Hypertension in pregnancy

Hypertension in pregnancy
Dr-Rashna Sharmin Juthi
MBBS
Eastern Medical College and Hospital

Introduction
Hypertension is one of the most common complication
during pregnancy
Increased maternal and perinatal morbidity and
mortality
It is a sign of an underlying pathology that may be pre-
existing or appears for the first time during pregnancy
that is why it is also called asTOXEMIA OF PREGNANCY
Journals of the American college of obstetricians and gynecologists
Module of dr. Ayeshwara Ravindra Kaur
ASH position article

Hypertension
Blood pressure of 140/90 mmHg or more or an increase of 30 mmHg
in systolic and/or 15 mmHg in diastolic blood pressure over the pre-
or early pregnancy level.
DC Dutta`s textbook of obstetrics 8th edition, p- 255

Incidence
6% to 8% of all the pregnancies
Complicates 10-20% of pregnancies
District I ACOG Medical Student Education Module 2011

Prevalence
Hypertensive disorders during pregnancy occur in women with
preexisting primary or secondary chronic hypertension, and in
women who develop new-onset hypertension in the second half
of pregnancy
The present study was undertaken to study the prevalence and
correlates of hypertension in pregnancy in a rural area

Prevalence (cont.)
• A total of 931 pregnant women were included in the
present study. Prevalence of hypertension in pregnancy
was found to be 6.9%. Maternal age ≥25 years,
gestational period ≤20 weeks, history of cesarean section,
history of preterm delivery, and history of hypertension in
previous pregnancy were found to be significantly
associated with prevalence of hypertension in pregnancy

Risk Factors for
Hypertension in Pregnancy
Nulliparity
Pre-eclampsia in a previous pregnancy
Age >40 years or <18 years
Family history of pregnancy-induced hypertension
Chronic hypertension
Chronic renal disease
Anti-phospholipid antibody syndrome or inherited
thrombophilia

Vascular or connective tissue disease
Diabetes mellitus (pre-gestational and gestational)
Multi-fetal gestation
High body mass index
Male partner whose previous partner had preeclampsia
Hydrops-fetalis
Unexplained fetal growth restriction
Risk Factors for
Hypertension in Pregnancy (cont.)

Classification of Pregnancy induced
hypertension
According to national high blood pressure education program
2000 and ACOG-2013
1. Chronic hypertension
2. Pre-eclampsia
3. Chronic hypertension with superimposed pre-eclampsia and
eclampsia
4. Gestational Hypertension
5.Transient Hypertension
The Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation andTreatment of High Blood Pressure

Classification (cont.)
6. HELLP syndrome-
a. Hemolysis (H)
b. Elevated liver enzymes (EL)
c. Low platelet count (LP)
7. Eclampsia
8. Superimposed pre-eclampsia or eclampsia
9. Proteinuria
DC Dutta`s textbook of obstetrics 8th edition, p-255

Chronic hypertension in pregnancy
 The presence of hypertension of any cause antedating or before the
20th week of pregnancy beyond the 12 weeks after delivery
 Women with CH are low risk and have satisfactory maternal and fetal
outcome without any hypertensive therapy by life-style modification
 With life-style modification, aerobic exercise should be restricted based
on theoretical concerns.
 Risk factors:
 Age (>40 years)
 Duration of hypertension (>15 years)
 Level of BP (>160/110 mm of Hg)
 Presence of any medical disorder
 Presence of thrombophilias

Effect of Chronic Hypertension on Pregnancy
Maternal:
superimposed pre-eclampsia/
eclampsia in 15-20% of cases
Foetal:
Intrauterine growth
retardation.
Intrauterine foetal death.
module of dapinderjit gill, rose university

Prenatal Care for Chronic Hypertensives
 Electrocardiogram should be obtained in women with long-
standing hypertension.
 Baseline laboratory tests
Urinalysis, urine culture, and serum creatinine,
glucose, and electrolytes
Tests will rule out renal disease, and identify
comorbidities such as diabetes mellitus.
Women with proteinuria on a urine dipstick should
have a quantitative test for urine protein
The American college of obstetricians and gynocolists

Treatment
General and medical treatment
As pre-eclampsia regarding the following:
 Rest
 Antihypertensives
 Observation
DC Dutta`s textbook of
obstetrics 8th edition, p- 277

Definition
It is a multisystem disorder of unknown etiology characterized by
development of hypertension to the extent of 140/90 mm of Hg or
more with proteinuria after the 20th week in a previously
normotensive and non-proteinuric women

