Hypertensive Disorders of Pregnancy

Learning objectives

After completing this chapter, you should be able to distinguish chronic hypertension, gestational hypertension, preeclampsia, superimposed preeclampsia, eclampsia, and HELLP syndrome; recognize severe features even when proteinuria is absent; explain the placental and endothelial pathophysiology; identify cerebral, pulmonary, renal, hepatic, hematologic, and fetal complications; integrate magnesium and antihypertensive therapy; manage fluid cautiously; recognize postpartum disease; and make transport, escalation, and destination decisions based on maternal and fetal risk.

Opening transport scenario

A 36-year-old patient at 32 weeks is transferred for blood pressure 168/112 mm Hg, severe headache, right-upper-quadrant pain, platelets 88,000/µL, AST 142 U/L, creatinine 1.2 mg/dL, and fetal growth restriction. Urine protein is only trace. She has received magnesium and IV labetalol. During transport she becomes dyspneic, oxygen saturation falls, and crackles develop. The team must recognize that the absence of marked proteinuria does not exclude severe preeclampsia and that pulmonary edema changes both fluid and destination strategy.

1. Hypertensive-disorder spectrum

2. Diagnostic thresholds and severe features

Hypertension in pregnancy is generally defined as systolic blood pressure at least 140 mm Hg or diastolic blood pressure at least 90 mm Hg on appropriately repeated measurements. Acute severe hypertension is systolic pressure at least 160 mm Hg, diastolic pressure at least 110 mm Hg, or both, confirmed as persistent according to the emergency-treatment pathway. It requires prompt treatment to reduce maternal stroke risk.

Preeclampsia can be diagnosed without proteinuria when new hypertension is accompanied by significant organ dysfunction. Severe features include:

• Severe-range blood pressure.
• Platelet count below 100,000/µL.
• Serum creatinine above 1.1 mg/dL or doubling of baseline without another renal cause.
• Liver transaminases approximately twice normal or persistent severe right-upper-quadrant/epigastric pain not explained by another diagnosis.
• Pulmonary edema.
• New persistent headache, visual symptoms, altered mental status, or other concerning cerebral symptoms.

3. Pathophysiology

Preeclampsia begins with abnormal placentation and impaired remodeling of the uterine spiral arteries. The placenta remains relatively high-resistance and may release inflammatory and antiangiogenic factors into the maternal circulation. The result is widespread endothelial dysfunction, vasoconstriction, capillary leak, platelet activation, and altered organ perfusion.

4. Transport assessment

• Use the correct cuff size and repeat severe values promptly without creating treatment delay.
• Ask about baseline hypertension, previous preeclampsia, medication adherence, headache, vision, dyspnea, chest pain, RUQ pain, nausea, fetal movement, bleeding, and contractions.
• Perform mental-status, cranial-nerve, strength, reflex, clonus, lung, cardiac, edema, and abdominal assessment.
• Review platelets, creatinine, AST/ALT, LDH, bilirubin, urine protein, hemoglobin, fibrinogen, and coagulation when clinically relevant.
• Trend fetal heart rate, variability, decelerations, growth information, amniotic fluid, and Doppler findings when available.
• Identify magnesium indication, loading dose, maintenance rate, antihypertensive doses, response, urine output, and rescue medications.

5. Immediate treatment priorities

Acute severe hypertension requires prompt first-line antihypertensive therapy such as IV labetalol, IV hydralazine, or immediate-release oral nifedipine according to the established algorithm. Magnesium sulfate is used for seizure prophylaxis or eclampsia treatment, but it does not replace blood-pressure treatment.

1. Position to support venous return and oxygenation.
2. Treat persistent severe blood pressure promptly and document treatment intervals.
3. Continue or initiate magnesium as ordered; monitor respirations, reflexes, urine output, and mental status.
4. Use oxygen for maternal hypoxemia, not routinely for a normal saturation.
5. Avoid excessive crystalloid; pulmonary edema risk is increased.
6. Prepare for seizure, stroke, difficult airway, pulmonary edema, hemorrhage, placental abruption, and urgent delivery.
7. Notify the receiving obstetric, anesthesia, critical-care, blood-bank, and neonatal teams as indicated.

