- Clinical science
Hypertensive pregnancy disorders are the most common medical complication during pregnancy. There are four major types of hypertensive pregnancy disorders. The most common is gestational hypertension, also referred to as pregnancy-induced hypertension (PIH), which occurs after 20 weeks gestation. Preeclampsia is a form of hypertensive pregnancy disorder with multiorgan involvement. It is characterized by new-onset hypertension and proteinuria after 20 weeks gestation. Risk factors include nulliparity, a positive family history, and African-American ethnicity. Eclampsia is a severe form of preeclampsia, characterized by new-onset of eclamptic seizures (grand mal seizures). Preeclampsia may also progress to the life-threatening HELLP syndrome, which is characterized by Hemolysis, Elevated Liver enzymes, and Low Platelet count.
Hypertensive pregnancy disorders are usually diagnosed in the course of regular prenatal care, which includes regular surveillance of blood pressure, weight and urine tests. Initial treatment for all hypertensive pregnancy disorders consists of maternal and fetal monitoring until delivery is feasible. Antihypertensive treatment (e.g., labetalol, hydralazine) is indicated in severe hypertension. Magnesium sulfate is important to prevent seizures in severe preeclampsia and eclampsia. Patients with eclampsia and HELLP syndrome require immediate stabilization followed by delivery if the pregnancy is ≥ 34 weeks gestation. Delivery is the only curative option for preeclampsia and eclampsia, which are both associated with increased maternal and fetal morbidity and mortality. HELLP syndrome has a poor fetal prognosis.
These disorders are on a spectrum from less to more severe, and occur after 20 weeks gestation.
Gestational hypertension: pregnancy-induced hypertension with onset after 20 weeks gestation
- Defined as a systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg on 2 separate measurements at least 4 hours apart
- Chronic hypertension: hypertension diagnosed < 20 weeks gestation or before pregnancy
- Preeclampsia: gestational hypertension with proteinuria, renal insufficiency, thrombocytopenia, evidence of liver damage (e.g., elevated liver enzymes, epigastric pain), pulmonary edema, and/or cerebral edema (headache, visual blurring, vomiting, an altered mental status)
- Eclampsia: : severe form of preeclampsia with convulsive seizures and/or coma
- Postpartum hypertension: new-onset hypertension up to 6 months postpartum after normotensive gestation
- Etiology: not fully understood
- General risk factors
- Pregnancy-related risk factors
Smoking actually decreases the risk of developing preeclampsia!
Overview: Multiple maternal, fetal, and placental factors are involved in placental hypoperfusion, which leads to maternal hypertension and other consequences.
- Abnormal placental (or trophoblast) implantation or development in the uterus → hypoperfusion of placenta and fetus (see “Placenta” in the learning card for normal placenta formation)
- Arterial hypertension with systemic vasoconstriction causes placental hypoperfusion → release of vasoactive substances → ↑ maternal blood pressure to ensure sufficient blood supply of the fetus
- Systemic endothelial dysfunction causes placental hypoperfusion → ↑ placental release of factors → endothelial lesions that lead to microthrombosis; ;
Consequences of vasoconstriction and microthrombosis
- Organ ischemia and damage
- Chronic hypoperfusion of the placenta → insufficiency of the uteroplacental unit and fetal growth restriction
Normal placenta formation: cytotrophoblast implant into the uterus (decidua and myometrium) → infiltrate the endothelium and tunica media of the maternal spiral arteries → the spiral arteries remodel into large vessels with lower resistance → ensures sufficient blood supply for the fetus
- Asymptomatic hypertension
- Nonspecific symptoms (e.g., morning headaches, fatigue, dizziness) can occur.
- Onset: 90% occur after 34 weeks of gestation
- Usually asymptomatic
- Nonspecific symptoms may include:
- Severe hypertension (systolic ≥ 160 mmHg or diastolic BP ≥ 110 mmHg)
- Proteinuria, oliguria
- Visual disturbances (e.g., blurred vision, scotoma)
- RUQ or epigastric pain
- Cerebral symptoms (e.g., altered mental state, nausea, vomiting, hyperreflexia, clonus)
- Onset: most commonly > 27 weeks gestation (30% occur postpartum)
- Preeclampsia usually present (∼ 85%)
- Nonspecific symptoms: nausea, vomiting, diarrhea
- RUQ pain (liver capsule pain; liver hematoma)
- Rapid clinical deterioration (DIC, pulmonary edema, acute renal failure, stroke, abruptio placentae)
- Onset: the majority of cases occur in the intrapartum and postpartum period
- Most often associated with severe preeclampsia (but can be associated with mild preeclampsia)
- Eclamptic seizures: generalized tonic-clonic seizures (usually self-limited)
Prenatal screening for hypertensive pregnancy disorders
Early detection to prevent maternal and fetal complications.
