The catabolic triad: case report of fasting,major cardiac surgery and sodium–glucose co-transporter 2 inhibitors leading to perioperative euglycaemic ketoacidosis

Sodium-glucose co-transporter-2 inhibitors (SGLT2i) are novel oral hypoglycaemic agents. For patients with diabetes mellitus, without a prior history of myocardial infarction or atherosclerotic disease, SGLT2i have been shown to reduce incident heart failure and worsening renal function. SGLT2i therapy is increasing among patients presenting for cardiac surgery. However, the perioperative use of SGLT2i carries a significant risk of euglycaemic diabetic ketoacidosis, due to their catabolic mechanism of action. This case report demonstrates euglycaemic ketoacidosis post-coronary artery bypass grafting secondary to SGLT2i, highlighting the multiple risk factors and consequences of this iatrogenic complication.     

Use of sodium bicarbonate and blood gas monitoring in diabetic ketoacidosis: A review

Diabetic ketoacidosis (DKA) is a severe and too-common complication of uncontrolled diabetes mellitus. Acidosis is one of the fundamental disruptions stemming from the disease process, the complications of which are potentially lethal. Hydration and insulin administration have been the cornerstones of DKA therapy; however, adjunctive treatments such as the use of sodium bicarbonate and protocols that include serial monitoring with blood gas analysis have been much more controversial. There is substantial literature available regarding the use of exogenous sodium bicarbonate in mild to moderately severe acidosis; the bulk of the data argue against significant benefit in important clinical outcomes and suggest possible adverse effects with the use of bicarbonate. However, there is scant data to support or refute the role of bicarbonate therapy in very severe acidosis. Arterial blood gas (ABG) assessment is an element of some treatment protocols, including society guidelines, for DKA. We review the evidence supporting these recommendations. In addition, we review the data supporting some less cumbersome tests, including venous blood gas assessment and routine chemistries. It remains unclear that measurement of blood gas pH, via arterial or venous sampling, impacts management of the patient substantially enough to warrant the testing, especially if sodium bicarbonate administration is not being considered. There are special circumstances when serial ABG monitoring and/or sodium bicarbonate infusion are necessary, which we also review. Additional studies are needed to determine the utility of these interventions in patients with severe DKA and pH less than 7.0.     

Sodium-glucose co-transporter 2 inhibitors induced euglycemic diabetic ketoacidosis within four days of initiation

Euglycemic diabetic ketoacidosis (EDKA) is a well-known complication of sodium-glucose co-transporter 2 inhibitors, and many cases with variable onset following the initiation of these agents are reported before, with a median onset of approximately 2 wk. This letter discusses a 45-year-old lady who initially presented with ischemic stroke but developed EDKA 4 d after starting empagliflozin, a rare occurrence. The patient had severe metabolic acidosis that necessitated admission into the intensive care unit. Prompt discontinuation of empagliflozin and DKA management resulted in clinical recovery.     

Effect of obstructive sleep apnea on type 2 diabetes mellitus: A comprehensive literature review

Obstructive sleep apnea (OSA) is frequently associated with obesity and metabolic syndrome. Also frequently associated with metabolic syndrome is type 2 diabetes mellitus (T2DM). Therefore, it is common to find OSA and T2DM together in individuals with metabolic syndrome. Additionally, both OSA and T2DM have a common pathophysiological link with development of insulin resistance. Individuals with severe insulin resistance are likely to have inadequate glycemic control. Long standing poorly controlled T2DM is associated with debilitating microvascular complications such as retinopathy, nephropathy, neuropathy and macrovascular complications such as coronary artery and cerebrovascular disease. There is extensively published literature exploring the cause-effect relationship between OSA and T2DM. In this article we provide an in-depth review of the complex pathophysiological mechanisms linking OSA to T2DM. Specifically, this review focusses on the effect of OSA on the microvascular complications of T2DM such as retinopathy, nephropathy and neuropathy. Additionally, we review the current literature on the effect of continuous positive airway pressure use in individuals with T2DM and OSA.