Diabetic Ketoacidosis (DKA) – Possible Acute Complication of Diabetes Mellitus

Overview

• More common in Type 1 diabetes.
• Results from prolonged insulin deficiency.
• Can occur if insulin injections are missed, or during times of insulin deficiency, when cells are requiring more glucose, which may occur during times of stress, infection, or excessive exercise.

Causes of DKA

• Missed insulin doses.
• Prolonged exercise without insulin.
• Overeating or high carbohydrate intake, especially if insulin is unavailable.
• Stressors like infection or illness increase fat breakdown and ketone production.

Pathophysiology

• Lack of insulin prevents glucose from entering cells via GLUT4 channels.
• Blood glucose levels rise (hyperglycemia).
• Cells starve for glucose, leading to reduced ATP production → reduced cellular function.
  • results in increased catabolism of fat and protein to produce ATP

• Muscle cells and other tissues break down fats (lipolysis) producing ketones.
• Ketones are acidic wastes (e.g., beta-hydroxybutyric acid, acetoacetic acid, acetone).
  • Acetone (fruity smell on breath)
• Excess ketones build up in the blood (ketonemia), leading to blood acidosis (ketoacidosis).

• Ketones accumulate and bind serum bicarbonate, reducing the blood’s buffering capacity.
• Blood pH drops below pH 7.3 (acidic blood).
• High ketone levels cause toxicity, impairing enzyme functions.

Progression of DKA

• Water loss from osmotic diuresis due to, polyuria, glucosuria and ketonuria causes dehydration.
• Electrolyte imbalance (potassium, sodium).
• Decreased renal function leads to oliguria and less ketone excretion.
• Accumulation causes decompensated metabolic acidosis and potential coma.

Signs and Symptoms

• Rapid breathing (Kussmaul respiration) to compensate for acidosis
  • breathing out CO₂ reduces carbonic acid in blood.
• Fruity smell on the breath (acetone).
• Nausea, vomiting, abdominal pain
• Frequent urination (polyuria) initially, followed by oliguria
• Dehydration signs:
  • Dry mouth and mucous membranes
  • Thirst (polydipsia)
  • Low blood pressure
  • Thready, rapid pulse and/or tachycardia
  • Confusion, headache, and weakness
  • Can lead to coma and be life-threatening.

Urinalysis

• Ketonuria (ketones in urine).
• Glucosuria (glucose in urine).

Nervous System and Brain Effects

• Dehydration reduces brain perfusion.
• Electrolyte imbalances impair neuron and muscle function.
• Decreased responsiveness, lethargy, and risk of coma.

Progression and Risks

• Water loss causes decreased blood volume (hypovolemia).
• Reduced renal function limits acid excretion.
• Blood pH drops further → decompensated metabolic acidosis.
• Fatal dehydration and brain edema possible if untreated.
• Loss of consciousness and potentially coma.

Severe Consequences

• Cerebral edema due to brain swelling.
• Cardiac dysrhythmias caused by electrolyte disturbances.
• Low blood volume reduces perfusion.
• Increased intracranial pressure can impair brain function.
• Potential death if untreated.

Treatment

• Administer insulin to restore glucose uptake.
• Hydrate with IV fluids to replace water and electrolytes.
• Correct acidosis with bicarbonate.
• Treat underlying cause (infection, diet change).
• Continuous monitoring is vital to prevent progression.

Prevention

• Blood glucose monitoring is essential to avoid both hypoglycemia and hyperglycemia.

Summary

• DKA is a life-threatening emergency.
• Rapid recognition and intervention are crucial for survival.
• Proper treatment prevents severe dehydration, acidosis, and brain damage.
• Rapid recognition and treatment are critical:
  • Rehydrate with IV fluids.
  • Correct electrolyte imbalances.
  • Administer insulin to reduce blood glucose and ketones.
• Wearing a medical alert bracelet is recommended for diabetics, especially those at risk for DKA.