- To diagnose PIH, blood pressure must be elevated on at least 2 occasions that are at least 4 hours apart
- Urine tests to determine proteinuria
- Laboratory analysis
- Further tests
|Gestational hypertension|| |
|Preeclampsia||Preeclampsia without severe features|
|Preeclampsia with severe features|| |
|HELLP syndrome|| |
- Ultrasound evaluates
Obstetric Doppler ultrasound: non-invasive method for monitoring placental and fetal blood flow
- Evaluate the uterine arteries, umbilical arteries, umbilical vein, fetal middle cerebral arteries, fetal aorta, and heart
- Cardiotocography (CTG): monitor fetal heart rate and uterine contractions (also called electronic fetal monitor)
Differential diagnosis of eclampsia
- Metabolic disorders (e.g., hypoglycemia, hyponatremia)
- Hemorrhagic stroke
- Ischemic stroke
- Withdrawal syndromes
Differential diagnosis of HELLP syndrome
- Definition: a rare disease most common in the third trimester characterized by extensive fatty infiltration of the liver, which can result in acute liver failure
- Epidemiology: < 1.4% of all deliveries
- Etiology: unknown
- Pathophysiology: dysfunction of fatty acid β-oxidation
- Laboratory analysis:
- Imaging: rule out other diagnoses (e.g., liver hematoma)
- Liver biopsy: confirms the diagnosis but biopsy during pregnancy is associated with high risk of complications for mother and fetus and should be avoided
- Therapy: : immediate Cesarean (C)-section
Intrahepatic cholestasis of pregnancy
- Definition: a rare disease most common in the third trimester that presents with pruritus, jaundice, and an elevation in serum bile acid concentrations
- Epidemiology: Intrahepatic cholestasis occurs in 0.1–0.2% of pregnancies.
- Etiology: Multifactorial Occasionally, intrahepatic cholestasis occurs in non-pregnant women using hormonal contraceptives.
- Prognosis: fully reversible postpartum
The differential diagnoses listed here are not exhaustive.
- Initial antepartum evaluation: assess maternal and fetal status and necessity for hospitalization and delivery
- Hospitalization and delivery indicated if:
- In all other cases, continue outpatient monitoring
- Maternal monitoring: (1–2 x/week): blood pressure, urine dipsticks, blood analysis (platelet count, liver enzymes, renal function)
- Fetal monitoring: ultrasound every 3 weeks and NST 1–2x weekly
- Patient education
- Antihypertensive drug therapy for severe hypertension (systolic BP ≥ 160 mmHg or diastolic BP ≥ 110 mmHg)
Delivery (only curative option!) is indicated if:
- Pregnancy is ≥ 34 0/7 weeks gestation
Pregnancy is < 34 0/7 weeks gestation with maternal or fetal instability
- Immediate delivery after stabilization (IV magnesium sulfate prophylaxis, antihypertensive drugs, corticosteroids ) if one of the following is present:
- Delivery 24–48 hours after corticosteroid administration and initial stabilization if one of the following is present:
- Procedure: vaginal delivery should be conducted if possible, but often cesarean delivery is needed for younger gestational age, immature cervix, or poor maternal or fetal condition.
Expectant management: if pregnancy < 34 weeks and mother and fetus are stable
- Monitor in facilities with maternal and neonatal ICU
- Oral antihypertensive treatment of severe hypertension
- Magnesium sulfate for prophylaxis of eclampsia
- Administer corticosteroids for fetal lung maturity
- Diuretics for pulmonary edema
Delivery is the only cure for preeclampsia.
- Airway management
- Supplemental oxygenation
- Anticonvulsive therapy
- Position patient on left lateral decubitus position → prevent placental hypoperfusion through compression of the inferior vena cava and reduce the risk of aspiration in the mother
- Expectant management in patients < 34 weeks gestation to allow time for corticosteroid administration can be considered in select cases, but the safety and benefits of this approach have not been confirmed (see “Expectant management” of preeclampsia with severe features above)
- Delivery: once the mother is stable and seizures have stopped.
Delivery is the only cure for eclampsia.
- Delivery: if ≥ 34 weeks gestation or at any gestational age with deteriorating maternal or fetal status (If the fetus is viable, delay labor until 24–48 h after corticosteroid administration)
- Maternal complications
- Fetal complications
ARDS and cerebral hemorrhage are the most common causes of death.
We list the most important complications. The selection is not exhaustive.
The prognosis of hypertensive pregnancy disorders depends on the severity of the condition and the complications that occur.
- In the majority of cases, the conditions resolve within hours or days after delivery.
- Recurrence rate in following pregnancies
- Maternal mortality
- Fetal mortality
- Prophylactic low-dose ASA PO from 12–14 weeks gestation for patients with a high risk of developing preeclampsia