Incidence:
In hospital:
varies widely from 5% to 15%
The incidence in primi-gravidae is about 10% and in multi-gravidae is
5%
More common in women with chronic hypertension, with an incidence
of approximately 25%
DC Dutta`s textbook of obstetrics 8th edition,p-256

Pre-disposing factors
Primigravidae more than multi-gravidae.
Pre-existing hypertension.
Previous pre-eclampsia.
Family history of pre-eclampsia.
Hyperplacentosis i.e. excessive chorionic tissue as in hydatidiform
mole, multiple pregnancy, uncontrolled diabetes mellitus and foetal
haemolytic diseases.
Obesity.
New paternity
Thrombophilias
DC Dutta`s textbook of obstetrics 8th edition.p-256

Pathophysiology
The uteroplacental bed
Immunological factor
Genetic factor
Renin- angiotensin system
Atrial natriuretic peptide (ANP)
Prostaglandins
Neutrophils

Diagnostic criteria:
- Hypertension
- Edema
- Proteinuria
Categories
Mild Preeclampsia
Severe Preeclampsia

Clinical features:
Symptoms:
Mild:
slight swelling over the ankle
Gradually swelling may be extend to the face, abdominal wall, vulva
even the whole body.
Alarming:
Headache
Disturbed sleep
Diminished urinary output
Epigastric pain
Eye symptoms- blurring, scotomata, dimness of vision or at times
complete blindness.Vision usually regained within 4-6 weeks following
delivery.

Signs:
Abnormal weight gain
Rise of blood pressure
Edema
There is no manifestation of chronic cardiovascular or renal
pathology
Pulmonary edema
Abdominal examination my reveal evidences of chronic
placental insufficiency such as scanty liquor or growth retardation
of the fetus

Investigations:
Urine:
24 hours urine collection for protein measurement is done.
Urine become solid on boiling (10-15 g/L)
A few hyaline cast, epithelial cells or few red cells.
Ophthalmoscopic examinations:
In severe cases- retinal edema, constriction of arterioles,
alteration of normal ration of vein, nicking the veins,
hemorrhage.

Blood values:
Serum uric acid level >4.5
mg/dl indicates presences of
pre-eclampsia
Blood urea level remains
normal
Abnormal coagulation
profile
Raised hepatic enzyme
levels
Antenatal fetal monitoring:
Done by clinical examination
Daily fetal kick count
USG of fetal growth
Liqour pockets
Cardiotocography
Umbilical artery flow
velocimetry
Bio-physical profile

Complications
Immediate:
Maternal:
 During prengnancy:
a. Eclampsia (2%)
b. Accidental hemorrhage
c. Oliguria and anuria
d. Dimness of vision even blindness
e. Pre-term labour
f. HELLP syndrome
g. Cerebral hemorrhage
h. Acute respiratoy distress syndrome
(ARDS)
 During labour:
a. Eclampsia
b. Post partum hemorrhage (PPH)
 Puerperium:
a. Eclampsia
b. Shock
c. Sepsis

Fetal:
a. Intrauterine death (IUD)
b. Intrauterine growth
retardation (IUGR)
c. Asphyxia
d. prematurity
Remote:
a. Residual hypertension
b. Recurrent pre-eclampsia
c. Chronic renal disease
d. Risk of placental abruption

Prediction
No screening test is really helpful
Various screening methods are:
Diastolic notch at 24weeks by Doppler ultrasonography
Absence or reversal of end diastolic flow
Average mean arterial pressure ≥ 90 mmHg in second trimester
Infusion test: angiotensin infusion required to raise the blood
pressure >20 mm Hg from baseline
Roll over test:
Rise in blood pressure >20 mmHg from baseline on turning supine at
28-32 weeks gestation is positive

General measures:
Maternal
Blood pressure twice daily
Urine volume and proteinuria
daily
Oedema daily
Body weight twice weekly
Fundus oculi once weekly
Blood picture including platelet
count, liver and renal functions
particularly serum uric acid on
admission
Daily foetal movement count
Serial sonography
Non-stress and stress test if
needed
Observation
Fetal

Medical treatment
Antihypertensives:
Decrease the maternal cerebral and cardiovascular complications but do
not affect the foetal outcome
Alpha-methyl-dopa:
It reduces the central sympathetic drive
Dose: 250-500 mg every 6-8 hours up to a maximum dose of 4 gm/day. Its
effect appears after 48 hours
A loading single dose of 2 gm may act within 1-2 hours
Side effects: headache, athenia and nightmares

