Case Presentation:

A 28–year–old woman, gravida2 para2, presented to the ER for abdominal pain and distention 2 weeks after cesarean section with total abdominal hysterectomy for placenta accreta. She was diagnosed with retrovesicular abscess which was percutaneously drained under fluoroscopic guidance. Intravenous antibiotics were given and she showed marked clinical improvement. On the fourth day, patient developed witnessed generalized tonic–clonic seizure, headache, and bilateral loss of vision which lasted for 3 hours and then resolved completely. Physical examination including fundus examination was unremarkable except for an elevated BP of 180/100 mmHg. Urine analysis revealed 3+ protein. With the impression of late postpartum eclampsia, patient was transferred to ICU while continuing labetalol, phenytoin and magnesium sulphate. T2–weighted and FLAIR images of brain MRI showed bilateral posterior parieto–occipital hyperdensities in the cortex and subcortical white matter consistent with Posterior Reversible Leukoencephalopathy Syndrome (PRES syndrome). Patient was observed for 24 hours in ICU and later transferred to a regular floor.

Discussion:

PRES syndrome was first described by Hinchey et al in 1996. It presents with headache, seizures, encephalopathy, and visual disturbances, as well as radiologic findings of focal reversible vasogenic edema presenting as hyper–densities in the posterior regions of the brain (mainly parieto–occipital). It has also been described in cases of hypertensive encephalopathy, eclampsia and as a complication of immune–suppressive therapy or antineoplastic medications. Eclampsia is the development of generalized convulsions in a pregnant or puerperal woman, usually between 20 weeks’ gestation and the first 48 hours postpartum. In contrast, Late Postpartum Encephalopathy (LPE) occurs between 48 hours and 1 month postpartum, frequently in women who have had a normal pregnancy and delivery and no signs of pre–eclamptic hypertension and proteinuria. Cerebral vasospasm is the proposed etiology of eclampsia. These features can make LPE difficult to recognize and can delay diagnosis. Because of overlapping symptoms in either condition, PRES is underdiagnosed in absence of brain imaging.

Conclusions:

LPE is very rare, with only a few reported cases to date. The presence of PRES syndrome in LPE makes this case very unique. Patients are routinely counseled about the signs and symptoms of preeclampsia during pregnancy. Likewise, before hospital discharge, patients should be educated about signs of an LPE prodrome in the postpartum period. Counseling should discuss the warning signs of severe persistent headache, nausea/vomiting, visual changes, and generalized or focal neurologic deficits. PRES syn–drome is reversible when the etiology is properly recognized and quickly treated; and if not, it can lead to irreversible neurologic sequelae.

Figure 1FLAIR image of Brain MRI showing hyperdensities in the cortex and subcortical white matter of parieto–occipital lobe consistent with Posterior Reversible Leukoencephalopathy Syndrome (PRES syndrome).