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Hypertensive disorders in pregnancy

Hypertension is the most common medical problem encountered during pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during pregnancy are classified into 4 categories,

1) chronic hypertension, 2) preeclampsia-eclampsia, 3) preeclampsia superimposed on chronic hypertension, and 4) gestational hypertension (transient hypertension of pregnancy )

You can get online consultation from Dr Sarika Jaiswal – Gynecologist in Indore

Chronic Hypertension in pregnancy

Chronic hypertension is high blood pressure that either precedes pregnancy, is diagnosed within the first 20 weeks of pregnancy, or does not resolve by the 12-week postpartum checkup. Two categories of severity are recognised: mild (up to 179 mm Hg systolic and 109 mm Hg) and severe (≥ 180 systolic or 110 diastolic).

Chronic hypertension complicates about 5% of all pregnancies, and prevalence rates are increasing due to delayed childbearing.Complication rates are directly related to the severity and duration of elevated blood pressures. For instance, patients with severe hypertension in the first trimester have a greater than 50% risk of developing superimposed preeclampsia.

Gestational Hypertension

Gestational hypertension, formerly known as pregnancy-induced hypertension or PIH, is the new onset of hypertension after 20 weeks of gestation. The diagnosis requires that the patient have:

  • Elevated blood pressure (systolic ≥ 140 or diastolic ≥ 90 mm Hg,
  • Previously normal blood pressure
  • No protein in the urine
  • No manifestations of preeclampsia eclampsia

Also known as transient hypertension, gestational hypertension is actually diagnosed retrospectively when the patient does not develop preeclampsia and if blood pressure returns to normal by the 12-week postpartum visit. Fifty percent of women diagnosed with gestational hypertension between 24 and 35 weeks develop preeclampsia


Preeclampsia is a multi-organ disease process of unknown aetiologycharacterised by the development of hypertension and proteinuria after 20 weeks of gestation.

There are various theories of pathogenesis of preeclampsia. The most popular theory is immunologic.

During a normal pregnancy, fetal syncytial trophoblasts penetrate and remodel maternal spiral arteries, causing them to dilate into large, flaccid vessels. This remodelling accommodates the vast, increased maternal circulation needed for adequate placental perfusion. This remodelling is somehow prevented in preeclamptic pregnancies: the placenta is unable to properly burrow into the maternal blood vessels, leading to intrauterine growth restriction and other fetal manifestations of the disorder. Investigators speculate that this incomplete placentation is due to maternal immunologic intolerance of foreign fetal genes.

Early onset preeclampsia (EOPE) is understood to be the onset of proteinuric (or aproteinuric)hypertension before 34 weeks of pregnancy. Maternal complications are more severe and low birth weight (LBW), fetal growth restriction (FGR), and iatrogenic prematurity are common. Late onset preeclampsia (LOPE) is the onset of proteinuric (or aproteinuric) hypertension after 34th week of pregnancy wherein the maternal as well as fetal complications are less severe:


Preeclampsia is defined as elevated blood pressure after 20 weeks of gestation (≥ 140 mm Hg systolic or ≥ 90 mm Hg diastolic) plus proteinuria (> 0.3 g/24 hours). In clinical practice, we usually use the criteria of two elevated blood pressure measurements 6 hours apart and a proteinuria of 300 mg in a 24-hour urine specimen. A 24-hour determination is most accurate because urine dipsticks can be affected by variable excretion, maternal dehydration, and bacteruria.

Preeclampsia used to be diagnosed by the

“30-15” rule: systolic pressure more thar 30 mm Hg above baseline and diastolic pressure more than 15 mm Hg above baseline

Severe preeclampsia is defined as any of the following:

  • Markedly elevated blood pressure measurements (systolic ≥ 160 mm Hg or diastolic ≥ 110 mm Hg) taken at least 6 hours apart with the patient on bed rest
  • Proteinuria ( 5 g/24 hours or ≥ 3+ on two random samples 4 hours apart)
  • Manifestations of end-organ disease: oliguria (< 500 mL in 24 hours), cerebral or visual disturbances, pulmonary oedema, cyanosis, epigastric or right-upper-quadrant pain, impaired liver function, thrombocytopenia, or fetal growth restriction.