Medical treatment (cont.)
Hydralazine:
It is a vasodilator, increases renal and uteroplacental blood flow
Dose: 20 mg slowly IV initially followed by 5mg every 20 min. until
diastolic blood pressure is 100-110 mmHg.This regimen is used for
severe and acute hypertension. Oral hydralazine can be used in the
chronic situation as a second line treatment in a dose of 25-75 mg/ 6
hours
Side effects: tachycardia, headache, flushing, nausea and vomiting
Calcium channel blockers (Nifedipine):
It is a vasodilator acting by blocking the Ca influx into smooth muscle
cells
It can be given sublingually (acts within 10 minutes) or orally (acts
within 30 minutes) in a dose of 10-20 mg 2-3 times daily
The higher the starting blood pressure the greater is the hypotensive
effect.
Side effects: headache and flushing

Prophylactic
Proper antenatal care:
To detect the high risk patients who may develop PIH through the
screening tests
Early detection of cases who have already developed PIH and
examine them more frequently
Low dose aspirin:
It inhibits thromboxane production from the platelets and the AII
binding sites on platelets
A low dose (60 mg daily) selectively inhibits thromboxane due to
higher concentration of such a low dose in the portal circulation
than systemic affecting the platelets when they pass through the
portal circulation.The Prostacyclin production from the systemic
vessels will not be affected
DC Dutta`s textbook of obstetrics 8th edition,p-265-66

Curative
Delivery of the foetus and placenta is the only real treatment of pre-
eclampsia. As the conditions are not always suitable for this, the
treatment aims to prevent or minimize the maternal and foetal
complications till reasonable maturation of the foetus.

Obstetric measures
Timing of delivery
Method of delivery
Intrapartum care
Postpartum care

Obstetric measures
Timing of delivery:
Severe pre-eclampsia is usually treated conservatively till the end of
the 36th week to ensure reasonable maturation of the foetus.
Indications of termination before 36th week include:
1. Aggravation of pre-eclamptic features
2. Hypertension persists
3. Acute fulminating pre-eclampsia
4. Tendency of pregnancy to overrum the expected date

Method of delivery
Vaginal delivery may be commenced in vertex presentation by:
Amniotomy + oxytocin if the cervix is favorable
Prostaglandin vaginal tablet (PGE2) if the cervix is not favorable
Caesarean section is indicated in:
Foetal distress
Late deceleration occurs with oxytocin challenge test
Failure of induction of labour
Other indications as contracted pelvis, and malpresentations

Intrapartum care
Close monitoring of the foetus is indicated
Proper analgesia to the mother
Anti-hypertensives may be given if needed
2nd stage of labour may be shortened by forceps

Postpartum care
Methergin (Ergometrine) is better avoided as it may increase the blood
pressure
Continue observation of the mother for 48 hours
Anti- hypertensive drugs are continued in a decreasing dose for 48 hours

Prevention of preeclampsia
• Identification of high-risk women
• Close clinical and laboratory monitoring aimed at its early
recognition
• Institution of intensive monitoring or delivery when indicated.

Note
Imminent eclampsia: It is a state in which the patient is about to
develop eclampsia. Usually there are:
Blood pressure much higher than 160 /110 mmHg
Heavy proteinuria (+++or ++++)
Hyperreflexia
Severe continuous headache
Blurring of vision
Epigastric pain
Fulminating pre-eclampsia: a rapidly deteriorating pre-eclampsia to
be imminent eclampsia

Chronic hypertension with
superimposed pre-eclampsia or
eclampsia
The common cause of chronic hypertension:
- Essential hypertension
- Chronic renal disease
- Coarctation of aorta
- Endocrine disorders (DM, pheochromocytoma,
thyrotoxicosis)
- Connective tissue disease (SLE)
Criteria for diagnosis of superimposed pre-eclampsia:
- New onset of proteinuria >0.5 g/24 hours specimen
- Aggravation of hypertension
- Development of HELLP syndrome
- Development of headache scotoma, epigastric pain

Gestational hypertension
A sustained rise of blood pressure to 140/90 mm of Hg or more on
at least two occasions 4 or more hours apart beyond the 20th week
of pregnancy or within the first 48 hours of delivery in a previously
normotensive women

Gestational hypertension (cont.)
It should fulfill the following criteria:
- Absence of any evidences for the underlying cause of hypertension
- Generally unassociated with other evidences of pre-eclampsia (edema
or proteinuria)
- Majority of cases are more than or equal to 37 weeks of pregnancy
- Generally not associated with hemo-concerntation or
thrombocytopenia, raised serum uric acid level or hepatic dysfunction
-The blood pressure should come down to normal within 12 weeks
following pregnancy

