HYPERTENSION IN PREGNANCY

By : Febriani Valentina

030.07.091

FACULTY OF MEDICINE

TRISAKTI UNIVERSITY

JAKARTA 2010

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CHAPTER I

INTRODUCTION

Hypertension or High blood pressure, defined as a repeatedly elevated blood pressure

exceeding 140 over 90 mmHg -- a systolic pressure above 140 with a diastolic pressure above

90. There are 2 types of chronic hypertension: essential hypertension and secondary

hypertension. We do not know the cause of essential hypertension, but because hypertension

commonly runs in families, we know that genes are involved. A minority of individuals have

secondary hypertension, which means that the hypertension is explained by another condition

such as kidney disease, narrowing of the artery to the kidney, and adrenal tumors. In many

such cases, the hypertension will resolve after treatment for the underlying problem. If you are

undergoing evaluation for a secondary form of hypertension, it is advisable to be treated for

the underlying condition before becoming pregnant. A third type of hypertension is called

pregnancy-induced hypertension. Some women develop new-onset hypertension in

pregnancy, which can present in the second half of pregnancy, usually in the third trimester.

Many women have been diagnosed with hypertension (blood pressure >140/90 mm

Hg) when they were in their childbearing years. Because the hypertension predates the

pregnancy, it is called chronic hypertension. This type of hypertension complicates at least 5%

of all pregnancies. When managed appropriately, most women with chronic hypertension can

experience healthy pregnancies and give birth to healthy babies. To accomplish this goal, it is

important that women with chronic hypertension let their doctors know when they are

planning a pregnancy so that they can receive pregnancy counseling and so that adjustments to

antihypertensive medications can be made if needed.

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A more worrisome complication of chronic hypertension is the development of

superimposed preeclampsia. Preeclampsia is a serious condition that can affect many organ

systems and cause liver dysfunction, kidney failure, and an increase in bleeding tendency, and

at times it can progress to eclampsia seizures. Superimposed preeclampsia is more likely to

occur in women who have poorly controlled hypertension, underlying renal disease, and

diabetes mellitus. At present, there is no treatment for preeclampsia except for delivery of the

baby; therefore, babies of women who have this condition are frequently born prematurely.

Another complication of chronic hypertension that may cause premature birth is placental

abruption. An abruption is an early separation of the placenta from the wall of the uterus,

usually leading to strong contractions, bleeding, and early delivery. Early delivery is

associated with prematurity. If an early delivery is planned, your body may not be ready to

deliver the baby vaginally, so there is a greater chance that you might need a cesarean section.

Hypertension may also affect the development of the placenta, which is important for the

nourishment and growth of the fetus. Thus, some babies may be affected by low amniotic

fluid levels and/or intrauterine growth restriction.

Preeclampsia occurs in up to 5% of all pregnancies, in 10% of first pregnancies, and in

20-25% of women with a history of chronic hypertension. Hypertensive disorders in

pregnancy may cause maternal and fetal morbidity, and they remain a leading source of

maternal mortality.

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CHAPTER II

HYPERTENSION IN PREGNANCY

1. Background

Hypertension is the most common medical problem encountered during

pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during

pregnancy are classified into 4 categories, as recommended by the National High

Blood Pressure Education Program Working Group on High Blood Pressure in

Pregnancy:

1) chronic hypertension,

2) preeclampsia-eclampsia,

3) preeclampsia superimposed on chronic hypertension, and

4) gestational hypertension (transient hypertension of pregnancy or chronic

hypertension identified in the latter half of pregnancy).1

This terminology is preferred over the older but widely used term pregnancy-

induced hypertension (PIH) because it is more precise.

The Society of Obstetricians and Gynecologists of Canada (SOGC) recently

released revised guidelines that simplified the classification of hypertension in

pregnancy into 2 categories, preexisting or gestational, with the option to add

"with preeclampsia" to either category if additional maternal or fetal symptoms,

signs, or test results support this.2

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Chronic hypertension is defined as blood pressure exceeding 140/90 mm Hg

before pregnancy or before 20 weeks' gestation. When hypertension is first

identified during a woman's pregnancy and she is at less than 20 weeks' gestation,

blood pressure elevations usually represent chronic hypertension. In contrast, new

onset of elevated blood pressure readings after 20 weeks' gestation mandates the

consideration and exclusion of preeclampsia. Preeclampsia occurs in up to 5% of

all pregnancies, in 10% of first pregnancies, and in 20-25% of women with a

history of chronic hypertension. Hypertensive disorders in pregnancy may cause

maternal and fetal morbidity, and they remain a leading source of maternal

mortality.

2. Epidemiology

In United States, Chronic hypertension occurs in up to 22% of women of

childbearing age, with the prevalence varying according to age, race, and body

mass index. Population-based data indicate that approximately 1% of pregnancies

are complicated by chronic hypertension, 5-6% by gestational hypertension

(without proteinuria), and 1-2% by preeclampsia.

