Diabetic Ketoacidosis
Endocrinology
Illness script · Endocrinology
Diabetic Ketoacidosis
Life-threatening triad of hyperglycemia, anion-gap metabolic acidosis, and ketonemia due to absolute insulin deficiency.
This illness script for Diabetic Ketoacidosis covers predisposing factors, classic presentation, mechanism, workup, management, and the clinical pivots that separate it from look-alikes—written for USMLE Step 1 and clerkship reasoning.
01
Predisposing factors
- Type 1 DM most common; also occurs in Type 2 (especially in illness/stress)
- New-onset T1DM (~25–30% present in DKA)
- Precipitants: infection (#1), missed insulin, MI, surgery, pregnancy, steroids
- Young age (T1DM peak), but any age if insulin-deficient
- SGLT2 inhibitors can cause euglycemic DKA (glucose may be near-normal)
02
Presentation
- Polyuria, polydipsia, nausea/vomiting, abdominal pain — hours to days
- Kussmaul respirations (deep, rapid) — respiratory compensation for metabolic acidosis
- Fruity (acetone) breath — pathognomonic
- Altered mental status in severe cases; dehydration signs (dry mucosa, tachycardia)
- Classic labs: glucose >250 mg/dL, pH <7.3, bicarb <18, anion gap >12, ketonuria/ketonemia
03
Pathophysiology
- Absolute insulin deficiency → unrestrained glucagon → hepatic glucose production + lipolysis
- Free fatty acids → hepatic ketogenesis (β-hydroxybutyrate, acetoacetate) → anion-gap acidosis
- Osmotic diuresis from hyperglycemia → profound dehydration and electrolyte losses
- Total body K⁺ depleted despite initially normal/high serum K⁺ (acidosis shifts K⁺ extracellularly)
04
Diagnostics
- BMP: high glucose, low bicarb, elevated anion gap (Na − [Cl + HCO₃])
- ABG: metabolic acidosis (pH <7.3); may show respiratory alkalosis overlay
- Serum/urine ketones: β-hydroxybutyrate preferred (more sensitive than dipstick acetoacetate)
- CBC, UA, blood cultures: identify precipitating infection
- EKG: assess for hyperkalemia (peaked T-waves) before insulin; K⁺ trends are critical
05
Management
- IV fluids first: 1–2 L NS bolus → correct dehydration and improve perfusion
- Insulin infusion (0.1 U/kg/hr): do NOT start until K⁺ ≥3.5 mEq/L — risk of fatal hypokalemia
- Potassium replacement: add K⁺ to all fluids once urine output confirmed; watch closely
- Transition to dextrose-containing fluids when glucose <200 to avoid hypoglycemia
- Resolution criteria: glucose <200, bicarb ≥15, pH >7.3, anion gap closed — then overlap SubQ insulin before stopping drip
06
Clinical pivots
How to separate this script from the look-alikes that show up on exams and on the wards.
Hyperosmolar Hyperglycemic State (HHS)
HHS: glucose >600, serum osm >320, minimal/no ketones, pH >7.3 — older T2DM patients
Alcoholic Ketoacidosis (AKA)
AKA: glucose normal or low, recent binge + starvation, no significant hyperglycemia
Starvation Ketosis
Starvation ketosis: mild ketonemia, glucose normal, no acidosis (pH/bicarb normal)
Other Anion-Gap Acidoses (MUDPILES)
Lactic acidosis, uremia, salicylate: no significant hyperglycemia or ketonemia as primary driver
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Educational use only. This illness script is a study framework, not medical advice. Confirm decisions with current guidelines and your clinical supervisors.