Gestational hypertension:
Pathophysiology
Cardiovascular effects
Elevated BP
Increased cardiac output
Hematologic effects
Third spacing of fluid due to increased blood
pressure and decreased plasma oncotic
pressure
Renal effects
Atherosclerotic like changes in renal vessels
(glomerular endotheliosis)  decreased
glomerular filtration rate and proteinuria
Uric acid filtration is decreased

Pathophysiology (cont.)
Neurologic effects
Hyper-reflexia/hypersensitivity (does not correlate with
severity of disease)
In severe cases, grand mal seizures
Pulmonary effects
Pulmonary edema may occur due
to decreased colloid oncotic pressure
Fetal effects (severe gestational HTN)
Vasospasm  Decreased intermittent placental perfusion 
IUGR, oligo-hydramnios, low birth weight

Mechanisms
Uterine vascular changes
Trophoblastic-mediated vascular changes  decreased
musculature in spiral arterioles  development of low
resistance, low pressure, high-flow system
Inadequate maternal vascular response
Endothelial damage is also noted within the vessels
Hemostatic changes
Increased PLT activation with increased endothelial fibro-nectin
and decreased anti-thrombin III and alpha-2-antiplasmin 
further endothelial damage is thought to promote further
vasospasm

Mechanisms
Changes in prostanoids
During pregnancy, both PGI2 (vasodilation and decreased PLT
aggregation) andTXA2 (vasoconstriction and PLT aggregation)
are increased with balance favored to PGI2
In preeclampsia,TXA2 is favored
Changes in endothelium-derived factors
Decrease in Nitric oxide  promoting vasoconstriction

Transient Hypertension
• Retrospective diagnosis
• BP normal by 12 weeks postpartum
• May recur in subsequent pregnancies
• Predictive of future primary hypertension

HELLP Syndrome
He-hemolysis
EL-elevated liver enzymes
LP-low platelets
DC Dutta`s textbook of obstetrics 8th edition,p- 258

HELLP Syndrome (cont.)
Is a variant of severe preeclampsia
Platelets < 100,000
LFT’s - 2 x normal
May occur against a background of what appears to be
mild disease

Management of HELLP syndrome:
Immediate hospitalisation
Stabilise mother
Antihypertensive
Anti-seizure prophylaxis
Correct coagulation abnormalities
Assess foetal condition- FHR, Doppler ultrasound,
biophysical profile

Definition
Pre-eclampsia when complicated with grandmal seizures
(generalized tonic clonic seizures) and/or coma is called eclampsia

Incidence and prevalence
•0.1- 5.5 per 10,000 pregnancies
•Decreasing incidence with time
•Antepartum(50%): mostly in third trimester
•Intrapartum (30%):
•Postpartum(20%): usually within 48hours, fits beyond
7days generally rules out eclampsia

Risk factors:
• Maternal age less than 20 years
• Multigravida
• Molar pregnancy
•Triploidy
• Pre-existing hypertension or renal disease
• Previous severe Preeclampsia or Eclampsia
• Nonimmune hydrops fetalis
• Systemic Lupus Erythematosus

Clinical Features
Eclamptic convulsions are epileptiform and consist of four stages
• Premonitory stage: twitching of muscles of face, tongue, limbs
and eye. Eyeballs rolled or turned to one side
•Tonic stage: opisthotonus, limbs flexed, hands clenched
• Clonic stage: 1-4 min, frothing, tongue bite, stertorous
breathing
• Stage of coma: variable period

Pathogenesis:
Loss of normal cerebral auto regulatory mechanisms cerebral
hyperperfusion leading to Edema & ↓cerebral blood flow.

Diagnosis:
Lab Investigations:
• Complete Blood Count
• Platelet count
• LFT
• RFT
• Urine analysis
• Serum electrolytes
• Peripheral blood smear
• Prothrombin time
• Type and screen antibody if present
• Angiotensin II test: a dose of 8mk/kg/body weight to increase
Diastolic Blood pressure by 20 mm of Hg is taken as positive

Differential diagnosis
Epilepsy
Hysteria
Encephalitis
Meningitis
Puerperal cerebral thrombosis
Poisoning
Cerebral malaria
Intracranial tumor

Management
 Control Hypertension
 Improve intravascular volume
 Prevent convulsions
 Prevent complications
 Deliver viable fetus

