Preeclampsia and Eclampsia

Preeclampsia and Eclampsia

Hypertensive Disorders of Pregnancy Classification

Disorder	Features
Chronic hypertension	Hypertension before pregnancy or before 20 weeks gestation
Gestational hypertension/Pregnancy-Induced Hypertension (PIH)	New HTN after 20 weeks, no proteinuria/end-organ dysfunction
Preeclampsia	HTN after 20 weeks with proteinuria and/or end-organ dysfunction
Eclampsia	Preeclampsia with seizures
Chronic hypertension with superimposed preeclampsia	Chronic HTN plus new proteinuria or end-organ dysfunction

Gestational Hypertension

New-onset hypertension after 20 weeks gestation without proteinuria or end-organ dysfunction.

BP ≥140/90 mmHg on two occasions at least 4 hours apart.

Preeclampsia

New-onset hypertension after 20 weeks gestation plus either:

A. Proteinuria

≥300 mg/24 h urine

Protein/creatinine ratio ≥0.3

Dipstick ≥2+

B. End-Organ Dysfunction (even without proteinuria)

Platelets <100,000/μL
Serum creatinine >1.1 mg/dL
Doubling of baseline creatinine
Elevated liver enzymes
Pulmonary edema
New-onset headache
Visual symptoms

Severe Preeclampsia

Presence of any severe feature:

Severe Feature	Criteria
Severe hypertension	≥160/110 mmHg
Thrombocytopenia	<100,000
Renal dysfunction	Cr >1.1 mg/dL
Liver dysfunction	AST/ALT >2× normal
Pulmonary edema	Present
Neurologic symptoms	Headache, visual changes
HELLP syndrome	Present

Eclampsia

Generalized tonic-clonic seizure in a woman with preeclampsia that cannot be attributed to another cause.

Pathophysiology

Normal Pregnancy

Trophoblasts invade spiral arteries.

Result:

Large vessels
Low resistance
High flow

Placental perfusion becomes adequate.

Preeclampsia

Defective trophoblastic invasion.

Spiral arteries remain:

Narrow
Muscular
High resistance

Result:Placental ischemia.

Stage 1: Placental Dysfunction

Ischemic placenta releases:

Antiangiogenic Factors

sFlt-1 (soluble Fms-like tyrosine kinase)
Soluble endoglin

These inhibit:

VEGF
PlGF

leading to endothelial dysfunction.

Stage 2: Maternal Endothelial Dysfunction

Vasoconstriction(↑ SVR)
Capillary Leak(Edema)
Coagulation Activation(Microangiopathy)
Organ Ischemia(Brain,Kidney,Liver,Placenta)

Why Proteinuria Occurs

Endotheliosis of glomerular capillaries causes:

Loss of filtration barrier
Increased protein leakage

Why Edema Occurs

Combination of:

Capillary leak
Hypoalbuminemia
Sodium retention

Why Seizures Occur

Cerebral endothelial dysfunction causes:

Vasospasm
Hyperperfusion
BBB disruption
Vasogenic edema

This produces:Posterior Reversible Encephalopathy Syndrome (PRES) which is the major mechanism of eclamptic seizures.

Risk Factors

Maternal Risk Factors	Obstetric Risk Factors	Previous History
First pregnancy (nulliparity)	Multiple gestation	Previous preeclampsia
Age >40 years	Hydatidiform mole	Family history of preeclampsia
Obesity	IVF pregnancy
Chronic hypertension
Diabetes mellitus
Chronic kidney disease (CKD)
Autoimmune disease

Clinical Features

Symptom	Details / Significance
Headache	Persistent, frontal or occipital headache
Visual disturbance	Blurring of vision, scotoma, diplopia
Epigastric pain	Due to stretching of Glisson capsule; highly concerning for severe disease/HELLP syndrome
Nausea and vomiting	Common symptom in severe preeclampsia
Dyspnea	May indicate pulmonary edema and severe disease

Sign	Details / Significance
Hypertension	Most common clinical sign of preeclampsia
Edema	Involves face, hands, and feet; common but not diagnostic of preeclampsia
Hyperreflexia	Common in severe preeclampsia and indicates increased neuromuscular excitability
Clonus	Suggests CNS irritability and increased risk of eclamptic seizures

