Diabetic Ketoacidosis (DKA): A Comprehensive Guide for Nurses

Diabetic Ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes mellitus, primarily seen in type 1 diabetes but occasionally in type 2 diabetes under extreme conditions. It is characterized by hyperglycemia, ketosis, and metabolic acidosis. Early recognition and timely intervention are critical in preventing severe complications and improving outcomes. Nurses play a pivotal role in the early identification, management, and education of patients with DKA.

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Definition and Diagnostic Criteria

DKA occurs due to an absolute or relative insulin deficiency, leading to:

• Hyperglycemia: Blood glucose >250 mg/dL.
• Ketosis: Elevated serum ketones or positive urine ketones.
• Metabolic Acidosis: pH <7.3 and bicarbonate <18 mEq/L.

Severity Classification:

• Mild DKA: pH 7.25–7.30, bicarbonate 15–18 mEq/L.
• Moderate DKA: pH 7.00–7.24, bicarbonate 10–15 mEq/L.
• Severe DKA: pH <7.00, bicarbonate <10 mEq/L.

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Pathophysiology

DKA develops due to an interplay of insulin deficiency and counterregulatory hormone excess (glucagon, cortisol, epinephrine, and growth hormone), leading to:

Hyperglycemia:

• Reduced glucose uptake by cells.
• Increased gluconeogenesis and glycogenolysis in the liver.

Lipolysis and Ketogenesis:

• Free fatty acids released from adipose tissue are converted into ketone bodies (beta-hydroxybutyrate and acetoacetate) in the liver.
• Results in ketosis and metabolic acidosis.

Osmotic Diuresis and Dehydration:

• Hyperglycemia exceeds the renal threshold, leading to glucosuria, water, and electrolyte losses.

Electrolyte Imbalances:

• Potassium shifts from intracellular to extracellular compartments due to acidosis, resulting in total body potassium depletion.

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Causes and Risk Factors

Common Causes:

• Infection (most common trigger): Pneumonia, urinary tract infections (UTIs), sepsis.
• Non-Adherence: Missed insulin doses or inadequate therapy.
• New-Onset Diabetes: Often the initial presentation in type 1 diabetes.
• Stress: Surgery, trauma, or psychological stress.
• Medications: Glucocorticoids, thiazides, SGLT2 inhibitors.

Risk Factors:

• Poor glycemic control.
• Previous history of DKA.
• Limited access to healthcare or insulin supplies.
• Concurrent illness or injury.

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Clinical Presentation

Early Symptoms:

• Polyuria, polydipsia, and dehydration.
• Nausea and vomiting.
• Abdominal pain (often mimics acute surgical conditions).

Advanced Symptoms:

• Kussmaul respirations: Deep, labored breathing as compensation for acidosis.
• Fruity breath odor: Due to acetone.
• Altered mental status: Ranges from confusion to coma in severe cases.
• Signs of hypovolemia: Tachycardia, hypotension, dry mucous membranes.

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Diagnosis

Key Diagnostic Studies:

Blood Tests:

• Serum Glucose: Elevated (>250 mg/dL).
• Serum Ketones: Elevated beta-hydroxybutyrate.
• Arterial Blood Gas (ABG): Low pH (<7.3) and bicarbonate (<18 mEq/L).
• Electrolytes: Hyperkalemia or normokalemia initially, but total body potassium depletion.
• Hyponatremia: Due to osmotic shifts.
• Elevated anion gap:(>12) indicates metabolic acidosis.

Urine Tests:

• Positive for glucose and ketones.

Additional Workup:

• CBC, blood cultures (if infection is suspected).
• Chest X-ray or urinalysis to identify infection sources.

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Management of DKA

Goals of Treatment:

• Correct dehydration.
• Restore normal blood glucose levels.
• Reverse ketosis and acidosis.
• Correct electrolyte imbalances.
• Identify and treat precipitating factors.

1. Fluid Resuscitation:

• Start with isotonic saline (0.9% NaCl): 15-20 mL/kg/hr during the first 1-2 hours.
• Switch to 0.45% NaCl: Based on hydration status, serum sodium levels, and corrected sodium.
• Add dextrose (D5) to fluids: When glucose levels fall to 200 mg/dL to prevent hypoglycemia.

2. Insulin Therapy:

• Administer a regular insulin IV infusion:
• Initial bolus: 0.1 units/kg (optional based on protocol).
• Continuous infusion: 0.1 units/kg/hour.
• Goal: Reduce glucose by 50-75 mg/dL/hour.
• Transition to subcutaneous insulin: Once DKA resolves (pH >7.3, bicarbonate >18 mEq/L, anion gap closure).

3. Potassium Replacement:

• Monitor potassium closely as insulin therapy and fluid resuscitation shift potassium intracellularly.
• If potassium is:
• <3.3 mEq/L: Replace potassium before starting insulin.
• 3.3–5.2 mEq/L: Add potassium to IV fluids.
• >5.2 mEq/L: Monitor levels but do not supplement initially.

4. Bicarbonate Therapy:

• Reserved for severe acidosis (pH <6.9) to minimize complications like arrhythmias.

5. Monitor for Complications:

• Frequent blood glucose, ABG, and electrolyte monitoring every 1-2 hours initially.
• Watch for signs of cerebral edema (especially in pediatric patients).

6. Treat Underlying Cause:

• Administer antibiotics for infection.
• Address nonadherence or education gaps in insulin use.

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Nursing Interventions

1. Initial Assessment:

• Monitor vital signs, respiratory status, and neurological function closely.
• Assess fluid balance by tracking intake, output, and weight.

2. Frequent Monitoring:

• Check glucose, electrolytes, and ketones regularly.
• Observe for signs of hypoglycemia or hypokalemia.

3. Fluid and Medication Administration:

• Ensure accurate administration of IV fluids, insulin, and potassium supplements as prescribed.
• Titrate insulin infusion based on glucose levels and provider orders.

4. Patient Education:

• Teach patients about recognizing early symptoms of DKA.
• Emphasize the importance of insulin adherence, even during illness (sick-day rules).
• Educate on proper glucose and ketone monitoring.

5. Prevent Complications:

• Implement fall precautions for patients with dizziness or confusion.
• Ensure appropriate oxygenation if respiratory distress is present.

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Complications of DKA

• Cerebral Edema:
  • Most common in pediatric patients.
  • Symptoms: Severe headache, altered mental status, bradycardia.
  • Requires immediate intervention (e.g., mannitol or hypertonic saline).
• Hypokalemia:
  • Result of insulin therapy and fluid shifts.
  • Can cause cardiac arrhythmias.
• Acute Kidney Injury (AKI):
  • Due to severe dehydration and hypoperfusion.
• Hypoglycemia:
  • From excessive insulin administration.

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Prevention of DKA

Patient Education:

• Teach proper use of insulin and monitoring of blood glucose/ketones.
• Discuss the importance of hydration and adjusting insulin during illness.

Early Recognition:

• Encourage patients to seek medical attention for persistent hyperglycemia, nausea, or vomiting.

Regular Follow-Up:

• Ensure routine diabetes care and monitoring to avoid lapses in therapy.

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Conclusion

Diabetic ketoacidosis is a serious but manageable complication of diabetes that requires prompt recognition and treatment. Nurses play a critical role in stabilizing patients, administering treatment, and educating them to prevent recurrence. By adhering to evidence-based guidelines, nurses can significantly improve outcomes and reduce the burden of this life-threatening condition.