Classic DKA in type I diabetes involves marked hyperglycemia, resulting in osmotic diuresis, severe dehydration, and lipolysis-driven ketoacidosis. In type II diabetics, some residual insulin activity may suppress lipolysis and ketogenesis, leading to HHS without acidosis. Both forms of hyperglycemia can result in severe volume depletion.

Two essential principles of DKA resuscitation are directly relevant in the perioperative setting:

1. Fluids before insulin: insulin drives potassium into cells, and in DKA, total body potassium is often critically low, despite normal or elevated serum levels.
   
2. Continue insulin infusions for at least 2 hours after administering long-acting insulin, as basal formulations take time to reach the effect-site concentrations. Premature discontinuation may result in rebound ketoacidosis.

The increasing use of SGLT-2 inhibitors (e.g., empagliflozin, dapagliflozin) has added complexity to perioperative glucose management. These drugs improve glycemic control and reduce cardiovascular mortality, possibly via mild ketone elevation and inhibition of the renin–angiotensin–aldosterone system. However, they also introduce the risk of euglycemic DKA (eDKA): a metabolic acidosis with a normal glucose level.

In eDKA, urinary glucose wasting puts a check on the usually high levels of hyperglycemia typically seen in DKA. Since glucose can remain normal or only slightly elevated, this tends to delay the diagnosis. eDKA is diagnosed by the presence of blood glucose levels below 200–250 mg/dL (often under 200 mg/dL), a high anion gap metabolic acidosis with arterial pH less than 7.3, serum bicarbonate below 18 mEq/L, and an anion gap greater than 10, along with elevated serum or urine ketones, preferably measured as -hydroxybutyrate. Management is the same as for traditional DKA, though the anion gap may close more slowly and reopen due to the long half-life of the drug.

To reduce risk, most centers recommend holding SGLT-2 inhibitors for 3–4 days preoperatively. If this isn’t done—and especially if the case is not minor—consider checking a basic metabolic panel preoperatively. An elevated anion gap in the absence of hyperglycemia should raise concern for eDKA.

Insulin infusions are commonly required in cardiac, transplant, and major vascular surgery. Glucose tends to get very high in settings of extreme physiologic stress, high-dose steroids, and inflammatory response associated with foreign tissue exposure or synthetic materials (e.g., during cardiopulmonary bypass). This is due to the release of catecholamines and cortisol. IV insulin in this setting is not only being used to mitigate hyperglycemia, but to play a protective role against hyperkalemia. This is particularly useful when related to cardioplegia solutions, blood transfusions, or liver dysfunction.

You’ll often be asked whether a patient “needs stress-dose steroids.” Always question phrases such as this one! The underlying concern at play is that patients on chronic corticosteroid therapy may have adrenal suppression. Thus, they may be unable to mount an appropriate physiologic stress response to surgery.

Despite this concern, most surgeries do not require large surges in steroid output, and most anesthetics are not especially hemodynamically stressful. The risks of unnecessary steroids—including hyperglycemia, infection, delirium, and poor wound healing—should not be overlooked.

According to the Endocrine Society Clinical Practice Guideline on Glucocorticoid-induced Adrenal Insufficiency, patients at risk of glucocorticoid-induced adrenal insufficiency include those who have taken the equivalent of ≥5 mg of prednisone daily for more than 3–4 weeks. In high-risk surgeries, these patients may benefit from supplemental hydrocortisone (typically 50–100 mg IV). Decisions should be individualized and discussed with the surgical team.