Hypertensive Disorders of Pregnancy

Hypertensive disorders complicate roughly 5–10% of pregnancies and remain a leading cause of maternal mortality in India (second only to haemorrhage). This is the single largest scoring topic in NEET PG obstetrics — diagnostic cut-offs, magnesium sulphate regimens, choice of antihypertensive, and the timing of delivery recur almost every year.

Classification (ACOG / ISSHP)

Four core entities are recognised. Getting the definitions exact is half the battle.

Entity	BP & timing	Proteinuria	Key point
Chronic (pre-existing) hypertension	≥140/90 before 20 weeks (or pre-pregnancy, or persists >12 weeks postpartum)	Variable	Predates pregnancy
Gestational hypertension	≥140/90 after 20 weeks, no proteinuria, no features	Absent	~25% progress to preeclampsia
Preeclampsia	≥140/90 after 20 weeks	Present OR end-organ involvement	See criteria below
Preeclampsia superimposed on chronic HTN	New proteinuria/worsening BP after 20 weeks in a chronic hypertensive	New/worsening	Worst prognosis

High-yield: Hypertension appearing before 20 weeks is chronic HTN (or molar pregnancy/multiple gestation if preeclampsia features appear early). Preeclampsia before 20 weeks = think hydatidiform mole.

BP thresholds: Mild = 140–159 / 90–109 mmHg. Severe = ≥160/110 mmHg. Two readings ≥4 hours apart confirm; in severe range, a shorter interval (minutes) suffices to start treatment.

Diagnostic criteria for preeclampsia

Proteinuria is no longer mandatory. Preeclampsia = new-onset HTN after 20 weeks plus proteinuria OR any severe/end-organ feature.

Proteinuria (any one):

• ≥300 mg in 24-hour urine (gold standard)
• Protein/creatinine ratio ≥0.3 mg/mg
• Dipstick ≥1+ (only if quantitative unavailable)

Features of preeclampsia with severe features (any one upgrades to "severe", regardless of proteinuria):

System	Severe feature
Cardiovascular	BP ≥160/110 mmHg
Renal	Creatinine >1.1 mg/dL (or doubling of baseline)
Hepatic	Transaminases ≥2× normal; severe persistent RUQ/epigastric pain
Haematological	Platelets <1,00,000/µL
CNS	Headache, visual disturbance, hyperreflexia, clonus
Pulmonary	Pulmonary oedema

High-yield: Massive proteinuria and fetal growth restriction are NO LONGER classified as "severe features" in current ACOG criteria — a favourite trick question. The five severe features are BP, platelets, liver, kidney, and CNS/pulmonary.

Etiology & pathophysiology

The disease is a two-stage disorder:

Stage 1 — abnormal placentation: Failure of the second wave of trophoblastic invasion (16–20 weeks) → spiral arteries remain narrow, high-resistance → placental ischaemia.

Stage 2 — maternal syndrome: Ischaemic placenta releases anti-angiogenic factors → sFlt-1 (soluble fms-like tyrosine kinase-1) ↑ and soluble endoglin ↑, while PlGF (placental growth factor) ↓ and VEGF ↓. Net result: widespread endothelial dysfunction, vasospasm, and capillary leak.

Stepwise cascade: Defective trophoblast invasion → placental ischaemia → ↑sFlt-1 / ↓PlGF → endothelial dysfunction → vasospasm + ↑capillary permeability → hypertension, proteinuria, oedema, end-organ damage.

High-yield: A high sFlt-1/PlGF ratio predicts preeclampsia. Ratio ≤38 has a strong negative predictive value (rules out PE in the next week).

Pathology hallmarks: glomerular endotheliosis (pathognomonic renal lesion — swollen endothelial cells occluding capillary lumen) and a vasospastic, volume-contracted state (haemoconcentration despite oedema).

Risk factors: Nulliparity, previous preeclampsia, chronic HTN, pre-existing diabetes, renal disease, antiphospholipid syndrome, obesity, age >40 or <18, multiple gestation, molar pregnancy, IVF/new paternity, family history.

Clinical features

• Symptoms of severity: persistent frontal/occipital headache, blurring of vision/scotomata, epigastric or right-upper-quadrant pain (Glisson capsule stretch), oliguria, rapidly rising oedema.
• Signs: rapid weight gain, brisk reflexes, clonus, papilloedema, generalised oedema.
• Eclampsia = preeclampsia + generalised tonic-clonic seizures not attributable to other cause. May occur antepartum (~50%), intrapartum (~25%), or postpartum (~25%, usually within 48 h but up to 4 weeks).

High-yield: Headache is the single most common premonitory symptom preceding an eclamptic fit. Epigastric pain suggests hepatic involvement / impending HELLP.

