What is the management algorithm for diabetic ketoacidosis?

Management Algorithm for Diabetic Ketoacidosis (DKA)

The management of diabetic ketoacidosis requires a systematic approach focusing on fluid resuscitation, insulin therapy, electrolyte replacement, and identification of precipitating causes to reduce morbidity and mortality.

Diagnosis and Initial Assessment

• Initial laboratory evaluation must include plasma glucose, blood urea nitrogen, creatinine, serum ketones, electrolytes with calculated anion gap, osmolality, urinalysis, arterial blood gases, complete blood count with differential, and electrocardiogram 1
• Direct measurement of β-hydroxybutyrate in blood is preferred for monitoring DKA, as nitroprusside methods only measure acetoacetic acid and acetone 1
• Continuous cardiac monitoring is crucial in severe DKA to detect arrhythmias early 2
• DKA is diagnosed when all three criteria are present: hyperglycemia or known diabetes, presence of ketones in blood or urine, and metabolic acidosis with elevated anion gap 3

Fluid Therapy

• Begin with balanced electrolyte solutions at 15-20 mL/kg/h during the first hour to restore circulatory volume and tissue perfusion 1
• Continue fluid replacement to correct estimated deficits within 24 hours, with induced change in serum osmolality not exceeding 3 mOsm/kg/h 1
• For mild DKA, administer 1.5 times the 24-hour maintenance requirements (5 mL/kg/h) for smooth rehydration; do not exceed twice the maintenance requirement 1
• Monitor fluid input/output, hemodynamic parameters, and clinical examination to assess progress with fluid replacement 1

Insulin Therapy

• After excluding hypokalemia, administer intravenous bolus of regular insulin at 0.15 U/kg body weight, followed by continuous infusion at 0.1 U/kg/h 1
• If plasma glucose does not fall by 50 mg/dL from initial value in the first hour, double the insulin infusion every hour until steady glucose decline between 50-75 mg/h is achieved 1
• Add dextrose to hydrating solution when blood glucose reaches 250-300 mg/dL while continuing insulin infusion at reduced rate 1
• Target blood glucose levels of 100-180 mg/dL 1
• For mild DKA, subcutaneous regular insulin may be given every 4 hours (5-unit increments for every 50 mg/dL increase in blood glucose above 150 mg/dL) 1

Electrolyte Management

• Monitor potassium levels closely as total body deficits are common despite potentially normal or elevated initial levels due to acidosis 1
• Begin potassium replacement after serum levels fall below 5.5 mEq/L, assuming adequate urine output 1
• Add 20-30 mEq potassium (2/3 KCl and 1/3 KPO₄) in each liter of infusion fluid to maintain serum potassium concentration within 4-5 mEq/L 1
• If significant hypokalemia is present initially, delay insulin treatment until potassium concentration is restored to >3.3 mEq/L to avoid arrhythmias, cardiac arrest, and respiratory muscle weakness 1
• Bicarbonate therapy is generally not recommended in DKA patients with pH >7.0 1
• For adult patients with pH <6.9, administer 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/h 1
• For patients with pH 6.9-7.0, administer 50 mmol sodium bicarbonate in 200 mL sterile water at 200 mL/h 1
• Consider phosphate replacement only in patients with cardiac dysfunction, anemia, respiratory depression, or serum phosphate <1.0 mg/dL 1

Monitoring During Treatment

• Draw blood every 2-4 hours to determine serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH 1
• Monitor blood glucose at least every 2-4 hours while the patient takes nothing by mouth 1
• Venous pH (typically 0.03 units lower than arterial pH) and anion gap can be followed to monitor resolution of acidosis 1
• Watch for complications, particularly electrolyte imbalances that can trigger cardiac arrhythmias 2

Resolution Parameters

• DKA resolution requires glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L 1

Transition from IV to Subcutaneous Insulin

• Transition from intravenous to subcutaneous insulin requires administration of basal insulin 2-4 hours before the intravenous insulin is stopped to prevent recurrence of ketoacidosis and rebound hyperglycemia 4, 1
• When DKA is resolved and the patient can eat, transition to a multiple-dose regimen using a combination of short/rapid-acting and intermediate/long-acting insulin 1
• For newly diagnosed patients, initiate a multidose regimen of short- and intermediate/long-acting insulin at approximately 0.5-1.0 units/kg/day 1

Identification and Treatment of Precipitating Causes

• Obtain bacterial cultures of urine, blood, and other sites as needed and administer appropriate antibiotics if infection is suspected 1
• Treat any correctable underlying cause of DKA, such as sepsis, myocardial infarction, or stroke 4
• SGLT2 inhibitors should be discontinued 3-4 days before surgery to prevent DKA 1

Special Populations Considerations

• In patients with chronic kidney disease, adjust fluid and electrolyte management carefully 5
• For pregnant patients, more intensive monitoring and specialized care are required 5
• In patients with heart failure, careful fluid administration is essential to prevent volume overload 6

Discharge Planning and Prevention

• Include education on recognition, prevention, and management of DKA for all individuals affected by or at high risk for these events 1
• Provide information on medication changes, pending tests, and follow-up needs 4
• Transmit discharge summaries to the primary care provider as soon as possible after discharge 4
• Schedule follow-up appointments prior to discharge to increase attendance likelihood 4

Common Pitfalls and Caveats

• Overzealous insulin treatment can lead to hypoglycemia 7
• Excessive fluid administration can cause pulmonary edema, especially in patients with cardiac or renal dysfunction 6
• Failure to replace potassium adequately can lead to life-threatening arrhythmias 2
• Cerebral edema is a rare but potentially fatal complication, especially in children 1
• Bicarbonate administration generally does not improve outcomes and may potentially worsen hypokalemia and cerebral acidosis 1