last authored: Dec 2011, David LaPierre
Gestational hypertension, previously known as pregnancy-induced hypertension, is hypertension of systolic BP >90mmHg, with onset after 20 weeks gesational age. It is one of the most common disorders of pregnancy, affecting 5-6% of all pregnancies (Sibai, Dekker, and Kupferminc, 2005).
Pre-eclampsia is the next step in the disease progression, representing end-organ damage. This can include proteinuria, cerebral symptoms, or epigastric or right-upper quadrant pain. It occurs in 1-2% of pregnant women (Sibai, Dekker, and Kupferminc, 2005). Severe pre-eclampsia is defined as onset before 34 weeks gestation, heavy proteinuria, or one or more adverse conditions other than proteinuria.
Eclampsia occurs in 1:2000 pregnancies. It is a life-threatening condition that can lead to rapid death of both mother and fetus. It is characterized by seizures and other organ dysfunction such as pulmonary embolism. HELLP syndrome, or Hemolysis, Elevated Liver enzymes, Low Platelets, is a devestating consequence that can accompany eclampsia.
Pre-existing hypertension is defined as hypertension <20 weeks gestation. It is present in 1% of pregnant women. Pre-eclampsia can develop secondary to pre-existing hypertension.
Given the potential mortality associated with hypertensive disease, screening during pregnancy is essential. Sufficient staff, diagnostics, and treatments should be available to women who are displaying evidence of worsening condition, and transport should be arranged as necessary.
Esther is a 34 year-old woman pregnant with her third child. She has not seen a health care provider during her pregnancy, and estimates herself to be 28 weeks gestation. She presents to the emergency department with an increasingly severe headache that as lasted 48 hours. The nurse takes her blood pressure, which is 176/98.
There is no single predictor of gestational hypertension or worsening disease, but identified risk factors include:
While the etiology of gestational hypertension is unknown, it appears that improper placental development and abnormal invasion of uterine vessels leads to vascular endothelial dysfunction, with an imbalance of thromboxane (vasoconstrictor) and prostaglandin (vasodilator). This results in increased permeability, hypercoagulability, and diffuse vasospasm. Increased vasospasm leads to increased systemic pressure. There also a belief that women prone to gestational hypertension have an increased sensitivity of their vasculature to the effects of angiotensin II.
The increased incidence observed in patients using barrier contraception, in multiparous women conceiving with a new partner, and in nulliparous women, suggests a potential immunologic role.
Increased risk with family history suggests the role of genetics in some cases.
Cardiovascular and Pulmonary
As described above, symptoms of preeclampsia include:
Eclampsia symptoms include:
Ensure accurate blood pressure is taken. Non-severe hypertension should be confirmed with readings >6 hours apart, while severe hypertension should only be diagnosed with two readings >15 min apart.
Hypertension in a previously normotensive woman is defined as greater than diastolic 90mmHg.
Systolic prssure above 140mmHg, or 30 mmHg above preterm levels, should be carefully noted. However, as sBP can normally vary, it is not diagnostic.
Severe hypertension is defined as sBP >160 mmHg or dBP >110 mmHg.
Findings of worsening disease can include:
Fetal evaluation should be done, as available:
Lab investigations should include (with associated abnormal findings in brackets):
24 hour urine collection or a protein/creatinine ratio
As described, imaging of the fetus may include:
Screening is important to identify women who are developing signs and symptoms. Regular prenatal visits should be provided, assessing for symptoms, blood pressure and proteinuria. Further investigations may be carried out as clinical suspicion suggests.
Other conditions that can resemble preeclampsia include:
Conditions that can resemble HELLP syndrome include:
While the evidence of measures for prevention are not convincing, the following is recommended:
Low risk: calcium supplementation if diet is poor.
Increased risk: low-dose ASA, started before 16 weeks; calcium supplementation, regardless of dietary intake.
For all patients: avoid weight gain between pregnancies
Hypertensive disease can be life-threatening and should be aggressively managed, with a goal of 130-155 mmHg systolic. If severe hypertension or other findings are present, blood pressure, proteinuria, and fetal well-being should be closely monitored, initially as an inpatient until stable.
Mild disease can be followed as an outpatient, with weekly visits (or more frequent). This should include clinical assessment, labs, and non-stress test. Bed rest in the left lateral decubitus position may be helpful but is unproven. Sodium and fluid restriction are not as helpful as in essential hypertension. Low-dose aspirin and calcium should be given.
Always get repeat readings and assess the status of the baby before instituting medication treatment. Drugs to consider include methyldopa, labetolol, hydralazine, or nifedipine.
Avoid diuretics and ACE inhibitors due decreased intravascular volume, risk of uterine ischemia and teratogenicity for ACE.
Women with severe hypertension, preeclampsia, or eclampsia should be hospitalized.
Acute control of blood pressure should be obtained with labetalol or nifedipine. Hydralazine is a third line choice. Methyldopa is not helpful, given its long time of onset. Avoid reducing the blood pressure too quickly, however, to avoid hypoperfusion of the placenta.
Magnesium sulfate (MgSO4) should be used for prevention of worsing eclampsia and seizures.
Give fluid cautiously, as fluid overload can result in pulmonary edema. Fluid status should be monitored via Foley catheter.
Control pain, anxiety, and nausea and vomiting, as these have a significant impact on blood pressure.
If seizures begin, call for help. Maintain the mother in the lateral position. Protect the airway and provide oxygen. Treat with magnesium bolus, followed by continuous infusion. Do not give magnesium too quickly, as it can cause toxicity (loss of reflexes, flushing, somnolence, paralysis, respiratory distress, and heart block). Calcium gluconate is the antidote for toxicity. Assess for abruption following a seizure.
Delivery is the definitive treatment. If under 34 weeks, treat with glucocorticoids for fetal lung development if possible. If a decision is made to wait, perform daily non-stress tests. Weigh the risks and benefits of induction vs Cesarean section.
A drop in platelets, as seen with HELLP syndrome, can result in significant risk for bleeding. Consider transfusion of blood, platelets, or corticosteroids prior to delivery.
Risk of seizures is high in first 24 hours postpartum, requiring continued MgSO4 for 12-24 hours. Seizures can occur up to 30 days postpartum. Blood pressure control should continue as an outpatient as necessary.
Treatment with prophylaxis for thromboembolism should be considered, especially in cases of C/S, obesity, or bedrest.
A clear care plan needs to be in place for outpatient follow-up to ensure blood pressure normalizes.
If treated early, the prognosis is usually good. However the following can also occur:
British Columbia Reproductive Care Program. 2006. Hypertension in Pregnancy Guideline.
Merck manual of medical information.
authors: Reuben Kiggundu, David LaPierre