1. Africa international university
faculty of medicine and health sciences
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Hypertensive
Disorder of
Pregnancy
Presented by:
Dr. Elwaleed Mudather
Gyae. & obs

2. Hypertensive disorders of
pregnancy
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o Hypertensive disorders in pregnancy are a
major cause of maternal and fetal mortality
- In the developing countries the maternal
mortality is about 70-120 per 100.000
maternities
- in UK it is about 0.9 per 100.000 maternities
accounting for about 16% of all maternal death
- The over all perinatal mortality is around 35 per
1000 total birth but may reach 160 per 1000
total birth is severe disease

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o Definition of hypertension:-
-BP should be measured in the sitting position .
- The sphygmomanometer at the level of the
heart .
- Using a cuff wide enough to cover 80% of arm
- Hypertension is defined as:-
o BP 140 over 90 mmHg or more measured in
two consecutive occasions 4 hours or more
apart
Increase of 30 mmHg systolic or 15 mmHg DBP.
From the pre pregnancy BP

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Definition of proteinuria
o 300 mg or more total protein excretion in
24hours urine collection.
Classification
- Based on these definitions hypertensive
disorders of pregnancy can be classified in to

5. 1) GESTATIONAL HYPERTENSION
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Onset of Hypertension without proteinuria
arising for the first time after 20 week of
gestation with resolution to baseline by 12
week postpartum .

6. 2) pre-eclampsia
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Hypertension of at least 140 over 90 mmHg
recorded on two separate occasions at least 4
hours apart & in the presence of at least
300mg of protein in 24 hours collection of
urine arising de novo after the 20th week of
gestation in a previously normotensive women
& resolving completely by the 6th postpartum
week

7. 3)Pre existing Chronic hypertension with or
without renal disease:-
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hypertension. diagnosed before pregnancy or in the first
20th week of pregnancy.
Can be ;-
o 1- Essential hypertension or
o 2-Secondary hypertension.
o --glomerulonephritis.
o --renal artery stenosis.
o --diabetic nephropathy.
o --Polycystic kidneys.
o --SLE.
o --conns syndrome
--Coarctation of the aorta. -

8. 4) Chronic hypertension superimposed by pre-
eclampsia
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proteinuria ,or other symptoms &signs of pre-
eclampsia developing for the first time in
pregnancy in a women with a chronic
hypertension.

9. GESTATIONAL HYPERTENSION
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1-more in multi than primigravida
2- frequency and severity increases with
maternal age.
3- often recurs and familial
4- those women have a high incidence of
hypertension later in life.
.

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pre- eclampsia
- It is a multi system disease specific to
pregnancy in human.
- Affecting 10-
15% of PG and 5 –
7% of multigravida .

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o Risks factors includes:-
- 1-More common at the extremes of age
- 2-More common in PG
- 3-More common in the short and obese women
- 4-Is familial and may recur
- 5-More common in cases with excessive
amount of chorinic tissue such as:-
---hydatidiform mole 70% of cases
- ---multiple pregnancy 25% of cases
- ---hydrops fetalis
- ---poorly controlled diabetes

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- 6--more common in patient with pre existing
chronic renal disease and previous PE.
- 7-Is not associated with increase incidence of
hypertension in later life.
- Clinical feature:-
PE is characterized by lack of symptoms until an
advanced stage reached. Patient may report.
Swelling of feet and ankle, difficulty in putting
on her shoes, tightness of rings and tightness
and puffiness of the face.
Sign includes hypertension and non dependent
oedema. urine may show proteinuria

13. Aetiology of pre-eclampsia:-
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- Cause is unknown
- Genetic factors together with an abnormal
immunological reaction to the first pregnancy
have been postulated this leads to defective
trophoblast invasion of the spiral arteries and as a
result the spiral arteries remain muscular, un
dilated and respond to presser agent such as
angiogenesis2. placental blood flow is therefore
reduced & this results in release of factors in the
maternal circulation that targeted the vascular
endothelium which result in wide vascular
endothelial dysfunction

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with the development of hypertension, altered
vascular reactivity, Activation of the
coagulation cascade and multi system
damage.
- generalized maternal endothelial damage
affects every system in the body with the
following effects.

