Internal MedicineEndocrinologyDiabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA)

Must-Not-Miss / Red Flags

  • Cerebral edema – especially in children (headache, altered mental status, bradycardia)
  • Severe hypokalemia – risk of cardiac arrhythmia during insulin therapy
  • pH <6.9 – severe acidosis requiring bicarbonate?
Patient Explanation
“Your blood sugar is very high because your body doesn’t have enough insulin. We’ll give you IV fluids and insulin to bring it down safely.”
Board Fact
“DKA is the initial presentation in 20‑30% of new‑onset type 1 diabetes mellitus.”
ICD-10
E11.10

Definition & Core Concept

Diabetic ketoacidosis is a life‑threatening complication of diabetes mellitus characterized by hyperglycemia, metabolic acidosis, and ketosis, resulting from absolute or relative insulin deficiency and increased counter‑regulatory hormones.

Epidemiology & Risk Factors

  • Annual incidence 4‑8 per 1,000 patients with diabetes
  • Most common in type 1 DM, but increasingly seen in type 2 (ketosis‑prone)
  • Precipitants: infection (30‑40%), missed insulin, new‑onset DM, myocardial infarction

Pathophysiology (Rule of 3)

  1. Insulin deficiency → decreased glucose uptake → hyperglycemia
  2. Counter‑regulatory hormone excess (glucagon, cortisol, catecholamines) → lipolysis → free fatty acids
  3. Hepatic fatty acid oxidation → ketone bodies (β‑hydroxybutyrate, acetoacetate) → high anion gap metabolic acidosis

Clinical Presentation

  • Polyuria, polydipsia, weight loss
  • Nausea, vomiting, abdominal pain (may mimic acute abdomen)
  • Kussmaul respirations (deep, labored breathing), fruity breath (acetone)
  • Altered mental status in severe cases

Diagnostic Workup

Serum glucose: >250 mg/dL (may be normal in “euglycemic DKA”). Anion gap: elevated (>12). Serum ketones: positive β‑hydroxybutyrate. ABG: pH <7.30, bicarbonate <18 mEq/L. Urinalysis: ketonuria.

Management Protocol

  1. IV fluids: 0.9% NaCl at 15‑20 mL/kg/hour initially, then switch to 0.45% NaCl
  2. Insulin: regular insulin IV bolus 0.1 U/kg, then continuous infusion 0.1 U/kg/hour
  3. Potassium replacement: start when K⁺ <5.2 mEq/L (insulin drives K⁺ intracellularly)
  4. Glucose: add D5W when glucose falls below 200 mg/dL to prevent hypoglycemia
  5. Treat underlying cause: antibiotics for infection, etc.

Complications & Prognosis

  • Cerebral edema (more common in children)
  • Hypokalemia and cardiac arrhythmia
  • Hypoglycemia from aggressive insulin therapy
  • Acute respiratory distress syndrome (rare)

ICU Criteria

ICU admission if: pH <7.0, altered mental status, pregnancy, or severe electrolyte disturbances.

Clinical Vignette

A 19‑year‑old with type 1 diabetes presents with 3 days of nausea, vomiting, and diffuse abdominal pain. He missed his last two insulin doses due to a viral illness. Glucose is 480 mg/dL, pH 7.12, and β‑hydroxybutyrate is elevated.

Pearls & Pitfalls

  • Bicarbonate therapy is controversial – only consider if pH <6.9, as it may worsen intracellular acidosis.
  • Monitor potassium closely – the drop during insulin therapy is predictable and can be profound.

Discharge & Follow-Up

Transition to subcutaneous insulin when anion gap closes and patient tolerates oral intake. Diabetes education and endocrinology follow‑up.

Literature & Guidelines

ADA Standards of Medical Care in Diabetes 2024. PMID: 38078590.

Personal Clinical Notes