Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, there has been a growing and justifiable fear of catching the virus from the emergency rooms, thus decreasing the hospital visits. With Virginia State slowly reopening and HCA local hospitals resuming elective procedures, the number of emergency room visits, are recovering and increasing. We report a sad and unfortunate case of an 87-year-old female who was experiencing pressure-like chest pain but presented to the emergency room five days later out of fear of catching COVID-19 from the hospital. On presentation to the ED, she was found to have an non-ST-elevation myocardial infarction, which required urgent stenting of the left anterior descending artery. Unfortunately, several hours later, she developed fatal cardiogenic shock due to ventricular septal rupture. We are reporting this case to highlight one of the many potential bad outcomes as a result of a delay in seeking necessary medical attention due to the fear of contracting the virus.

Focal seizures related to non-ketotic hyperglycemia (NKH) are rare in clinical practice. Plasma glucose levels are usually above 16.6 mmol/L and with normal or slightly elevated serum osmolality. The occurrence of focal seizures may be augmented by the absence of ketoacidosis. Electroencephalogram (EEG) during seizures usually confirms the diagnosis, however, the absence of epileptiform discharges does not rule out seizures. A non-ketotic hyperglycemiaassociated occipital lobe seizure can manifest itself as color flashes, blurry vision with periodic confusion, and usually resolves with insulin treatment and rehydration. We are reporting a 65year-old male patient who presented with intermittent confusion and left-sided visual disturbances, found to have a blood glucose of 33.7 mmol/L with a normal anion gap of 10 and calculated serum osmolality of 303 mOsm/L. The patient's visual disturbances responded very well to rehydration and insulin treatment.

No abstract

Pituitary macroadenoma usually presents with visual field defects. Oculomotor nerve palsy is a rare presentation, and usually a sign of para-sellar growth and cavernous sinus extension. The oculomotor nerve is more susceptible to laterally transmitted pressure by pituitary mass expansion because of its anatomical location. A slow onset oculomotor nerve palsy results from either gradual compression of the nerve in the sinus wall or direct infiltration of the nerve by the pituitary tumor. We are reporting a unique case of a 68-year-old African American patient who presented to an ophthalmology clinic with left eye complete ptosis, blurry vision, and a progressive headache for a few weeks. He was found to have a nonfunctioning pituitary adenoma (NFPA) that required urgent transnasal transsphenoidal tumor resection. The patient's ocular movements significantly improved a few days postoperatively, and repeated computed tomography (CT) of the head showed complete resection of the pituitary adenoma. The postoperative morning cortisol level was significantly low, confirming the diagnosis of secondary adrenal insufficiency. The patient was treated with corticosteroid replacement therapy.

Fabry disease (FD) is an X-linked recessive lysosomal storage disease caused by a mutation of the galactosidase alpha (GLA) gene, leading to deficiency of α-galactosidase A (alpha-Gal A). This deficiency results in a progressive, multiorgan accumulation of glycolipids, most notably globotriaosylceramide (Gb3), leading to multiorgan failure and subsequently premature death. Gb3 accumulation in the podocytes, epithelial, and mesangial cells of the glomeruli results in progressive renal disease and eventually renal failure and hemodialysis (HD). There are two types of FD: early-onset classical type 1 and late-onset type 2. Although nearly a thousand mutations of the GLA gene have been identified, the majority of them are of unknown significance. Herein we report the case of a 25-year-old Caucasian male with no significant medical history who presented with peripheral neuropathy and end-stage renal failure, requiring HD. He was diagnosed with FD based on the electron microscopy findings of renal biopsy and severely reduced alpha-Gal A activity (<0.4 nmol/mL/hour). A novel mutation of c.281G>T; p.Cys94Phe was identified. On discharge from our facility, he was referred to a renal transplant center and genetic counseling.