15% of maternal deaths). It is the second most common cause of
maternal mortality in Iraq.
» It is also a major cause of perinatal morbidity and mortality.
Because the blood pressure falls in the first trimester, pregnancy may mask pre-existing hypertension. Blood
pressure rises again in the third trimester and therefore, if hypertension is noted for the first time in the third
trimester, this may be due to unrecognized pre-existing hypertension, pregnancy – induced hypertension or pre-
eclampsia. Often a clear diagnosis is only possible several months after delivery when the blood pressure dose
or dose not revert to normal.
Classification:
(I)
Pre-existing (chronic) hypertension or chronic renal disease:
Hypertension is present before pregnancy, detected in early pregnancy (before 20 weeks in absence of
(Hydatidiform mole), Examples: essential hypertension, secondary to chronic renal disorders, coarctation of
the aorta, systemic lupus erythematosus and pheochromocytoma.
- CHT (chronic hypertension)
- CRD (chronic renal disease)
- CHT with superimposed PET (pre-eclampsia): Development of pre-eclampsia or eclampsia in a
pre-existing hypertension.
(II)
(PIH) pregnancy induced hypertension & /or protinuria (only during pregnancy,
during labour, or puerperium) after 20 weeks of pregnancy.
- PIH without proteinuria- usually not associated with adverse pregnancy outcome.
- PI proteinuria
- PI proteinuric hypertension (pre-eclampsia): which is a disease of pregnancy characterized by
a BP of 140/90 or more on two occasion at least 4 hours apart after the 20
th
week of pregnancy in a
previously normotensive woman and in the presence of significant proteinuria (> 300mg in 24 hours)
and resolve completely by the 6
th
postpartum week.
(III) Unclassified HT and proteinuria: where the patient seen for the first time after 20
weeks.
Pre-eclampsia:
Incidence
: 3-5%.
Aetiology
: Although pre-eclampsia had been described since 200 years, no definite aetiology is found
for it and it is still a disease of theories.
Predisposing factors
:

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1. It is more in Primigravidae than multigravidae, as feto-maternal transfusion that occurs during
pregnancy and especially labour expose the mother to the fetal and (hence the paternal genome),
protecting her in subsequent pregnancies.
2. Pre-existing hypertension.
3. Previous pre-eclampsia.
4. Family history of pre-eclampsia / genetic predisposition
5. Hyperplacentosis i.e. excessive chorionic tissue as in hydatidiform mole, multiple pregnancy,
uncontrolled diabetes mellitus and fetal haemolytic diseases.
6. Obesity.
7. Climate variations: more in cold weather than hot weather.
• Theories of pathogenesis
:
(I) The uteroplacental bed:
In early normal pregnancy, the trophoblasts invade the decidual arteries making their musculature more
flaccid and dilated. During the second trimester of normal pregnancy, a second wave of invasion occurs into
the myometrial segments of the spiral arteries. If the second invasion does not occur, pre-eclampsia will
develops. So in pre-eclampsia, the spiral arteries retain their muscular wall and this will prevent the
development of high flow – low impedence uteroplacental circulation. This will result in under perfusion of
the placenta which will causing release of certain factors into the maternal circulation that targets the
vascular endothelium
(II) Immunological factor:
Stimulation of the maternal immune system by the early conceptus is essential for production of the
blocking factors that prevent rejection of the fetus and placenta. Hypoimmune response results in damage of
the placenta and subsequent pre-eclampsia.
The evidences for this theory are that: Pre eclampsia is less common in previously stimulated immunity
conditions as in:
- Previous pregnancy.
- Previous blood transfusion.
- Consanguineous marriages.
- Increased maternal anti-HLA (human leucocyte antigen) antibodies.
(III) Genetic factor:
A maternal autosomal recessive gene or a fetal genetic component could be responsible.
(IV) Renin-angiotensin system:
It was found that the vascular sensitivity to angiotensin II is reduced in normal pregnancy while it increases
in PIH.
(V) Prostaglandins: Prostacyclin is a vasodilator and an inhibitor for platelets aggregation while
thromboxane is a vasoconstrictor and platelets aggregator. In PIH, there is imbalance towards an increase in
thromboxane production.
• Pathological Changes:
the clinical picture of pre-eclampsia is due to an activation or dysfunction of
vascular endothelial cells.
(I) Vasospasm: In normal pregnancy there is a marked peripheral vasodilatation which causing decrement
in the total peripheral resistance despite the increase of cardiac output and circulating volume and that is