Haematology changes include

  • Thrombocytopenia-platelets are dramatically reduced, probably consumed by endothelial injury. Counts can be as low as 20000 to 50000 per micro-litre of blood.
  • Hemoconcentration-doctors used to follow preeclampsia with serial hematocrits.
  • Microangiopathic hemolysis—eventually, red cells are sheared through the microcirculation.

Hepatic changes are usually limited to hepato cellular necrosis, demonstrated by elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels.

Occasionally there is sub-capsularhaemorrhage and even hepatic rupture, which has a 60% maternal mortality rate.

Neurologic changes are common and include headache, blurred vision, scotoma , hyperreflexia and rarely cortical blindness and generalised seizures or eclampsia.

Fetal changes:

Intrauterine growth restriction is very common. Oligohydramnios also occurs, because the amniotic fluid is essentially fetal urine; with poor perfusion through the placenta, the foetus has diminished urine output. Intrauterine demise and placental abruption are not uncommon.

Doppler waveforms are typically abnormal, and antenatal testing suggests that the foetus is in jeopardy. We use the ratio of forward flow of blood in the umbilical artery during systole to that during diastole (the “umbilical artery S:D ratio”) to assess the degree of resistance to flow in the placenta. The higher the ratio, the less diastolic flow. The greater the resistance to flow, the greater the peril to the foetus.

HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) occurring in about 20% of severe cases. It is associated with significant maternal and perinatal morbidity.


The mainstay of treatment is early detection and managed delivery to minimise both maternal and fetal risks. If the pregnancy is at term, the decision is easy: the baby should be delivered. The decision to deliver involves balancing the risks of worsening preeclampsia against those of prematurity. Delivery is generally not indicated for women with mild preeclampsia until 37 to 38 weeks of gestation and should occur by 40 weeks.If remote from term, the mother should be admitted for evaluation. She will need:

  • Baseline and serial laboratory tests (complete blood cell count, BUN, creatinine, uric acid, ALT, AST).
  • Ultrasonography to measure fetal growth and amniotic fluid volume and Doppler ultrasonography. Umbilical artery systolic/diastolic ratios measured by Doppler ultrasonography may detect early uteroplacental insufficiency .
  • Antenatal testing (non-stress test or biophysical profile).
  • A 24-hour urine collection for protein.
    The goals of treatment are to prevent seizures, lower blood pressure to avoid maternal end-organ damage, and expedite delivery

Magnesium sulphate is still the drug of choice for preventing and arresting eclamptic seizures. It has the additional benefit of reducing the incidence of placental abruption (Serum magnesium levels should be monitored in women with elevated serum creatinine levels, decreased urine output, or absent deep tendon reflexes.

Magnesium toxicity can lead to respiratory paralysis, central nervous system depression, and cardiac arrest. The antidote is calcium gluconate, 1 g infused intravenously over two minutes .

Antihypertensive medications are used solely to prevent maternal morbidity and have no effect on disease progression or preventing eclampsia. Medications must be given with caution: if blood pressure is lowered too fast, it can have a dramatic effect on uteroplacental perfusion and can cause an already compromised fetus to rapidly decompensate and become bradycardic Preferred medications are hydralazine (5-10 mg intravenous bolus every10-15 minutes), labetalol, nicardipine, and sodium nitroprusside. Intravenous labetalol and hydralazine are commonly used for the acute management of preeclampsia.

Diuretics are usually contraindicated because of the already collapsed intravascular volume. However, if the pulmonary capillary wedge pressure is high, diuretics are necessary.

Intravenous hydration for oliguria must be given cautiously to avoid pulmonary oedemaascites and cardiopulmonary overload.

If there is no evidence of pulmonary oedema, a trial of fluid resuscitation (500 mL

over an hour) should be given.

