Endocrinology · USMLE Step 1 and Step 2

Diabetic Ketoacidosis song

Diabetic Ketoacidosis - Labs & Management, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

Diabetic Ketoacidosis

Full song on YouTube ↗Spotify ↗

Key points in this song10

DKA is defined by the triad of hyperglycemia (glucose >250 mg/dL), anion gap metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L), and ketonemia/ketonuria.
Absolute insulin deficiency drives unopposed glucagon, causing increased lipolysis and hepatic beta-oxidation of fatty acids into ketone bodies (acetoacetate and beta-hydroxybutyrate).
DKA occurs most commonly in Type 1 diabetes; the most common precipitating factors are infection and medication non-compliance (missed insulin doses).
Beta-hydroxybutyrate is the predominant ketone in DKA and is NOT detected by the nitroprusside reaction, so urine ketone dipstick may underestimate severity.
Kussmaul respirations (deep, rapid breathing) are a compensatory response to metabolic acidosis, and fruity (acetone) breath reflects exhaled acetone.
DKA causes a total body potassium deficit despite initial hyperkalemia; insulin therapy shifts K⁺ intracellularly, so potassium must be repleted before starting insulin if K⁺ is below 3.5 mEq/L.
First-line treatment is aggressive IV isotonic saline (0.9% NaCl) for volume resuscitation, followed by insulin infusion (0.1 units/kg/hour IV regular insulin).
The anion gap is calculated as Na⁺ − (Cl⁻ + HCO₃⁻); a gap >12 mEq/L confirms an anion gap metabolic acidosis characteristic of DKA.
Cerebral edema is the most feared complication of DKA treatment, occurring most commonly in children due to overly rapid fluid correction.
DKA resolution criteria require closure of the anion gap, not normalization of serum glucose, which typically normalizes before the acidosis resolves.