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associated with reduced vascular sensitivity to vasoconstrictors but this insensitivity to vasoconstrictors lost
in pre-eclampsia and on the contrary it shows enhanced sensitivity.
Vasospasm with endothelial cell dysfunction, and subsequent platelet activation and micro-aggregate
formation, account for many of the pathological features of pre-eclampsia which seen mostly in every major
system
The organs mostly affected are:
1. Central nervous system: Ischaemia, haemorrhages and oedema.
2. Liver: Subcapsular haemorrhage, periportal necrosis and infarctions.
3. Endocrine glands: Necrosis and haemorrhage in pituitary, pancreas and adrenal glands.
4. Cardiovascular: Generalized vasospasm, increase peripheral resistance and reduce central venous
pressure. Myocardial and endocardial haemorrhage and necrosis. Lungs show haemorrhage and
secondary bronchopneumonia.
5. Kidney: Decrease in renal blood flow with glomerular damage (glomerular endotheliosis – specific
leasion for pre-eclampsia) leading to:
- Decrease glomerular filtration rate by about 50%.
- Loss of protein in urine (albuminuria),
- Elevated serum levels of uric acid, urea and creatinine. Serum uric acid level is
diagnostic and prognostic for severe pre-eclampsia.
6. Placenta: Reduced utero-placental blood flow leading to intrauterine growth restriction (IUGR) and
even death. Acute atherosis in the spiral arteries, infarction and abruption placentae.
7. Retina: Vascular spasm, haemorrhage, exudates and rarely retinal detachment in severe cases,
papilledema may occur.
(II) Coagulation status:
1. Fibrin production is increased.
2. Fibrinolytic activity is increased.
3. Factor VII, factor VIII-related antigen and fibrin/fibrinogen degradation products (FDP) concentrations
in the plasma are all increased.
4. Fibrin and platelet deposition is increased particularly in the placental arteries.
5. Platelets are activated and depleted.
The end result of these changes in association with decrease plasma volume and increase blood viscosity is
hypercoagulability and disseminated intravascular coagulation (DIC) in severe pre-eclampsia and
eclampsia.
(III) Sodium and water retention:
Loss of endothelial cell integrity result in an increase in vascular permeability and contribute to the
formation of generalized oedema. There is haemoconcentration with fluid shift from the intravascular to
the extravascular compartment.
Diagnosis:
(A) Symptoms:
These are usually depend on severity as may be symptomless.
1. Headache: usually frontal but may be occipital. It is due to cerebral oedema and hypertension.
2. Visual disturbances: blurring of vision flashes of light or blindness.
3. Epigastric or right upper quadrant pain: due to enlargement and subcapsular haemorrhage of the liver.

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4. Nausea and vomiting: due to congestion of gastric mucosa and /or cerebral oedema.
5. Oliguria or anuria: due to kidney pathology.
(B) Signs:
(I) Hypertension:
Blood pressure of 140/90 mmHg or more in two occasions 4 hours apart.
(II) Oedema: generalized accumulation of fluid and it affect more than 50 % of pregnant population.
It is weight gain of more than 1kg in any one week or 2.25kg in any one month.
Clinical oedema is present in about two-thirds of patients with PIH. However, two-thirds of pregnant
women with clinical oedema do not develop hypertension, so it is nonspecific.
Other causes of oedema:
1. General causes: cardiac, hepatic, renal or nutritional oedema.
2. Local causes: as inflammatory or deep vein thrombosis (usually unilateral).
3. Pressure of the gravid uterus: on the pelvic veins may produce ankle oedema.
(C) Investigations:
1. General urine examination: for proteinuria, pus cells, RBCs, casts, specific gravity, culture and
sensitivity. (dipstick measurement is inaccurate quantitatively, then 24 hours urine collection will be better).
Proteinuria (albuminuria):
Significant proteinuria is a urinary protein of 300 mg or more in a 24 hours collection or greater than 1 gm/L
in two random samples obtained at least 4 hours apart. It indicates glomerular damage and almost always
occurs after hypertension.
Other causes of proteinuria
- Contamination of urine by vaginal discharge.
- Urinary infection: excluded by microscopic examination and culture of urine.
- Congestive heart failure and severe anemia due to hypoxia of the kidney.
- Orthostatic proteinuria: Proteinuria is detected at the end of the day while it is absent in the morning.
2. Full blood count (platelets & haematocrit)
3. Blood chemistry (renal function & protein concentration)
4. Serum uric acid > 6mg% is abnormal during pregnancy. It is more specific for pre-eclampsia than
creatinine.
5. Coagulation status: fibrinogen and FDP as DIC may develop.
6. Eye fundus examination.
7. Tests for fetal wellbeing as:
- Daily fetal movement count
- Non-stress test
- Ultrasound, serial bipariatal diameter (BPD)/abdominal circumference (AC)
- Biophysical Profiles (fetal movement, fetal breathing movement, amniotic Fluid Vol. & fetal tone)
- Doppler ultrasound
Types:
1. Mild pre-eclampsia: blood pressure ≥ 140/90 mmHg + mild proteinuria ± oedema.

