Notes on Diabetic Ketoacidosis (DKA)

Overview

• DKA is a critical metabolic complication of diabetes mellitus.
• It often leads to coma if not managed properly.

Definition and Triggering Events

• DKA occurs when the body starts ketogenesis due to a lack of insulin, resulting in acidosis.
• Key point: DKA most commonly occurs in patients with Type 1 Diabetes Mellitus (T1DM).
  • T1DM patients have a higher risk due to severe or absolute deficiency of insulin.
  • Some Type 2 Diabetes Mellitus (T2DM) patients may also experience DKA, but it is less frequent and usually less severe.

Causes of DKA

1. Absolute or Severe Insulin Deficiency:

   • Primary reason for DKA development.
   • Can arise from:
     • Undiagnosed T1DM (first presentation of the disease).
     • Known T1DM patients experiencing a demand for more insulin due to stressors (e.g., infections, trauma).

2. Non-compliance with Insulin Treatment:

   • Failure to take insulin can lead to an increase in ketogenesis and, subsequently, DKA.
   • Common among adolescents who may skip insulin during illness or emotional distress.

3. Increased Insulin Demand:

   • Situations that increase insulin needs include:
     • Severe infections (e.g., pneumonia, sepsis).
     • Trauma or surgeries.
     • Myocardial infarctions and other acute illnesses.

Pathogenesis of DKA

• Insulin Deficiency Effects:

  • Reduced glucose utilization by peripheral tissues, causing hyperglycemia.
  • Increased levels of counter-regulatory hormones (glucagon, epinephrine, cortisol, growth hormone) due to low insulin.

• Counter-regulatory Hormone Actions:

  • In the absence of sufficient insulin, the liver undergoes:
    1. Glycogenolysis: Breakdown of glycogen into glucose.
    2. Gluconeogenesis: Formation of glucose from non-carbohydrate sources (amino acids and free fatty acids).
  • Muscle tissue breaks down proteins for amino acids, which contribute to gluconeogenesis.
  • Fat cells undergo lipolysis, leading to the release of free fatty acids, which can overwhelm the liver and lead to ketogenesis.

• Ketogenesis:

  • Excess free fatty acids are converted into ketone bodies in the liver, contributing to acidosis.
  • Types of ketone bodies produced:
    • Beta-hydroxybutyric acid (most abundant), acetoacetate, and acetone.

Clinical Presentation and Diagnosis

1. Key Indicators:

   • Plasma glucose > 250 mg/dL.
   • Blood pH < 7.3 and bicarbonate < 15 mEq/L.
   • Presence of ketone bodies > 5 mmol/L.

2. Classic Signs:

   • Sweet, fruity odor on breath due to acetone.
   • Kussmaul breathing (deep, labored breathing) due to metabolic acidosis.

Management of DKA

• Treatment typically includes:
  • Fluid replacement to address dehydration.
  • Insulin therapy to lower blood glucose levels gradually.
  • Electrolyte management, particularly monitoring potassium levels, as they may initially rise but can rapidly drop with treatment.

Key Takeaways

• Important Causes of Mortality in DKA:

  1. Rapidly falling potassium levels leading to cardiac issues.
  2. Severe acidosis due to accumulated ketone bodies.
  3. Persistent hyperglycemia if not managed properly.

• Patient Education:

  • Importance of adherence to insulin therapy and recognizing signs of DKA early.