Background: Continuous glucose monitoring (CGM) is widely used in the outpatient setting for people with diabetes and has been limited to investigational use only for the inpatient population. In April 2020, the US FDA exercised enforcement discretion for the temporary use of inpatient CGM during the pandemic, thus hospitals were presented the opportunity to implement this technology. Methods: We sought to investigate the accuracy of CGM in hospitalized patients on general care floors and the intensive care unit (ICU) in attempts to decrease healthcare professional exposure to COVID-19 and ultimately improve glycemic management of patients affected by COVID-19. Point of care (POC) and laboratory (Lab) glucose values were matched with simultaneous CGM glucose values and measures of accuracy were performed to evaluate the safety and usability of CGM in this population. Our data are presented drawing a distinction between POC and Lab as reference glucose sources. Results: In 808 paired samples obtained from 28 patients (10 ICU, 18 general floor), overall mean absolute relative difference (MARD) for all patients using either POC or Lab as reference was 13.2%. When using POC as the reference glucose MARD was 13.9% and using Lab glucose as reference 10.9%. Using both POC and Lab reference glucose pairs the overall MARD for critical care patients was 12.1% and for general floor patients 14%. Conclusion: We determined, with proper protocols and safeguards in place, use of CGM in the hospitalized patient is a reasonable alternative to standard of care to achieve the goal of reducing healthcare professional exposure. Further study is necessary to validate safety, accuracy, and efficacy of this technology. Investigation and analysis are necessary for the development of protocols to utilize CGM trend arrows, alerts, and alarms.

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Pituitary apoplexy is a rare endocrine emergency due to acute infarction or hemorrhage of the pituitary gland. It most often involves an underlying adenoma. Precipitating factors include hypertension, major surgery, coagulopathy, or medications. Fulminant liver disease giving rise to a coagulopathy can lead to an increased risk of hemorrhage into the pituitary. A 20-year-old female was transferred from British Overseas Territory for evaluation of fulminant liver failure after presenting with worsening of longstanding abdominal pain and vomiting. She was taking ciprofloxacin and metronidazole for colitis and Tylenol for pain. She denied alcohol abuse, illicit drugs or herbal supplements. Her blood pressure was 107/72 mmHg and physical exam was notable for jaundice. Labs were significant for Alanine Aminotransferase (ALT) 10277 IU/L (n<35 IU/L), Aspartate aminotransferase (AST) 10886 IU/L (n<40 IU/L), total bilirubin 15 mg/dl (n<1.2 mg/dl), alkaline phosphatase 160 IU/L (n<115 IU/L) and INR 4.9 (n<1.3). She was given 100 mg of methylprednisolone. CT head without contrast (WO) completed prior to transfer showed no abnormal findings. The next day, she reported new onset severe headache and diplopia. Bilateral wrist asterixis and worsening lethargy was noted on exam. Ammonia was 278 umol/L (<n 42 umol/L). CT head WO showed a 0.6 x 0.9 x 1.0 cm hyperdense area in the posterior aspect of pituitary gland concerning for apoplexy. Additional labs showed cortisol 11 ug/dL (n<22 ug/dL), ACTH 2.9 pg/mL (n 7.2-63.3 pg/mL), TSH 0.04 uIU/mL (n 0.3-4.5 uIU/mL), free (F) T4 1.4 ng/dl (n 0.6-1.5 ng/dl), FT3 1.2 ng/dl (n 2.4-4.2 ng/dl), FSH 1.8 mIU/ml (n 3.5-12.5 mIU/ml), LH <0.1 mIU/mL (n 2.4-12.6 mIU/ml), prolactin 49 ng/mL (n 5-23 ng/mL), and IGF-1 141 ng/mL (n 109-372 ng/mL). She was managed conservatively with hydrocortisone for secondary adrenal insufficiency and hypopituitarism. With extensive work up, no underlying cause was found for her fulminant hepatic disease. She underwent a deceased donor liver transplant. Perioperatively, she was given 200 mg methylprednisolone which was subsequently tapered to 5 mg prednisone. Postoperative course was complicated by a new right parietal lobe hemorrhage. There was no change in pituitary hemorrhage size. As her FT4 trended down to 0.6 ng/dl, along with suppressed TSH, she was started on 50 mcg of levothyroxine. Upon discharge, she was advised to follow with an endocrinologist and have her hormones revaluated once the acute phase has resolved. Pituitary apoplexy as a consequence of coagulopathy caused by liver failure has not been described before. Although she was given methylprednisolone which can suppress ACTH for up to 48 hours, ACTH deficiency is the most critical endocrine dysfunction and is present in nearly 70% of cases of pituitary apoplexy. Therefore, urgent treatment of secondary adrenal insufficiency is warranted along with thyroid hormone replacement.

Summary Central diabetes insipidus (DI) is characterized by decreased release of antidiuretic hormone, resulting in a variable degree of polyuria. The etiologies are variable, with the vast majority of cases either being idiopathic or resulting from primary or secondary tumors. Such tumors include craniopharyngioma, Langerhans cell histiocytosis, or a variety of inflammatory, vascular, or granulomatous diseases. It is exceptionally rare for pituitary adenomas to present with DI. We describe a young patient who first presented with symptoms consistent with DI. He was tested for DI and found to have panhypopituitarism due to a metastatic pineal germ cell tumor causing thickening of his pituitary stalk. Learning points New onset central diabetes insipidus requires dedicated pituitary MRI for determination of etiology. Germ cell tumors in the pineal and suprasellar regions most commonly cause central diabetes insipidus. Determining the etiology of new-onset central diabetes insipidus can radically affect treatment.