What are we waiting for? A review of early basal insulin therapy in diabetic ketoacidosis management.

Diabetic ketoacidosis (DKA) remains a significant challenge for healthcare systems due to prolonged lengths of stay and rising costs. The current American Diabetes Association (ADA) guidelines recommend starting basal insulin after resolution of DKA. However, these guidelines have not been updated since 2009, which can potentially limit optimal care. Meanwhile, the Joint British Society guidelines on DKA management, which were more recently updated in March 2023, do advocate for early administration of basal insulin in their treatment algorithm. This article assesses the rationale and literature associated with the recommendation for early basal insulin administration in the management of DKA. Benefits of early basal insulin in this cohort appears to be associated with less rebound hyperglycemia, reduction in time to DKA resolution, reduced intravenous insulin requirements, and reduced length of stay without associated increases in hypoglycemic or hypokalemic events.

Propofol and Clevidipine-induced Hypertriglyceridemia.

Hypertriglyceridemia and related pancreatitis due to the use of lipid emulsions such as propofol has been documented, but less is known about the additive adverse effects of propofol and clevidipine lipid emulsions in the literature. We report an unusual case, highlighting the trend of serum triglyceride and pancreatic enzymes (amylase/lipase) with the administration of propofol and clevidipine for a prolonged period in the neurocritical care setting. We present a case of a 27-year-old male who was admitted to the neuroscience intensive care unit (NSICU) for management of severe subarachnoid hemorrhage (SAH) with six-millimeter (mm) midline shift to the left from the rupture of anterior communicating artery aneurysm. The patient was given propofol infusion to maintain sedation and manage intracranial pressures, and clevidipine was chosen over other antihypertensive class for blood pressure management secondary to renal impairment. To focus on the risk of hypertriglyceridemia and associated pancreatitis with the combined use of lipid emulsions we quantified the effect of lipid emulsions on serum triglycerides. We calculated the total calorie and fat content the patient received from the propofol and clevidipine along with the calorie intake from enteral nutrition (Fibersource® tube feed). The patient received a total propofol infusion of 44,391.2 milligrams (mg) over 16 days which accounts for 4,882.99 kilocalories (kcal) and 443.91 grams of fat. He received a total clevidipine infusion of 297 mg over the 48-hour period which contributes 594 kcal and 59.4 grams of fat. The required daily calorie intake through enteral nutrition of Fibresource® was titrated to a goal of 80 mL/hour which provided 2,304 kcal and 76.8 grams of fat each day. We also graphically depicted the rise in the serum triglyceride level after continuous infusion of propofol and clevidipine and subsequent improvement in the amylase and lipase level after the propofol was discontinued. Hence we conclude, careful and periodic monitoring of the serum triglyceride levels and limitation on the total calories from other fat sources such as enteral nutrition can help to mitigate the drug-induced effects.