HYPERTENSIVE DISORDERS IN PREGNANCY

INTRODUCTION

Hypertension is one of the commonest medical complications of the pregnancy and

contributes significantly to the maternal and perinatal morbidity and mortality. Hypertension
is a sign of an underlying pathology, which may be re-existing or appears for the first time
during pregnancy. The identification of this clinical entity and effective management play a
significant role in the outcome of pregnancy, both for the mother and baby.

DEFINITION

Hypertension is characterised by increase in blood pressure more than or equal to

140/90 mm Hg measured two times with at least 6 hours interval.

CLASSIFICATION OF HYPERTENSIVE DISORDERS IN PREGNANCY

S.No TYPES DESCRIPTION

Pregnancy Induced
1
Hypertension
Development of hypertension and proteinuria
1. Preeclampsia in previously normotensive patient after 20
wks of gestation
Development of convulsion or coma in
2. Eclampsia
preeclamptic patients
Development of hypertension after 20 wks of
3. Gestational hypertension gestation in previously normotensive patient
without proteinuria
Known hypertensive before pregnancy or
2 Chronic hypertension hypertension diagnosed first time before 20
wks of pregnancy

PREGNANCY INDUCED HYPERTENSION

DEFINITION

The hypertension develops as a direct result of the gravid states. The woman does not
have a history of previous hypertension

CLASSIFICATTION

The clinical types of PIH are:

1. Preeclampsia
2. Eclampsia
3. Gestational hypertension
 PREECLAMPSIA

DEFINITION

Preeclampsia is a multisystem disorders of unknown etiology characterized by

development of hypertension to the extent of 140/90 mmHg or more with proteinuria after the
20th week in a previously normotensive and non proteinuric woman.

INCIDENCE

The incidence of preeclampsia in hospital practice varies from 5-15%. The incidence
in primigravida is about 10% and in multigravida 5%.

CLINICAL CLASSIFICATION OF PREECLAMPSIA

MILD PREECLAMPSIA SEVERE PREECLAMPSIA

Diastolic blood
90-110mmHg 110 mmHg
pressure
Proteinuria 0.3-4 g/24hr 5 g/24hr
Dipstick 1+ 2+
Urinary output >30ml/hr <20 ml/hr
Reflexes Normal Hyperreflexia
Pulmonary edema Absent Present
Epigastric pain Absent Present
Cerebral or Visual
Absent Present
disturbances
HELLP syndrome Absent Present

RISK FACTORS

Young or elderly primigravida

Elevated body mass index (Obesity BMI >35 kg/m2 )
Family history of hypertension & family obstetrical history of preeclampsia
Previous history of preeclampsia

Placental abnormalities

Antiphospholipid antibody syndrome

Diabetes mellitus
Multiple gestation
Chronic renal disease
Pre-existing vascular disease

ETIOLOGY
The causes of preeclampsia remains unknown.
Failure of trophoblast invasion (abnormal placentation)
Vascular endothelial damage
 Inflammatory mediators (cytokines)
Immunological intolerance between maternal and fetal tissues.
Coagulation abnormalities
Increased oxygen free radicals
Imbalance of angiogenic and anti angiogenic proteins
Genetic predisposition (polygenic disorder)
Dietary deficiency or excess

IN NORMAL PREGNANCY
To understand the pathophysiology of preeclampsia the nurse should be familiar with
the normal physiologic changes of pregnancy.
Angiotensin II is destroyed by angiotensinase, which is liberated from the placenta.
Thus the blood pressure is stabilized.
The vascular system becomes refractory, selectively to pressoor agent angiotensin
II. This is probably brought out by vascular synthesis of prostaglandin I2 and Nitric
oxide (NO) which has got vasodilator effect. The interaction between the two
systems stabilizes the blood pressure in normal pregnancy.
Vascular endothelial growth factor (glycoprotein) which restores the uteroplacental
blood flow to normal level.

