PRES in Eclampsia (Posterior Reversible Encephalopathy Syndrome)

Definition & Overview

"PRES is thought to be due to abnormal cerebral vascular autoregulation resulting in vasogenic edema." — Bradley and Daroff's Neurology in Clinical Practice

Pathophysiology

1. Loss of Cerebral Autoregulation (Hyperperfusion Theory)

• Severe, sudden hypertension overwhelms the brain's ability to autoregulate blood flow
• Forced vasodilation → hyperperfusion → fluid extravasation into the interstitium
• Results in vasogenic edema — predominantly in posterior (parieto-occipital) white matter
• The posterior circulation is more susceptible because it has less adrenergic innervation

2. Endothelial Dysfunction (Vasospasm Theory)

• In eclampsia, circulating anti-angiogenic factors (e.g., sFlt-1) and endothelial activation cause endothelial injury
• Damage to capillary endothelial tight junctions → fluid extravasation
• Vasodilatation and vasogenic edema occur
• This is analogous to the mechanism seen with calcineurin inhibitors (tacrolimus, cyclosporine)

Clinical Features (Classic Tetrad)

"Cortical visual deficits can occasionally be the presenting feature, others including headache and seizures." — Kanski's Clinical Ophthalmology

MRI Findings

• Modality of choice: MRI with FLAIR sequence
• Signal: T2/FLAIR hyperintensities (vasogenic edema) — hypointense on T1
• Location: Predominantly parietal and occipital lobe white matter, bilateral and roughly symmetric
• Gray matter (cortex, basal ganglia) can also be involved
• Frontal and temporal lobes may be affected in atypical/severe cases
• DWI: Typically shows no diffusion restriction (distinguishing vasogenic from cytotoxic/ischemic edema) — though areas of true infarction may show restriction in severe cases

Diagnosis

• Clinical + MRI confirmation
• CT may show cerebral edema but is less sensitive than MRI
• Lumbar puncture: not routinely required; may show elevated opening pressure
• Blood work: assess for HELLP (CBC, LFTs, LDH), renal function, proteinuria
• Exclude stroke (DWI positive) and other encephalopathies

Association with Eclampsia

• PRES is found in a significant proportion of women with severe preeclampsia and eclampsia
• The pathophysiology overlaps: both involve endothelial dysfunction and disrupted cerebral autoregulation
• Postpartum eclampsia accounts for ~25% of eclamptic seizures and can occur up to 8 weeks postpartum, even without preceding hypertension — PRES must be considered in this window
• Long-term: women with preeclampsia have more white matter lesions and are more likely to report cognitive dysfunction compared to normotensive pregnancies
• Severe cases can progress to cytotoxic edema and infarction (irreversible injury)

Management

Definitive Treatment

Seizure Control

"Magnesium is the therapy of choice to treat acute eclamptic seizures and prevent recurrence. It is more effective and has a better safety profile than phenytoin." — Rosen's Emergency Medicine

Blood Pressure Control

• Target: reduce BP by no more than 25% in the first hour, then gradually to ~160/105 mmHg
• Agents: labetalol (IV), hydralazine (IV), nifedipine (oral)
• Avoid nitroprusside in pregnancy (fetal cyanide toxicity)

General Supportive Care

• Airway management, O₂ supplementation
• Continuous fetal monitoring (>24 weeks)
• ICU-level monitoring in severe cases

Prognosis & Reversibility

• With prompt treatment, imaging and clinical findings typically resolve (the "R" in PRES)
• Irreversible infarction can occur if treatment is delayed or hypertension is extreme
• The name changed from "reversible posterior leukoencephalopathy" because gray matter involvement and frontal/temporal extension are recognized

Differential Diagnosis

• Creasy & Resnik's Maternal-Fetal Medicine, 8th ed. — Chapter 45
• Bradley and Daroff's Neurology in Clinical Practice — Chapter 40
• Rosen's Emergency Medicine — Chapter 88
• Kanski's Clinical Ophthalmology, 10th ed. — Chapter on neuro-ophthalmology