No abstract

The current widespread use of sodium-glucose co-transporter 2 (SGLT2) inhibitors has triggered an increase in reported cases of euglycemic diabetic ketoacidosis (EDKA), often characterized by a protracted metabolic acidosis that is resistant to conventional DKA treatment. We report a case of empagliflozin-induced EDKA with severe metabolic acidosis intractable to aggressive fluid resuscitation and boluses of bicarbonate infusion. Following the introduction of high-calorie glucose infusion coupled with tight glycemic control, the recalcitrant acidosis was successfully corrected. This is the first case report that adopts the above approach, representing a paradigm shift in the management of SGLT2 inhibitor-induced EDKA.

medical records in the hospital information system. Results were analyzed using SPSS version 23. Results: A total of 78 patients fulfilled the inclusion criteria. The mean age was 52.4 and predominantly male (66.6%). Comorbidities identified in this cohort were diabetes mellitus, hypertension and ischemic heart disease bringing to a total of 52.5%, followed by patients with preexisting CKD stage 2 to 4 (23%), retroviral disease (RVD) (7.7%) and there were 2 patients with underlying malignancy. 13 patients (16.7%) had no known medical illness. Main causes of AKI requiring HD in the group with comorbidities were sepsis (56.4%), cardiogenic shock(12.7%), obstructive uropathy(7.7%), trauma related(6.4%), ingestion of traditional medicine and nephrotoxic drugs(6.4%), hypertensive emergency(6.3%), burn related disease(2.5%) and radiocontrast agents(1.6%). Amongst the cohort with no medical illness, non-sepsis cause (medication and trauma related) predominated (76.4%). 17.9% of the study group developed hospital acquired AKI requiring HD. Within 90 days, 39.7% died during hospitalization. Amongst those alive at 90 days, 51.3% achieved full renal recovery, 29.7% were rendered end stage renal disease requiring regular dialysis and 19% were diagnosed with new onset chronic kidney disease or developed progression of their chronic kidney disease but did not require regular dialysis. Conclusion: AKI requiring HD should be identified as a predictor of inpatient mortality and long term morbidity. It is imperative that early recognition and intervention is undertaken to reduce the burden of disease.

Background: Insulinoma is the most common type of functioning pancreatic neuroendocrine tumor (NET). Polyhormonal secretions from the NET, giving rise to distinct clinical symptoms such as carcinoid symptoms are rare. Clinical Case: We report a 68-year-old woman who presented with four months history of recurrent diaphoresis, palpitations, tremors and chest tightness. These were associated with episodic paroxysms of flushing and diarrhoea. The physical examination was unremarkable. She was a well-nourished woman with BMI of 28 kg/m2. Initial laboratory tests ruled out any renal, liver abnormalities with normal cortisol and thyroid function test. Further evaluation confirms insulin mediated hypoglycaemia with low random blood sugar 2.5 mmol/l (4.4-7.8) and failure to suppress C-peptide, 1092 pmol/L (298-2350) and insulin levels, 12.7 mU/L (3-25). Urine 5-HIAA was markedly elevated 2430.37 µmol/day (3.66-42.89) with borderline elevation of serum chromogranin A level 122 ng/mL (27-94). IGF-1 was also raised at 416 ug/L (91-282). Two months later she presented with new onset of delirium, incoherence, agitation and restlessness independent of her hypoglycaemic events. These symptoms deteriorated and fluctuates throughout the day with period of normalcy in between. This has led to requirement of a full time caregiver for her. Cranial CT excluded any brain pathology. We are faced with a diagnostic challenge to localize the primary lesion as radiological imaging so far were normal. GALLIUM-68 PET CT showed physiological uptake in the uncinate process of the pancreas (SUVmax 14.4). Endoscopic ultrasound of the pancreas was normal. An intra-arterial calcium stimulation test with hepatic venous sampling (ASVS) confirms a lesion at the head of pancreas with two times increment of insulin from baseline at the gastroduodenal artery distribution. Despite elimination of hypoglycaemic events with Diazoxide 100mg twice daily, her neuropsychiatric symptoms persisted. We postulate that this might be from excessive peripheral production of serotonin by the pancreatic carcinoid tumour or a niacin deficiency state because of metabolic diversion of its precursor, tryptophan. Conclusion: This case highlights the occurrence of debilitating neuropsychiatry manifestations in a likely neuroendocrine tumour arising from the head of pancreas secreting insulin, serotonin and IGF-1.