What are the key differences in radiological findings and clinicopathology between Posterior Reversible Encephalopathy Syndrome (PRES) and eclampsia, and how do their management strategies differ?

PRES vs Eclampsia: Radiological and Clinicopathological Distinctions

PRES is present in nearly all eclampsia cases (up to 100%), representing the underlying neuroimaging manifestation of eclamptic seizures rather than a separate entity, though PRES can occur without eclampsia in preeclamptic patients. 1, 2

Radiological Findings

PRES Imaging Characteristics

• Parietal lobe involvement occurs in 78% of cases, occipital lobe in 76%, frontal lobe in 63%, temporal lobe in 28%, and basal ganglia/brainstem/cerebellum in 26% 1
• Cerebral edema predominantly affects the posterior circulation territories (parietal and occipital lobes), though anterior involvement is common 2
• MRI without contrast is the most sensitive modality (87% detection rate), followed by MRI with contrast (57%), CT without contrast (34%), and CT with contrast (15%) 1
• Petechial cortical hemorrhages may be present on autopsy 2
• White matter lesions may persist long-term on follow-up imaging, though their clinical significance remains unclear 3

Eclampsia-Specific Imaging

• 97.9% of eclamptic patients demonstrate PRES on neuroimaging using standard radiological criteria 1
• The radiographic pattern is identical to PRES seen in non-obstetric conditions (hypertensive crisis, immunosuppression, chemotherapy) 4, 3

Critical distinction: Eclampsia is the clinical syndrome (seizures in preeclampsia), while PRES is the radiological manifestation—they represent the same pathophysiological process rather than separate entities 1, 4

Clinicopathological Features

Clinical Presentation

• Headache is the most common presenting symptom (87%), followed by altered mental status (51%), visual disturbances (34%), and nausea/vomiting (19%) 1
• Severe systolic hypertension (≥160 mmHg) is present in only 47% of eclamptic patients, meaning 53% have eclampsia without severe hypertension 1
• Seizures define eclampsia but are not required for PRES diagnosis 4, 2
• Occipital lobe blindness, hyperreflexia, and clonus indicate severe disease 5

Pathophysiology

Two mechanisms explain the cerebrovascular injury: 2

• Vasogenic theory: Severe hypertension exceeds cerebral autoregulation limits, causing endothelial dysfunction, blood-brain barrier breakdown, and vasogenic edema
• Vasospasm theory: Endothelial injury triggers cerebral vasoconstriction, leading to ischemia and cytotoxic edema

Both mechanisms likely coexist, with the posterior circulation being more vulnerable due to less sympathetic innervation 2

Laboratory Correlates

• HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) may coexist and represents severe preeclampsia manifestation 6
• Proteinuria ≥300 mg/24 hours defines preeclampsia but does not predict PRES severity 5, 7
• Thrombocytopenia <100×10⁹/L increases risk of abnormal coagulation and hemorrhagic complications 6

Management Differences

Acute Treatment (Identical for Both)

Blood pressure control is the cornerstone: 6, 7

• Severe hypertension (≥160/110 mmHg) requires urgent treatment with IV labetalol (20 mg bolus, then 40 mg at 10 minutes, then 80 mg every 10 minutes to maximum 220 mg) or IV hydralazine (5 mg bolus, then 10 mg every 20-30 minutes to maximum 25 mg) 6
• Non-severe hypertension can be managed with oral labetalol, nifedipine, or methyldopa targeting diastolic BP 85 mmHg and systolic 110-140 mmHg 6, 7

Seizure management: 6, 7

• Magnesium sulfate is mandatory for all eclamptic patients: 4 g IV loading dose, then 1 g/hour maintenance for 24 hours postpartum 6, 7
• Lorazepam may be required if seizures occur despite magnesium or in magnesium toxicity settings 8
• Magnesium provides both seizure prophylaxis and fetal neuroprotection if delivery occurs <32 weeks 5, 6

Delivery Timing

• Definitive treatment is delivery of the placenta and fetus once maternal stabilization is achieved 7
• Deliver at 37 weeks or earlier if severe hypertension is refractory, thrombocytopenia progresses, liver/renal function deteriorates, pulmonary edema develops, or fetal status is non-reassuring 7
• Immediate delivery is indicated once coagulopathy and severe hypertension are corrected 6

Monitoring Requirements

• High-dependency or ICU monitoring for 24-48 hours postpartum with central venous pressure, urinary output, BP, ECG, and oxygen saturation monitoring 6
• Fluid restriction to 60-80 mL/hour to prevent pulmonary edema 7
• Blood pressure monitoring every 4 hours (more frequently if severe) and laboratory tests (CBC, platelets, liver enzymes, renal function) at least twice weekly 7

Prognosis and Long-Term Outcomes

Reversibility

• Clinical and neuroimaging manifestations are reversible in the majority of patients with prompt treatment 2
• Mean hospitalization is brief (3.9 days) with appropriate therapy including antihypertensives, magnesium sulfate, diuretics, and corticosteroids for fetal lung maturity 1

Potential Complications

• Permanent vision loss and other disabling sequelae can occur in survivors, particularly with delayed diagnosis or inadequate treatment 2, 3
• Intracranial hemorrhage represents the most severe complication 4
• Long-term cognitive failures are reported by previously eclamptic women, though formal neurocognitive testing has not consistently demonstrated impairment 3

Cardiovascular Risk

• Women with preeclampsia/eclampsia history have increased lifetime risks of cardiovascular disease, stroke, diabetes mellitus, venous thromboembolism, and chronic kidney disease 7
• Follow-up at 3 months postpartum is mandatory to ensure BP, urinalysis, and laboratory normalization; persistent abnormalities require further investigation 7

Critical Pitfalls to Avoid

• Do not assume severe hypertension is required for eclampsia—53% of eclamptic patients have BP <160/110 mmHg 1
• Do not use serum uric acid or proteinuria level to guide delivery timing 7
• Do not attempt to classify as "mild" versus "severe" preeclampsia clinically—all cases can rapidly become emergencies 7
• Do not delay neuroimaging in eclamptic patients with persistent neurological symptoms, as early recognition prevents devastating sequelae 2
• Do not give corticosteroids to improve maternal outcomes in HELLP syndrome—reserve for fetal lung maturity only 6