Orris

Hypertensive diseases of pregnancy. Etiology,pathophysiology,management diagnosis and antihypertensive and anti convulsive therapy

Reading File
Reading File
Finding Sources
Finding Sources
Finding Sources
Searching PubMed

preeclampsia AND management

Searching the Web

ACOG clinical practice guideline chronic hypertension pregnancy severe hypertension preeclampsia magnesium sulfate

Reading File
Reading File
Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Searching the Web

ACOG emergent therapy acute onset severe hypertension pregnancy labetalol hydralazine nifedipine dosage magnesium sulfate

Hypertensive diseases of pregnancy: topic map

  1. Classification
    • Chronic hypertension
    • Gestational hypertension
    • Preeclampsia with or without severe features
    • Preeclampsia superimposed on chronic hypertension
    • Eclampsia and HELLP syndrome
  2. Etiology and risk factors
    • Abnormal placentation, maternal vascular disease, immune and genetic contributors
    • Risk factors such as prior preeclampsia, chronic hypertension, diabetes, renal disease, multifetal pregnancy, obesity, and antiphospholipid syndrome
  3. Pathophysiology
    • Failed spiral-artery remodeling and uteroplacental ischemia
    • Placental release of anti-angiogenic factors, especially sFlt-1, with reduced PlGF
    • Maternal endothelial dysfunction, vasospasm, capillary leak, platelet activation, and multiorgan injury
  4. Diagnosis
    • Blood-pressure criteria
    • Proteinuria criteria
    • Severe features, laboratory evaluation, maternal assessment, and fetal surveillance
  5. Management and delivery planning
    • Monitoring in non-severe disease
    • Indications for admission, corticosteroids, delivery, and postpartum surveillance
    • Prevention with low-dose aspirin for appropriate high-risk patients
  6. Antihypertensive therapy
    • Acute severe hypertension: IV labetalol, IV hydralazine, or immediate-release oral nifedipine
    • Maintenance therapy: labetalol, nifedipine extended release, methyldopa
  7. Anticonvulsant therapy
    • Magnesium sulfate for preeclampsia with severe features and eclampsia
    • Toxicity monitoring and calcium gluconate rescue

High-level overview

Hypertension in pregnancy is diagnosed when BP is ≥140/90 mmHg on two measurements at least 4 hours apart. Preeclampsia is new hypertension after 20 weeks plus proteinuria, or, even without proteinuria, evidence of maternal end-organ dysfunction. Severe BP, ≥160 systolic or ≥110 diastolic mmHg, is an obstetric emergency because of maternal stroke risk. Harrison’s Principles of Internal Medicine, 22e, pp. 3942-3943.
Preeclampsia originates primarily from placental dysfunction. Defective trophoblast invasion and incomplete spiral-artery remodeling reduce placental perfusion. The ischemic placenta releases factors such as sFlt-1 that impair angiogenesis and damage maternal endothelium. This produces hypertension, renal injury and proteinuria, thrombocytopenia, liver injury, pulmonary edema, cerebral edema, and seizures.
Delivery of the fetus and placenta is definitive treatment. In general, preeclampsia without severe features is monitored closely and delivered at 37 weeks. Preeclampsia with severe features is delivered at 34 weeks or later, or sooner after maternal stabilization if there is maternal or fetal deterioration, eclampsia, HELLP syndrome, pulmonary edema, abruption, or uncontrolled severe BP. Harrison’s Principles of Internal Medicine, 22e, p. 3943.
For persistent severe hypertension, treatment should begin promptly with IV labetalol, IV hydralazine, or oral immediate-release nifedipine. Magnesium sulfate prevents and treats eclamptic seizures but is not an antihypertensive. The usual IV magnesium regimen is 4-6 g loading over 20-30 minutes, then 1-2 g/hour infusion. Monitor respiratory rate, urine output, and deep-tendon reflexes; give IV calcium gluconate for clinically significant magnesium toxicity. Barash, Cullen, and Stoelting’s Clinical Anesthesia, 9e, p. 1926.
Which section should I expand into a detailed exam-style note?
  1. Classification and diagnosis
  2. Etiology and pathophysiology
  3. Management and timing of delivery
  4. Antihypertensive and anticonvulsant therapy

Explained in detail

Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Searching PubMed

preeclampsia AND management

Searching the Web

ACOG gestational hypertension preeclampsia practice bulletin 222 diagnosis severe features treatment magnesium sulfate