HELLP syndrome

A severe variant — a microangiopathic process that may occur without marked hypertension or proteinuria (15–20% have neither, a classic exam trap).

HELLP = Haemolysis + Elevated Liver enzymes + Low Platelets.

Tennessee (Sibai) criteria — all three required:

Component	Cut-off
Haemolysis	Abnormal peripheral smear (schistocytes), LDH ≥600 IU/L, bilirubin ≥1.2 mg/dL
EL (Elevated liver enzymes)	AST ≥70 IU/L
LP (Low platelets)	Platelets <1,00,000/µL

Mississippi classification (by platelet count):

Class	Platelets	AST/ALT	LDH
I	≤50,000	≥70	≥600
II	50,000–1,00,000	≥70	≥600
III	1,00,000–1,50,000	≥40	≥600

High-yield: The most dreaded complication of HELLP is subcapsular hepatic haematoma → rupture (sudden shock + abdominal pain). Definitive management of HELLP is delivery; corticosteroids may transiently raise platelets but do not improve maternal/perinatal outcomes per the latest evidence.

Investigations

• CBC — platelets, haematocrit (haemoconcentration; falling Hb may signal haemolysis).
• LFT — AST/ALT, LDH, bilirubin.
• Renal — serum creatinine, uric acid (rises early; reflects severity), urea.
• Urine — protein/creatinine ratio or 24-h protein.
• Peripheral smear — schistocytes, burr cells (microangiopathic haemolysis).
• Coagulation — PT/aPTT, fibrinogen if DIC suspected.
• Angiogenic markers — sFlt-1/PlGF ratio (prediction/rule-out).
• Fetal surveillance — USG for growth/liquor, umbilical artery Doppler (absent/reversed end-diastolic flow = ominous), NST/BPP.

High-yield: Serum uric acid is an early and useful marker of preeclampsia severity and correlates with perinatal outcome.

Management

General principles

The only definitive cure is delivery of the placenta. Everything else buys time, controls BP, and prevents seizures.

1. Seizure prophylaxis & treatment — Magnesium sulphate (DOC)

MgSO₄ is the drug of choice for prevention and treatment of eclamptic seizures (superior to diazepam and phenytoin — Collaborative Eclampsia Trial / MAGPIE). Given to all women with preeclampsia with severe features and to all eclampsia cases.

Feature	Pritchard regimen (IM)	Zuspan regimen (IV)
Loading	4 g IV (20%) over 5 min + 10 g IM (5 g each buttock)	4–6 g IV over 15–20 min
Maintenance	5 g IM every 4 h (alternate buttocks)	1–2 g/hour IV infusion
Setting	Resource-limited (no infusion pump)	Where pumps & monitoring available
Duration	Continue 24 h after last fit or after delivery	Same

High-yield: Pritchard = intramuscular; Zuspan = intravenous infusion. Continue MgSO₄ for 24 hours after delivery or after the last convulsion, whichever is later.

Magnesium toxicity monitoring — therapeutic level 4–7 mEq/L. Monitor before each dose:

1. Knee/patellar reflex present (lost at ~10 mEq/L — first sign of toxicity)
2. Respiratory rate ≥12–16/min (depression at ~12–15 mEq/L)
3. Urine output ≥30 mL/h (≥100 mL in 4 h — Mg is renally excreted)

Toxicity flow: loss of deep tendon reflexes → respiratory depression → cardiac/conduction arrest.

High-yield: Antidote = Calcium gluconate 1 g (10 mL of 10%) IV slowly. Stop MgSO₄ first. Loss of patellar reflex is the earliest sign of overdose.

2. Control of blood pressure

Treat severe hypertension (≥160/110) to prevent maternal stroke. Target ≈140–150 / 90–100 (avoid precipitous drops that compromise placental perfusion).

Drug	Class	Notes
Labetalol	α/β-blocker	First-line IV for acute severe HTN
Hydralazine	Arteriolar vasodilator	IV; watch maternal hypotension/tachycardia
Nifedipine	CCB (oral)	Effective oral acute agent
Methyldopa	Central α2-agonist	First-line oral/chronic outpatient agent; safest long-term

High-yield: ACE inhibitors, ARBs, and atenolol are CONTRAINDICATED in pregnancy (fetal renal damage, oligohydramnios, growth restriction). Methyldopa is the safest long-term oral agent; labetalol, hydralazine, or oral nifedipine for acute severe hypertension.

3. Timing of delivery — the decisive intervention

Condition	Deliver at
Gestational HTN / preeclampsia without severe features	37 weeks
Preeclampsia with severe features (stable)	34 weeks
Eclampsia, HELLP, uncontrollable BP, pulmonary oedema, DIC, abruption, non-reassuring fetus	Deliver after maternal stabilisation, regardless of gestation

• Antenatal corticosteroids (betamethasone/dexamethasone) if <34 weeks for fetal lung maturity — but never delay delivery for steroids when mother is unstable.
• Vaginal delivery preferred if feasible; caesarean for obstetric indications.
• Fluids restricted (~80 mL/h) — these women are volume-contracted but leak; over-hydration → pulmonary oedema.

