Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes characterized by hyperglycemia, ketosis, and metabolic acidosis. It occurs more commonly in individuals with type 1 diabetes, though it can also be seen in type 2 diabetes under stress or in severe insulin deficiency.

Pathophysiology:

DKA results from a deficiency of insulin and an excess of counter-regulatory hormones (glucagon, cortisol, catecholamines, growth hormone). This hormonal imbalance leads to:

1. Increased gluconeogenesis and glycogenolysis in the liver, raising blood glucose levels.
2. Lipolysis and free fatty acid release, which are converted into ketone bodies (acetoacetate and β-hydroxybutyrate) in the liver.
3. Ketosis and metabolic acidosis, due to the accumulation of these ketone bodies.

Diagnostic Criteria:

DKA is diagnosed based on the presence of:

• Hyperglycemia: Blood glucose levels >250 mg/dL (13.9 mmol/L).
• Ketosis: Elevated serum ketones or positive urine ketones.
• Metabolic Acidosis: Arterial blood pH <7.3 and serum bicarbonate <18 mEq/L, with an increased anion gap (>12).

Clinical Presentation:

• Symptoms: Polyuria, polydipsia, nausea, vomiting, abdominal pain, fatigue, weakness, confusion, or coma.
• Signs: Dehydration, tachycardia, hypotension, Kussmaul respiration (deep, labored breathing), fruity breath odor (due to acetone), altered mental status.

Initial Evaluation:

Blood Tests:

• Serum glucose: Typically >250 mg/dL (13.9 mmol/L).
• Electrolytes: Check sodium, potassium, chloride, bicarbonate levels. Calculate the anion gap (AG = [Na+] – [Cl- + HCO3-]).
• Serum ketones: β-hydroxybutyrate is preferred for its accuracy.
• Blood gas analysis: Arterial or venous blood gas to assess pH and bicarbonate.
• Renal function tests: BUN, creatinine, to evaluate dehydration and renal impairment.

Urine Tests:

• Urine ketones: Positive for ketones.
• Urinalysis: To rule out infections.

Other Investigations:

• Complete blood count (CBC): For leukocytosis.
• Electrocardiogram (ECG): To detect cardiac effects of hyperkalemia or hypokalemia.
• Serum osmolality: To assess the degree of hyperosmolarity.

Management:

DKA management involves correcting dehydration, hyperglycemia, and electrolyte imbalances while addressing the underlying precipitating factor.

1. Fluid Replacement:

Initial Fluid Resuscitation:

• Start with 0.9% normal saline (NS) at 15-20 mL/kg/hr (approximately 1-1.5 L) during the first hour.
• If corrected serum sodium is normal or elevated, switch to 0.45% saline (half-normal saline) at 250-500 mL/hr. If corrected sodium is low, continue with 0.9% NS.
• Once blood glucose reaches 200-250 mg/dL (11-13.9 mmol/L), switch to 5% dextrose with 0.45% saline (D5-½NS) at 150-250 mL/hr to prevent hypoglycemia.

2. Insulin Therapy:

Intravenous (IV) Insulin:

• Administer a regular insulin bolus of 0.1 units/kg body weight, followed by a continuous insulin infusion of 0.1 units/kg/hr.
• If blood glucose does not decrease by at least 50-70 mg/dL in the first hour, the insulin infusion rate may be doubled.
• When blood glucose reaches 200-250 mg/dL, reduce the insulin infusion rate to 0.02-0.05 units/kg/hr and continue the infusion along with dextrose-containing fluids.

3. Potassium Replacement:

• Potassium shifts out of cells during acidosis, resulting in normal or elevated serum potassium despite total body depletion.
• Potassium <3.3 mEq/L: Hold insulin therapy and give 20-30 mEq of potassium per hour until serum potassium is >3.3 mEq/L.
• Potassium 3.3-5.2 mEq/L: Add 20-30 mEq/L of potassium to each liter of IV fluid to maintain potassium levels within the normal range.
• Potassium >5.2 mEq/L: Do not give potassium. Monitor serum levels every 2 hours.

4. Bicarbonate Therapy (Controversial):

• Indicated only if arterial pH <6.9 to prevent severe acidosis complications.
• Give 100 mEq of sodium bicarbonate in 400 mL of sterile water with 20 mEq of potassium chloride over 2 hours. Repeat every 2 hours until pH >7.

5. Phosphate Replacement:

• Phosphate levels may fall during insulin therapy.
• Replace if serum phosphate <1.0 mg/dL or if there is severe respiratory depression, cardiac dysfunction, or muscle weakness. Administer 20-30 mEq of potassium phosphate per liter of IV fluid.

Monitoring:

• Vital Signs: Every 15-30 minutes until stable, then every 1-2 hours.
• Serum Glucose and Electrolytes: Check glucose, sodium, potassium, bicarbonate, and anion gap every 1-2 hours during the initial phase.
• Urine Output: Monitor hourly to assess renal function.
• Blood Gas Analysis: Periodically recheck pH, bicarbonate, and CO2 to assess the resolution of acidosis.
• Neurologic Status: Monitor for signs of cerebral edema, particularly in younger patients.

Resolution Criteria for DKA:

• Blood glucose <200 mg/dL (11 mmol/L).
• Serum bicarbonate ≥18 mEq/L.
• Venous pH >7.3.
• Anion gap ≤12.

Transition to Subcutaneous Insulin:

• Once DKA resolves, and the patient can tolerate oral intake:
• Overlap the IV insulin infusion with the first dose of subcutaneous insulin by 1-2 hours to prevent rebound hyperglycemia.
• Subcutaneous insulin dosage: Calculate the patient’s daily requirement based on weight (0.5-0.8 units/kg/day) or their previous insulin regimen.

Complications:

1. Hypoglycemia or Hypokalemia: Can occur due to overzealous correction.
2. Cerebral Edema: More common in children and young adults. Present with headache, altered consciousness, or seizures.
3. Acute Kidney Injury: Due to severe dehydration.
4. Thrombosis: Due to hyperosmolarity and dehydration.

Prevention:

• Educate patients on the early signs of DKA, proper insulin administration, and management of sick days.
• Regular monitoring of blood glucose and ketones during illness.
• Adjustment of insulin therapy during times of increased stress (infection, surgery).

Effective DKA management requires prompt recognition and a systematic approach to correcting metabolic derangements while carefully monitoring and managing potential complications.