Quick answer

Explained in detail

Hypertensive diseases of pregnancy

Hypertensive disorders complicate pregnancy after 20 weeks most commonly, but chronic hypertension may be present before conception or appear earlier in pregnancy. They can cause maternal stroke, heart failure, acute kidney injury, liver injury, seizures, placental abruption, fetal growth restriction, prematurity, and fetal death.
The major disorders are:
  1. Chronic hypertension
  2. Gestational hypertension
  3. Preeclampsia with or without severe features
  4. Preeclampsia superimposed on chronic hypertension
  5. Eclampsia
  6. HELLP syndrome

1. Classification and definitions

A. Chronic hypertension

Hypertension that:
  • Is known before pregnancy, or
  • Is detected before 20 weeks of gestation, or
  • Persists beyond the postpartum period.
It may be primary (essential) hypertension or secondary to renal disease, endocrine disease, renovascular disease, etc.

B. Gestational hypertension

New hypertension after 20 weeks' gestation, without proteinuria or maternal end-organ dysfunction.
Diagnostic threshold
  • Systolic BP ≥140 mmHg and/or diastolic BP ≥90 mmHg
  • On two readings at least 4 hours apart
It is a provisional diagnosis because some patients subsequently develop preeclampsia.

C. Preeclampsia

New-onset hypertension after 20 weeks plus either proteinuria or evidence of maternal organ dysfunction.
Hypertension
  • BP ≥140/90 mmHg on two occasions at least 4 hours apart
Proteinuria: any one
  • ≥300 mg in a 24-hour urine collection
  • Urine protein:creatinine ratio ≥0.3
  • Dipstick 2+ only if quantitative testing is unavailable
Preeclampsia may be diagnosed without proteinuria if hypertension occurs with one or more signs of end-organ involvement:
  • Platelet count <100,000/µL
  • Serum creatinine >1.1 mg/dL or doubling of baseline creatinine without another explanation
  • Liver transaminases at least twice normal
  • Persistent severe right upper quadrant or epigastric pain
  • Pulmonary edema
  • New-onset headache not relieved by medication and not explained otherwise
  • Visual disturbances
Harrison’s Principles of Internal Medicine, 22e, pp. 3942-3943.

D. Preeclampsia with severe features

Preeclampsia is considered severe if there is any of the following:
  • Severe hypertension: systolic BP ≥160 mmHg or diastolic BP ≥110 mmHg
  • Thrombocytopenia: platelets <100,000/µL
  • Progressive renal insufficiency
  • Impaired liver function or persistent severe epigastric/right upper quadrant pain
  • Pulmonary edema
  • Persistent headache or visual symptoms
  • Eclampsia
Important: massive proteinuria and fetal growth restriction alone are not severe features. Creasy & Resnik’s Maternal-Fetal Medicine, 9e, hypertensive disorders chapter.

E. Superimposed preeclampsia

This occurs in a patient with chronic hypertension when there is:
  • New proteinuria after 20 weeks, or
  • A sudden worsening of BP control or proteinuria, plus
  • Thrombocytopenia, elevated liver enzymes, renal dysfunction, pulmonary edema, neurologic symptoms, or fetal growth restriction.
Creasy & Resnik’s Maternal-Fetal Medicine, 9e, pp. 1055-1056.

F. Eclampsia

Eclampsia is the occurrence of new generalized tonic-clonic seizures in a patient with preeclampsia that cannot be explained by another neurologic cause.
It can occur:
  • Before delivery
  • During labor
  • After delivery, including during the first postpartum week

G. HELLP syndrome

HELLP means:
  • Hemolysis
  • ELevated liver enzymes
  • LP: low platelet count
It is usually considered a severe form or variant of preeclampsia. Hypertension and proteinuria may be absent, so it requires a high index of suspicion in a pregnant or postpartum patient with epigastric pain, nausea, vomiting, malaise, thrombocytopenia, or abnormal liver tests.

2. Etiology and risk factors

The precise cause of preeclampsia is not fully known. It is a placenta-related multisystem disorder resulting from an interaction between abnormal placentation and a susceptible maternal vascular, metabolic, genetic, or immunologic background.