Black women have higher rates of preeclampsia complicating their pregnancies

compared with other racial groups, mainly because they have a greater prevalence

of underlying chronic hypertension. Among women aged 30-39 years, chronic

hypertension is present in 22.3% of African Americans, 4.6% of non-Hispanic

white persons, and 6.2% of Mexican Americans. Hispanic women generally have

blood pressure levels that are the same as or lower than those of non-Hispanic

white women.

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Table 1.Study characteristics and incidence of pre-eclampsia/eclampsia in developing and developed countries.( * Placebo group only, NR:not reported)

Country Year No of women(n)

Incidence  of Pre-eclampsia  (%)

Incidence  of Eclampsia  (%)

Jamaica 1992-94 3026* 6.3 NR

Saudi Arabia 1994 10407 1.68 NR

Zimbabwe 1992-95 51206 7.1 NR

Colombia 1993-95 20277 NR 0.81

Norway 1967-98 1869388 2.77 NR

UK 1992 774436 NR 0.049

Barbados 1992-94 1822* 2.2 NR

3. Pathophysiology

3.1. Chronic Hypertension

Chronic hypertension may be either essential (90%) or secondary to some

identifiable underlying disorder, such as renal parenchymal disease (eg,

polycystic kidneys, glomerular or interstitial disease), renal vascular disease

(eg, renal artery stenosis, fibromuscular dysplasia), endocrine disorders (eg,

adrenocorticosteroid or mineralocorticoid excess, pheochromocytoma,

hyperthyroidism or hypothyroidism, growth hormone excess,

hyperparathyroidism), coarctation of the aorta, or oral contraceptive use.

About 20-25% of women with chronic hypertension develop preeclampsia

during pregnancy.

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3.2. Pre-eclampsia

Although the exact pathophysiologic mechanism is not clearly understood,

preeclampsia is primarily a disorder of placental dysfunction leading to a

syndrome of endothelial dysfunction with associated vasospasm. In most

cases, pathology demonstrates evidence of placental insufficiency with

associated abnormalities such as diffuse placental thrombosis, an

inflammatory placental decidual vasculopathy, and/or abnormal

trophoblastic invasion of the endometrium. This supports abnormal

placental development or placental damage from diffuse microthrombosis as

being central to the development of this disorder.

The widespread endothelial dysfunction may manifest as a maternal

syndrome, fetal syndrome, or both. Endothelial damage leads to pathologic

capillary leak that can present in the mother as rapid weight gain,

nondependent edema (face or hands), pulmonary edema,

hemoconcentration, or a combination thereof. The diseased placenta can

also affect the fetus via decreased utero-placental blood flow. This decrease

in perfusion can manifest clinically as nonreassuring fetal heart rate testing,

low scores on a biophysical profile, oligohydramnios, or as fetal growth

restriction.

The hypertension occurring in preeclampsia is due primarily to vasospasm,

with arterial constriction and relatively reduced intravascular volume

compared to normal pregnancy. The vasculature of normal pregnant women

typically demonstrates decreased responsiveness to vasoactive peptides such

as angiotensin-II and epinephrine. In contrast, women who develop

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preeclampsia typically show a hyperresponsiveness to these hormones, an

alteration that may be seen even before the hypertension and other

manifestations of preeclampsia become apparent. In addition, blood

pressures in preeclampsia are labile, and the normal circadian blood

pressure rhythms may be blunted or reversed. One study found increased

arterial stiffness in women with preeclampsia, as well as in those with

gestational hypertension, compared with normotensive controls; treatment

with alpha methyldopa significantly improved the vascular stiffness in

preeclampsia but did not normalize it.3

3.3. Gestational Hypertension

Gestational hypertension refers to hypertension with onset in the latter part

of pregnancy (>20 weeks’ gestation) without any other features of

preeclampsia, and followed by normalization of the blood pressure

postpartum. Of women who initially present with apparent gestational

hypertension, about one third develop the syndrome of preeclampsia. As

such, these patients should be observed carefully for this progression. The

pathophysiology of gestational hypertension is unknown, but in the absence

of features of preeclampsia, the maternal and fetal outcomes are usually

normal. Gestational hypertension may, however, be a harbinger of chronic

hypertension later in life.

4. Clinical

4.1. Symptoms of Pre-eclampsia

4.1.1. Visual disturbances

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4.1.2. Headache or similar to a migraine headache.

4.1.3. Epigastric pain

4.1.4. Mild lower extremity edema

4.1.5. Rapid weight gain

4.2. Physical

4.2.1. Blood pressure

4.2.1.1. Blood pressure should be measured in the sitting position, with

the cuff at the level of the heart. Inferior vena caval compression by

the gravid uterus while the patient is supine can alter readings

substantially, leading to an underestimation of the blood pressure.