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- Maternal effects
- Cardio vascular and pulmonary effect:-
* hypertension
* Peripheral oedema due to leaking endothelium
*Cardiac failure due to the high systemic vascular
resistance
*Pulmonary oedema may arise due to an imbalance
between a reduced colloid osmotic pressure, and the
pulmonary capillary wedge pressure
- *Acute adult respiratory distress syndrome also can
occur.

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The kidneys:-
- glomerular endothelial cells swell- block the
capillaries.
- Impaired renal function may result in a rise in
plasma urate (an early feature), urea, and
creatinine.
- Proteinuria develops.

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o The liver:_
- Hepato-celluar damage can occur due to fibrin
deposits in the sinusoids.
- In some cases jaundice and severe liver
damage can follow.
- The potentially dangerous HELLP syndrome
(haemolysis, elevated liver enzyme and low
platelets) must be considered in severe cases.
- Subcapsular haemorrhage and even liver
rupture my occur

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o Coagulation:-
- Increasingly generalized endothelial damage
commonly causes slight intravascular
coagulation.
- Disseminated intravascular coagulation (DIC) is
rare but serious
Central nervous system:-
- Sudden elevation of BP can causes arterial damage and
loss of vascular auto regulation which may leads to
cerebral oedma, haemorrhages and infacts

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- Cerebral haemorrhage & pulmonary oedema
are the commonest causes of maternal death
from eclampsia.
o Placenta:-
- Hypertension is associated with constriction of
uterine blood vessel. Pathological change in
spiral arteries and fibrin deposition, infacts and
other pathological change.

20. Complication of pre-eclampsia:-
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A- feto- placental
- Abruptio placenta
- IUGR
- IUFD
- Preterm labour
B- maternal complication:-
 Eclampsia
 Pulmonary oedema:-
--- secondary to hypertension
---Adult respiratory distress syndrome

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- --- following prolonged hypoxia
- --- fluid over load
- Cardiac failure
- CVA and other haemorrhages
due to fibrinoid necrosis and rupture of wall of
small vessels.
- HELLP syndrome
o Renal failure due to :
---ischaemia
--- tubular necrosis
--- cortical necrosis

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o DIC.
o blindness
o Micro angiopathic haemolytic anaemia acute
or sub acute haemolysis with the appearance
of fragmented RBCs and reticuloytes in the
prephral blood smear associated with
thrombocytopenia haemoglobinaemia and
hemoglobinuria

23. Management of pre-eclapsia:-
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o The aim of management is:-
o To minimize the hazards both to the mother
and to the fetus until such a time as the fetus
stand a better chance of survival outside the
uterus than inside, or until further prolongation
of pregnancy creates a threats to the mother
life or health

24. Antenatal manangement
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- Initial assessment
- all patient found to have hypertension
should be admitted to hospital or obstetric day
unit for full initial assessment and plan of
management should be formulated according
to the severity of disease and the duration of
pregnancy.

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- Classification according to severity:
- hypertensive disorders can be classified
according to severity to
1.mild:-
DBP 90 and more but less than 110 mmHg
No significant proteinuria
Normal fetal growth
2. sever:-
- DBP 110 mmHg and more or
- DBP 90 and more with significant proteinuria or
fetal growth restriction.

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- 3- imminent eclampsia:-
- -DBP 90 or more with symptoms such as
- Severe persisting headache usually frontal but
may be occipital.
- Visual disturbance (flash of light diplopia)
- -upper abdominal pain, nausea, vomiting (due
to oedema of gastric mucosa, subcapsular Hge
and stretching of liver capsule ).
- Oliguria (urine less than 30 ml per hour)
- Hyperflexia or clonus
-

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- 4- eclampsia:-
- -DBP 90 and more +convulsion (grand
mal epileptiform convulsion).
Eclampsia
- In majority of cases it occur
antepartum usually in the last quarter
of pregnancy.
- In few case it occurs intrapartum or
postpartum
- Haemorrhagic complication are
common.

