This document discusses hypertensive disorders of pregnancy, which are a leading cause of maternal mortality worldwide. It defines the different types of hypertensive disorders like gestational hypertension, preeclampsia, and chronic hypertension. Preeclampsia is characterized by new onset hypertension and proteinuria after 20 weeks of gestation. The document outlines risk factors, pathogenesis, clinical manifestations, investigations, management including delivery timing, and complications like eclampsia and HELLP syndrome for different hypertensive disorders of pregnancy. Magnesium sulfate is the primary treatment for seizures of eclampsia. Delivery is usually required to resolve preeclampsia symptoms.

1. 1
Hypertensive disorders of
pregnancy
Prof. Adel Abul-Heija

2. 2
Introduction
1. Hypertensive disorders of pregnancy are
one of the leading causes of maternal
mortality.
2. Worldwide: 50,000 women die each year.
3. Jordan: 4th. Cause of maternal death after
(hemorrhage, thrombo-embolism, and
sepsis. (Jordan MMR 19.1 per 100000 live
birth, 2007-2008)

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Diagnosis of hypertension in
pregnancy
 A systolic BP of > 140 mmHg, a diastolic BP
of > 90 mmHg, or both.
 Hypertension is considered severe when BP >
160 for systolic or > 110 for diastolic.
 It required at lest two determinations with at
least 6 hours apart of bed rest.

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How to measure BP in pregnant
woman
 Women should be allowed to sit quietly for 10-20 minutes before
each blood pressure measurement.
 Blood pressure should be measured in the sitting position, with the
cuff at the level of the heart.
 Korotkoff sounds I (the first sound) and V (the disappearance of
sound) should be used to denote the systolic blood pressure
(SBP) and DBP, respectively.
 In about 5% of women, an exaggerated gap exists between the
fourth (muffling) and fifth (disappearance) Korotkoff sounds, with
the fifth sound approaching zero. In this setting, both the fourth
and fifth sounds should be recorded (eg, 120/80/40, with sound I =
120, sound IV = 80, and sound V = 40), because the fourth sound
will more closely approximate the true DBP.

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Diagnosis of Protienurea in
pregnancy
 Proteinuria:
 ≥ 300mg/24 hours urine.
 ≥ +1 dipstick. (only applicable if the others are not
avialables)
 Urinary Protein:creatinine ratio:
 At least 0.3 (each measured as mg/dl)

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Classifications
 Gestational hypertension.
 Preeclampsia-Eclampsia.
 Chronic hypertension with pregnancy.
 Chronic hypertension with
Superimposed preeclampsia.

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Definitions
 Gestational hypertension:
– Hypertension for first time after 20 w, without
Proteinuria. BP returns to normal before 12
weeks postpartum.
 Chronic hypertension with pregnancy:
– Hypertension antedates pregnancy and detected
before 20 w, & lasts more than 12 weeks
postpartum.

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Definitions
– Preeclampsia:
 The development of hypertension and Proteinuria after
20 weeks.
 May occur earlier in vesicular mole or multiple
pregnancy.
 Preeclampsia is diagnosed also in the presence of
sever features even in the absence of protienurea (see
next slide).
– Eclampsia:
 The occurrence of tonic-clonic convulsions (without
any neurological disease) in a woman with pre-
eclampsia.

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Definitions
 Superimposed pre-eclampsia:
¤ It is the new development of Proteinuria
after 20 weeks gestation in a patient with
chronic hypertension

10. 10

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Incidence of hypertensive disorders in
pregnancy
 Gestational hypertension occurs in around 5-6% of all
pregnancies. More common in primigravida. Most cases are
diagnosed after 34 weeks.
 PE complicates 1-2% of all pregnancies. 4-7% of first
pregnancies (1 in 4 of PIH) and 1% of subsequent
pregnancies, rising to 16% with history of preeclampsia in
first pregnancy.
 Around 5-10% of PE cases are severe.
 Approximately 1% of pregnancies are complicated by
chronic hypertension and 20-25% of women with chronic
hypertension develop preeclampsia during pregnancy.

