Hypertensive Disorders

Last updated On August 2nd, 2020

Hypertensive disorders of pregnancy are the second most common cause of maternal death, accounting for 15% of all maternal deaths.

Effects of pregnancy on the maternal cardiovascular system:

• Blood volume increases 800 ml by 12 weeks (1.5 l in twins).
• Blood pressure (BP) decreases in early pregnancy (due primarily to a decrease in systemic vascular resistance secondary to progesterone), nadirs in mid-pregnancy, and returns to baseline by term.

Classification:

1 Chronic hypertension

• Definition. Hypertension before pregnancy. The diagnosis should also be entertained in women with BP ≥140/90 mmHg before 20 weeks’ gestation.
• Complications. Such pregnancies are at increased risk of superimposed preeclampsia, intrauterine fetal growth restriction (IUGR), placental abruption, and stillbirth.

• Management. Continue antihypertensive medications except for angiotensin-converting enzyme (ACE) inhibitors. These drugs have been associated with progressive and irreversible renal injury and possibly other structural anomalies in the fetus. Diuretic therapy is generally discouraged.

• Fetal testing (serial ultrasound examinations for fetal growth with or without fetal non-stress testing) should be initiated after 32 weeks’ gestation. Delivery should be achieved by 40 weeks.

2 Gestational hypertension

• Also known as gestational non-proteinuric hypertension.
• Diagnosis. Persistent elevation of BP ≥140/90 mmHg in the third trimester without evidence of pre-eclampsia. It is a diagnosis of exclusion that is best made retrospectively.
• Etiology. It probably represents an exaggerated physiologic response of the maternal cardiovascular system to pregnancy.
• Rarely associated with adverse maternal or fetal outcome.

3 Chronic hypertension with superimposed pre-eclampsia

• Also known as gestational proteinuric hypertension, preeclamptic toxemia (PET).
• Definition. A multisystem disorder specific to pregnancy and the puerperium. More precisely, it is a disease of the placenta because it occurs in pregnancies where there is trophoblast but no fetal tissue(complete molar pregnancies).

• Incidence. Six to eight percent of all pregnancies.
• Risk factors.

Nulliparity
African-American/African race
Prior history of pre-eclampsia
Extremes of maternal age (<15 or >35 years)
Family history of pre-eclampsia
Multiple gestation
Chronic hypertension
Chronic renal disease
Antiphospholipid antibody syndrome
Collagen vascular disease
Angiotensinogen gene T235 mutation

• Diagnosis. A clinical diagnosis with two elements:

1 New-onset hypertension defined as a sustained sitting BP ≥140/90 mmHg in a previously normotensive woman (a prior definition included an elevation in systolic BP ≥30 or diastolic BP ≥15 mmHg over first trimester BP, but these criteria have now been dropped).

2 New-onset significant proteinuria defined as >300 mg/24 h or ≥1+ on a clean-catch urine in the absence of urinary tract infection.

Note. A definitive diagnosis of preeclampsia should only be made after 20 weeks’ gestation. Evidence of gestational proteinuric hypertension before 20 weeks should raise the possibility of an underlying molar pregnancy, drug withdrawal, or (rarely) chromosomal abnormality in the fetus.

• Classification. Preeclampsia is classified as “mild” or “severe.” There is no category of “moderate” pre-eclampsia.

• Etiology. The cause of preeclampsia is not known. Theories include an abnormal maternal immunologic response to the fetal allograft, an underlying genetic abnormality, an imbalance in the prostanoid cascade, and the presence of circulating toxins and/or endogenous vasoconstrictors.

What is known is that the blueprint for the development of preeclampsia is laid down early in pregnancy. The primary event is a failure of the second wave of trophoblast invasion from 8 weeks to 18 weeks,

which is responsible for remodeling of the spiral arterioles in the myometrium adjacent to the developing placenta, and establishment of the definitive uteroplacental circulation. As pregnancy progresses and the metabolic demand of the fetoplacental unit increases, the spiral arterioles are therefore unable to accommodate the necessary increase in blood flow. This then leads to the development of “placental dysfunction” which manifests clinically as preeclampsia. Although attractive, this hypothesis remains to be validated. Whatever the placental abnormality, the end-result is widespread vasospasm and endothelial injury.

• Complications. Eclampsia – defined as one or more generalized convulsions or coma in the setting of preeclampsia and in the absence of other neurologic conditions – was thought to be the end stage of preeclampsia, hence the nomenclature. It is now clear, however, that seizures are but one clinical manifestation of “severe” pre-eclampsia; 50% of eclampsia occurs preterm. Of those at term, 75% occur either intrapartum or within 48 hours of delivery.
• Management. Delivery is the only effective treatment for preeclampsia, and is recommended:

1 in women with “mild” preeclampsia once a favorable gestational age has been reached (>36–37 weeks).

2 in all women with “severe” preeclampsia regardless of gestational age (except for “severe” preeclampsia due to proteinuria alone or intrauterine growth restriction [IUGR] remote from term with good fetal testing). There has also been a recent trend toward expectant management of “severe” preeclampsia by BP criteria alone at <32 weeks’ gestation.

• There is no proven benefit to routine delivery by cesarean section. However, the probability of vaginal delivery in a patient with preeclampsia remote from term with an unfavorable cervix is only 15–20%.
• BP control is important to prevent cerebrovascular accidents (usually associated with BP ≥170/120 mmHg) but does not affect the natural course of preeclampsia.
• Intravenous magnesium sulfate should be given intrapartum and for at least 24 hours postpartum to prevent eclampsia.
• Prevention. Despite promising early studies, low-dose aspirin (acetylsalicylic acid or ASA) and/or supplemental calcium does not prevent preeclampsia in either high- or low-risk women.
• Prognosis. Preeclampsia and its complications always resolve after delivery (except for cerebrovascular accident). Diuresis (>4 L/day) is the most accurate clinical indicator of resolution. Fetal prognosis is dependent largely on gestational age at delivery and problems related to prematurity.