Important risk factors

High-risk factors

  • Previous preeclampsia, especially if severe or early-onset
  • Chronic hypertension
  • Chronic kidney disease
  • Diabetes mellitus, type 1 or type 2
  • Antiphospholipid syndrome
  • Systemic lupus erythematosus
  • Multifetal pregnancy
  • Assisted reproductive pregnancy in some settings

Moderate-risk factors

  • First pregnancy
  • Obesity
  • Maternal age ≥35 years
  • Family history of preeclampsia
  • Previous adverse pregnancy outcome, such as fetal growth restriction or stillbirth
  • Long interval since prior pregnancy
  • Social and demographic factors associated with reduced access to antenatal care

Etiologic mechanisms

1. Abnormal trophoblast invasion and placentation

Normally, extravillous trophoblasts invade the maternal spiral arteries early in pregnancy. These vessels become wide, low-resistance channels that provide a large, steady blood supply to the placenta.
In preeclampsia:
  • Trophoblast invasion is shallow.
  • Spiral arteries remain narrow, muscular, and responsive to vasoconstriction.
  • Uteroplacental perfusion is reduced.
  • Placental ischemia and oxidative stress result.

2. Angiogenic imbalance

The ischemic placenta releases anti-angiogenic factors, particularly:
  • Soluble fms-like tyrosine kinase-1, or sFlt-1
  • Soluble endoglin
sFlt-1 binds and reduces the activity of vascular endothelial growth factor and placental growth factor, or PlGF. This leads to impaired endothelial health and impaired vascular relaxation.
Preeclampsia is associated with increased sFlt-1 and reduced PlGF. Harrison’s Principles of Internal Medicine, 22e, pp. 3942-3943.

3. Maternal endothelial dysfunction

Generalized endothelial injury produces:
  • Vasoconstriction and hypertension
  • Increased capillary permeability and edema
  • Platelet activation and consumption
  • Microangiopathy
  • Reduced organ perfusion
  • Activation of coagulation pathways

4. Immunologic and genetic influences

Normal placentation requires appropriate maternal immune tolerance to fetal and paternal antigens. Abnormal immune adaptation may contribute to defective placentation in some pregnancies. There is also familial predisposition, and fetal/placental genetic variation near the FLT1 locus has been associated with preeclampsia. Creasy & Resnik’s Maternal-Fetal Medicine, 9e.

3. Pathophysiology and organ effects

A useful sequence is:
Abnormal placentation → placental hypoperfusion/ischemia → anti-angiogenic and inflammatory factor release → maternal endothelial dysfunction → vasospasm, capillary leak, coagulation activation, and multiorgan injury.

A. Blood vessels and cardiovascular system

Endothelial dysfunction causes arteriolar vasospasm and increased systemic vascular resistance.
Consequences:
  • Hypertension
  • Reduced uteroplacental perfusion
  • Risk of placental abruption
  • Risk of intracranial hemorrhage and stroke in severe hypertension
  • Pulmonary edema due to capillary leak, low oncotic pressure, left ventricular dysfunction, excessive IV fluid, or a combination

B. Kidney

Renal endothelial injury causes glomerular endotheliosis, characterized by swollen glomerular endothelial cells and narrowed capillary lumina.
Consequences:
  • Reduced glomerular filtration rate
  • Proteinuria
  • Oliguria in severe disease
  • Increased creatinine
  • Sodium retention and edema

C. Liver

Hepatic vasospasm and microvascular injury cause:
  • Elevated transaminases
  • Right upper quadrant or epigastric pain
  • Subcapsular hepatic hematoma
  • Rarely, liver rupture
In HELLP syndrome, microangiopathic hemolysis and platelet consumption are prominent.

D. Brain

Cerebral vasospasm, endothelial dysfunction, loss of autoregulation, cerebral edema, and posterior reversible encephalopathy syndrome can occur.
Clinical manifestations:
  • Severe headache
  • Hyperreflexia or clonus
  • Visual disturbance
  • Altered mental status
  • Seizures, namely eclampsia
  • Intracranial hemorrhage in severe hypertension

E. Placenta and fetus

Reduced uteroplacental blood flow can cause:
  • Fetal growth restriction
  • Oligohydramnios
  • Non-reassuring fetal testing
  • Placental abruption
  • Prematurity because delivery may become necessary
  • Stillbirth in severe untreated disease

4. Clinical assessment and diagnosis

History

Ask about:
  • Headache, especially persistent or severe
  • Blurred vision, flashing lights, scotomata
  • Right upper quadrant or epigastric pain
  • Nausea and vomiting
  • Dyspnea, chest pain, cough
  • Reduced urine output
  • Sudden swelling of hands or face
  • Reduced fetal movements
  • Past hypertension, renal disease, diabetes, lupus, thrombophilia, or prior preeclampsia
Edema is common in normal pregnancy and is not diagnostic by itself.