PATHOPHYSIOLOGY

Risk factors/etiological factors

Genetic
Nutritional
Immunological

Deficient trophoblast invasion

Shallow
Failed endovascular remodelling
Thrombosis

Placental injury / stress

Ischemia
Oxidative stress
Overgrowth / undergrowth

Circulating toxin causes endothelial damage

Antiangiogenic Factor (tyrosine kinase &
endoglin)
Inflammatory mediators cytokines,
interleukins
Free radicals (abnormal lipid metabolism)
 Damaged endothelial cells releases
vasoconstrictive agents
Thromboxane (TXA2 )
Increased vascular sensitivity to pressor
agent angiotensin II
Endothelin I
Deficiency of nitric oxide & PGI2

Development of hypertension
Vasospasm
Capillary leak
DIC

End-organ injury
Proteinuria
Hepatic injury
IUGR / Abruption
Seizures

CLINICAL FEATURES
1. The diagnosis of a new onset of hypertension during pregnancy is based on atleast
two measurements at least 4 to 6 hours apart
The systolic blood pressure is 140 mmHg or greater on any one occasions
The diastolic blood pressure is 90 mmHg or greater on two occasion 6 hours apart
The mean arterial pressure is 105 mmHg or greater
Women must be in upright of left lateral recumbent position with arm at heart
level
2. Proteinuria
3. With or without generalized edema
WARNING SIGNS
Systolic BP 160 mmHg or diastolic BP 110 mmHg
Severe headache
Visual disturbances/blurred vision
Diminished urine output (400ml/24hrs)
Rapid weight gain 2kg/month
Generalized edema over ankles, face, abdominal wall, vulva and even whole body
that is not responsive to 12 hours of bed rest.
 Epigastric pain
Pulmonary edema or cyanosis

DIAGNOSIS

1. History collection medical history includes presence of DM, renal disease and
hypertension. Family history of DM and other chronic conditions. Family obstetrical
history of preeclampsia. Also collect information about the womans support system,
nutritional status, cultural beliefs, activity level and lifestyle behaviours. Review the
systems is important to note whether the woman is having unusual, frequent or severe
headaches, visual disturbances or epigastric pain and abnormal pattern of weight gain
and increased signs of edema.

2. Physical examination

Assess and record BP measurement in standardized manner

Observation of edema distribution, degree and pitting and sites of edema
Assess for epigastric pain and oliguria
Assess respirations for crackles indicates pulmonary edema
Assess deep tendon reflexes
Opthalmic examination for retinal edema, constriction of arterioles of retinal
haemorrhage
Determination of fetal status - assess daily fetal movement count (DFMC),
FHR by Doppler.

3. Laboratory tests
Complete blood count - Haemoglobin level (), haematocrit,
Platelets(<100000/mm3), Prothrombin time(PT), Partial prothrombin
time(PTT), Fibrinogen level (300-600 mg/dl), Blood urea nitrogen (),
Creatinine ( 1.2mg/dl), Uric acid (5.9mg/dl), Liver enzymes (LDH, AST &
ALT), Blood glucose level.
Urine examination - Output atleast 30 ml/hr or 120 ml/4hr.. 24 hr urine
collection reflect the true renal status. Proteinuria is determined from dipstick
method (0-negative, 1+ - 30mg/dl, 2+ - 100mg/dl, 3+ - 300mg/dl, 4+ -
1000mg/dl)

4. Ultrasonography to assess the fetal growth and liquor level.

5. Cardiotocography to assess the fetal status.
6. Doppler flow velocimetry studies for evaluating maternal and fetal wellbeing

MANAGEMENT

The definite treatment for preeclampsia is the termination of pregnancy. The aim of
treatment is to continue the pregnancy if possible, without affecting the maternal prognosis
until the fetus become mature enough to survive in the extra uterine environment. If the
pregnancy far from the term, the treatment is continued with weekly assessment. If the
pregnancy at term the women is kept in the hospital until completion of 37 weeks. Those the
women does not responding to the treatment termination of pregnancy done irrespective of
the period of gestations.
Objectives are:
To stabilize hypertension and prevent its progression to severe preeclampsia
To prevent eclampsia and other complications.
To deliver a healthy baby in optimal time
To restore the health of the mother in puerperium
MEDICAL MANAGEMENT

Antihypertensive Therapy

Antihypertensive drugs have limited value in controlling blood pressure due to preeclampsia.
Indications are:
1. Persistent rise of blood pressure especially where the BP is over 140/90 mm Hg.
2. In severe preeclampsia to bring down the blood pressure during pregnancy and labour.
The common oral drugs used are

S.No DRUG MODE OF ACTION DOSE

Central and peripheral antiadrenergic

1. Methyl dopa 250-500 mg bd or tds
action

2. Labetalol Adrenoceptor antagonist 250 mg bd or tds

3. Nifedipine Calcium channel blocker 10-20 mg bd
4. Hydralazine Vascular smooth muscle relaxant 10-25 mg bd

Note: Magnesium sulphate is the drug of choice in the prevention or treatment of

convulsions caused by severe preeclampsia. The routine use of MgSO4 is indicated for
severe preeclampsia, eclampsia and HELLP syndrome.