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neurological complications may include coma focal
motor deficits and cortical blindness.
Differential Diagnosis:-
o Cerebral malaria
o CVA
o Amniotic fluid embolism
o Water intoxication
o Meningitis
Pathology of Eclampsia:-
Is thought to involve cerebral vasospasm leading to
ischaemia, disruption of the blood brain barrier

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1) Mild hypertension without IUGR or
impairment of fetal well being:-
- In general implies minimal or no added risk to
the mother or fetus.
- No immediate indication for antihypertensive
or other treatment.
- Out patient surveillance on weekly ANC visits
with assessment of symptoms. Weight, BP,
fetal size & movement. Amniotic fluid volume,
Urine for protein CTG, scan for growth at 28-
34wks

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- Rest at home but it benefits have never been
clearly defined.
- Sedation is not necessary.
- If labour has not commenced at term induction
may be advocated largely on empirical ground.
2) severe PIH:-
o Admission to hospital
o BP and other vital sign 6 hourly
o Urine for protein daily

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- Fetal movement (kick chart)
- Clinical examination includes fundal height and
amount of liquor.
- Weekly renal and liver function test as well as
platelets count, coagulation status and protein
excretion. Elevated urate levels and falling
platelets reflect worsening of the clinical
condition.
- Fetal size and liquor volume are assessed by
ultra sound.

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- CTG is repeated at intervals determined by
clinical status and can be enforced by a
biophysical profile
- Doppler ultra sound :- absent or reversed flow
in the umbilical artery during diastoly is
associated with high perinatal mortality.
- Antihypertensive:-
- Is to protect the mother from the risk of
cerebral haemorrhage,
- left Ventricular failure, renal failure, DIC and
convulsion.

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- Is indicated when the mean arterial BP
exceed the threshold for vessel
injury(140mmHg)
- The drugs have no effect on the progress of
the disease.
Therapeutic options include the following.
1. Methyldopa
- central alpha stimulants
- Dose up to 2gm/day

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- Side effect include
sedation ,headache, nightmares depression,
dizziness, haemolytic anaemia positive
coombs test.
- 2- calcium channel blockers e.g. Nifedipine
- 3- vasodilators e.g hydrallazine
- 4- labetolol (100—200mg)
- has both Beta and alfa adrenoceptor
blocking action

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- Termination of pregnancy:-
- The definitive treatment of severe PIH is
delivery of the fetus.
- In most cases labour should be induced at
completed 37wks
- Elective C/S may be considered in patient less
than 34wks and when there is some additional
obstetric indication.

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- Management of imminent eclampsia and Eclampsia:-
- Left lateral position, secure air way, oxygen.
- Control of fits with anticonvulsants :
- 1- diazpam dose
10mg I.V in 4min. Followed by 40mg in 500cc
of 5%Dext.water 2-4ml/hour. Safe-
immediate action, but it has short action& can
sedate the fetus & the patient
- Magnezium sulphate: is the drug of first choice it is
- - Anti convulsant ,Antihypertensive and
tocolytic with prolong .action

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- Therapeutic dose is close to toxic dose.
- Dose ;--
intravenous;-
loading dose 4gm in 100ml over 15 -20 min.
Maintenance dose 1 - 1.5gm hourly for 24 hours
from the last fit.
intramuscular;-
loading dose10 gm as 50% sol. 5gm in each
buttock. maintenance 5gm as 50% sol. 4houly
- Monitoring by reflexes, respiratory rate (>16/min)
. urinary out put ( >30ml/ hour) and blood level.
- Toxic effect include
hypotension and respiratory failure.
- Antidote is Calcium. gluconate.
- 3- phenytoin
- 4- thiopentone

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o Control of hypertension:-
1- hydralazine : 5mg intravenous repeated every 20 min
to a maximum cumulative dose 20 mg.
2- labetolol :- 40mh I.V escalated to 40, 80 every 10
min to cumulative dose of 300mg
3- diazoxide (300mg).
- Maintenance of fluid, electrolytes and acid- base
balance by monitoring CVP, urea electrolytes and
blood gases
- Monitoring of Hb, platelets count, transaminases and
coagulation profiles

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o Delivery of fetus:-
o The definitive treatment of eclampsia is delivery
o Attempts to prolong pregnancy in order to improve
maturity are unlikely to be of value.
o However it is in appropriate to deliver an unstable
mother even if there is fetal distress.
o Once seizures are controlled, severe hypertension
treated and hypoxia corrected delivery can be
expedited

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o Vaginal delivery should be considered but caesarean
section is likely to be required in PG remote from
term with an unfavorable cervix.
o After delivery high dependency cares should be
continued for a minimum of 24 hours
o Treatment of complication.

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 Prophylaxis :-
o Regular and efficient ANC is the best weapon in
prevention early detection and reduction of the
hazards of Pre-eclampsia
o Reduction of sodium is of no benefit