Examination

  • Measure BP with appropriate cuff size and correct technique.
  • Repeat severe BP promptly, often within minutes, rather than waiting 4 hours.
  • Check reflexes and ankle clonus.
  • Assess lungs for pulmonary edema.
  • Assess for right upper quadrant tenderness.
  • Measure oxygen saturation and urine output in severe disease.
  • Perform fetal heart rate assessment.

Investigations

Maternal tests

  • Complete blood count, especially platelets
  • Serum creatinine and electrolytes
  • AST and ALT
  • LDH, bilirubin, peripheral smear if HELLP suspected
  • Urine protein:creatinine ratio or 24-hour urine protein when needed
  • Coagulation profile if abruption, DIC, severe HELLP, or major bleeding is suspected

Fetal tests

  • Ultrasound for growth and amniotic fluid volume
  • Nonstress testing or cardiotocography
  • Biophysical profile where indicated
  • Umbilical artery Doppler in fetal growth restriction
Once preeclampsia is established, repeatedly measuring proteinuria does not guide severity or management as well as BP, symptoms, platelet count, renal function, liver tests, and fetal condition. Creasy & Resnik’s Maternal-Fetal Medicine, 9e.

5. General management principles

Immediate priorities in severe disease

For severe preeclampsia or eclampsia:
  1. Admit to labor and delivery or a high-dependency/critical-care setting.
  2. Stabilize airway, breathing, and circulation.
  3. Establish IV access and monitor oxygen saturation.
  4. Measure BP frequently.
  5. Assess urine output. A Foley catheter is usually needed in severe disease.
  6. Obtain CBC, platelets, creatinine, AST/ALT, and other relevant tests.
  7. Treat persistent severe hypertension urgently.
  8. Give magnesium sulfate for seizure prevention or seizure treatment.
  9. Assess maternal and fetal status.
  10. Plan delivery once the patient is stabilized if delivery is indicated.
Avoid routine large-volume IV fluid administration because these patients have increased pulmonary-edema risk.

Definitive treatment

The only definitive cure for preeclampsia is delivery of the fetus and placenta. However, timing balances maternal safety with fetal maturity.

Preeclampsia or gestational hypertension without severe features

  • Monitor closely if before 37 weeks and maternal/fetal status is reassuring.
  • Deliver at 37 weeks 0 days.

Preeclampsia with severe features

  • Deliver at 34 weeks 0 days or later, after maternal stabilization.
  • Before 34 weeks, carefully selected stable patients may receive expectant inpatient management in a tertiary unit with maternal and neonatal intensive-care capability.
  • Give antenatal corticosteroids if preterm birth is likely, but do not delay necessary delivery solely to complete steroids.

Deliver regardless of gestational age after stabilization if there is:

  • Uncontrolled severe hypertension despite treatment
  • Eclampsia
  • Pulmonary edema
  • Stroke or persistent severe neurologic symptoms
  • HELLP syndrome with deterioration
  • Disseminated intravascular coagulation
  • Placental abruption
  • Non-reassuring fetal status
  • Fetal demise
  • Persistent severe epigastric/right upper quadrant pain or worsening liver/renal function
Harrison’s Principles of Internal Medicine, 22e, p. 3943.

Mode of delivery

The diagnosis itself is not an indication for cesarean delivery. The route depends on gestational age, cervical status, urgency, fetal presentation, fetal condition, and obstetric indications. Induction of labor is appropriate when feasible.

6. Antihypertensive therapy

Purpose

Antihypertensive drugs do not cure preeclampsia and do not prevent seizures. Their immediate role in severe hypertension is to prevent maternal complications, especially:
  • Hemorrhagic stroke
  • Hypertensive encephalopathy
  • Myocardial ischemia
  • Heart failure
  • Renal injury
  • Placental abruption

When to treat urgently

Treat acute-onset persistent severe hypertension, defined as:
  • Systolic BP ≥160 mmHg, and/or
  • Diastolic BP ≥110 mmHg,
when persistent for approximately 15 minutes. Treatment should be started as quickly as possible, generally within 30-60 minutes.
The aim is to reduce BP below the severe range, commonly to around 140-150/90-100 mmHg, while avoiding sudden hypotension that could reduce placental perfusion.

