A primigravida at 35 weeks of pregnancy is admitted with a BP of 180/110 mm Hg and diplopia. What is the name of this condition? How will you stabilize her? What may be the complications of such a case? How can you predict this disease? (1+5+4+5=15)

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I now have comprehensive information from authoritative obstetric and nephrology textbooks to answer all four parts. Let me compile the complete answer.

Severe Pre-eclampsia with Impending Eclampsia


1. Name of the Condition (1 mark)

This is Severe Pre-eclampsia with Features of Impending Eclampsia.
  • Severe pre-eclampsia is defined by BP ≥ 160/110 mm Hg after 20 weeks of gestation
  • Diplopia (double vision) is a prodromal neurological symptom indicating impending eclampsia — it signals hypertensive encephalopathy and cortical visual disturbance
  • The classical triad of impending eclampsia includes: severe headache, visual disturbances (blurring/diplopia/amaurosis), and epigastric pain

2. Stabilization (5 marks)

Management follows the Parkland Protocol for severe pre-eclampsia/eclampsia. The four pillars are:

A. Seizure Prophylaxis / Control — Magnesium Sulfate (MgSO₄)

StepDose
Loading dose4–6 g IV over 15–20 minutes
Maintenance2 g/hour IV infusion
  • MgSO₄ is the drug of choice — it is the most effective anticonvulsant, maintains uterine and fetal blood flow, and has a wide safety margin
  • Monitor continuously for signs of hypermagnesaemia: loss of deep tendon reflexes (at ~10 mg/dL), respiratory depression (at ~12 mg/dL)
  • Antidote: 1 g IV calcium gluconate (given slowly) reverses toxicity immediately
  • If seizures persist despite therapeutic MgSO₄: add diazepam or phenytoin as second-line

B. Antihypertensive Therapy (once seizure control is established)

Target: Bring diastolic BP to 90–105 mm Hg (avoid sharp drops → uteroplacental insufficiency)
DrugDose
Labetalol20 mg IV bolus, repeat q10 min PRN up to 300 mg total
Hydralazine5–10 mg IV push, repeat every 2–4 hours
Nifedipine (oral)10–20 mg orally, can be used if IV access not immediately available
ACE inhibitors and ARBs are absolutely contraindicated in pregnancy (fetal renal dysplasia, oligohydramnios).

C. Monitoring — Assess End-Organ Involvement

Baseline investigations mandatory:
  • CBC + platelets (thrombocytopenia → HELLP)
  • LFTs (hepatitis, hepatic rupture risk)
  • Serum creatinine, BUN (renal involvement)
  • Urine output — maintain ≥ 25 mL/hour
  • LDH + peripheral smear (haemolysis in HELLP)
  • Fetal heart rate monitoring + biophysical profile

D. Fluid Management

  • Restrict IV fluids — pre-eclampsia patients are at high risk for pulmonary oedema due to low oncotic pressure and capillary leak
  • Avoid diuretics and hyperosmotic agents
  • CT head if: reduced consciousness, persistent seizures, or lateralising neurological signs

E. Delivery

  • Definitive treatment is delivery of the placenta; plan timing based on gestational age, fetal maturity (35 weeks here = consider delivery after stabilisation)
  • At 35 weeks, risk of prematurity is low — proceed to delivery after maternal stabilisation

3. Complications (4 marks)

Maternal Complications

SystemComplication
NeurologicalEclamptic seizures, hypertensive encephalopathy, intracerebral oedema/haemorrhage, cortical blindness
HaematologicalHELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets), DIC
HepaticHepatitis, periportal necrosis, subcapsular haematoma, hepatic rupture (life-threatening)
RenalAcute kidney injury, acute tubular necrosis (can cause oliguria/anuria)
PulmonaryPulmonary oedema (from capillary leak + low oncotic pressure)
CardiovascularHypertensive crisis, future risk of chronic hypertension, ischaemic heart disease
DeathMaternal mortality historically 5–10%; caused mainly by eclampsia, hepatic rupture, abruption
HELLP syndrome is a particularly severe variant:
  • Microangiopathic haemolytic anaemia (schistocytes, ↑LDH, ↑bilirubin, ↓haptoglobin)
  • AST > 70 U/L
  • Platelets < 100 × 10⁹/L
  • Perinatal mortality: 7–34%

Fetal/Neonatal Complications

ComplicationDetails
IUGR (Intrauterine Growth Restriction)Placental insufficiency, most common with severe/early-onset disease
Placental abruption1–4% incidence; can cause sudden fetal demise
Preterm birthIatrogenic (indicated delivery) or spontaneous
Neonatal deathTwofold increased risk
StillbirthRelative risk 2.7× compared to normotensive controls

4. Prediction of Pre-eclampsia (5 marks)

Prediction uses a combined first-trimester screening approach (around 11–13+6 weeks):

A. Maternal Risk Factors

  • Nulliparity (primigravida — as in this case)
  • Age < 20 or > 40 years
  • BMI > 35 kg/m²
  • Personal/family history of pre-eclampsia
  • Multiple gestation
  • Chronic hypertension, diabetes, CKD, antiphospholipid antibody syndrome
  • New paternity (immunological factor)

B. Biophysical Markers

  • Uterine artery Doppler (uterine artery pulsatility index, UtA-PI): Elevated PI indicates impaired trophoblastic invasion of spiral arteries; predicts early-onset pre-eclampsia
  • Mean arterial pressure (MAP): Elevated MAP in first trimester is predictive

C. Biochemical Biomarkers

MarkerFinding in Pre-eclampsia
PAPP-A (Pregnancy-Associated Plasma Protein-A)↓ Low levels
PlGF (Placental Growth Factor)↓ Markedly reduced (< 100 pg/mL before 35 weeks has 98% NPV for ruling out delivery due to PE within 2 weeks)
sFlt-1 (Soluble fms-like tyrosine kinase-1)↑ Elevated — anti-angiogenic factor
sFlt-1:PlGF ratioRatio < 38 has 99% NPV for ruling out PE within 1 week and 95% NPV for next 4 weeks
sEng (Soluble endoglin)↑ Elevated; augments sFlt-1 effects

D. Combined Screening Performance

Using all modalities together — maternal characteristics + PAPP-A/PlGF + UtA-PI + MAP — the detection rate for early-onset pre-eclampsia (delivery < 34 weeks) reaches:
  • Maternal characteristics alone: 50%
    • Biochemical markers: 75%
    • Biophysical markers: 90%
    • Both biochemical & biophysical: 95%

E. Prevention in High-Risk Women

  • Low-dose aspirin (75–150 mg/day), started between 12–16 weeks and continued until delivery, reduces the risk of pre-eclampsia in high-risk women by ~50% for early-onset disease (ASPRE trial)
  • The sFlt-1 screening strategy was used to identify high-risk women in the ASPRE RCT with a 77% detection rate

Sources: Rosen's Emergency Medicine, 9th ed. • Comprehensive Clinical Nephrology, 7th ed. • Creasy & Resnik's Maternal-Fetal Medicine • National Kidney Foundation Primer on Kidney Diseases, 8th ed.
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