4. Prevention

• Low-dose aspirin (75–150 mg) started at 12–16 weeks (before 16 weeks) in high-risk women — the single most effective preventive measure.
• Calcium supplementation in populations with low dietary calcium.

High-yield: Aspirin works only if started early (12–16 weeks); it reduces preeclampsia risk by inhibiting thromboxane and restoring the prostacyclin:thromboxane balance.

Eclampsia — acute management flow

ABC / airway + left lateral, padded tongue depressor, oxygen → MgSO₄ loading dose (Pritchard or Zuspan) → control severe BP (labetalol/hydralazine) → stabilise & investigate → deliver (only definitive treatment) → continue MgSO₄ 24 h post-delivery.

High-yield: Do not try to deliver during or immediately after a fit — first control convulsions and BP, then plan delivery. Magnesium is not an antihypertensive.

Complications

Maternal: eclampsia, PRES (posterior reversible encephalopathy syndrome — occipital oedema, cortical blindness), cerebral haemorrhage (commonest cause of death), pulmonary oedema, HELLP / hepatic rupture, abruptio placentae, DIC, acute kidney injury (cortical necrosis), retinal detachment, postpartum collapse / future cardiovascular disease.

Fetal: IUGR, oligohydramnios, prematurity (iatrogenic), abruption, intrauterine death, increased perinatal mortality.

Key differentials

Mimic	Distinguishing feature
Acute fatty liver of pregnancy (AFLP)	Hypoglycaemia, prolonged PT, ↑ammonia, marked coagulopathy; Swansea criteria
TTP / HUS	Pentad (TTP), profound thrombocytopenia, normal LFTs, ADAMTS13 ↓; renal failure dominant in HUS
Epilepsy	Pre-existing seizure history, normal BP, no proteinuria
Chronic HTN	Onset <20 weeks
Gestational thrombocytopenia	Mild (>70,000), no haemolysis/organ damage

High-yield: AFLP vs HELLP — both with raised liver enzymes, but AFLP shows hypoglycaemia, hyperammonaemia, and prolonged PT/INR (true synthetic liver failure), whereas HELLP has near-normal glucose and coagulation early. TTP has normal liver enzymes and very low ADAMTS13.

Recently asked / exam angle

• Pritchard vs Zuspan — IM vs IV; loading and maintenance doses verbatim.
• First sign of magnesium toxicity = loss of patellar reflex; antidote = calcium gluconate.
• Platelet threshold for "severe feature" and for HELLP = <1,00,000/µL.
• Which features are NOT severe features now: proteinuria amount and fetal growth restriction.
• Delivery timing: 37 weeks (non-severe) vs 34 weeks (severe).
• Contraindicated antihypertensives = ACEi/ARB/atenolol; DOC chronic = methyldopa.
• Aspirin prophylaxis window = 12–16 weeks.
• Pathophysiology marker = ↑sFlt-1, ↓PlGF; ratio ≤38 rules out.
• Pathognomonic renal lesion = glomerular endotheliosis.
• Commonest cause of maternal death in eclampsia = cerebral haemorrhage.
• Preeclampsia before 20 weeks → suspect molar pregnancy.

Rapid revision

1. Preeclampsia = new HTN >20 wk + proteinuria OR end-organ damage (proteinuria not mandatory).
2. Severe BP = ≥160/110; severe platelets = <1,00,000**; severe creatinine **>1.1 mg/dL.
3. MgSO₄ is DOC for seizure prophylaxis and treatment — beats diazepam/phenytoin.
4. Pritchard = IM (4 g IV + 10 g IM, then 5 g IM q4h); Zuspan = IV (4–6 g load, 1–2 g/h).
5. Continue magnesium 24 h after delivery or last fit.
6. Mg toxicity order: lost reflexes → respiratory depression → cardiac arrest; antidote calcium gluconate.
7. Acute severe BP: labetalol / hydralazine / oral nifedipine; chronic: methyldopa.
8. Avoid ACEi, ARB, atenolol in pregnancy.
9. HELLP can occur without HTN/proteinuria; dread hepatic rupture; treatment = delivery.
10. Deliver non-severe at 37 wk, severe at 34 wk; eclampsia/HELLP/instability → deliver now after stabilising.
11. Low-dose aspirin at 12–16 wk is best prevention in high-risk women.
12. ↑sFlt-1 / ↓PlGF drives endothelial dysfunction; glomerular endotheliosis is pathognomonic.