Control Hypertension:
Most commonly, for acute control:
 Hydralazine
 Labetalol
 Nifedipine may be used, but unexpected hypotension may occur
when given with MgSO4
 For refractory hypertension: nitroglycerin or nitroprusside may be
used
 Nitroprusside dose and duration should be limited to avoid fetal
cyanide toxicity
 Usually require invasive arterial pressure monitoring
 Angiotensin-converting enzyme (ACE) inhibitors contraindicated
due to severe adverse fetal effect

Improve intravascular volume:
Main aim is to increase CVP & PCWP range 4-6 cm H2O & 5-10
mm HG and to increase urine output to 1 ml/kg/hr.
There is a controversy between colloid and crytalloid as both
complicates the condition causing low colloid oncotic
pressure and leaky capillary predisposing them to risk of non-
carcinogenic pulmonary oedema
Fluid recommendation: crystalloids to be administered at
the rate of 1-2 ml/kg/hr. and alternating according to CVP,
PCWP and Urine Output.

Seizure Prophylaxis &Treatment: Magnesium
sulphate therapy. Magnesium sulfate has many
effects; its mechanism in seizure control is not clear.
It is an NMDA (N-methyl-D-aspartate) antagonist
vasodilator
Brain parenchymal vasodilation demonstrated in
preeclamptics by Doppler ultrasonography increases
release of prostacyclin

Potential adverse effects:
• Toxicity from overdose (respiratory, cardiac)
• Bleeding
• Hypotension with haemorrhage
• Uterine contractility
Renally excreted
Preeclamptics prone to renal failure
Magnesium levels must be monitored frequently either clinically
(patellar reflexes) or by checking serum levels for 6-8 hours

Treatment of magnesium toxicity:
- Stop MgSO4
- IV 1 g 10% calcium gluconate slow
- Administer Oxygen
- Secure airway
- Ventilation

Anaesthetic Implication:
MgSo4 potentiate and prolongs both actions of depolarizing and
non-depolarizing Muscle relaxants. Intubating dose of
succinylcholine should not be decreased as onset and duration of
action of single dose does not alter in preeclamptic patients. NDMR
when used neuromuscular monitoring with peripheral nerve
stimulation and dose titration should be done accordingly.
DC Dutta`s textbook of obstetrics 8th edition

Various Regime of Magnesium
Therapy
• Pritchard Regime:
- Loading dose: 4g (20 ml of 20%) MgSo4 IV over 4 min. immediately
followed by 10g (20 ml of 50%) IM i.e. 5 gm in each buttocks
- If convulsion persists after 15 min 2 g IV over 2 min
- Maintenance dose: 5g IM every 4 hours alternate side
• Zuspan or Sibai regime:
- Loading dose: 6 g IV over 20 min
- Maintenance dose: 2-3 g/hr. IV every 6 hr

Treatment of Eclampsia:
Seizures are usually short-lived.
• If necessary, small doses of barbiturate or benzodiazepine
(STP, 50 mg, or midazolam, 1-2 mg) and supplemental oxygen
by mask
• If seizure persists or patient is not breathing, rapid sequence
induction with cricoid pressure and intubation should be
performed
• Patient may be extubated once she is completely awake,
recovered from neuromuscular blockade, and magnesium
sulfate has been administered
The American college of obstetricians and
gynocolists

Superimposed pre-eclampsia or eclampsia
Occurrence of new onset of proteinuria in women with chronic
hypertension
Risk factors:
Renal insufficiency
History of hypertension for 4 years or more
Hypertension in previous pregnancy

Proteinuria (albuminuria)
It is urinary protein greater than 0.3gm/L in 24 hours
collection or greater than 1gm/L in two random samples
obtained at least 6 hours apart
It indicates glomerular damage and almost always occurs
after hypertension
Proteinuria is usually in the range of 1-3 gm daily, of
which 50-60% is albumin but in severe cases it may
exceed 15gm

Treating hypertension during
lactation
Hypertensive mothers can usually breast-feed safely.
Antihypertensive drugs are excreted into human breast milk.
Therefore, in mothers with stage 1 hypertension who wish to
breast-feed for a few months, it might be prudent to withhold
antihypertensive medication, with close monitoring of BP, and
reinstitute antihypertensive therapy following discontinuation of
nursing. No short-term adverse effects have been reported from
exposure to methyldopa or hydralazine. Propanolol and labetalol
are preferred if a beta-blocker is indicated. ACEIs and ARBs
should be avoided, based on reports of adverse fetal and
neonatal renal effects. Diuretics may reduce milk volume and
thereby suppress lactation. Breast-fed infants of mothers taking
antihypertensive agents should be closely monitored for
potential adverse effects.

Hypertension in pregnancy

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