Blood pressures measured in the left lateral position similarly may

yield falsely low values if the blood pressure is measured in the

higher arm, unless the cuff is carefully maintained at the level of

the heart.

4.2.1.2. Many automated blood pressure cuffs provide reasonable

estimates of true blood pressure during normal pregnancy

(especially those validated for pregnancy) but tend to underestimate

blood pressure in preeclamptic women. Only a few automated BP

cuffs have been validated in preeclampsia. Manual blood pressure

measurement with a mercury sphygmomanometer remains the

criterion standard in this setting.

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4.2.1.3. Home and ambulatory BP measurements are increasingly being

used in the pregnant population. Assuming the BP device is

accurate (validated relative to an office measurement) they may

provide valuable additional data regarding hypertension severity

and control during pregnancy.

4.2.2. Retinal vasospasm is a severe manifestation of maternal disease;

consider delivery.

4.2.3. Retinal edema is known as serous retinal detachment. This can

manifest as severely impaired vision if the macula is involved. It

generally reflects severe preeclampsia and should lead to prompt

consideration of delivery. The condition typically resolves upon

completion of pregnancy and resolution of the hypertension and fluid

retention.

4.2.4. Right upper quadrant (RUQ) abdominal tenderness stems from liver

swelling and capsular stretch. Consider delivery.

4.2.5. Brisk, or hyperactive, reflexes are common during pregnancy. Clonus

is a sign of neuromuscular irritability that usually reflects severe

preeclampsia.

4.2.6. In most normal pregnancies, the woman has some lower extremity

edema by the third trimester. In contrast, a sudden worsening in

dependent edema, edema in nondependent areas (such as the face and

hands), or rapid weight gain suggest a pathologic process and warrant

further evaluation for preeclampsia.

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5. Investigation

5.1. Laboratory Studies

5.1.1. Laboratory testing to evaluate chronic hypertension includes testing for

target organ damage, potential secondary causes of hypertension, and

other risk factors.

5.1.1.1. Studies include: urinalysis; CBC; and serum sodium, potassium,

creatinine, and glucose levels

5.1.1.2. Other suggested tests include creatinine clearance,

microalbuminuria, 24-hour urinary protein, serum calcium, uric

acid, glycosylated hemoglobin, thyroid-stimulating hormone

(TSH), and an ECG.

5.1.1.3. Serum lipids predictably increase during pregnancy, so

measurement should be deferred until the postpartum period.

5.1.1.4. The increase in endogenous corticosteroid levels during normal

pregnancy makes it difficult to evaluate for secondary

hypertension due to adrenal corticosteroid excess.

5.1.2. Routine tests when evaluating a patient for preeclampsia include: CBC

count, electrolytes, BUN, creatinine, liver enzymes and bilirubin, and a

urine dip for protein.

5.1.3. Researchers in the United Kingdom have developed a method for first-

trimester screening to identify women at risk for the development of

preeclampsia or gestational hypertension. The screening algorithm uses

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a combination of maternal variables, including mean arterial pressure,

uterine artery pulsatility index, pregnancy-associated plasma protein–

A, and placental growth factor. The algorithm proved especially

effective for predicting early preeclampsia (ie, requiring delivery

before 34 weeks).4

5.2. Imaging Studies

5.2.1. Chest radiograph

Obtain chest radiographs to evaluate for pulmonary edema in the

setting of dyspnea or hypoxia occurring in a woman with preeclampsia.

5.2.2. CT scan of the brain

5.2.3. MRI of the brain

5.2.4. Ultrasonography or CT scan of the liver

5.2.5. Limited echocardiography may be performed to evaluate for left

ventricle hypertrophy (LVH) in chronic hypertension.

5.2.6. Electroencephalogram

5.2.7. Fetal monitoring

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6. Treatment

6.1. Medical Care

If a pregnant woman’s blood pressure is sustained greater than 160 mm Hg

systolic and/or 110 mm Hg diastolic at any time, lowering the blood pressure

quickly with rapid-acting agents is indicated for maternal

safety. Anticonvulsant therapy may be undertaken in the setting of severe

preeclampsia (primary prophylaxis) or in the setting of eclamptic seizures

(secondary prophylaxis). The most effective agent is IV magnesium sulfate;

phenytoin is an alternative, although less effective, therapy.

