Abstract
Background
Posterior Reversible Encephalopathy Syndrome (PRES) is an acute neurological entity characterized by headache, altered mental status, visual loss and seizures. It can be triggered by multiple aetiologies including hypertension, eclampsia, cytotoxic and immunosuppressant drugs and, rarely, hypercalcaemia.
Case Report
A 64 years old woman presented with five weeks history of fatigue, poor appetite, dry mouth, constipation and abdominal discomfort and one-week history of nausea and vomiting. She was hypertensive at 177/88 mmHg with dry mucous membranes. Physical examination and neurological examination were unremarkable.
Laboratory investigation showed corrected calcium of 4.83 mmol/L (2.25-2.54) with
Ionized calcium of 2.62 mmol/L (1.15-1.27), parathyroid hormone (PTH) of 1330 ng/l (15-68), phosphate of 1.16 mmol/L(0.8-1.5), magnesium of 0.51 mmol/L (0.7-1.0) urea of 10.7 mmol/L (2.8-8.4), creatinine of 119 umol/L (49-90), potassium 3.4 mmol/L(3.5-5.1). She was aggressively rehydrated, commenced on Intravenous (IV) frusemide and was given IV zoledronic acid. Cinacalcet was commenced and titrated gradually up according to corrected calcium level (target corrected calcium level between 2.5-3.0 mmol/L).Electrolytes deficiencies corrected with replacement therapy.Ultrasound neck and parathyroid MIBG scan showed large 5.1cm heterogeneous lesion posterior to the right lobe of the thyroid extending inferiorly into the superior mediastinum consistent with parathyroid mass. Histology confirmed benign parathyroid adenoma.
38 hours after admission, the patient became intermittently confused and complained of visual symptoms followed by complete visual loss in the left eye. This was followed shortly by status epilepticus which required treatment with intravenous antiepileptic therapy and mechanical ventilation.Corrected calcium at that time was 3.82 mmol/L.Patient was noted to have left upper limb weakness.Computed tomography of the brain was normal and magnetic resonance imaging (MRI) of the brain showed bilateral symmetrical subcortical T2 hyper- intensities in the occipital- parietal lobes consistent with PRES.
By day five, corrected calcium was 2.52 mmol/L. On day six patient had successful parathyroidectomy. Post operatively PTH was 7.73 ng/L and corrected calcium 2.27 mmol/L. Repeated Brain MRI showed resolution of symmetrical subcortical T2 hyperintensities within both occipital lobes. She made a complete neurological recovery. DEXA scan showed osteoporosis (T score in left forearm of -3.8). She was commenced on bisphosphonate therapy.
In conclusion, we demonstrated hypercalcemia-induced PRES. This can be a life-threatening condition and can be reversed by proper treatment of hypercalcemia.
Posterior reversible encephalopathy syndrome presenting with atypical findings: case study