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Pre-eclampsia (PE):
Definition:
A diastolic BP > 90 mmHg, on at least two
occasions after 20 weeks of gestation
accompanied by significant proteinuria (>
300 mg/24h) and/or other systemic severe
manifestations mentioned before.

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Aetiology of PE:
PE is the disease of theories:
1. Damage to the vascular endothelial cells.
2. Abnormal lipid metabolism.
3. Reduced anti-oxidant status.
4. Altered catecholamine homeostasis.
5. Abnormal dietary calcium, magnesium, or selenium.
6. Reduced production of nitric oxide.
7. Abnormal immune response to pregnancy.

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Patho-physiology of PE:
 Abnormal placentation is central to the pathogenesis
of PE.
 In PE there is reduction in the synthesis of nitric
oxide and prostacyclin and increased production of
endothelin and sensitivity to angiotensin. This result
in to vasospasm and endothelial dysfunction, with
subsequent platelet activation and micro thrombus
formation. These are responsible for features of PE.

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Multi-system Features Of
Preeclampsia
Multi-organ disease
Kidney
Systemic blood vessels
Liver
Fetus
Cerebral blood vessels
HELLP syndrome
IUGR
Eclampsia
Proteinuria
Hypertension

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Clinical features of PE:
Maternal syndrome:
1. PIH.
2. Proteinuria.
3. Generalized oedema.
4. Hyperuricaemia.
5. Increased haematocrit.
6. Thrombocytopenia & DIC.
7. Reduced antithrombin III.
8. Abnormal liver function tests.
9. Hypocalciuria.
10. Seizures, cortical blindness,
retinal detachment (eclampsia).
Fetal syndrome:
1. IUGR.
2. Fetal hypoxaemia.

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Prevention of PE:
 Aspirin: Low dose (81mg/day) increases the
prostacycline to thromboxan ratio and prevent platelets
aggregation. It should be used from 12 weeks of
pregnancy in women at risk.
 Calcium supplementation ( may reduce severity in
women with low intake of calcium.
 Antioxidant: vit.C or vit.E (not effective)
 Restriction of dietary salt (not effective)

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High risk women that need aspirin
 Maternal disorders:
– Chronic hypertension
– Renal diseases
– Diabetes
– Autoimmune conditions
 First pregnancy
 Multiple pregnancy
 Maternal BMI > 25
 H/O preeclampsia
 Age > 40 years

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Investigations for PE:
 Urinalysis.
 24 h urine collection for total protein.
 Renal function (urea,uric acid,s. creatinine).
 Full blood count (platelets and haematocrit).
 Liver function tests.
 Coagulation profile if delivery is indicated.
 Fetal biophysical profile and Doppler study.

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Management of PE:
 Diagnosis of PE requires admission for bed
rest and close monitoring for mother and fetus.
 If the diastolic BP is 90-95mmHg with only 1+
protein in the urine, out-patient management
could be followed.
 The definitive treatment for PE is delivery. But
this depend on gestational age and feto-
maternal well-being.

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Management of PE (cont.):
Antihypertensive therapy:
 Treating the hypertension is mainly to reduce the maternal
complications. It will not improve fetal condition.
Acute treatment of severe hypertension:
 Hydralazine: 5mg IV repeated every 20-30 min.
 Nifedipine: 10mg orally repeated at 30 min. IV infusion can be
used in severe cases.
 Labetalol:10-20mg IV .
 The dose can be doubled every 10 minutes if proper
response is not achieved.
 Magnesium Sulphate should be given in the management of
all cases of severe preeclampsia to prevent eclampsia.

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Indications for delivery in PE:
 Term pregnancy.
 Severe uncontrolled hypertension (>160/110).
 Haemolysis with thrombocytopenia.
 Progressive symptoms (headache, visual disturbances,
epigastric pain).
 Pulmonary oedema.
 Renal failure with oliguria.
 Eclampsia.
 Fetal compromise ( abnormal biophysical profile).

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Management of labour and
delivery:
 The mode of delivery is determined by Bishop’s score
and feto-maternal well-being.
 Induction of labour is commonly used, but CS is
needed in large number of cases.
 Fluids input and output should be monitored.
 Prolonged pushing by the mother should be avoided.
 Ergometrine should be avoided.
 Pain relief is optimal (epidural analgesia if no signs of
DIC).

