Kufa university

medical collage

Hypertensive Disorder
of Pregnanc
Presented by
Dr. nada alibrahim
Gyae. & obs
:

Hypertensive disorders of pregnancy

o Hypertensive disorders in pregnancy are a major

cause of maternal and fetal mortality.
o Hypertensive disease complicates 5-7 per cent of all
pregnancies.
o Definition of hypertension:-

-Hypertension is defined as:

o Systolic BP 140 over diastolic BP 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.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

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-

◻ Clasification of hypertension disorder in pregnancy.it

is important because fetal and maternal
complication differ according to the types.

◻ But the management and follow up the same for all

types

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1) GESTATIONAL HYPERTENSION

Onset of Hypertension without proteinuria arising for

the first time after 20 week of gestation with
resolution to baseline by 12 week postpartum .

2-GESTATIONAL protein urea with out

hypertension rare

 3-pre-eclampsia
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.
4-)Pre existing Chronic hypertension with or without renal disease:-

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.

.

5) Chronic hypertension superimposed by pre-

eclampsia

proteinuria ,or other symptoms &signs of pre-

eclampsia developing for the first time in pregnancy
in a women with a chronic hypertension.
GESTATIONALHYPERTENSION

1-more in multi than primigravid

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.
.

 pre- eclampsia

- It is a multi system disease specific to pregnancy in

human.
- Affecting 15%
of PG and
7%multigravida .

o Risks factors for preeclampsia 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 diabetes6--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.
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PIH is almost entirely a disease of primigravidae.

◻ Pre-eclampsia only occurs in multigravid women under the

following conditions:
◻ Those who have had it severely in the first pregnancy.

◻ Those who have changed their partner between

pregnancies.
◻ Pregnancies complicated by hydatidiform mole.

◻ Multiple pregnancies.

◻ Gestational diabetes.

◻ Those with antiphospholipid syndrome.

◻ Those with family history.

Fact about the disease
◻ unknownAetiology:it is adisease of thoeries.
◻ It is disease of primigravida.

◻ It is multi systemic disorder.

◻ Antenatal care can reduce the incidence of disease.

◻ It is progressive disorder.

◻ Definitive treatment termination of pregnancy.

It is progressive disorder.
◻ Prevent Blood pressure >160/105 which may prevent
complications to the mother for example cerebral
hemorrhage

◻ It has not been shown that it is possible to prevent the

development of preeclampsia

◻ It has not been shown that it is possible to improve the

fetomaternal circulation and growth of the baby.
Aetiology of pre-eclampsia:-
- 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
 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.
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.
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
o Coagulation:-
- Increasingly generalized endothelial damage
commonly causes slight intravascular coagulation.
- Disseminated intravascular coagulation (DIC) is rare
but serious complication
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 infaction.
- 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.

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Complication of pre-eclampsia:-

A- feto- placental
- Abruptio placenta
- IUGR
- IUFD
- Preterm labour

B- maternal complication:-
○ Eclampsia
○ Pulmonary oedema:
--- secondary to hypertension
---Adult respiratory distress syndrome

- --- 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
:

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

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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.
- -impaired renal and liver function (HELLP syndrom
- -Aprubtio placentea.
- -Eclamptic fit
- 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
-
 - 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.

Pathology of Eclampsia:-
Is thought to involve cerebral vasospasm leading to ischaemia, disruption of the blood brain
barrier

neurological complications may include coma focal motor

deficits and cortical blindness.
Differential Diagnosis:-
o CVA
o Amniotic fluid embolism
o Water intoxication
o Meningitis
o Cerebral malaria www.doctor.sd
- 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
Antenatal manangement
- 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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Management of pre-eclampsia:-

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

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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
- 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

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

- 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(oraly,parantral)
- 4- labetolol (100—200mg)
- has both Beta and alfa adrenoceptor blocking
action
- 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.
- Management of imminent eclampsia and
Eclampsia:

- Quiet roo
- Left lateral position, secure air way, oxygen,catheter
for input and output.
- Control of fits with anticonvulsants :
- 1- diazpam dose 10mg I.V in 4min. Safe- immediate
action, but it has short action& can sedate the fetus &
the patient
- Magnezium sulphate: is the drug of first choice it i
- - Anti convulsant ,Antihypertensive and tocolytic with
prolong action.
Also have neuroprotective effect on fetus
m

- 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..
- Toxic effect include hypotension and respiratory
failure.
- Antidote is Calcium. gluconate.
3- phenytoin
4- thiopentone
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).
Farther mamegemen
- Maintenance of fluid, electrolytes and acid- base
balance by monitoring CVP, urea electrolytes and
blood gase
- Monitoring of Hb, platelets count, transaminases and
coagulation profiles
s

◻ Prophylaix anticoagulation like inoheparin

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 o Delivery of fetus:

o The definitive treatment of eclampsia is deliver

o

o Once seizures are controlled, severe

hypertension treated and hypoxia corrected
delivery can be expedited
.

o Vaginal delivery should be considered but

caesarean section is likely to be required in PG
remote from term with an unfavorable cervix
o Or other obestatric indication
o After delivery high dependency cares should be
continued for a minimum of 24 hours because
risk of complication .

○ Prophylaxis :-

o Regular and efficient ANC is the best weapon in prevention early

detection and reduction of the hazards of Pre-eclampsi
o Low dose of aspirin
Reduction of sodium is of no benefit
Women with a low dietary intake of calcium given calcium
supplements at a dose of at least g before and during
pregnancy can halve their risk of developing pre-
eclampsi
.
.

Select correct answer

◻ 1- Pre-eclampsia is more common in except:
◻ Multigravid women.
◻ Women with congenital cardiac disease.
◻ Multiple pregnancy.
◻ Women with diabetes insipidus.
◻ Women with pre-existing renal disease.
◻ 2- all steps of treatment of sever pre-eclampsia correct excepts :
◻ Hospital admission.
◻ labetolol.
◻ Early delivery.
◻ Frusemide

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3- 30 years old primigravida 36 weeks her blood
presure 160/110 and urinary protien is 3++ her
platlet count 8000/mm3 what be the management?
◻ a-magnisium sulfat.

◻ b-labetalol.

◻ C-urgent L.S.C.S

◻ D-labour induction.

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4-Which of the following not important in diagnosis of
preeclampsia
◻ A hypertension

◻ B protienurea

◻ C convulsion

◻ D leg oedema

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5-Indicator of sever preeclampsia
◻ A-I.U.G.R

◻ B-Diastolic BP>110.

◻ C-pulmonary oedema.

◻ D-oligurea

◻ E-all of above

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Preterm delivery in preeclampsia indicated in
◻ A-diaystolic BP>110mmHg despite the adequat use
of antihypertensive drug.
◻ B-laboratory evidence of end organ involment
despit good blood pressure control.
◻ C- platlate count between 5000and 10000/mm3.

◻ D-elevated liver enzymes.

◻ E-all of above.

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Thank
you