SURGICAL MANAGEMENT
Indications for Caesarean section (LSCS) are
When an urgent termination is indicated and the cervix is unfavourable
Severe preeclampsia with a tendency of prolonged labour
Associated complicating factor CPD, malpresentations, elderly primi etc

NURSING MANAGEMENT

During pregnancy:
Monitoring of BP, morning urine dipstick protein estimation, daily fetal kick count
and weight checking.
 Rest - The woman should be in bed preferably in left lateral position as much possible
to lessen the effects of venacaval compression. Rest increases the renal blood flow
causing increased diuresis, increases the uterine blood flow causing improved
placental perfusion and reduces the blood pressure.
Diet - Omission of salty food and extra salt in the dish is desirable. Fluids need not be
restricted. Total calorie may be approximately 1,600 per day with about 100 gm
proteins.

During labour:
The patient should be in the bed
Liberal sedatives should given in the form of pethidine 75-100mg intramuscularly
between 4 and 7cm cervical dilatation.
Administer antihypertensive drugs as prescribed
Monitor BP hourly
Urinary output are to be noted. In severe preeclampsia patient should be
catheterized
Carefully monitor the FHR every 15mts
Labour duration is curtailed by low rupture of the membrane
Ergometrine should be avoided as it cause rise in blood pressure, Syntocinon IM
or slow IV can be used following the delivery of the anterior shoulder
The patient should be sedated immediately after delivery to prevent postpartum
eclampsia.

During puerperium:
Patient is watched closely for atleast 48hrs, the period during which convulsions
usually occur
Antihypertensive drugs should be continued if the BP is high. In breast feeding
women labetalol, nifedipine or enalapril can be used. Methyldopa should be voided
due to the risks of postpartum depression.
The patient should be in the hospital, till the blood pressure is brought down to a safe
level and proteinuria disappears

COMPLICATIONS
Mother
Eclampsia
Abruption placenta
Dimness of vision and even blindness
Preterm labour
HELLP syndrome
Cerebral haemorrhage
Pulmonary edema
Postpartum haemorrhage
Fetal
 Intrauterine death
IUGR
Asphyxia
Prematurity

PREVENTION
Avoid early marriage
Regular antenatal check up for early detection of rapid weight gain and tendency of
rising blood pressure.
Antithrombotic agents low dose aspirin 60 mg daily in beginning early in pregnancy
in potentially high risk patients.
Calcium supplementation reduces the risk of hypertension
Antioxidants Vitamin C,E & D are effective
Balanced diet rich in protein reduces the risk
 ECLAMPSIA

DEFINITION

Preeclampsia when complicated with grandma seizures (generalized tonic-clonic

convulsions) and or coma called eclampsia.

INCIDENCE
The incidence is ranges from 1 in 500 to 1 in 30. It is more common in primigravida
(75%), five times more common in twins than in singleton pregnancies and occurs between
the 36th week and term in more than 50% cases.

Onset of convulsion
It is more frequently beyond 36 weeks.
Antepartum 50% fits occur before the onset of the labour.it is difficult to differentiate
it from intrapartum fits.
Intrapartum 30% fits occur for the first time during labour
Postpartum 20% fits occur for the first time in the puerperium usually within 48
hours.
CAUSES OF CONVULSION
Cerebral irritation causes convulsion. The irritation may be provoked by 1. Anoxia
spasm of the cerebral vessels, which leads to increased vascular resistance and fall in cerebral
oxygen consumption and 2. Cerebral edema also contribute to the irritation. Also there is
excessive release of excitory neurotransmitters (glutamate).

PATHOPHYSIOLOGY
Since the eclampsia is a severe form of preeclampsia the histopathological and
biochemical changes are similar although intensified than those of preeclampsia.

CLINICAL FEATURES (STAGES OF CONVULSION)

Expect on rare cases an eclamptic patient always shows previous manifestation of
acute fulminating preeclampsia called premonitory symptoms.

