BackgroundIn-hospital glycaemic management can reduce post-transplant morbidity, but is not always part of transplant care.ObjectiveWe aimed to reduce the mean number of postoperative days in hyperglycaemia (≥2 blood glucose >12 mmol/L in 24 hours) in kidney and liver transplant recipients by 30%. We also aimed to reduce the mean number of days between transplant admission to endocrine consult by 2.0 days.Design, setting, participantsWe conducted a quality improvement project in liver and kidney transplant recipients admitted to an academic transplant unit in Canada between 1 March 2019 and 1 May 2021.InterventionWe developed a bedside algorithm to monitor post-transplant capillary blood glucose; the algorithm also included thresholds for nursing-initiated inpatient endocrinology consultation.Main outcome and measuresWe examined outcome (postoperative days in hyperglycaemia, days to inpatient endocrine consultation), process (nursing documentation of postoperative blood sugars) and balancing measures (nursing workload, postoperative days in hypoglycaemia) following implementation of our algorithm. We used Plan-Do-See-Act cycles to study three iterations of our algorithm, and used box plots to present outcomes before and after algorithm implementation.ResultsIn the pre-intervention period, 21 transplant recipients spent a mean of 4.1 (SD 2.4) postoperative days in hyperglycaemia before endocrine consultation. The mean number of days between hospital admission to endocrine consult was 10.7 (SD 13.0) days.In the post-intervention period, we observed a 62% reduction in postoperative days in hyperglycaemia. The mean number of days between admission and endocrine consult was reduced by 6.3 days (59% reduction).ConclusionsImplementation of a simple, bedside algorithm for postoperative glucose monitoring and detection of hyperglycaemia in transplant patients, reduced the mean number of postoperative days in hyperglycaemia and time to inpatient endocrine consultation. Our algorithm continues to be used in our academic transplant unit.

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Introduction Acromegaly is a chronic disorder characterized by excess growth hormone production, withclinical manifestations ranging from subtle signs to significant systemic complications. We describe a patient who presented with diplopia as initial symptom of acromegaly. Clinical case: A 72-year-old female patient was referred for diplopia. Upon questioning, she reported headache, muscle aches and heavy sweating. On physical assessment, she had coarse facial features, thickened tongue and hand enlargement. Orbital CT images revealed a mild to moderate symmetric enlargement of the extraocular muscle which spared myotendinous junction. MRI sella showed a 12 mm pituitary adenoma. The diagnosis of acromegaly was confirmed with high IGF-1 and oral glucose tolerance test. The patient underwent endoscopic debulking of the pituitary tumor and pathology showed a densely granulated GH producing adenoma. Upon follow up, she reported improvement of the diplopia which was completely corrected with prism glasses. Remission of acromegaly was confirmed biochemically and repeated MRI sella showed no residual tumor. Conclusion Acromegaly is the most likely cause of extraocular muscle enlargement with subsequent diplopia in this patient. Ocular manifestations in patients with acromegaly include visual field defect, excessive lacrimation, proptosis and double vision. This case adds to previous literature that diplopia could be the presenting manifestation of acromegaly. This is the first case reporting of improvement of diplopia following remission of acromegaly. Comprehensive ophthalmic assessment of patients presenting with eye symptoms and features suggestive of acromegaly is of value as it helps with early diagnosis as well as improving the outcome of this condition. Presentation: No date and time listed

Background: To determine whether acromegaly is associated with increased extraocular muscle (EOM) size at time of presentation. Methods: Patients with a new diagnosis of acromegaly in a single tertiary care clinic with a CT scan that adequately delineated the EOMs were included. Control subjects were age- and sex-matched patients with a new diagnosis of nonfunctioning pituitary adenoma. Retrospective chart review was performed to extract baseline clinical and laboratory parameters including growth hormone, insulin-like growth factor 1, thyroid stimulating hormone, free T3, and free T4. A single neuroradiologist analyzed all CT scans and measured the maximum diameter and cross-sectional area of the superior rectus, inferior rectus, medial rectus, and lateral rectus in both eyes of all patients. Results: We evaluated 17 patients with acromegaly and 18 control subjects. Mean maximum diameter of the superior, inferior, medial, and lateral recti were 4.80 mm (SD = 0.81), 4.67 mm (SD = 0.54), 4.86 mm (SD = 0.77), and 4.53 mm (SD = 0.70) respectively, in the acromegaly group. In the control group, they were 3.62 mm (SD = 0.58),3.71 mm (SD = 0.46), 3.66 mm (SD = 0.32), and 3.21 mm (SD = 0.44), respectively. The maximum diameter and cross-sectional area of all 4 EOMs measured in the acromegaly group were significantly larger (P < 0.001) compared with the control group. Conclusions: Patients with acromegaly present with significantly enlarged EOMs compared with control subjects with nonfunctioning pituitary adenomas.

Background: Immune checkpoint inhibitors are immunomodulatory antibodies directed against programmed cell death 1 (PD-1), Nivolumab, or cytotoxic T-lymphocyte antigen-4 (CTLA-4) Ipilimumab. They have improved outcomes in patients with advanced cancers including renal cell carcinoma, non-small cell lung cancer and melanoma. Several immune related adverse events (irAEs) have been recognized with use of immune checkpoint inhibitors, including those involving the endocrine system. We present a case of a patient presenting with isolated central adrenal insufficiency in the context of Nivolumab use. Clinical Case: Our patient is a 54-year old man with pre-existing primary hypothyroidism and metastatic renal cell carcinoma treated with Nivolumab. After receiving a total of 14 cycles of Nivolumab, he presented to the Emergency room with his sister, who found him confused and lethargic. On presentation, he was found to be hypoglycemic (random glucose was 2.2 mmol/L). On physical examination, his vital signs were stable and he appeared euvolemic. He was disoriented without focal neurological deficits. Initial blood work revealed sodium 134 mmol/L, (Normal 135-145mmol/L), potassium 4.5 mmol/L (Normal 3.5-5 mmol/L), and TSH being 12.6 mIU/L (Normal 0.4-4 mIU/L). He was resuscitated with IV Dextrose 50% bolus then admitted to hospital and kept on an IV dextrose infusion. While his glucose improved, he was found to have hyponatremia, and confusion persisted. His nadir sodium was 116 mmol/L without seizures or loss of consciousness and required treatment with hypertonic saline. Giving hypoglycemia and hyponatremia, morning cortisol and ACTH were checked and came back 4 nmol/L (Normal 133-537 nmol/L) and undetectable (&lt; 0.7 pmol/L, Normal 1.6-13.9 pmol/L) respectively. The diagnosis of central adrenal insufficiency was made likely secondary to Nivolumab. He was started on Dexamethasone 8 mg daily. Sodium level normalized and glucose level improved with steroids. He was discharged home on prednisone 50 mg and then switched to hydrocortisone. Further work up confirmed preserved other anterior pituitary hormones. MRI of Sella did not show pituitary enlargement or inflammation. Conclusion: Our patient presented with hypoglycemia and hyponatremia; both could be the presenting manifestations of central adrenal insufficiency. Nivolumab has been commonly associated with thyroid dysfunction and thyroiditis. Given lack of expression of PD-1 in the pituitary, PD-1 inhibitors are less likely to be associated with hypopituitarism in general, or central adrenal insufficiency in particular. However, our report adds to the growing body of literature associating it with central adrenal insufficiency, which can be isolated. In so doing, it underscores the need for early recognition this association with Nivolumab, so as to avoid the potentially life threatening consequences of this condition.