Evidence-based guidelines from the American Association of Clinical

Endocrinologists single out methyldopa, labetalol or nifedipine as preferable

antihypertensive medications in pregnancy, with magnesium sulfate for

women with preeclampsia who are at high risk for seizures, but they

recommend all major antihypertensive agents with the exception of

angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor

blockers (ARBs).5

ACE inhibitors should be avoided during pregnancy, as they are associated

with fetal renal dysgenesis or death when used in the second and third

trimesters and with increased risk of cardiovascular and central nervous

system malformations when used in the first trimester.6 Angiotensin II

receptor antagonists/blockers are not used during pregnancy because they

have a mechanism of action similar to that of ACE inhibitors. Diuretics do

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not cause fetal malformations but are generally avoided in pregnancy, as they

prevent the physiologic volume expansion seen in normal pregnancy. They

may be used in states of volume-dependent hypertension, such as renal or

cardiac disease.

6.2. Non-medical

6.2.1. Consultation

Women with chronic hypertension in pregnancy should be monitored

by an obstetrician. Women with moderate or severe hypertension may

benefit from referral to an experienced internist (obstetric medicine

specialist), hypertension subspecialist, and/or a specialist in maternal-

fetal medicine (perinatologist).

6.2.2. Diet

Multiple dietary interventions and supplements have been investigated

for a role in preventing preeclampsia, but none has shown any

consistent beneficial effect.

6.2.3. Activity

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Women with worsening hypertension during pregnancy often are

placed on bed rest or restricted activity, although no scientific evidence

demonstrates that this is beneficial in prolonging gestation or reducing

maternal or fetal morbidity/mortality.

7. Complication

7.1. Life-threatening complications in preeclampsia

7.1.1. Seizures

7.1.2. Cerebral hemorrhage

7.1.3. Pulmonary edema – Due to pulmonary capillary leak, excess IV fluid

administration, or myocardial dysfunction

7.1.4. Acute renal failure – Due to renal vasospasm, ATN, or renal cortical

necrosis

7.1.5. Disseminated intravascular coagulopathy

7.1.6. HELLP syndrome – Microangiopathic hemolysis, elevated liver

enzymes, and thrombocytopenia (platelets [PLT] <100)

7.1.7. Hepatic infarction/rupture and subcapsular hematoma – May lead to

massive internal hemorrhage and shock

7.2. Acute fatty liver of pregnancy: Although a distinct and rare disorder, acute

fatty liver has some clinical features similar to, and often overlapping with,

severe preeclampsia.

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7.3. TTP and HUS: While unrelated to preeclampsia, consider these important

disorders in the setting of presumed severe HELLP syndrome.

8. Prognosis

Women who develop preeclampsia are at increased risk for cardiovascular disease

later in life. Whether the preeclampsia increases cardiovascular risk or the 2

conditions share a common underlying cause remains unclear.7

Transient hypertension of pregnancy is the development of isolated hypertension

in a woman in late pregnancy without other manifestations of preeclampsia, is

associated strongly with later development of chronic hypertension.

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CHAPTER III

CONCLUSION

Hypertension is the most common medical problem encountered during pregnancy,

complicating 2-3% of pregnancies. Hypertensive disorders during pregnancy are classified

into 4 categories, chronic hypertension, preeclampsia-eclampsia, preeclampsia superimposed

on chronic hypertension, and gestational hypertension.

Preeclampsia is primarily a disorder of placental dysfunction leading to a syndrome of

endothelial dysfunction with associated vasospasm. The hypertension occurring in

preeclampsia is due primarily to vasospasm, with arterial constriction and relatively reduced

intravascular volume compared to normal pregnancy.

If a pregnant woman’s blood pressure is sustained greater than 160 mm Hg systolic

and/or 110 mm Hg diastolic at any time, lowering the blood pressure quickly with rapid-

acting agents is indicated for maternal safety. Evidence-based guidelines from the American

Association of Clinical Endocrinologists single out methyldopa, labetalol or nifedipine as

preferable antihypertensive medications in pregnancy, with magnesium sulfate for women

with preeclampsia who are at high risk for seizures, but they recommend all major

antihypertensive agents with the exception of angiotensin-converting enzyme (ACE)

inhibitors and angiotensin II receptor blockers (ARBs).5

When treating chronic hypertension during pregnancy, maintaining a balance between

uncontrolled blood pressure and adverse medication effects is paramount. Optimal

management for both mother and fetus is best achieved via frequent monitoring, especially in

the final month of gestation.

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REFERENCES

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of the Hypertensive Disorders of Pregnancy. Journal of Obstetrics and Gynaecology

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http://www.sogc.org/guidelines/documents/gui206CPG0803_001.pdf.

3. Khalil A, Jauniaux E, Harrington K. Antihypertensive therapy and central

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prediction of hypertensive disorders in

pregnancy. Hypertension. May 2009;53(5):812-8.

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doc_id=9338&nbr=005007. Accessed June 1, 2009.

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al. Major congenital malformations after first-trimester exposure to ACE inhibitors. N

Engl J Med. Jun 8 2006;354(23):2443-51.

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