Antihypertensive medication:

1)Methyldopa is the most studied of all antihypertensive medications and is generally the first choice in pregnancy because it has a limited effect on uteroplacental blood flow.

2)Labetalol, a combined alpha and beta-blocker, is the first alternative to methyldopa and is becoming a first-line choice as experience with the drug during pregnancy increases. It is generally well tolerated and has an easier (twice-a-day) dosing schedule than methyl-dopa.

3)Calcium channel blockers, particularly nifedipine, are being used more frequently, probably because doctors have become familiar with their use to stop premature labor. They seem to be safe and effective, but evidence is sparse.

4)Atenolol and other pure beta-blockers should be avoided: they have been associated with babies born small for their gestational age.

5)Angiotensin-converting enzyme (ACE)inhibitors are contraindicated in the second and third trimester because they are associated with a myriad of congenital anomalies, including renal failure, oligohydramnios, renal dysgenesis, reduced ossification, pulmonary hypoplasia, and fetal and neonatal death. Patients presenting in the first trimester on an ACE inhibitor should either be taken off antihypertensive medications or switched to another agent. Exposure during this time is not an indication for pregnancy termination, however.

Delivery Decisions in Severe Preeclampsia

Delivery is the only cure for preeclampsia.

Corticosteroids are administered to accelerate fetal lung maturity  and induction or cesarean delivery 12 to 24 hours after corticosteroid administration ). Contraindications to expectant management include persistent severe symptoms, multi-organdysfunction, severe IUGR (i.e., estimated fetal weight below the 5th percentile), suspected placental abruption, or non reassuring fetal testing .

Method of delivery can be vaginal delivery or caesarean section. Vaginal delivery may be commenced in vertex presentation by: amniotomy + oxytocin if the cervix is favourable or prostaglandin vaginal tablet (PGE2) if the cervix is not favourable. Caesarean section is indicated in foetal distress, late deceleration occurs with oxytocin challenge test, failure of induction of labour and other indications as contracted pelvis and malpresentation.

Some experts recommend cesarean delivery for fetuses younger than 30 weeks when the cervix is not ripe.

In patients with HeLLP syndrome, cesarean delivery carries special risks, such as bleeding from thrombocytopenia and difficulty controlling blood pressure because of depleted intravascular volume .

Postpartum Management:

Eclampsia may occur postpartum; the greatest risk of postpartum eclampsia is within the first 48 hours .

Magnesium sulphate is continued for 12 to 24 hours, or occasionally longer if the clinical situation warrants. Generally, once the placenta is delivered, the disease rapidly improves. Large fluid shifts should occur immediately postpartum, and diuresis indicates that the syndrome is resolving.


Eclampsia is the development of convulsions in a preexisting pre-eclampsia or it may appear unexpectedly in a patient with minimally elevated blood pressure and no proteinuria. The exact cause is unknown but cerebral ischaemia and oedema were suggested. The timing of an eclamptic seizure can be antepartum (53 percent), intrapartum  or postpartum .

Management of eclampsia

General measures include:

  • Care for respiratory system by:
    head-down tilt to help drainage of bronchial secretion,
    frequent change of patient position, keep upper respiratory tract clear by aspiration of mucous through a plastic airway, prophylactic antibiotic and oxygen is administered during and after fits.
    a medical professional skilled in performing intubations should be immediately available .
  • The tongue is protected from biting by a plastic mouth gauge.
  • After sedation, a self-retained Foley’s catheter is applied. The hourly output of urine is charted. Proteinuria, haematuria and specific gravity are noticed.
  • Efficient nursing in a single quiet semi-dark room to prevent any auditory or visual stimuli.

Magnesium sulphate is the drug of choice because it is more effective in preventing recurrent seizures than phenytoin (Dilantin) or diazepam (Valium) . If a patient has already received a prophylactic loading dose of magnesium sulphate and is receiving a continuous infusion, an additional 2 g should be given intravenously.