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2. Severe pre-eclampsia:
- BP > 140/90 mmHg + significant proteinuria ± oedema or
- Diastolic blood pressure > 110 mmHg or
- Cerebral or visual disturbances.
3. Imminent eclampsia
or fulminating pre-eclampsia: is a transitional condition characterized by increasing
symptoms and signs and rapidly could deteriorate to eclampsia, so it is a state in which the patient is
about to develop eclampsia.
Complications of pre-eclampsia:
(A) Maternal:
1. Convulsions and coma (eclampsia).
2. Cerebral haemorrhage.
3. Renal Failure.
4. Heart Failure.
5. Liver failure, HELLP syndrome described in severe PET which consists of:
H = Haemolysis, EL = Elevated Liver enzymes, LP = Low Platelet count. Seen in 2-4 % of women with
pre-eclampsia, may associated with DIC, placenta abruption & fetal death of up to 60% & maternal
mortality up to 24%
6. Disseminated intravascular coagulation
7. Abruption placentae.
8. Residual chronic hypertension in about 1/3 of cases.
9. Recurrent pre-eclampsia in next pregnancies.
(B) Fetal: may appear small with oligohydraminous and reduced fetal movement
1. Intrauterine growth restriction (IUGR).
2. Intrauterine fetal death.
3. Prematurity and its complications.
Prophylaxis
:
(1) Proper antenatal care:
- To detect the high risk patients.
- Early detection of cases who are already developed PIH and examine them more frequently.
(2) Low dose aspirin: (75 mg daily)
Inhibit platelets activation and thromboxane production from the platelets. It had showed some effect if given
to the high risk population. For that a second trimester screening tests had been developed as Doppler
ultrasound uterine artery waveform (characteristic notch can be seen in the waveform pattern in women with
incomplete trophoblast invasion of the spiral arteries), so aspirin could be prescribed to those cases.
Treatment:
Depends on the gestational age and severity of the disease. In mild cases we can deal with them as an
outpatient and can await spontaneous labour or attempt vaginal delivery at 38 completed weeks. While
in severe cases termination can be done regardless the gestational age.
Delivery of the fetus and placenta is the only real treatment of pre-eclampsia.
(I) General Measures:

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1. Hospitalization: with bed rest more in left lateral position to prevent compression of the inferior vena cava.
This lowers the blood pressure, induces diuresis, reduces oedema and increases renal and placental blood
flow.
2. High protein, low sodium diet.
3. Observation:
I- Maternal:
- Daily chart for blood pressure, urine volume, proteinuria and oedema.
- Body weight twice weekly.
- Fundus oculi once weekly.
- Blood picture including platelet count, liver and renal functions particularly serum uric
acid…according to severity.
II- Fetal:
- Daily fetal movement count
- Serial sonography
- Non-stress and stress test if needed
(II) Medical treatment:
If the BP is consistently > 150 / 100 mmHg, antihypertensive medication need to be given. To reduce the risk of
sever hypertension and its complications. Care should be taken not to reduce the BP so much as this may
adversely affecting the fetus by reducing placental blood flow. The aim is to reduce systolic BP below 160
mmHg & diastolic BP below 100 mmHg.
1. Antihypertensive: It decrease the maternal cerebral and cardiovascular complications but do not affect
the fetal outcome.
i) Alpha-methyl-dopa (Aldomet): only given orally
- It is centrally acting, maximum dose of 4 gm/day. Its effect appears after 24 hours.
- Side effects: headache, nightmares & postural hypotension.
ii) Hydralazine (Apresoline):
- It is a vasodilator, increases renal and uteroplacental blood flow. Can be given orally and intravenous.
- Side effects: tachycardia, headache, flushing, nausea and vomiting.
iii) Calicium channel blockers (Nifedipine): has rapid onset of action but can cause severe headache which
may mimic worsening of the features
- It is vasodilator acting by blocking the Ca influx into smooth muscle cells.
iv) Alpha & Beta -Adreno-receptor blockers:
- Labetalol, causes vasodilatation and given orally and intravenously.
2. Diuretics:
Need to be avoided in pregnancy. It aggravates the haemoconcentration. We only use them in heart failure.
3. Anticonvulsant therapy: e.g. magnesium sulphate may be started in case of imminent eclampsia and
eclampsia.
(III) Obstetric measures:
(1) Timing of delivery:
Severe pre-eclampsia is usually treated conservatively till the end of the 36
th
week to ensure reasonable
maturation of the fetus.
Indications for urgent delivery:
- BP persistently at 160/100 or more with significant proteinuria

