Diabetic ketoacidosis is a perennial USMLE favorite because it ties pathophysiology directly to a structured management protocol, and because the 2024 ADA consensus report refreshed the diagnostic criteria. This review covers DKA the way the boards test it, reflecting current US practice. Follow current guidelines and institutional protocols clinically; this reflects guidance as of mid-2026.
What DKA is
DKA results from an absolute or relative insulin deficiency, usually in type 1 diabetes, that drives unrestrained lipolysis and hepatic ketogenesis. Counter-regulatory hormones — glucagon, catecholamines, cortisol and growth hormone — amplify hyperglycemia and ketone production, producing the triad of hyperglycemia, ketosis and high anion gap metabolic acidosis. Common precipitants, the classic "I"s, include infection, insulin nonadherence, ischemia (myocardial infarction) and intoxication, along with new-onset diabetes. DKA is far more typical of type 1 diabetes but can occur in type 2, including a ketosis-prone phenotype. The pathophysiology explains the labs: insulin lack plus excess counter-regulatory hormones produces hyperglycemia (osmotic diuresis, dehydration and electrolyte loss) and ketogenesis (the acidosis), so volume, glucose, ketones and electrolytes all move together.
Presentation
The patient is typically polyuric, polydipsic, nauseated and vomiting, with abdominal pain, and may be drowsy or comatose. Look for Kussmaul respirations (deep, labored breathing compensating for the acidosis), a fruity acetone odor on the breath, and signs of dehydration — tachycardia, hypotension and dry mucous membranes. Abdominal pain is common and can mimic a surgical abdomen. The degree of dehydration is often underappreciated, with fluid deficits of several liters common, and the apparent sodium is falsely lowered by hyperglycemia, so a corrected sodium should be calculated.
Diagnosis
The 2024 ADA consensus defines DKA by three components: hyperglycemia (glucose above 200 mg/dL, or known diabetes), ketosis (a beta-hydroxybutyrate of 3.0 mmol/L or higher is preferred, since it is more specific than urine ketones), and metabolic acidosis (a pH below 7.3 and/or a bicarbonate below 18 mEq/L). A key update: the anion gap is no longer a first-line diagnostic criterion, because the large volumes of normal saline used in treatment cause a hyperchloremic acidosis that confounds it — though an anion gap above 12 still signals a high anion gap acidosis if ketone measurement is unavailable. HHS sits at the other end of the spectrum — marked hyperglycemia (often above 600 mg/dL) with high serum osmolality but minimal ketosis or acidosis — and the two can overlap.
The initial workup includes a basic metabolic panel, serum and capillary ketones, a venous blood gas, and a search for the precipitant — an ECG and troponin, urinalysis and cultures, and a pregnancy test where relevant.
Management
Treatment runs on three parallel tracks — fluids, insulin and potassium — with close monitoring.
- Fluids: start isotonic saline (0.9% sodium chloride) for volume resuscitation, then switch to half-normal saline (0.45%) once the corrected sodium is normal or high. Add dextrose-containing fluid once the glucose falls below about 200 mg/dL, so insulin can continue without causing hypoglycemia.
- Insulin: a continuous IV infusion of regular insulin at 0.1 units/kg/hr, sometimes preceded by a 0.1 units/kg bolus. The goal is to close the gap and clear ketones, not simply to normalize glucose.
- Potassium: total-body potassium is depleted even when the serum level looks normal or high. Replace potassium once it falls below 5.2 mEq/L with adequate urine output, and crucially, hold insulin if the potassium is below 3.3 mEq/L until it is repleted, because insulin drives potassium intracellularly and can precipitate fatal hypokalemia.
- Bicarbonate: reserved for severe acidosis with a pH below 6.9; it is not given routinely.
- Continue any long-acting basal insulin, and treat the precipitating cause.
Resolution is defined by a beta-hydroxybutyrate below 0.6 mmol/L and a venous pH of 7.3 or higher (or a bicarbonate of 18 mEq/L or higher), with glucose below 200 mg/dL. Transition to subcutaneous insulin with an overlap before stopping the infusion. Overlapping subcutaneous insulin with the infusion by an hour or two prevents rebound hyperglycemia and recurrent ketosis once the IV insulin stops.
High-yield exam points and traps
- The board answer for a depleted but normal-looking potassium is to replace it — and to hold insulin if potassium is below 3.3 mEq/L.
- Add dextrose when glucose falls below about 200 mg/dL; do not stop the insulin, which is needed to clear ketones.
- The 2024 criteria favor beta-hydroxybutyrate over urine ketones and drop the anion gap as a first-line criterion.
- Bicarbonate is reserved for a pH below 6.9 — a frequent distractor.
- Cerebral edema is a feared complication, especially in children, and is linked to overly rapid correction.
- Euglycemic DKA occurs with SGLT2 inhibitors — the glucose can be near-normal, so check ketones if the patient is acidotic.
- Watch for a falsely normal or high serum potassium at presentation that masks total-body depletion.
- Distinguish DKA from HHS, which has minimal ketosis but extreme hyperglycemia, hyperosmolality and a substantially higher mortality.
Common questions
What are the diagnostic criteria for DKA? Hyperglycemia (glucose above 200 mg/dL or known diabetes), ketosis (beta-hydroxybutyrate 3.0 mmol/L or higher), and metabolic acidosis (pH below 7.3 and/or bicarbonate below 18 mEq/L), per the 2024 ADA consensus.
Why hold insulin if potassium is low? Insulin is held because it shifts potassium into cells: giving it when potassium is below 3.3 mEq/L can cause dangerous hypokalemia and arrhythmia, so potassium is repleted first.
When do you add dextrose? Once the glucose falls below about 200 mg/dL, so the insulin infusion can continue to clear ketones without causing hypoglycemia.
When is bicarbonate indicated in DKA? Only for severe acidosis with a pH below 6.9; it is not given routinely.
What is euglycemic DKA? DKA with a near-normal glucose, classically with SGLT2 inhibitors, which is why ketones and pH should be checked in any acidotic diabetic patient even when the glucose looks unremarkable.
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