Diabetic Ketoacidosis (DKA) – Study Notes

Medical emergency, especially in Type 1 DM, but can also occur in Type 2 DM.

• Characterized by hyperglycemia, ketonemia/ketonuria, and metabolic acidosis.

• Results from absolute or relative insulin deficiency + counterregulatory hormone excess.

Clinical Features

Symptoms:

• Nausea, vomiting

• Polyuria

• Polydipsia

• Weight loss

• Abdominal pain

• Hyperventilation (Kussmaul respirations)

Signs:

• Dehydration (dry mucous membranes, tachycardia, hypotension)

• Altered mental status (confusion → coma if severe)

• Fruity odor to breath (acetone)

Etiology – The 5 I’s (common triggers)

1. Infection

2. Intoxication (alcohol, drugs)

3. Inappropriate withdrawal of insulin

4. Infarction (MI, stroke)

5. Intercurrent illness (e.g., pancreatitis, trauma, surgery)

Pathophysiology

Insulin Deficiency

• Autoimmune destruction of pancreatic β-cells (Type 1 DM) → ↓ insulin.

• Without insulin:

  • ↑ Gluconeogenesis → ↑ blood glucose

  • ↑ Glycogenolysis → ↑ blood glucose

  • ↓ Glycolysis → ↓ cellular glucose uptake

• Result: Severe hyperglycemia → osmotic diuresis → polyuria, glycosuria, dehydration, polydipsia

Lipolysis & Ketogenesis

• Adipose tissue breakdown → free fatty acids (FFA) released.

• FFAs transported to liver → undergo ketogenesis → ketone bodies (β-hydroxybutyrate, acetoacetate, acetone).

• Ketones = acidic → ketonemia + metabolic acidosis.

• Ketones excreted in urine → ketonuria + further electrolyte loss.

Investigations

Bedside

• Vitals (hypotension, tachycardia, tachypnea)

• Capillary glucose

• Urine dipstick (glucose, ketones, infection screen)

Laboratory

• ABG → metabolic acidosis (↓ pH, ↓ HCO₃⁻, ↓ CO₂ as compensation).

• Serum glucose: typically > 14 mmol/L (250 mg/dL).

• Serum ketones: elevated.

• Electrolytes:

  • Potassium: total body ↓, but may be normal or ↑ initially (due to acidosis + insulin deficiency shifting K⁺ extracellularly).

  • Risk of severe hypokalemia once insulin therapy starts.

• FBC: look for infection.

• U&E: check renal function, dehydration.

• ECG: arrhythmias from hyper- or hypokalemia.

Management

Initial Priorities – ABC

• Airway, Breathing, Circulation.

• Secure IV access for fluids, bloods, and medications.

1. Fluids

• Start with IV saline (0.9% NaCl) → correct hypovolemia and dehydration.

• Once glucose falls to ~14 mmol/L → switch to 0.45% saline + 5% dextrose to prevent hypoglycemia while continuing insulin.

2. Insulin Therapy

• Low-dose IV insulin infusion (0.1 U/kg/hr).

• Aim: lower glucose gradually (avoid rapid shifts → cerebral edema).

• Insulin also stops ketogenesis and promotes cellular glucose uptake.

3. Potassium Management

• Check serum K⁺ before insulin.

  • K⁺ < 3.3 mmol/L → hold insulin, replace potassium first.

  • K⁺ 3.3–5.0 → start insulin + IV K⁺ replacement.

  • K⁺ > 5.0 → start insulin, monitor closely.

• Insulin + correction of acidosis drive K⁺ into cells → risk of dangerous hypokalemia.

• Calcium gluconate may be given to stabilize myocardium if arrhythmias develop.

4. Monitoring

• ABG every 1–2 hrs (pH, HCO₃⁻, CO₂).

• Serum electrolytes (especially K⁺) every 2–4 hrs.

• Urine output (strict I&O chart).

• Blood glucose hourly.

• ECG monitoring (potassium shifts).

Resolution Criteria

• Patient is alert and eating.

• Anion gap closed.

• Serum bicarbonate > 18 mmol/L.

• Venous pH > 7.3.

• Ketones cleared.

Key Points for Exams & Clinical Practice

• DKA = hyperglycemia + ketosis + acidosis.

• Always correct potassium first before starting insulin.

• Fluids first, then insulin, then potassium = classic teaching.

• Search for triggers (infection, MI, insulin omission).

• Close monitoring is essential to prevent complications (cerebral edema, hypokalemia, arrhythmias).