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- Elevated liver enzyme
- Low platelet count
- Eclamptic fit
- Anuria
- Significant fetal distress
(2) Method of delivery:
i) Vaginal delivery ii) Caesarean section for obstetrical causes only.
(3) Intrapartum care:
- Close monitoring of the fetus is indicated.
- Proper analgesia to the mother. Hypotensives drugs may be given if needed (intravenously)
- 2
nd
stage of labour may be shortened by forceps or vacuum.
- With normal clotting study then can use epidural anaesthesia as it help to control the BP
(4) Postpartum care:
- Methergin is avoided as it increases the blood pressure.
- Continue observation of the mother for 48 hours as blood pressure may increase again on the 3
rd
or 4
th
day.
- Hypotensive drugs are continued in a decreasing dose for 48 hours.
- Breast feeding is encouraged, non of the standard antihypertensive medication is contraindicated in
pregnancy.
- Such patient has high risk for thromboembolism, so she need prophylactic anticoagulant
( subcutaneous heparin) is indicated.
Eclampsia:
Definition: It is the development of grand mal convulsions in a pre-existing pre eclampsia, however other
causes of fits such as epilepsy need to be excluded. Any convulsion in pregnancy is eclamptic fit until prove
otherwise.
Incidence: About 1/2000 pregnancies in UK. Sever pre -eclampsia is much more common than eclampsia.
Aetiology: The exact cause is unknown but cerebral ischaemia and oedema were suggested.
Clinical Picture:
Premonitory stage: the eyes are rolled up with twitches of the face and hands. It lasts for about ½ min.
Tonic stage: generalized tonic contraction of the whole body muscles with. It lasts for about ½ min.
Clonic Stage: convulsions occur where there is alternative contraction and relaxation of the body
muscles. The face is congested, tongue may be bitten, blood-stained frothy saliva appears on the mouth,
breathing is stertorous, urine and stool may pass involuntarily, temperature rises due to increased
muscular activity patient is unconscious. This lasts for about 1 min.
Coma which may last for few hours. Other fits may occur during coma, after recovery or may not recur
again.
Types:
1. Antepartum eclampsia 40%.
2. Intrapartum eclampsia 20%.
3. Postpartum eclampsia 40% occurs within 48 hours of delivery. It is usually the most dangerous one.
Differential Diagnosis:
(1) Epilepsy.
(2) Intracranial haemorrhage.

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(3) Meningitis.
(4) Brain tumours.
Management
(A) General Measures:
1. Hospitalization is mandatory.
2. Efficient nursing in a single quiet semi-dark room to prevent any auditory or visual stimuli.
3. A self-retained Foley’s catheter is applied. The hourly output of urine is charted. Proteinuria,
haematuria and specific gravity is noticed.
4. Care for respiratory system by: Turn the woman onto her side with the head down tilt to help
drainage of bronchial secretion, frequent change of patient position, keep upper respiratory tract clear by
aspiration of mucous through a plastic airway and oxygen is administered during and after fits.
5. The tongue is protected from biting by a plastic mouth gauge.
6. Call for help, senior obstetrician and anesthetic staff must be involve. The mother condition need to
be stabilized before delivery.
7. Observation for:
a- Maternal:
- Pulse, temperature, blood pressure, respiratory rate, tendon reflexes, urine volume, number of fits and
duration of coma, uterine contraction, tests for urine, clotting studies, liver function tests, urea, electrolytes and
cross-matching with blood preparation.
b- Fetal:
Fetal heart monitoring.
(B) Medical measures:
(1) Anticonvulsant therapy: to prevent fit or further fits.
a) Magnesium sulphate:
Action: inhibits neuromuscular transmission,
- Sedation,
- Peripheral & cerebral vasodilatation & membrane stabilizer.
- Diuresis.
Dose: A loading dose 4 gm over 5 minutes, followed by 1gm/hour infusion for 24 hours. Recurrent attacks
should be treated with a further dose of 2-4 gm over 5 minutes. And diazepam should be given only if fit
continue despite Magnesium sulphate use but sometime diazepam could be used to arrest the fit when Mg
sulphate is not available.
Before each maintenance does of Magnesium sulphate, the following criteria should be checked as the
therapeutic level is near to the toxic level:
i-
Knee jerk should be present,
ii-
Respiratory rate not less than 16 / min.
iii-
Urine output not less than 30 ml/hour.
(2) Antihypertensives:
Potent and rapidly acting drugs are used when needed, usually use injectable one, as hydralazine or labetalol.
Give bolus dose and then as infusion. No much reduction of BP is needed. The aim is to return not to
normality, but to safety.
(3)Dexamethazone: to enhance lung maturity if delivery is needed before term.