Otherwise,  4g loading dose is given intravenously over 15 to 20 minutes, followed by maintenance infusion of 1-2 g per hour. A total of 8 g of magnesium sulphate should not be exceeded over a short period of time .

Recent advances in screening of preeclampsia

1st step is gestosis scoring

Low Risk Factors – 1 Point for each Risk
Maternal Anaemia
Age >35 years
Age <19 years
Woman born as Small for Gestational Age
Obesity (BMI > 30 kg/m2)
Short duration of Paternity (Cohabitation)
Family History of PE and Cardiovascular Diseases
• Inter-pregnancy Interval >5 years
• Excessive Maternal Weight Gain during Pregnancy*
  Mean aterial pressure > 85 mm Hg  


Moderate Risk Factors – 2 Points for each Risk
1. Gestational Diabetes Mellitus*
2. Obesity Grade II (BMI > 40 kg/m2)
3. Multiple Pregnancy
4. Hypertensive Disease during Previous Pregnancy



High Risk Factors – 3 Points for each Risk

1. Pre-Gestational Diabetes Mellitus
2. Chronic Hypertension
3. Mental Disorders (Schizophrenia)
4. Inherited/Acquired Thrombophilia
5. Maternal Chronic Kidney Disease
6. Autoimmune Disease (SLE/APLAS/RA)
7. Assisted Reproductive (OD) Treatment


Scoring: 1-3 At Low Risk: Be more vigilant. ≥3 At High Risk: Surveillance


  • PAPP-A- pregnancy associated plasma protein A is a large gycosylated protein prodeced by the developing trophoblast cells and lower levels are associated with high incidence of PE and FGR.
  • PLGF ( placental growth factor ) is a member of tge vascular endothelial growth factors family . Maternal serum levels are reduced at 11 to 13 weeks pregnancy with aneuploidies and thise with impaired placentation
  • Sflt 1- ( soluble fms like tyrosine kinase 1)- Its level is increased almost 5 weeks prior to onset of PE.
  • Glycosylated Fibronectin (GlyFN)is a relatively new biomarker that has recently been introduced in India. Oxidative stress and cellular matrix dysfunction are just a couple of causes of preeclampsia that involves glycosylation of glycoproteins by an enzymatic process.Fibronectin is an extracellular matrix glycoprotein with a wide spectrum of physiological functions. Multiple isoforms of Fibronectin are generated through alternate splicing and proteolysis. The majority of Fibronectin present in serum or plasma is termed plasma Fibronectin (pFn), which is soluble and produced by hepatocytes. Cellular Fibronectin (cFn) is produced by numerous cell types including fibroblasts, endothelial cell and smooth muscle cells. Specific variants of Fibronectin have the potential to serve as informative biomarkers reflecting the identified roles of Fibronectin in homeostasis,Cell migration. Vessel remodelling, inflammation and embryonic differentiation . Maternal serum glycosylated Fibronectin levels are ekevated in PE and it’s complications

The preeclampsia pathology is based on excessive production of antiangiogenic proteins like sFlt-1, soluble Endoglin (sEng), and GlyFN and reduced production of angiogenic proteins vasculoendothelial growth factor (VEGF) and PIGF. Alterations in absolute levels of VEGE, PIGE, sFIt-1, sEng in maternal blood and urine precede the onset of clinical preeclampsia by several weeks to months, and also correlate with disease severity. They normalize after delivery.

Doppler studies:

Impedance to flow in the uterine arteries normally decreases as pregnancy progresses. Increased impedance for gestational age is an early radiographic feature of preeclampsia and reflects vascular resistance due to defective differentiation of trophoblast, which leads to defective invasion of spiral arteries and failure of these vessels to transform into low resistance vessels. Two types of techniques to analyse Doppler waveforms have emerged for prediction of preeclampsia as well as other disorders associated with impaired placentation (e.g., FGR, pregnancy loss):

  • Presence or absence of unilateral and/or bilateral diastolic notching of the uterine arcuate vessels
  • Flow waveform ratios (e.g., high resistance or pulsatility index (PI), systolic/ diastolic ratio).
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