6. Eclampsia

During an eclamptic seizure, protect from injury, position when possible, support airway and oxygenation, suction as needed, and administer magnesium according to protocol. Most seizures are self-limited, but recurrent or prolonged seizure requires additional therapy and evaluation for other causes such as intracranial hemorrhage, cerebral venous thrombosis, epilepsy, toxicologic exposure, hypoglycemia, or posterior reversible encephalopathy syndrome.

Do not force objects into the mouth or delay magnesium while attempting a prolonged neurologic examination. After the seizure, reassess blood pressure, oxygenation, ventilation, glucose, trauma, fetal status, and the need for emergent delivery.

7. HELLP syndrome

HELLP may present with malaise, nausea, vomiting, right-upper-quadrant or epigastric pain, headache, or nonspecific illness. Hypertension or proteinuria may be absent or mild. The key pattern is hemolysis, liver injury, and thrombocytopenia. Transport risks include abrupt platelet decline, DIC, hepatic hematoma or rupture, placental abruption, renal injury, hemorrhage, and the need for urgent operative delivery.

8. Pulmonary edema and fluid management

New dyspnea, crackles, hypoxemia, orthopnea, or frothy sputum is not normal pregnancy physiology. Stop unnecessary fluid loading, position upright or laterally as tolerated, provide oxygen and positive pressure when indicated, and consult regarding diuresis, vasodilator therapy, or critical-care support. Differentiate preeclampsia-related pulmonary edema from cardiomyopathy, pulmonary embolism, pneumonia, aspiration, and iatrogenic overload.

9. Postpartum hypertension

Preeclampsia, severe hypertension, pulmonary edema, stroke, and eclampsia can first appear or worsen after birth. Do not dismiss headache, visual symptoms, dyspnea, epigastric pain, or severe BP because the patient is postpartum. Medication history should include drugs stopped after delivery, NSAID exposure, magnesium completion, and antihypertensive access.

10. Transport and destination decisions

Patients with severe features require a destination capable of obstetric delivery, anesthesia, blood products, critical care, and neonatal support appropriate to gestational age. Diversion should be considered for seizure, stroke signs, airway failure, pulmonary edema, persistent severe BP despite therapy, suspected abruption, hepatic rupture, hemorrhage, or sustained fetal deterioration.

11. Evolving case study

Phase 1

The patient’s trace urine protein does not reduce concern. Platelets, liver enzymes, creatinine, severe BP, headache, and RUQ pain establish severe multi-organ disease. Magnesium and antihypertensive therapy are continued with close monitoring.

Phase 2

She becomes hypoxemic with crackles after receiving two liters of crystalloid at the sending facility. Further routine fluid is stopped. She is positioned, supported with oxygen and positive pressure, and evaluated for pulmonary edema versus cardiomyopathy or embolism.

Phase 3

Severe BP recurs and fetal bradycardia develops. The original tertiary destination is 40 minutes away; a comprehensive obstetric surgical center is 9 minutes away. Immediate consultation and diversion are indicated.

12. High-yield summary

• Proteinuria is not required when qualifying organ dysfunction is present.
• Severe-range BP requires prompt treatment to reduce stroke risk.
• Magnesium prevents or treats seizure; antihypertensives treat BP.
• HELLP may occur with modest hypertension or proteinuria.
• Pulmonary edema and renal dysfunction require cautious fluid strategy.
• New postpartum symptoms can represent severe hypertensive disease.
• Fetal growth restriction and abnormal testing reflect placental disease.
• Delivery is definitive treatment, but stabilization and destination capability determine transport safety.

References

1. American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia. Practice Bulletin No. 222.
2. American College of Obstetricians and Gynecologists. Emergent Therapy for Acute-Onset, Severe Hypertension During Pregnancy and the Postpartum Period.
3. Alliance for Innovation on Maternal Health. Severe Hypertension in Pregnancy Patient Safety Bundle.
4. Society for Maternal-Fetal Medicine. Guidance on hypertensive disorders and maternal critical care.
5. International Board of Specialty Certification. Maternal Fetal Transport Microcredential Candidate Handbook. Updated April 2026.