First-line drugs for acute severe hypertension

1. IV labetalol

A combined alpha- and beta-adrenergic blocker.
Typical regimen
  • 20 mg IV over 2 minutes
  • If BP remains severe after 10 minutes: 40 mg IV
  • After another 10 minutes: 80 mg IV
  • Maximum cumulative dose commonly 220-300 mg, depending on local protocol
An alternative is IV infusion, such as 1-2 mg/min in monitored settings.
Avoid or use cautiously in:
  • Asthma or active bronchospasm
  • Bradycardia
  • Heart block
  • Decompensated heart failure
  • Significant cardiac disease

2. IV hydralazine

A direct arteriolar vasodilator.
Typical regimen
  • 5-10 mg IV
  • Repeat 5-10 mg every 20 minutes as required
  • Maximum cumulative dose commonly 20 mg
Adverse effects
  • Maternal hypotension
  • Reflex tachycardia
  • Headache
  • Nausea
  • Fetal heart rate abnormalities if BP falls rapidly

3. Immediate-release oral nifedipine

A calcium-channel blocker. It is particularly useful when IV access is delayed or unavailable.
Typical regimen
  • 10 mg orally
  • Repeat 10-20 mg after 20 minutes if BP remains severe
  • Further doses according to the institutional regimen
Do not give sublingually because absorption is unpredictable and may cause an abrupt dangerous fall in BP.
Adverse effects
  • Headache
  • Flushing
  • Tachycardia
  • Hypotension
IV labetalol, IV hydralazine, and immediate-release oral nifedipine are accepted first-line acute options. Goldman-Cecil Medicine, Table: Urgent Management of Severe Hypertension in Pregnancy; Creasy & Resnik’s Maternal-Fetal Medicine, 9e.

Maintenance antihypertensive treatment

Used mainly for chronic hypertension, persistent hypertension, or after acute BP control.
DrugTypical useImportant considerations
LabetalolCommon first-line oral drugAvoid in asthma, bradycardia, heart block, decompensated heart failure
Nifedipine extended releaseCommon first-line oral drugUseful if beta-blockers are unsuitable
MethyldopaLong safety recordLess potent; may cause sedation, depression, dry mouth
HydrochlorothiazideOccasionally continued in selected chronic hypertension casesNot a usual treatment for preeclampsia-related edema
Common maintenance doses vary by local protocol and individual response. Typical regimens include oral labetalol 100-200 mg twice daily, titrated as needed, or nifedipine extended release 30 mg daily, titrated as needed.

Drugs generally avoided during pregnancy

  • ACE inhibitors: enalapril, lisinopril, captopril
  • Angiotensin receptor blockers: losartan, valsartan
  • Direct renin inhibitor: aliskiren
  • Mineralocorticoid receptor antagonists such as spironolactone, unless specialist-directed in exceptional circumstances
  • Sodium nitroprusside except as a last resort in refractory, life-threatening hypertension because of fetal cyanide/thiocyanate toxicity risk

Important point about diuretics

Diuretics do not treat the underlying pathophysiology of preeclampsia and should not be used simply for edema. They may be used for pulmonary edema under appropriate monitoring.

7. Anticonvulsant therapy: magnesium sulfate

Indications

Magnesium sulfate is indicated for:
  • Eclampsia: treatment of the seizure and prevention of recurrent seizures
  • Preeclampsia with severe features: seizure prophylaxis
  • Gestational hypertension with severe-range BP is usually managed similarly to preeclampsia with severe features
Routine magnesium sulfate in preeclampsia without severe features is individualized because the absolute seizure risk is lower.

Why magnesium sulfate?

Magnesium sulfate:
  • Reduces the risk of eclampsia
  • Is more effective than phenytoin or diazepam for prevention and treatment of recurrent eclamptic seizures
  • Has only minor BP-lowering activity and must not replace antihypertensive treatment

Standard IV regimen

Loading dose
  • Magnesium sulfate 4-6 g IV over 20-30 minutes
Maintenance
  • 1-2 g/hour IV infusion
Continue for:
  • Usually 24 hours after delivery, or
  • 24 hours after the last seizure in eclampsia
Barash, Cullen, and Stoelting’s Clinical Anesthesia, 9e, p. 1926.

If a seizure recurs

  • Give an additional 2 g IV magnesium sulfate slowly.
  • Check for other causes of seizure if it persists or is atypical.
  • Secure airway and provide oxygen.
  • Consider benzodiazepine or other antiepileptic therapy only if seizures continue despite adequate magnesium or another cause is suspected.
  • Expedite delivery after maternal stabilization. Do not attempt delivery during an uncontrolled convulsion.

