Posterior Reversible Encephalopathy Syndrome in a Postpartum Preeclamptic Woman without Seizure

Posterior reversible encephalopathy syndrome (PRES) is a cliniconeuroradiological entity presenting with headache, confusion, visual disturbances or blindness, and seizures. Parieto-occipital white matter changes due to vasogenic oedema can be observed on imaging modalities. It rarely occurs without seizures and after delivery. We report a 33-year-old multigravida with a history of preeclampsia in term pregnancy complicated by PRES without seizures at the postpartum period. Clinical improvement with complete resolution without any complications was observed on the 6th day after delivery. Posterior reversible encephalopathy syndrome is reversible when early diagnosis is established and appropriate treatment is started without delay. 1. Introduction Posterior reversible leukoencephalopathy syndrome (PRES) is a clinical and radiological syndrome which is also known as reversible posterior cerebral edema syndrome, hyperperfusion encephalopathy, or brain capillary leak syndrome [1]. PRES has been accompanied by a number of medical conditions such as hypertensive encephalopathy, preeclampsia, eclampsia, acute or chronic renal diseases, hemolytic uremic syndrome, use of cytotoxic and immunosuppressant drugs, blood transfusion, and electrolyte disturbances [2]. Preeclampsia and eclampsia are among the most common causes of PRES. Prompt recognition and treatment are crucial to avoid the permanent damage leading to sequelae and even mortality. Clinical and radiological features of PRES include headache, encephalopathy, seizures, cortical visual changes, and parieto-occipital white matter edema visualized on neuroimaging modalities [3]. Even though PRES is increasingly recognized and reported in the current literature, its incidence is still obscure. In this case report, we present a preeclamptic pregnant woman complicated by PRES after delivery without seizures. 2. Case Report A 33-year-old multigravida at the 38th week of gestation was admitted to our clinic with complaints of headache. She had no visual abnormalities and her blood pressure was 210/120？mmHg with pulse rate of 108/minute. Urinalysis revealed 2+ proteinuria and she had bilateral pedal oedema. There was no past history of hypertension, vision abnormalities, seizures, or any other pathologies. Complete blood count revealed a hemoglobin level of 9.1？g/dL and a platelet count of 162.000/mm3. Renal and hepatic function tests as well as electrocardiogram were within normal limits. Magnesium sulphate 4？g loading dose was administered intravenously, followed by continuous intravenous infusion at 2？g per