DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by hyperglycemia, ketonuria, acidosis, and dehydration.
Pathophysiology and Etiology
- Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for fuel.
- Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver.
- Ketone bodies are organic acids that cause metabolic acidosis.
- Increase in the secretion of glucagon, catecholamines, growth hormone, and cortisol, in response to the hyperglycemia caused by insulin deficiency, accelerates the development of DKA.
- Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium, sodium, phosphate, and water.
- Caused by inadequate amounts of endogenous or exogenous insulin.
- Frequently occurs due to failure to increase the dose of insulin during periods of stress (eg, infection, surgery, pregnancy).
- May occur in previously undiagnosed or untreated diabetics.
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Clinical Manifestations
Early
- Polydipsia, polyuria
- Fatigue, malaise, drowsiness
- Anorexia, nausea, vomiting
- Abdominal pains, muscle cramps
Later
- Kussmaul respiration (deep respirations)
- Fruity, sweet breath
- Hypotension, weak pulse
- Stupor and coma
Diagnostic Evaluation
- Serum glucose level is usually elevated over 300 mg/dL; may be as high as 1,000 mg/dL.
- Serum and urine ketone bodies are present.
- Serum bicarbonate and pH are decreased due to metabolic acidosis, and partial pressure of carbon dioxide is decreased as a respiratory compensation mechanism.
- Serum sodium and potassium levels may be low, normal, or high due to fluid shifts and dehydration, despite total body depletion.
- BUN, creatinine, hemoglobin, and hematocrit are elevated due to dehydration.
- Urine glucose is present in high concentration and specific gravity is increased, reflecting osmotic diuresis and dehydration.
NURSING ALERT
Severity of DKA cannot be determined by serum glucose levels; acidosis may be prominent with glucose level of 200 mg/dL or less.
Management
- I.V. fluids to replace losses from osmotic diuresis, vomiting.
- I.V. insulin drip- regular insulin infused only to increase glucose utilization and decrease lipolysis.
- Electrolyte replacement- sodium chloride and phosphate as required, potassium chloride and bicarbonate based on laboratory results.
Complications
- Premature discontinuation of I.V. insulin can result in prolongation of DKA.
- Too-rapid infusion of I.V. fluids in cases of severe dehydration can cause cerebral edema and death.
- Failure to institute subcutaneous insulin injections before discontinuation of I.V. insulin can result in extended hyperglycemia.
Nursing Assessment
- Assess skin for dehydration- poor turgor, flushing, dry mucous membranes.
- Observe for cardiac changes reflecting dehydration, metabolic acidosis, and electrolyte imbalance- hypotension; tachycardia; weak pulse; electrocardiographic changes, including elevated P wave, flattened T wave or inverted, prolonged QT interval.
- Assess respiratory status- Kussmaul breathing, acetone breath characteristic of metabolic acidosis.
- Perform GI assessment- nausea, vomiting, extreme thirst, abdominal bloating and cramping, diarrhea.
- Determine GU symptoms- nocturia, polyuria.
- Observe for neurologic signs- crying, restlessness, twitching, tremors, drowsiness, lethargy, headache, decreased reflexes.
- Interview family or significant other regarding precipitating events to episode of DKA.
- Patient self-care management before hospitalization
- Unusual events that may have precipitated episode (eg, chest pain, trauma, illness)
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Nursing Diagnoses
- Deficient Fluid Volume related to hyperglycemia
- Ineffective Therapeutic Regimen Management related to failure to increase insulin during illness
Nursing Interventions
Restoring Fluid and Electrolyte Balance
- Assess BP and heart rate frequently, depending on patient's condition; assess skin turgor and temperature.
- Monitor intake and output every hour.
- Replace fluids as ordered through peripheral I.V. line.
- Monitor urine specific gravity to assess fluid changes.
- Monitor blood glucose frequently.
- Assess for symptoms of hypokalemia - fatigue, anorexia, nausea, vomiting, muscle weakness, decreased bowel sounds, paresthesia, arrhythmias, flat T waves, ST-segment depression.
- Administer replacement electrolytes and insulin as ordered. Flush the entire I.V. infusion set with solution containing insulin and discard the first 50 mL because plastic bags and tubing may absorb some insulin and the initial solution may contain decreased concentration of insulin.
- Monitor serum glucose, bicarbonate, and pH levels periodically.
- Provide reassurance about improvement of condition and that correction of fluid imbalance will help reduce discomfort.
NURSING ALERT
Electrolyte levels may not reflect the total body deficit of potassium (primarily) and sodium (to a lesser extent) due to compartment shifts and fluid volume loss. Replacement is necessary despite normal to high values.
DRUG ALERT
Interruption in insulin administration may result in reaccumulation of ketone bodies and worsening acidosis. Glucose will normalize before acidosis resolves so I.V. insulin is continued until bicarbonate levels normalize and subcutaneous insulin takes effect and the patient starts eating.
Preventing Further Episodes of DKA
- Review with patients precipitating events and causes of DKA.
- Assist patient in identifying warning signs and symptoms of DKA.
- Instruct patient in sick-day guidelines
Patient Education and Health Maintenance
- Make sure that patient and caretakers can demonstrate drawing up and administering insulin in the proper dose, blood glucose monitoring, and urine ketone testing.
- Make sure that patient and caretakers know whom to notify in the event of hyperglycemia, stressful situation, or symptoms of DKA.
Evaluation: Expected Outcomes
- BP and heart rate stable; glucose and bicarbonate levels improving
- Verbalizes sick-day guidelines correctly
