Post Partum Eclampsia with Atypical Posterior Reversible Encephalopathy Syndrome - Case Report

Abstract

Posterior reversible encephalopathy syndrome (PRES) is a rare but serious clinical-neuroradiological entity characterized by headache, vomiting, visual disturbances, altered mental status, seizures, and unconsciousness, as well as characteristic imaging findings such as subcortical vasogenic edema in the bilateral parietal and occipital lobes. Eclampsia, a common obstetric emergency in pregnant or postpartum women, is a risk factor for posterior reversible encephalopathy syndrome. The majority of eclampsia cases develop after childbirth. We report a woman with PRES associated with eclampsia 15 Days post-delivery.

Keywords

Introduction

Posterior Reversible Encephalopathy Syndrome (PRES) is a rare neurological condition characterized by symptoms such as seizures, visual disturbances, headaches, and altered consciousness. It is often linked to severe hypertension, which disrupts cerebral autoregulation, leading to vasogenic edema—fluid accumulation in the brain's white matter [1]. PRES frequently occurs in postpartum eclampsia, a condition where systemic inflammation and uncontrolled blood pressure exacerbate endothelial dysfunction, resulting in a leaky blood-brain barrier and associated neurological symptoms [2]. The postpartum period is a high-risk phase due to hormonal and vascular changes that can further impair cerebral perfusion. Early diagnosis of PRES through Magnetic Resonance Imaging (MRI) is crucial, as MRI often reveals reversible edema patterns. Prompt treatment, including effective blood pressure control, seizure management, and supportive care, is essential to ensure full recovery and prevent long-term complications. The strong association between PRES and postpartum eclampsia underscores the importance of monitoring at-risk individuals during and after childbirth[1]. In around 1% of births, eclampsia occurs. [3]  Some individuals exhibit eclampsia between 48 hours and 4 weeks postpartum, even though the majority of cases occur between 20 weeks of pregnancy and 48 hours postpartum. [3–6]  Early postpartum eclampsia, which happens within 48 hours of giving birth, is therefore different from late postpartum eclampsia, which happens more than 48 hours later. [6,7]  Fifteen days after birth, we saw a woman who had both PRES and late onset postpartum eclampsia.  It is quite uncommon for PRES to coexist with late-onset postpartum eclampsia.  By raising awareness of PRES brought on by delayed onset of eclampsia, our case study may assist emergency doctors in diagnosing patients early and administering the right care.

Case Presentation

A 32-year-old female with reproductive age P₂L₁D₁ with PND-15 presented to the emergency department, with a 2-day history of severe headache, visual disturbances, seizures since 3 days associated with uprolling of eyes and confusion. She had a history of preeclampsia during pregnancy, diagnosed at 7 months of pregnancy, which was managed with antihypertensive medications and Magnesium Sulphate (MgSO?) 20cc in 30ml NS for seizure prophylaxis. There was no history of recent medication changes, infections, or significant stressors. On examination, the patient was alert but disoriented, irritable. She had bilateral visual field defects and mild left-sided weakness. Blood pressure was elevated at 170/100 mmHg. Laboratory tests revealed normal renal function and electrolyte levels, presence of proteins (++) in the urine. A lumbar puncture was performed, which showed normal cerebrospinal fluid (CSF) findings. A brain MRI with contrast revealed hyperintense signals in the subcortical white matter of both cerebral hemispheres, predominantly in the frontal lobes, without significant edema. This atypical pattern raised the suspicion of PRES. Based on the clinical presentation, imaging findings, and exclusion of other differential diagnoses, the patient was diagnosed with atypical PRES secondary to post-partum -eclampsia. The patient was managed with antihypertensive agents – Tab. Amlodipine 5mg OD to control her blood pressure, Inj. Levetiracetam 500mg IV BD, Inj. Lacosamide 100mg IV BD, Tab. Clabazam 10mg HS OD, Midazolam 2ml in 3ml NS/ SOS to control seizure activity and MgSO? with a dose of 20cc in 30ml NS was also given to patient. She was also given supportive care, including intravenous fluids and electrolyte management. Over the next few days, her blood pressure normalized, and her neurological symptoms gradually improved. A follow-up MRI showed resolution of the hyperintense signals, confirming the reversibility of the condition.

