Beyond hypertension: current concepts in postpartum posterior reversible encephalopathy syndrome - a narrative review
TL;DR
The available evidence suggests that postpartum Posterior Reversible Encephalopathy Syndrome is more appropriately viewed as the cerebral manifestation of systemic endothelial dysfunction occurring within a uniquely vulnerable postpartum physiological environment rather than solely as a neurological complication of hypertensive pregnancy.
Abstract
Background: Posterior Reversible Encephalopathy Syndrome (PRES) is an acute neurovascular syndrome characterized by vasogenic cerebral edema and heterogeneous neurological manifestations. Although most commonly associated with hypertensive disorders of pregnancy, PRES may also develop during the postpartum period, when persistent cerebrovascular vulnerability and atypical clinical presentations can delay diagnosis and increase the risk of severe maternal neurological complications. Objective: To critically review the evidence on postpartum PRES, focusing on its clinical presentation, pathophysiological mechanisms, diagnostic approach, neuroimaging characteristics, management strategies, and maternal outcomes, while examining the evolving concept of PRES as the cerebral manifestation of systemic maternal endotheliopathy. Methods: A critical narrative review was conducted through a structured literature search of the PubMed, Scopus, and Google Scholar databases. Case reports, case series, observational studies, neuroradiological investigations, and review articles addressing postpartum PRES were critically appraised and synthesized using a thematic approach. Key findings: Postpartum PRES is increasingly recognized as a heterogeneous neurovascular syndrome whose clinical spectrum extends beyond the classical triad of headache, seizures, and hypertension. Recognition of normotensive presentations, atypical neuroimaging patterns, and delayed postpartum onset has challenged the traditional view of PRES as a disorder driven exclusively by severe hypertension. Emerging evidence increasingly suggests that systemic endothelial injury, inflammatory activation, angiogenic imbalance, and impaired cerebral autoregulation may act synergistically in the pathogenesis of the syndrome. Magnetic resonance imaging is the diagnostic cornerstone, while early recognition, appropriate blood pressure control, magnesium sulfate administration when indicated, and multidisciplinary management are associated with favorable neurological outcomes. Conclusion: The available evidence suggests that postpartum PRES is more appropriately viewed as the cerebral manifestation of systemic endothelial dysfunction occurring within a uniquely vulnerable postpartum physiological environment rather than solely as a neurological complication of hypertensive pregnancy. This integrated perspective helps explain the clinical heterogeneity of the syndrome and underscores the importance of early diagnosis, continued postpartum surveillance, and timely intervention to optimize maternal outcomes.