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Complications of severe PE:
Eclampsia: Occurrence of convulsions in association with
PE.
 Incidence: 5 in 10 000 deliveries and 1-2% of severe
PE cases.
 High maternal and fetal mortality.
 It can occur ante-natally, intra-partum and post-partum.
 The patho-physiology is cerebral vasospasm leading to
ischemia and cerebral edema.

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Eclampsia:
Diagnosis:
 Women manifest excitability or hyperflexia prior
to onset of seizure.
 Tonic-clonic convulsions with small period of
coma.
 Prolonged coma mains CVA.

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Management of eclampsia:
 During seizure: Maintain airway, Administer oxygen
and avoid supine hypotension.
 Anticonvulsant therapy:
1. Magnesium sulphate 4-6 g IV followed by a
maintenance infusion of 1-2 g / h.
2. Diazepam 20mg IV followed by a maintenance
infusion as required.
3. Phynenton
 Anticonvulsant should be continued for at least 24 h
after the last convulsion.
 CS is indicated unless the mother is in active labour.

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Magnesium Sulfate (MgSO4):
 It can be given IV or IM or SC
– The therapeutic level is 4-7mEq/L.
– The total dose of MgSO4 should not exceed 24 gms in 24
hours .
 The dose of MgSO4 is monitored by:
 Preserved patellar reflex. (7-10 mEq/L)
 Respiratory rate >16/min. (10-13 mEq/L)
 Urine output >100ml/4hours. (15-25 mEq/L)
 Serum Mg++ level.
 Is stopped 24 hours after delivery.
 Antidote is ca gluconate

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Complications of severe PE:
HELLP syndrome: Occurs in the absence of hypertension.
H: haemolysis.
EL: elevated liver enzymes.
LP: low platelet count.
 Present with epigastric pain, tender liver, nausea & vomiting.
 Headache and arterial hypertension.
 Carries high maternal (acute renal failure & pulmonary odema)
and fetal mortality.
 Treatment similar to eclampia & DIC. Platelet transfusion and
cortico-steroids are necessary.
 Delivery is the treatment of choice.

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Chronic hypertension in pregnancy
Causes of CHT:
1. Essential hypertension.
2. Renal diseases (glomerulonephritis, polycystic
disease, diabetic nephropathy, renal artery stenosis).
3. Collagen vascular diseases ( systemic lupus
erythematosus, scleroderma).
4. Coarctation of the aorta.
5. Phaeochromocytoma.

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Chronic hypertension in pregnancy
 The main concern that one third of these women will
develop superimposed PIH.
Risk factors for preeclampsia in CHT:
1. Renal disease.
2. Maternal age > 40 years.
3. Diabetes.
4. SLE.
5. Coarctation of the aorta.
6. BP > 160/100 mmHg in early pregnancy.

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Chronic hypertension in pregnancy
Feto-Maternal risks:
1. Eclampsia.
2. Abruptio-placenta.
3. Heart failure.
4. Intracerebral haemorrhage.
5. IUGR.

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Long-term treatment of hypertension
This is used mainly in CHD.
 Methyldopa is the most common in use (least
side effects). 1-2 g / day in three divided doses.
 Nifedipine 40 mg / day in two divided doses.
 Labetolol and Hydralazine can also be used.
 ACE inhibitors, Angiotensin II blocker, and
Chlorothiazide should be avoided because of
teratogenic effect.

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Chronic hypertension in pregnancy
Management:
 Investigations should be performed to diagnose the
cause of hypertension.
 If the woman is on antihypertensive drugs, she should
continue on it, except for angiotensin converting
enzyme inhibitors (captoprel) because of risk of fetal
damage. Care should be taken not to excessively
lower the BP as this may affect the fetal healthy.
 Maternal and fetal well-being should be monitored
through the pregnancy.

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Chronic hypertension in pregnancy
Management (cont.):
 In severe cases admission is needed.
 The obstetric management is similar to that of
preeclampsia.
 Timing the delivery must be individualized
according to the feto-maternal well-being.
 Induction of labour or CS should be selected
according to the case.

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