Eclamptic convulsion or fitz consists of four stages

Premonitory stage: The patient becomes unconscious. There is twitching of the
muscles of the face, tongue, and limbs. Eye ball roll or are turned to one side and
become fixed. This stage lasts for 30 sec.
Tonic stage; The whole body goes into tonic spasm- the trunk opisthotonus, limbs are
flexed and hands clenched. Respiration ceases and the tongue protrudes between the
teeth. Cynosis appear. Eye balls become fixed. This stage lasts for 30 sec.
Clonic stage: All the voluntary muscles undergone alternate contraction and
relaxation . The twitching start in the face then involve one side of extremities and
ultimately the whole body involved in the convulsion. Biting of tongue occurs.
 Breathing is stertorous and blood stained frothy secretions fill the mouth. Cyanosis
disappears. This stage lasts for 1-4 min.
Stage of coma: Following the convulsion, the patient passes on the stage of coma. It
may last for a brief period or in others deep coma or may persist until another
convulsion. At times patient appears to be confused state and fails to remember the
happenings.

MANAGEMENT

GENERAL MANAGEMENT (Nursing Management)

Immediate care during convulsion
Patient is kept in a railed cot and a tongue blade is inserted between the teeth.
The patient should be in lateral position to prevent aspiration of vomitus and
supine hypotension syndrome.
Oral suctioning should be done to remove secretions
Oxygen is administered by face mask 8-10L/mt to improve oxygenation and
prevent respiratory acidosis
Oxygenation is monitored by pulsoximetry.
FHR should be checked every 15 mts
After convulsion
Once the patient is stabilized, a thorough but quick general, abdominal and
vaginal examinations are made.
A self retaining catheter is introduced and urine is tested for protein
Monitor hourly urine output
Monitor hourly pulse, respiration rate and blood pressure

MEDICAL MANAGEMENT

Name of the
Dose/Route Action Toxicity
medicine
MgSO4 Loading dose 4-6g It interferes with the Loss of deep
over 15-20mts/IV release of acetylcholine at tendon reflexes
Maintenance dose- the synapses, decreasing Decreased
2g/hr/IV CN irritability, depressing respiratory rate
Therapeutic MgSO4 cardiac conduction, Chest pain
level is 4-7mEQ/L induces cerebral Heart block
vasodilation
Labetalol 20mg /IV Adrenoceptor antagonist
Hydralazine 5-10mg/IV Vascular smooth muscle
relaxant
Furosemide 20- 40mg/IV Diuretics
Ceftriaxone 1 gm/IV Antibiotics
OBSTETRICAL MANAGEMENT
Assess the uterine activity, cervical status and fetal status, then proceed to labour

Less than 37 weeks Beyond 37 weeks

Corticosteroids
administered to
promote fetal lung Induction o labour
maturity
Fits controlled by oxytocin
Induction of labour infusion and ARM
after 48 hrs of steroid
therapy
If fits not controlled by anticonvulsants with
in 6-8hrs

Termination of pregnancy

Fits not controlled

Cervix Cervix not
favourable favourable

Induction of LSCS
Labour by ARM &
Oxytocin infusion

SURGICAL MANAGEMENT
Caesarean section is indicated when fits is not controlled, patient becomes
unconscious, poor scope for vaginal delivery and obstetrical indications such as
malpresentations, etc

COMPLICATIONS OF ECLAMPSIA
Injuries tongue bites, injuries due to falling out of bed.
Heart failure
Anuria
Hyperpyrexia
Psychosis
Fetal placental abruption, fetal distress & intrauterine death.

PREVENTION

In the majority of cases, eclampsia is preceded by a severe preeclampsia. Hence the

prevention of eclampsia rests on early detection, prophylactic anticonvulsant therapy and
effective institutional management with judicious termination of pregnancy. Adequate
sedation and or prophylactic anticonvulsant therapy soon after delivery in preeclampsia and
meticulous observation for 24- 48 hours are definite steps to prevent postpartum eclampsia.
 GESTAIONAL HYPERTENTION

Gestational hypertention is a substained rise of blood pressure to 140/90 mmHg or more on at

least two occasion, 4 or more hours apart beyond the 20th week of pregnancy or during the
first 24 hours after delivery in a previously normotensive woman.

Essential features of this condition are:

Absence of any evidence for the underlying cause of hypertention
Unassociated with other evidences of preeclampsia such as edema or proteinuria
The blood pressure returns to normal within 12 weeks following delivery.
Generally not associated with hemoconcentration or thrombocytopenia
The hypertention may be stress response.

Management includes antihypertensive drugs