1. Eclampsia (Preeclampsia with Severe Features)

Quick Recap

Obstetrics System, Protocol 1/6. Covers preeclampsia with severe features and eclampsia; HELLP syndrome has its own dedicated protocol (2/6) with cross-reference here.

1. Definitions

Preeclampsia: new-onset hypertension (SBP >140 or DBP >90 mmHg on at least 2 occasions >=4h apart) presenting AFTER 20 WEEKS gestation, WITH significant proteinuria. Complicates 5-10% of all pregnancies (as part of the broader hypertensive-disorders-of-pregnancy spectrum: preeclampsia, chronic hypertension, preeclampsia superimposed on chronic hypertension, gestational hypertension).

Usually seen after 34 weeks and progresses until delivery, but can develop earlier, intrapartum, or even POSTPARTUM.

Delivery of the placenta usually resolves maternal organ dysfunction and restores normotension — the placenta is the disease driver, and delivery remains the only definitive treatment.

Eclampsia: new-onset grand mal seizures in a woman with preeclampsia, without another attributable cause.

Severe features (any one defines severe preeclampsia): severe hypertension refractory to treatment, persistent CNS symptoms (headache, visual disturbance, hyperreflexia), pulmonary edema, HELLP syndrome, coagulopathy, abruptio placentae, acute kidney injury, hepatic capsule irritation/RUQ pain (rare hepatic rupture risk).

2. Organ System Manifestations

CNS: eclampsia and intracranial hemorrhage drive INCREASED MATERNAL MORTALITY — temporary blindness, headache, blurred vision, scotomata, hyperreflexia are severe-feature signs.

Hepatic: hepatic hemorrhage with capsule irritation causes RUQ pain; hepatic rupture is rare but catastrophic.

Renal: normal pregnancy INCREASES GFR/renal blood flow, LOWERING baseline creatinine (typically <=0.8 mg/dL) — preeclampsia-associated vasospasm REVERSES this normal physiologic change, so oliguria and rising creatinine can occur even at "normal-for-nonpregnant" absolute values. Renal dysfunction defined as creatinine >1.1 mg/dL OR doubling of baseline (absent other renal disease) — use the PATIENT'S OWN pregnancy baseline, not a generic nonpregnant reference range.

Fetal: intrauterine growth restriction, oligohydramnios, placental infarction can occur but are NO LONGER considered diagnostic criteria for preeclampsia itself.

3. Immediate Stabilization (ABCDE)

Airway: ALWAYS anticipate a DIFFICULT AIRWAY in pregnant patients — airway edema, increased aspiration risk, and physiologic changes of pregnancy all contribute. Intubation should be performed by a SENIOR intensivist/anesthesiologist, with difficult airway equipment checked in advance and a surgical airway backup plan identified BEFORE proceeding. Target SpO2 >95%.

Circulation: two large-bore IVs (14-16G); Foley catheter for urine output monitoring; judicious fluid administration — optimize preload while avoiding overload (Section 6); nurse in the LEFT LATERAL position (30-degree right hip wedge) to prevent supine hypotension syndrome (gravid uterus compressing the IVC).

Checklist:

4. Seizure Control — Magnesium Sulfate

Magnesium sulfate is the PREFERRED antiseizure drug in preeclampsia/eclampsia — mechanism not fully elucidated, but magnesium suppresses excitatory neurotransmitter release by replacing calcium at nerve endings.

Dosing: initial IV load 4-6g over 15-20 minutes, followed by continuous infusion 1-2 g/h, maintained through 24 HOURS POST-DELIVERY (extend if no evidence of improvement).

During an active seizure: protect the airway, ensure adequate oxygenation FIRST, then treat.

Recurrent seizure on magnesium: repeat bolus of 2-4g given over 5 minutes, concurrent with the ongoing infusion. If seizures persist despite repeat magnesium bolus, use diazepam or lorazepam as an adjunct/alternative. Amobarbital is an older alternative option.

Postpartum preeclampsia with severe features: magnesium sulfate is STILL indicated for eclampsia prevention even when the diagnosis first appears after delivery.

5. Magnesium Toxicity — Monitoring Reference Table

Narrow therapeutic range — target serum level 4-8 mg/dL (some sources cite up to 4-7 mEq/L / 2-4 mmol/L).

Meticulous monitoring: pulmonary status (respiratory rate/effort) AND deep tendon reflexes on every clinical exam — loss of patellar reflex is the EARLIEST clinically detectable warning sign before progression to respiratory/cardiac toxicity, making DTR checks a simple, essential bedside surveillance tool.