Laboratory Abnormalities

Investigation	Purpose / Findings
Urine protein-creatinine ratio (UPCR)	≥0.3 supports diagnosis of proteinuria
24-hour urinary protein	Gold standard; ≥300 mg/24 h diagnostic
Urine dipstick	Rapid screening; ≥2+ suggests significant proteinuria
Complete blood count (CBC)	Hemoconcentration, thrombocytopenia, evidence of HELLP syndrome
Peripheral blood smear	Schistocytes suggest microangiopathic hemolysis
Platelet count	Assess severity; <100,000/μL is a severe feature
Liver function tests (AST, ALT)	Elevated levels indicate hepatic involvement
Serum bilirubin	Elevated in hemolysis/HELLP syndrome
LDH	Elevated in hemolysis and tissue injury; often >600 U/L in HELLP
Serum creatinine	Assess renal dysfunction; >1.1 mg/dL is a severe feature
Blood urea nitrogen (BUN)	Renal assessment
Serum uric acid	Often elevated; supports diagnosis but not diagnostic
Electrolytes	Baseline renal and metabolic assessment
Coagulation profile (PT, INR, aPTT)	Evaluate DIC or severe disease
Fibrinogen level	May decrease in DIC or placental abruption
Blood group and crossmatch	If severe disease, HELLP, or anticipated delivery
Arterial blood gas (ABG)	If respiratory distress or pulmonary edema develops
Chest X-ray	Suspected pulmonary edema or heart failure
ECG	If severe hypertension or cardiac symptoms
Echocardiography	Suspected cardiomyopathy, pulmonary edema, or cardiac dysfunction
Fundus examination	Hypertensive retinopathy, retinal edema, hemorrhage
CT/MRI brain	Severe headache, focal deficits, altered sensorium, suspected PRES, stroke, or intracranial hemorrhage

Fetal Evaluation

Investigation	Purpose / Findings
Fetal movement count	Simple assessment of fetal well-being
Non-stress test (NST)	Fetal heart rate reactivity
Obstetric ultrasound	Fetal growth, amniotic fluid volume, placental assessment
Umbilical artery Doppler	Assess placental insufficiency
Middle cerebral artery Doppler	Fetal adaptation to hypoxia

Management

Three major goals:

Prevent seizures
Control blood pressure
Deliver fetus at appropriate time(Delivery of the placenta is the only definitive cure for preeclampsia.)

Blood Pressure Control

Severe Hypertension

≥160/110 mmHg Persistent for ≥15 minutes

Must be treated urgently.

Target

SBP 140–150

DBP 90–100

Avoid excessive reduction.(Placental perfusion may fall.)

Antihypertensive Drugs Used in Preeclampsia

Drug	Dose	Onset	Adverse Effects / Contraindications
Labetalol (IV)(first line)	20 mg IV → 40 mg after 10 min → 80 mg every 10 min (max 300 mg)	5–10 min	Bradycardia, hypotension, bronchospasm; avoid in asthma, severe bradycardia, heart block
Labetalol (Oral)	100–200 mg BD/TDS, can increase up to 2400 mg/day	1–2 hr	Bradycardia, fatigue, bronchospasm
Hydralazine (IV)-(Alternative first-line agent)	5–10 mg IV every 20 min until target BP achieved	10–20 min	Reflex tachycardia, headache, flushing, maternal hypotension, fetal distress if BP falls rapidly
Nifedipine Immediate Release (PO)	10 mg orally; repeat after 20–30 min if needed	10–20 min	Headache, flushing, tachycardia
Nifedipine Extended Release (PO)	30–60 mg daily	30–60 min	Peripheral edema, headache
Methyldopa (PO)	250–500 mg 2–4 times daily (max 3 g/day)	4–6 hr	Sedation, depression, fatigue, dry mouth
Nicardipine (IV Infusion)	5 mg/hr IV infusion; titrate every 15 min (max 15 mg/hr)	5–15 min	Reflex tachycardia, headache
Urapidil (IV)	Variable infusion protocols	Rapid	Hypotension, dizziness
Nitroglycerin (IV)	5–10 mcg/min infusion; titrate upward	1–2 min	Headache, hypotension
Sodium Nitroprusside (IV)	0.25–5 mcg/kg/min	Seconds	Cyanide/thiocyanate toxicity, fetal toxicity
Esmolol (IV)	Rarely used	Rapid	Fetal bradycardia
Enalapril (Postpartum)	5–20 mg/day	1 hr	Contraindicated during pregnancy
Captopril (Postpartum)	12.5–25 mg TDS	15–30 min	Contraindicated during pregnancy

