What is the treatment for ketoacidosis?

Treatment of Diabetic Ketoacidosis

Begin immediate treatment with aggressive intravenous fluid resuscitation using isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour, while closely monitoring and replacing potassium to maintain levels between 4-5 mEq/L. 1, 2

Initial Fluid Resuscitation

• Start with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in adults) during the first hour to restore intravascular volume and tissue perfusion 1, 2

• After the first hour, continue fluid replacement at 4-14 mL/kg/hour based on hemodynamic status and hydration assessment 1

• When serum glucose reaches 200-250 mg/dL, switch to 5% dextrose with 0.45-0.75% saline while continuing insulin infusion to prevent hypoglycemia and ensure complete resolution of ketoacidosis 1, 2

• Aim to correct estimated fluid deficits within 24 hours, but avoid overly rapid correction of osmolality (should not exceed 3-8 mOsm/kg/hour) to prevent cerebral edema 2, 3

Insulin Therapy Protocol

• Administer continuous IV regular insulin infusion at 0.1 units/kg/hour after initiating fluid resuscitation 1, 2

• If plasma glucose does not fall by 50-75 mg/dL in the first hour, check hydration status and double the insulin infusion rate hourly until achieving steady glucose decline 1, 2

• Continue insulin infusion until DKA resolves (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L, and glucose <200 mg/dL), regardless of glucose levels 1, 2

• For mild-to-moderate uncomplicated DKA, subcutaneous rapid-acting insulin analogs combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin, though continuous IV insulin remains standard for critically ill and mentally obtunded patients 2

Critical Potassium Management

• Monitor serum potassium every 2-4 hours throughout treatment 1, 2

• If potassium is <3.3 mEq/L, delay insulin therapy and aggressively replace potassium first to prevent life-threatening cardiac arrhythmias and respiratory muscle weakness 2

• When potassium is 3.3-5.5 mEq/L, add 20-30 mEq potassium per liter of IV fluid (use 2/3 KCl and 1/3 KPO₄) once adequate urine output is confirmed 1, 2

• If potassium is >5.5 mEq/L, withhold potassium initially but monitor closely, as levels will drop rapidly with insulin therapy 2

• Target serum potassium of 4-5 mEq/L throughout treatment, recognizing that total body potassium depletion averages 3-5 mEq/kg body weight despite potentially normal or elevated initial levels 2

Common pitfall: Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA. Despite total body potassium depletion being universal, only a small percentage present with hypokalemia, making this a high-risk scenario. 2

Bicarbonate Administration

• Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0, as multiple studies show no difference in resolution of acidosis or time to discharge 1, 2

• Bicarbonate may worsen ketosis, cause hypokalemia, and increase cerebral edema risk 2

• Only consider bicarbonate if pH is <6.9 1

Monitoring During Treatment

• Check blood glucose every 1-2 hours until stable 1

• Monitor electrolytes, blood urea nitrogen, creatinine, and venous pH every 2-4 hours 1, 2

• Direct measurement of β-hydroxybutyrate in blood is preferred over urine ketones, as the nitroprusside method only measures acetoacetic acid and acetone, not β-hydroxybutyrate (the strongest and most prevalent acid in DKA) 1, 2

• Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor resolution of acidosis 2

Treatment of Precipitating Factors

• Identify and treat underlying causes concurrently: infection (most common precipitant), myocardial infarction, stroke, pancreatitis, trauma, insulin omission, or SGLT2 inhibitor use 1, 2, 3

• Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics 2

• Discontinue SGLT2 inhibitors immediately if being used, as they can cause euglycemic DKA 4

Transition to Subcutaneous Insulin

• Once DKA resolves (glucose <200 mg/dL, bicarbonate ≥18 mEq/L, pH >7.3, anion gap ≤12 mEq/L), administer basal insulin (intermediate or long-acting) 2-4 hours BEFORE stopping IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2

• Continue IV insulin for 1-2 hours after starting subcutaneous insulin to ensure adequate plasma insulin levels 1

• Start multiple-dose schedule using combination of short/rapid-acting and intermediate/long-acting insulin once patient can eat 2

• Recent evidence shows adding low-dose basal insulin analog during IV insulin infusion may prevent rebound hyperglycemia without increasing hypoglycemia risk 2

Critical pitfall: Premature termination of insulin therapy before complete resolution of ketosis is a common cause of recurrent DKA. Never stop IV insulin just because glucose levels normalize. 2

Complications to Monitor

• Cerebral edema (more common in children and adolescents): Monitor for headache, altered mental status, seizures, or bradycardia; treat immediately if suspected 1, 2

• Hypoglycemia: Prevent by adding dextrose to IV fluids when glucose falls below 200-250 mg/dL while continuing insulin 1, 2

• Hypokalemia: The leading preventable cause of mortality in DKA; requires aggressive monitoring and replacement 2

• Recurrence of DKA: Prevent with proper 2-4 hour overlap when transitioning to subcutaneous insulin 1, 2

Discharge Planning

• Identify outpatient diabetes care providers before discharge 2

• Educate patients on glucose monitoring, insulin administration, recognition and treatment of hyperglycemia/hypoglycemia, and sick day management 2

• Schedule follow-up appointment prior to discharge 1, 2