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Introduction
Hypertensive disorders of pregnancy, including chronic hypertension, with or without
superimposed pre-eclampsia/eclampsia, gestational hypertension, or preeclampsia with or
without severe features or eclampsia present a significant risk of morbidity to both mother
and fetus. Although appropriate prenatal care with close observation to detect signs of pre-
eclampsia and prompt delivery to reduce or avoid adverse effects have produced reduced
morbidity and mortality, they still exist. While hypertension itself presents concerns during
pregnancy, adverse effects from progression to pre-eclampsia/eclampsia present the primary
concern. [1][2][3]
Etiology
Conditions that reduce uteroplacental blood flow and vascular insufficiency including pre-
existing hypertension, renal disease, diabetes mellitus, thrombophilia, and autoimmune
disease have demonstrated an increased risk for hypertensive disease in pregnancy.
Additionally, women with a previous history of preeclampsia, previous history of HELLP
syndrome, twin or other multiple pregnancies, obesity, autoimmune disease, are women who
are less than 20 years of age or more than 40 years of age, are first-time mothers, or have a
mother or sister who has had gestational hypertension have been shown to be at higher risk
for developing gestational hypertension and are at an elevated risk of progressing to pre-
eclampsia.[4][5]
Epidemiology
Hypertensive disorders complicate between 5% and 10% of all pregnancies. Pre-eclampsia
complicates 3% of all pregnancies in the United States and 4% of pregnancies worldwide.
The incidence of hypertension is increasing due to changes in maternal demographics (e.g.
advancing maternal age, increased pre-pregnancy weight). Eclampsia, however, has declined
due to improved prenatal care, and the increased use of antenatal therapies (e.g. blood
pressure control, magnesium seizure prophylaxis) as well as timely delivery by induction of
labor or cesarean section which serve as a cure for pre-eclampsia/eclampsia.[6][7]
Pathophysiology
The pathophysiology of hypertension in pregnancy is not completely understood. Current
research demonstrates that improper trophoblast differentiation during endothelial invasion
due to abnormal regulation and/or production of cytokines, adhesion molecules, major
histocompatibility complex molecules, and metalloproteinases plays a key role in the
development of a gestational hypertensive disease. Abnormal regulation and/or production of
these molecules leads to abnormal development and remodeling of spiral arteries in the deep
myometrial tissues. This leads to placental hypoperfusion and ischemia. Antiangiogenic
factors are released by placental tissue causing systemic endothelial dysfunction which can
result in systemic hypertension. Organ hypoperfusion from endothelial dysfunction is most
commonly seen in the eyes, lungs, liver, kidneys and peripheral vasculature. [8]
Evaluation
Chronic hypertension is diagnosed per USPSTF guidelines as an in-office measurement with
a systolic blood pressure greater than 140mmHg or diastolic blood pressure greater than
90mmHg confirmed with either ambulatory blood pressure monitoring, home blood pressure
monitoring, or blood pressure evaluation with serial office visits, or with a single blood
pressure greater than 180mmHg systolic or 110mmHg diastolic with or without emergent
symptoms. Clinical symptoms are usually only noted when blood pressure is greater than
180/110 and may signify end organ damage.[9][10][11]
Gestational hypertension is defined per ACOG guidelines as blood pressure greater than or
equal to 140mmHg systolic or 90mmHg diastolic on two separate occasions at least four
hours apart after 20 weeks of pregnancy when previous blood pressure was normal.
Alternatively, a patient with a systolic blood pressure greater than 160mmHg or diastolic
blood pressure greater than 110mmHg can be confirmed to have gestational hypertension if
they have a similar pressure after a short interval. This is in order to ensure timely
antihypertensive treatment. As above, clinical symptoms are usually only noted when blood
pressure is greater than 160/110 and may signify end organ damage.
Pre-eclampsia is defined per ACOG guidelines as meeting either above hypertension criteria
with greater than or equal to 300mg urine protein excretion in a 24-hour period, a
protein/creatinine ratio of greater than or equal to 0.3, or a urine dipstick protein reading of at
least 1+ (only used if above methods are unavailable). In the absence of the above findings,
patients meeting criteria for chronic or gestational hypertension and having new onset of
severe features of pre-eclampsia meet criteria for the diagnosis of pre-eclampsia. Severe
features are defined as cerebral symptoms (unremitting/severe headache, altered mental
status), visual symptoms (scotomata, photophobia, blurred vision, or temporary
blindness/visual field defect), pulmonary edema, impaired liver function as indicated by liver
transaminases elevated to greater than twice the normal concentration, progressive renal
insufficiency as demonstrated by serum creatinine greater than 1.1 or a doubling of serum
creatinine in the absence of another renal disease, or a platelet count of less than 1.0x10^5/ml
meet criteria for pre-eclampsia. Any of these findings or a systolic blood pressure greater
than 160mmHg or diastolic blood pressure greater than 110mmHg constitute severe features
suggestive of end organ damage. Pre-eclampsia can be superimposed with chronic
hypertension, or as an advancement along the spectrum of gestational hypertensive disease.
Per ACOG guidelines, systolic blood pressure of greater than 160mmHg or diastolic blood
pressure greater than 110mmHg on two separate readings at least four hours apart while the
patient is on bed rest is also considered a severe feature.
Eclampsia refers to the pre-eclamptic patient who progresses to have generalized tonic-clonic
seizures secondary to her untreated/undertreated pre-eclampsia. Eclampsia occurs in
approximately 2-3% of women with severe features who are not receiving anti-seizure
prophylaxis and up to 0.6% of women with preeclampsia without severe features. Maternal
complications occur in up to 70% of women experiencing eclamptic seizures with maternal
morbidity as high as 14%.
Treatment / Management
Treatment/management of gestational and chronic hypertension in pregnancy is always
indicated when blood pressures are in the severe range (>160/110). Several studies
recommend consideration for treatment of pressures in the mild to the moderately
hypertensive range (140-160/90-110). Commonly used therapies include calcium channel
blockers, beta blockers, and methyldopa. Thiazide diuretics can be continued if used to treat
chronic hypertension before pregnancy. Hydralazine and clonidine have been used in certain
circumstances, but are not commonly used in the longitudinal treatment of gestational or
chronic hypertension. ACE inhibitors, angiotensin receptor blockers, mineralocorticoid
receptor antagonists, and nitroprusside, are teratogenic and thus contraindicated in
pregnancy.[2][12][13]
When patients are diagnosed with chronic hypertension, gestational hypertension, or pre-
eclampsia, increased monitoring is recommended as concern for intrauterine growth
retardation, placental abruption and poor placental/umbilical blood flow are concerns. Up to
twice weekly BP monitoring, frequently combined with the fetal non-stress test, amniotic
fluid index evaluation, and laboratory evaluations may be indicated. Abnormal findings on
any of these evaluations may indicate the need for early delivery.
Differential Diagnosis
Antiphospholipid syndrome
Aortic coarctation
Cushing syndrome
Eclampsia
Glomerulonephritis
Hydatiform mole
Conn syndrome
Hyperthyroidism
Malignant hypertension
Complications
Eclamptic seizures
Intracranial hemorrhage
Pulmonary edema
Renal failure
Coagulopathy
Outcomes
Development of hypertension during pregnancy is associated with high maternal and fetal
morbidity and mortality. In the US, hypertension during pregnancy results in maternal
mortality rates of 2-7% each year. Transient hypertension during pregnancy can lead to
chronic hypertension development after pregnancy. Data also indicate that hypertension
during pregnancy is associated with fetal growth restriction and placental abruption.
[15][4](Level V)
Questions
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