LBSAT127 An Underrecognized Entity: Hypercalcemia Induced PRES

Abstract

Abstract Introduction Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiological entity that can present with headaches, focal neurological deficits, altered mental status, and seizures. Common etiologies are uncontrolled hypertension, preeclampsia/eclampsia, and chemotherapeutic agents. Hereby, we present a patient with status epilepticus secondary to PRES induced by hypercalcemia due to primary hyperparathyroidism. Clinical Case A 59-year-old Caucasian female with history of T2DM, GERD, gout, and bowel resection for an incarcerated abdominal hernia three weeks ago presented to the emergency department due to seizure-like movements. She had no history of seizures. Initial vitals showed HR of 96 bpm, BP of 148/67 mmHg, RR of 20 rpm, Temperature of 97.7F, and a BMI of 31.5 kg/m2. Physical exam revealed the presence of abdominal wound-vac and tonic-clonic movements that failed to improve with lorazepam, midazolam, and levetiracetam; hence she was intubated for airway protection and started on propofol. Lumbar puncture performed in the ED was unremarkable. Laboratory studies were pertinent for acute kidney injury (AKI) with a serum creatinine of 1.78 mg/dL, lactic acid of 6.1 mmol/L, and serum calcium of 14.5 mg/dL (8.7-10.4) with albumin of 4.2 g/dL. AKI and lactic acidosis rapidly improved with IV fluids. CT-head without contrast was negative for any acute pathologies. MRI-brain showed abnormal subcortical FLAIR signals within the bilateral parietal and occipital lobes with corresponding diffusion restriction in bilateral occipital lobes consistent with PRES. Continuous EEG (cEEG) showed ongoing epileptiform activity with an intermittent suppression pattern. Hypercalcemia workup revealed inappropriately normal intact-PTH of 45.9 pg/mL (10. 0-66. 0), PTHrP <2pmol/L, and 25-(OH)-Vitamin-D3 level of 34 ng/mL (30. 0-100. 0). Paraproteinemia work-up was negative. Thyroid ultrasound demonstrated an incidental nodule in the external aspect of the inferior right lobe measuring 6×3×3mm suggestive of parathyroid gland enlargement. Hypercalcemia was successfully treated with aggressive IV fluids and zoledronic acid. Repeat cEEG showed resolution of epileptiform discharges. She was successfully extubated without recurrence of seizures. She was determined to have hypercalcemia induced PRES secondary to primary hyperparathyroidism. Given the significant elevation of calcium and associated neurological symptoms, she met the surgical criteria and was discharged with outpatient parathyroidectomy plan. Conclusion PRES secondary to severe hypercalcemia has been described in the literature, albeit rarely. The exact pathophysiology is unclear but thought to be due to vasospasm based on cerebral angiogram studies. Early recognition of hypercalcemia as a culprit for PRES along with prompt treatment is crucial to treat life-threatening complications of PRES. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.