DISCUSSION

The clinical syndrome known as posterior reversible encephalopathy syndrome (PRES) is characterized by a focal neurologic deficit, acute headaches, seizures, vomiting, altered mental status, and visual impairment [1,8]. The syndrome can be caused by a number of conditions, but the most prevalent ones include systemic infections, chemotherapy, neoplasia treatment, acute blood pressure increase, transplantation, aberrant kidney function, and acute or chronic renal disease [9].  One of the most frequent situations mentioned in connection with PRES is a pregnant woman who has eclampsia, a coma, and/or convulsions without a different, recognizable reason. In this case, the patient's history of preeclampsia likely contributed to the development of atypical PRES. The absence of significant edema and the presence of hyperintense signals in the frontal lobes were atypical findings. On radiography, PRES usually reveals vasogenic edema that primarily affects the brain's bilateral parieto-occipital regions.  Even though PRES is known to have "reversible" foci and symptoms, it can sometimes develop into cytotoxic edema, which has sequelae and is irreversible.  Serious complications are avoided by early magnetic resonance imaging (MRI) diagnosis of PRES, prompt cause elimination, and antihypertensive and anticonvulsant medication. [10, 11] Even though the pathophysiology of PRES is still unclear, there are two conflicting pathophysiological mechanism explanations. The first hypothesis is the vasospasm/hypoperfusion theory.  This philosophy proposes that numerous risk factors generate vasospasm or vasoconstriction, which leads to brain hypoperfusion and cerebral ischemia, culminating in further brain vasogenic edema.  In contrast, the second theory is the hypertension/hyper perfusion hypothesis.  This theory proposes that when severe hypertension exceeds the vascular autoregulation range, it causes small artery passive expansion, vascular endothelial injury, and excessive perfusion, resulting in vasogenic edema in brain tissue. Based on an intuitive knowledge of hypertension dangers, and 75% PRES patients had moderate to severe hypertension, as well as the patients recovered following antihypertensive medication, hypertension/hyper perfusion hypothesis is widespread now. [12,13]  Eclampsia's pathophysiology is likewise not well understood. The pathophysiology of eclampsia is assumed to be influenced by a variety of variables, including altered immunological processes, placental abnormalities, oxidative stress, endothelial cell dysfunction, nutritional features, and hereditary predisposition. [14]  Eclampsia is also related with PRES, an anatomical substrate identified by neuroimaging.  Postpartum eclampsia is characterized by hyperintense foci in the occipital-parietal lobe on T2-weighted MRI.  Seizures, headaches, visual loss, and impaired sensorium are all unmistakable indicators of PRES. [3,15,16]  Focal neurological impairments other than cortical blindness are infrequent. In this case, the patient's history of preeclampsia likely contributed to the development of atypical PRES. The absence of significant edema and the presence of hyperintense signals in the frontal lobes were atypical findings. The patient's prognosis is typically favourable with a precise diagnosis and prompt and appropriate therapy.  Neurological symptoms, signs, and radiographic alterations often resolve entirely within 1-2 weeks, but delayed diagnosis and/or wrong treatment are likely to cause irreparable brain damage or even death [13,17,18]. Treatment consists of treating the underlying condition, controlling neurological symptoms, and managing hypertension. The occurrence of PRES in postpartum eclampsia remains uncertain with just a few case reports [19]. Magnesium sulphate is the preferred medication for managing seizures in postpartum eclampsia and it is also used as an anti-spasmodic agent In this case, the patient was treated with antihypertensive agents like Amlodipine 5mg OD to control her blood pressure, Inj. Levetiracetam 500mg IV BD, Inj. Lacosamide 100mg IV BD, Tab. Clabazam 10mg HS OD, Midazolam 2ml in 3ml NS and MgSO? to control seizure activity was given to patient.  The prognosis for PRES is generally favourable with appropriate and timely treatment. Most patients experience complete recovery, although some may have residual neurological deficits. In this case, the patient's symptoms resolved with treatment, and follow-up imaging confirmed the reversibility of the condition.

CONCLUSION

Atypical PRES is a rare but important condition to recognize, especially in patients with risk factors such as preeclampsia. Early diagnosis and management are crucial to prevent permanent neurological damage. This case highlights the need for a high index of suspicion and thorough evaluation in patients presenting with atypical neurological symptoms.

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