Check serum magnesium levels in any woman with impaired renal function; reduce infusion dose in renal dysfunction given magnesium's renal clearance.

Treatment of magnesium toxicity/cardiac arrest or severe cardiotoxicity: calcium gluconate 15-30mL of 10% solution IV over 2-5 minutes — the specific antidote, analogous in concept to calcium's role in hyperkalemia cardiac membrane stabilization.

Phenytoin may be used as an alternative in women with impaired renal function or compromised cardiopulmonary status where magnesium's toxicity risk is elevated.

Discontinue magnesium sulfate 24 hours after delivery (barring ongoing indication).

6. Fluid Management — A Genuine Paradox

Despite visible peripheral edema, preeclampsia patients are effectively VOLUME DEPLETED intravascularly, with HIGH peripheral vascular resistance — capillary leak and reduced oncotic pressure shift fluid into the interstitium, so total body water is increased while circulating volume is reduced. This paradox drives two management rules:

• AVOID diuretics (would worsen the already-reduced intravascular volume) EXCEPT specifically for treating pulmonary edema (Section 9)
• AVOID aggressive volume resuscitation — volume expansion has NO demonstrated benefit and risks precipitating pulmonary edema, a common cause of maternal morbidity/mortality; fluid-restrict where possible, at least until the postpartum diuresis period begins

Careful I/O measurement is essential, particularly in the immediate postpartum period. Central venous or other hemodynamic monitoring may be indicated in critical cases.

7. Blood Pressure Management

ICU-level BP control preferred, ideally with arterial line monitoring, performed WITH fetal monitoring — avoid a sudden BP fall, which can cause fetal distress.

Goal: 15-25% REDUCTION in MAP — do NOT normalize to <140/90 mmHg, as this can compromise placental perfusion. Unlike other hypertensive disorders, the underlying disease course is NOT influenced by antihypertensive therapy itself — treatment exists to prevent MATERNAL stroke and heart failure, not to treat the preeclampsia process, which only resolves with delivery.

Agents:

• Labetalol: 20mg IV initial, doubling every 10 min to a cumulative max of 300mg; can cause SEVERE BRADYCARDIA; continuous infusion 0.5-2mg/min alternative
• Hydralazine: 5-10mg IV every 20 min, max 40mg
• Nifedipine or nicardipine: effective but can cause a SUDDEN precipitous BP drop or tachycardia
• Nitroglycerin (10-100 mcg/min): prolonged use risks methemoglobinemia
• Sodium nitroprusside (0.2-8 mcg/kg/min): cyanide toxicity risk to BOTH mother and fetus — limit use to <4 hours, reserve as a last resort only

Vasodilation should be performed cautiously — organ perfusion (including uteroplacental) can be compromised, jeopardizing the undelivered fetus.

8. Fetal Assessment and Delivery Timing

Once maternal stabilization is achieved, assess fetal well-being via heart rate monitoring and ultrasound. Emergency cesarean may become necessary if fetal status worsens — but maternal stabilization is prioritized FIRST, particularly during active seizures, since fetal status often IMPROVES once the mother is stabilized.

Prematurity is the predominant cause of fetal morbidity/mortality — preeclampsia WITHOUT severe features may be managed expectantly to minimize prematurity and allow corticosteroids for fetal lung maturity.

Expedited delivery indications (regardless of gestational age given high maternal morbidity): eclampsia, persistent hypertension despite therapy, persistent CNS symptoms, pulmonary edema, HELLP syndrome, coagulopathy, abruptio placentae, acute kidney injury, refractory severe hypertension, nonreassuring fetal status, oligohydramnios (AFI <5cm), severe IUGR, oliguria (<500mL/24h), creatinine >=1.5 mg/dL, dyspnea/chest pain with SpO2 <94% room air, persistent severe headache, RUQ tenderness with worsening LFTs.

Severe hypertension AFTER 34 weeks with controlled BP and completed corticosteroid course: proceed with delivery.

BEFORE 34 weeks: offer delivery only after discussion with neonatal/anesthesia teams and after a corticosteroid course has been given (if maternal/fetal status allows this delay).

Preeclampsia is NOT an indication for cesarean delivery — many patients can have a normal vaginal delivery; mode of delivery is an obstetric decision independent of the preeclampsia diagnosis itself.

