DKA (Medical students)


Definition

Diabetic ketoacidosis (DKA) is a life-threatening metabolic state characterized by hyperglycaemia, ketosis, and metabolic acidosis, resulting from insulin deficiency and excess counter-regulatory hormones, particularly glucagon. This hormonal imbalance promotes gluconeogenesis, glycogenolysis, and lipolysis, leading to the formation of ketone bodies.

Pathophysiology

Hyperglycaemia induces osmotic diuresis, leading to significant loss of free water and electrolytes (including sodium, potassium, and phosphate).

Resulting hypovolaemia contributes to tissue hypoperfusion and can precipitate lactic acidosis.

Mortality is most commonly associated with cerebral oedema, severe hypokalaemia, and aspiration pneumonia.

Causes
  • New diagnosis of type 1 diabetes mellitus (IDDM)
  • Infection (most common precipitant)
  • Poor adherence to insulin therapy or missed doses
Clinical Presentation

Symptoms (often insidious, especially in young children):
  • Polydipsia
  • Polyuria
  • Weight loss
  • Nausea and vomiting
  • Abdominal pain
  • Fatigue or lethargy
Signs:
  • Altered mental status (e.g., drowsiness, irritability, coma)
  • Tachycardia
  • Tachypnoea with deep, laboured breathing (Kussmaul respiration)
  • Acetone (fruity) breath odour
  • Signs of shock: hypotension, poor perfusion
Diagnosis
  • Blood glucose (BG): >12 mmol/L
  • Venous blood gas (VBG):
  • pH < 7.3
  • Bicarbonate (HCO₃⁻) < 15 mmol/L
  • Positive ketonuria or blood ketones
Management

ICU admission is indicated if the patient is in coma, shock, or has severe electrolyte abnormalities.

Principles of treatment

Gradual correction of hyperglycaemia, acidosis, and dehydration

Fluid therapy:
Initial normal saline bolus if shocked.
Replace maintenance + deficit over 48 hours.
Start with normal saline, then transition to saline + dextrose when BG falls (~14 mmol/L).

Insulin infusion (after initial fluids)
Start low-dose IV insulin (e.g., 0.05–0.1 units/kg/hr).
Avoid insulin bolus.

Electrolyte monitoring and correction:
Frequent monitoring of capillary BG, serum potassium, sodium, and acid-base status.
Potassium replacement should begin once urine output is established and initial serum K⁺ is known. Even if initial serum K⁺ is normal or high, total body potassium is usually depleted. Bicarbonate is not routinely indicated and may worsen cerebral oedema.

Treat underlying infections with empiric antibiotics if clinically indicated.

Monitor for complications, especially cerebral oedema (headache, bradycardia, declining consciousness).