Mackintosh, Christopher

Abstract INTRODUCTION Locations of gliomas may influence clinical presentations, molecular profiles, treatment options, and prognoses. Using the Mayo Clinic Arizona Cancer Center registry, we analyzed the frequency at which gliomas were identified in different regions of the brain. We evaluated molecular profiles, clinical courses and survival by anatomic location. METHODS Registry was queried to include patients with glioma over a 10-year period. Statistical analyses were used to compare demographic, genetic, and clinical characteristics among patients with gliomas in different locations. RESULTS 182 gliomas were identified. Of the tumors confined to a single lobe, there were 51 frontal (28.0%), 50 temporal (27.5%), 22 parietal (12.1%), and 7 occipital tumors (3.8%) identified. Multifocal disease was noted in 38 patients (20.9%). Tumors affecting temporal lobe were associated with reduced overall survival when compared to all other tumors (11.0 months vs. 13.0 months, log-rank p=0.0068). However, this disparity became insignificant when adjusted for tumor grade, age, and surgical approach [HR(95% CI) 1.26(0.87, 1.82), p=0.212]. Out of 82 cases tested for IDH-1, 10 were mutated (5.5%). IDH-1 mutation was present in 6 frontal, 2 temporal, 1 thalamic, and 1 multifocal tumor. Out of 21 cases tested for 1p19q deletions, 12 were co-deleted, 9 of which were frontal lobe tumors. MGMT methylation was assessed in 45 cases; 7 of 14 frontal tumors and 6 of 13 temporal tumors were methylated. ATRX loss was detected in 2/42 assessed cases. CONCLUSION Our results support the hypothesis that the anatomical locations of gliomas influence patients’ clinical courses. Tumors involving the temporal lobe were associated with poorer survival, though this association appeared to be driven by these patients’ more aggressive tumor profiles and higher risk baseline demographics. Molecular analysis was limited by low prevalence of genetic testing in the study sample, highlighting the importance of capturing this information for all gliomas.

During preanesthesia evaluation, patient medications are reviewed and many are not administered on the day of surgery. Additionally, neurosurgical patients can develop postoperative encephalopathy from a variety of etiologies, including metabolic derangements. We report a case of postoperative neurosurgical euglycemic ketoacidosis which presented as unexplained encephalopathy and was the result of continued action of the patient’s serum glucose cotransporter-2 (SGLT-2) inhibitor combined with perioperative fasting. A 68-year-old woman with a history of type 2 diabetes mellitus was admitted to the neurocritical care service after resection of a left temporal meningioma. On postop day 1, she became lethargic and with worsening aphasia. Laboratory studies revealed blood glucose 140 to 160 mmol/L, bicarbonate 9 mmol/L, anion gap of 21, and pH of 7.2. Urine was positive for ketones and glucose, and serum was positive for β-hydroxybutyrate. Endocrinology was consulted and the patient was diagnosed with euglycemic diabetic ketoacidosis and treated with insulin until her anion gap closed. Over the next 2 days, her neurological examination improved to baseline. Although the patient did not take empagliflozin the day of surgery, the drug has a half-life of >12 hours, and other reports have described continued glycosuria for up to 10 days after drug discontinuation. This case illustrates the need for increased awareness of SGLT-2 inhibitors and “sweet pee encephalopathy” among neurosurgical and neurointensivist teams as well as potential modification of perioperative management of patients using newly emerging SGLT-2 inhibiting pharmaceuticals.