Monitoring during magnesium infusion

Monitor:
  • Respiratory rate, generally maintain >12/min
  • Oxygen saturation
  • Patellar deep-tendon reflexes
  • Urine output, commonly aim for >25-30 mL/hour
  • Level of consciousness
  • Serum magnesium concentration if renal impairment, oliguria, absent reflexes, or suspected toxicity

Magnesium toxicity

Progression may include:
  • Loss of deep-tendon reflexes
  • Somnolence
  • Respiratory depression
  • Respiratory arrest
  • Cardiac conduction abnormalities or cardiac arrest at very high concentrations

Management of toxicity

  1. Stop magnesium infusion.
  2. Support airway and ventilation.
  3. Give calcium gluconate 1 g IV over about 5 minutes as antidote.
  4. Consider diuresis or dialysis in severe toxicity, particularly with renal failure.
Tintinalli’s Emergency Medicine, calcium gluconate table.

Special cautions

Use magnesium cautiously with significant renal impairment because it is renally excreted. Lower maintenance doses and serum-level monitoring may be needed.
Magnesium may be contraindicated or require specialist input in:
  • Myasthenia gravis
  • Significant renal failure
  • Heart block
  • Severe myocardial dysfunction
If magnesium is contraindicated, alternatives such as phenytoin or benzodiazepines may be considered, but they are generally less effective for eclampsia.

8. Management of an eclamptic seizure

  1. Call for obstetric, anesthesia, and neonatal support.
  2. Place the patient in the left lateral position.
  3. Protect from injury. Do not force objects into the mouth.
  4. Ensure airway patency, provide oxygen, and suction secretions when needed.
  5. Establish IV access.
  6. Give magnesium sulfate: 4-6 g IV loading dose, then infusion.
  7. Treat persistent severe BP with labetalol, hydralazine, or oral immediate-release nifedipine.
  8. Assess fetal status after maternal resuscitation.
  9. Plan delivery once the mother is stabilized. Eclampsia itself is an indication for delivery after stabilization.
  10. Continue magnesium for 24 hours after delivery or the last seizure.

9. Prevention

Low-dose aspirin

Patients at high risk for preeclampsia should receive low-dose aspirin, commonly 81 mg daily, started between 12 and 28 weeks, preferably before 16 weeks, and continued until delivery according to local guidance.
High-risk indications include:
  • Previous preeclampsia
  • Multifetal gestation
  • Chronic hypertension
  • Diabetes
  • Chronic kidney disease
  • Autoimmune disease such as lupus or antiphospholipid syndrome
Low-dose aspirin reduces the risk of preeclampsia in high-risk groups. National Kidney Foundation Primer on Kidney Diseases, 8e, pp. 2880-2885.

Other preventive points

  • Optimize chronic hypertension before conception.
  • Review and discontinue teratogenic antihypertensives before pregnancy where possible.
  • Control diabetes and renal disease.
  • Ensure early and regular antenatal surveillance.
  • Calcium supplementation may be useful in populations with low dietary calcium intake, based on local recommendations.

10. Postpartum care

Preeclampsia can first appear or worsen postpartum. Monitor BP and symptoms carefully after delivery.
Advise urgent assessment for:
  • Severe headache
  • Visual symptoms
  • Epigastric or right upper quadrant pain
  • Shortness of breath
  • Chest pain
  • Seizures
  • BP ≥160/110 mmHg
Persistent postpartum hypertension may require medications such as labetalol, nifedipine, or other drugs selected with breastfeeding and comorbidities in mind.
A history of preeclampsia is associated with higher long-term cardiovascular and renal risk. Patients should receive follow-up for BP, metabolic risk factors, and cardiovascular prevention.

Exam summary

  • Preeclampsia = hypertension after 20 weeks + proteinuria or end-organ dysfunction.
  • Severe BP = ≥160/110 mmHg. Treat urgently.
  • Severe features include severe BP, thrombocytopenia, renal dysfunction, liver dysfunction/pain, pulmonary edema, headache, or visual disturbance.
  • Eclampsia = preeclampsia + seizures.
  • Definitive treatment = delivery of placenta and fetus.
  • Acute BP drugs = IV labetalol, IV hydralazine, or immediate-release oral nifedipine.
  • Seizure drug = magnesium sulfate, 4-6 g IV loading then 1-2 g/hour.
  • Antidote for magnesium toxicity = calcium gluconate 1 g IV.
  • Timing of delivery: 37 weeks if non-severe disease; 34 weeks or earlier if severe disease or maternal/fetal deterioration.
This is a shared conversation. Sign in to Orris to start your own chat.