Drugs Contraindicated During Pregnancy

Drug Class	Reason
ACE inhibitors (Enalapril, Ramipril, Lisinopril)	Fetal renal failure, oligohydramnios, fetal death
ARBs (Losartan, Telmisartan, Valsartan)	Fetopathy similar to ACE inhibitors
Direct renin inhibitors (Aliskiren)	Fetal toxicity
Mineralocorticoid antagonists (Spironolactone)	Potential fetal endocrine effects
Routine diuretics	May worsen intravascular depletion; use only for pulmonary edema or heart failure

Magnesium Sulfate

Gold Standard

Best drug for:

Seizure prevention
Seizure treatment

Mechanism

NMDA antagonism
Cerebral vasodilation
Reduces neuronal excitability
Magnesium sulfate is NOT an antihypertensive drug.

Why does BP sometimes fall after magnesium?

Magnesium causes:

Mild peripheral vasodilation
Reduced catecholamine release
Reduced vasospasm

Magnesium Sulfate Regimens

Pritchard Regimen (IV + IM)	Zuspan Regimen (IV Infusion)
Loading Dose: 4 g IV over 5–10 min plus 10 g IM (5 g in each buttock)	Loading Dose: 4–6 g IV over 15–20 min
Maintenance Dose: 5 g IM every 4 hours in alternate buttocks	Maintenance Dose: 1–2 g/hour continuous IV infusion
Continue only if RR >12/min, urine output >25–30 mL/hr, and patellar reflexes present	Continue only if RR >12/min, urine output >25–30 mL/hr, and patellar reflexes present
Preferred where infusion pumps are unavailable	Preferred in ICU and high-dependency units
More painful due to repeated IM injections	More comfortable for the patient
Widely used in resource-limited settings	Most commonly used in tertiary care and critical care settings

Duration of Therapy (Both Regimens)

Situation	Duration
Severe preeclampsia (seizure prophylaxis)	Continue for 24 hours after delivery
Eclampsia	Continue for 24 hours after the last seizure or 24 hours after delivery (whichever is later)

Timing of Delivery

Delivery Recommended Regardless of Gestation

Eclampsia
HELLP
Pulmonary edema
DIC
Placental abruption
Uncontrolled hypertension
Persistent neurologic symptoms
Fetal compromise

≥37 Weeks —Deliver.
34–37 Weeks— Usually deliver.
<34 Weeks—Selected cases may undergo expectant management in tertiary-center.

Fluids

Very cautious.
Preeclamptic patients are: Intravascularly depleted but simultaneously Extravascularly overloaded
Aggressive fluids precipitate pulmonary edema.

Fluid Strategy

Generally:80–100 mL/hr crystalloid unless bleeding.

High-Yield Exam Pearls

Delivery is the only definitive cure for preeclampsia.
Magnesium sulfate is superior to diazepam and phenytoin for eclampsia.
Most common cause of seizure in severe preeclampsia = PRES.
Most common cause of maternal death = Intracranial hemorrhage and complications of severe hypertension.
Most common fetal complication = Prematurity due to indicated early delivery.
HELLP syndrome may occur even without severe hypertension.
Pulmonary edema is a major cause of ICU admission in severe preeclampsia.
Loss of deep tendon reflexes is the earliest clinical sign of magnesium toxicity.
Severe hypertension (≥160/110 mmHg) requires urgent treatment within minutes, not hours.
The definitive treatment for eclampsia is stabilization followed by delivery, irrespective of gestational age once the mother is stabilized.