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(4)Management of fluid balance is a critical issue, due to intense peripheral vasoconstriction, decrease
blood volume, fall in urine output, so strict input /output balance must be maintained. If oliguria
developed ( < 20 ml of urine / h for 4 hours) so CVP line need to be inserted. Avoid diuretics.
(C) Obstetric measures: Once the patient has sever disease that need antihypertensive and
anticonvulsants, delivery should follow stabilization of the condition.
So no conservative treatment in eclampsia and the patient should be delivered but convulsions should be
controlled first. Spontaneous labour usually commences within 6 hours. If not, then induce labour by oxytocin
as long as there is no other indication for caesarean section and vaginal delivery is anticipated within 8-12
hours. Otherwise, caesarean section is indicated. Intra-and postpartum care: as in pre-eclampsia.
Causes of maternal death: mostly related to failure of recognition of deteriorating condition after delivery and
due to multiple organ failure:
- DIC
- Adult respiratory distress syndrome
- Renal failure
Pre-existing (chronic) hypertension
Causes
(i)
Essential hypertension: of unknown aetiology is the underlying cause in 90% of cases.
(ii)
Secondary to chronic renal disorder:
- Glomerulonephritis.
- Polycystic disease.
- Diabetic nephropathy.
- Renal artery stenosis.
(iii)
Secondary to cardiovascular disease:
- Coarctation of the aorta.
- Polyartheritis nodosa.
(iv) Secondary to collagen vascular disease:
- Systemic lupus erythematosus.
- Scleroderna.
(v) Secondary to endocrine disorders:
- Primary aldosternism.
- Phaeochromocytoma.
- Adrenocortical tumours.
- Diabetes mellitus.
Effect of Pregnancy on Chronic Hypertension:
1. Blood pressure falls by the second trimester in most of cases, but raises during the third trimester to a
level some what above that in early pregnancy.
2. Deterioration of the underlying disease.
3. These women may develop superimposed pre-eclampsia, may occur in up to 1/3 of women with pre-
existing hypertension, especially in cases of sever hypertension (diastolic BP of 110 mmHg and more or
renal disease).

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Effect of Chronic Hypertension on Pregnancy:
A- Maternal:
- Superimposed pre-eclampsia / eclampsia in 1/3 of cases.
- Abruption
- Heart failure
- Intracerbral Haemorrhage
B- Fetal:
- Intrauterine growth restriction.
- Intrauterine fetal death.
Investigations:
-
Creatinine, electrolytes
-
Liver function test
-
24 hs urinary protein/ creatinine clearance
-
Renal scan
-
Autoantibody screening
-
Complement study
-
Cardiac investigations ( ECG & Echo study)
Treatment
(1) General and medical treatment:
As pre-eclampsia regarding the following:
- Rest
- Antihypertensive
- Diuretics avoided
- Observation.
- Close monitoring looking for the development of superimposed pre-eclampsia
- If she using Angiotensin converting enzyme inhibitors (Captopril) before pregnancy,
then discontinue this drug with the start of pregnancy because of its side effect as fetal
renal failure and neonatal hypertension
(2) Obstetric measures:
a. Therapeutic abortion: in severe cases not responding to treatment.
b. Preterm delivery if there is:
- Marked deterioration of the underlying disease.
- Indication for termination as in pre-eclampsia if it is superimposed.
- Intrauterine growth restriction.
c. Early delivery rarely indicated, may need induction of labour at 38 weeks. In general it is
reasonable delivery at 38 completed weeks as intrauterine fetal death may result from
deteriorating placental functions.
d. Postnatal follow up for up to 48 hours because the BP tend to increase again at the 3
rd
or the 4
th
day.
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