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Pathophysiology and Management of Diabetic Ketoacidosis (DKA)


Pathophysiology of Diabetic Ketoacidosis

Diabetic Ketoacidosis (DKA) is a life-threatening complication, mainly associated with Type 1 Diabetes Mellitus. The primary mechanism involves a severe insulin deficiency, resulting in:

  • Hyperglycemia: Inadequate insulin means glucose cannot enter cells, leading to elevated blood sugar levels.
  • Lipolysis and Ketogenesis: Fat stores break down, releasing free fatty acids. The liver converts these fatty acids into ketone bodies (acetone, acetoacetate, beta-hydroxybutyrate).
  • Metabolic Acidosis: Ketones are acidic, leading to a drop in blood pH, causing metabolic acidosis.
  • Electrolyte Imbalance: High glucose causes osmotic diuresis, resulting in dehydration and loss of electrolytes like sodium, potassium, and magnesium.

This combination results in hyperglycemia, ketonemia, acidosis, dehydration, and electrolyte imbalance, forming the basis of DKA symptoms.


Factors Precipitating Diabetic Ketoacidosis

Several factors increase insulin demand or reduce insulin effectiveness, leading to DKA. These include:

  • Infection: The most common precipitating factor, increasing insulin requirements.
  • Insulin Therapy Non-compliance: Poor adherence to insulin regimens can precipitate DKA.
  • Acute Illness or Stress: Conditions like myocardial infarction or trauma increase counter-regulatory hormones.
  • Alcohol and Drug Abuse: Substances disrupt glucose metabolism, leading to poor blood sugar control.
  • Newly Diagnosed Diabetes: Many initial presentations of Type 1 Diabetes are in DKA due to delayed diagnosis.

Management of Diabetic Ketoacidosis

Effective management of DKA involves restoring normal glucose, fluid, electrolyte, and acid-base balance. The main steps include:

1. Initial Assessment and Monitoring

  • Monitor vital signs, mental status, and urine output.
  • Conduct laboratory tests (e.g., blood glucose, ketones, pH, electrolytes).

2. Fluid Replacement

  • Start with 0.9% NaCl (normal saline): Restore fluid balance and correct dehydration.
  • Switch to 0.45% NaCl after initial rehydration to avoid hypernatremia.

3. Insulin Therapy

  • IV insulin infusion (0.1 units/kg/hr): Reduce blood glucose gradually and inhibit ketone production.
  • Continue insulin infusion until ketonemia resolves and the anion gap normalizes.

4. Electrolyte Management

  • Potassium: Begin supplementation when levels fall below 5.5 mEq/L to prevent hypokalemia.
  • Sodium Bicarbonate: Administer only for severe acidosis (pH < 6.9), as routine use can interfere with electrolyte balance.

5. Addressing Underlying Causes

  • Treat infections or other precipitating factors (e.g., medication non-compliance).

6. Transition to Subcutaneous Insulin

  • When DKA resolves and the patient can eat, transition to subcutaneous insulin therapy.

7. Patient Education

  • Educate the patient on diabetes management, monitoring, and recognizing early signs of DKA.

Monitoring and Prognosis

Close monitoring of vital signs, oxygen saturation, and cardiac rhythm is critical. Patients should be observed for at least 48–72 hours due to the risk of recurrence. With timely management, mortality rates from DKA are significantly reduced.


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