9. Acute Pulmonary Edema (Complication-Specific Management)

Management similar to nonpregnant patients: IV furosemide 20-40mg bolus over 2 minutes, repeat doses 40-60mg after 30 min or infusion if inadequate response (max 120mg/h). Careful fetal monitoring, fluid restriction, strict I/O, and positioning (head elevated) required throughout.

10. Investigations

BP series (documenting the 2-reading, >=4h-apart criterion), urinalysis for proteinuria, CBC (platelet count — HELLP screen), LFTs (AST/ALT), renal function (creatinine relative to pregnancy baseline), coagulation panel, LDH/haptoglobin (hemolysis screen if HELLP suspected), serum magnesium (renal impairment or toxicity concern), fetal heart rate monitoring and ultrasound (growth, amniotic fluid index).

11. Organ Support

Magnesium sulfate for seizure control/prophylaxis; judicious, restrictive-leaning fluid management; BP control per the 15-25% MAP reduction target; furosemide specifically for pulmonary edema; standard ICU supportive care; multidisciplinary delivery planning.

12. Consultation Matrix

13. Monitoring Framework

Continuous BP monitoring (arterial line preferred), serial deep tendon reflex and respiratory status checks (magnesium toxicity surveillance), serum magnesium level if renal impairment, strict I/O, fetal heart rate monitoring, serial labs (platelets, LFTs, renal function) tracking for HELLP/severe-feature evolution.

14. Complications

Abruptio placentae, DIC, renal insufficiency/AKI, HELLP syndrome (see dedicated protocol), eclampsia/recurrent seizure, cerebral hemorrhage, magnesium toxicity, pulmonary edema, fetal IUGR/death. Prevention: appropriate magnesium dosing with DTR/respiratory monitoring, restrictive fluid strategy, 15-25% (not full) BP reduction target, timely delivery per expedited-delivery criteria. Rescue: calcium gluconate for magnesium toxicity, standard eclamptic seizure escalation (diazepam/lorazepam), emergency cesarean for fetal deterioration, standard DIC/AKI management.

15. Escalation & De-escalation

Escalate: any severe feature develops or expedited-delivery criteria met -> proceed to delivery regardless of gestational age; recurrent seizures despite magnesium -> benzodiazepine adjunct, reassess for magnesium toxicity vs treatment failure.

De-escalate: delivered, 24h magnesium course completed, BP controlled, no evolving severe features -> discontinue magnesium, transition to standard postpartum monitoring.

16. ICU Discharge Criteria

Delivered (or safely continuing expectant management under multidisciplinary follow-up if pre-delivery and appropriate), magnesium course completed (24h post-delivery), BP controlled on oral agents, no evolving severe features, renal/hepatic function stable or improving, no ongoing seizure activity.

17. Documentation & Medicolegal Checklist

18. Key Guidelines

Magee LA, Pels A, Helewa M, et al. Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy: executive summary. J Obstet Gynaecol Can. 2014;36(5):416-441. NICE Clinical Guideline: Hypertension in pregnancy — diagnosis and management (2010, updated 2018).

19. Landmark Evidence

Martin JN Jr, Thigpen BD, Moore RC, Rose CH, Cushman J, May W. Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol. 2005;105:246-254 — shifted emphasis toward SBP as the key stroke-risk parameter.

20. Controversies

The precise BP target (15-25% MAP reduction) reflects consensus guidance balancing maternal stroke prevention against uteroplacental perfusion risk, rather than a single RCT-derived number, and some variation exists across society guidelines. Expectant management thresholds for severe preeclampsia remote from term involve genuine maternal-fetal risk tradeoffs requiring individualized, multidisciplinary decision-making rather than a fixed protocol.

21. References

1. Preeclampsia/Eclampsia chapter. Washington Manual of Critical Care, 4th ed, 2025 (Ch. 72).
2. Chawla R, Nasa P, Chawla R, Jagiasi BG. Severe Preeclampsia. ICU Protocols: A Step-wise Approach, 2nd ed. Springer; 2020 (Ch. 20).
3. Magee LA, Pels A, Helewa M, et al. Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy. J Obstet Gynaecol Can. 2014;36(5):416-441.
4. Martin JN Jr, Thigpen BD, Moore RC, Rose CH, Cushman J, May W. Stroke and severe preeclampsia and eclampsia. Obstet Gynecol. 2005;105:246-254.
5. NICE. Hypertension in pregnancy: diagnosis and management. Clinical guideline, 2010 (updated 2018).

See also: HELLP Syndrome (Obstetrics System) for the closely related hepatic/hematologic complication with its own dedicated management detail.