A 70-year-old immunocompetent male in South Carolina was admitted secondary to altered mental status and headache without focal neurological deficits. Head CT was negative. Lumbar puncture (LP) revealed normal glucose, elevated protein, and lymphocytosis. Opening pressure was 15 cm of H20. CSF lateral flow assay was negative for cryptococcal antigen; CSF cultures showed no growth. The patient rapidly improved on acyclovir and was diagnosed with presumed viral meningitis, as viral PCR and fungal culture were pending at time of discharge. The patient’s condition quickly worsened and the patient returned one day later with right arm weakness and dysarthria. Brain MRI revealed T2/flair signal abnormalities in the left frontal lobe with associated parenchymal enhancement. Repeat LP revealed increasing white blood cell count with a worsening lymphocytosis and decreasing glucose, and opening pressure remained normal. CSF fungal culture from the first admission grew Cryptococcus gattii, and repeated CSF cryptococcal antigen and culture returned positive. The patient was started on IV steroids, induction Amphotericin and Fluconazole, followed by maintenance oral Fluconazole. The patient’s clinical course was complicated by a brainstem lacunar infarction, which led to demise. We present this case of Cryptococcus gattii meningoencephalitis to highlight the risk factors, characteristics, and challenges in diagnosis and treatment of an emerging disease in the Southeastern United States.

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Ketamine has played a versatile role in medicine due to its wide spectrum of uses in history including use in sedation, catalepsy, somatic analgesia, bronchodilation, and recent trial in complex chronic pain syndromes. There is very little, if any, discussion in the literature of ketamine use in stroke, particularly in improving symptoms of pain after stroke. We present a case of a 40-year-old female with a past medical history of right-sided thalamic ischemic stroke complicated by Central post-stroke pain syndrome (CPSP) presented for refractory severe diffuse pain causing debility and immobility. The patient failed outpatient medical therapy consisting of anxiolytics, serotonin, and norepinephrine reuptake inhibitors. This led to increased opioid use which resulted in dependence and opioid-hyperalgesia. Upon admission, the patient was unable to sit still, with severe, sharp 10/10 pain localized to her left lower extremity. Palliative medicine was consulted for management of refractory central neuropathic pain. Inpatient oral ketamine was initiated, and titrated over the patient's hospital course. During this time, the patient showed marked improvement in GAD-7, PHQ-9, and Short Mcgill pain scores while significantly decreasing opioid requirements. We present this case to demonstrate how oral ketamine usage in centrally mediated neuropathic pain such as in CPSP can lead to pain control, decreased opioid usage, and overall improved quality of life.

A 40-year-old male smoker with HIV was admitted for cough, hypotension, and abdominal pain for 5 days. Chest radiography showed a right lower lobe consolidation. CT of the chest, abdomen, and pelvis revealed paratracheal adenopathy, a 5.8×4.5 cm mass invading the right bronchus intermedius, and dense bilateral adrenal masses, measuring 5.4×4.0 cm on the right and 4.8×2.0 cm on the left. Laboratory studies showed white blood cell count of 18.5 K/mm3, sodium of 131 mmol/L, creatinine of 1.6 mg/dL, and CD4 count of 567 cells/mm3. The random morning cortisol level was 7.0 μg/dL, the ACTH stimulation test yielded inappropriate response, and a random serum ACTH was elevated at 83.4 pg/mL. MRI brain revealed no pituitary adenoma confirming primary adrenal insufficiency. The adrenal CT washout study was consistent with solid mass content, concerning for metastasis. Bronchoscopy with endobronchial mass and paratracheal lymph node biopsy confirmed small-cell lung cancer (SCLC). Intravenous steroids, 100 mg hydrocortisone every 8 hours, improved his hypotension and abdominal pain. PET scan revealed metabolically active right paratracheal mass, right hilar mass, and bilateral adrenal masses. Treatment included palliative chemotherapy consisting of carboplatin/etoposide/atezolizumab and chest radiation. We present this novel case to demonstrate SCLC’s ability to cause primary adrenal insufficiency, as well as evaluate clinical response to chemotherapeutics.