Management of Diabetic Ketoacidosis in a 7-Year-Old Child
Begin immediate fluid resuscitation with 0.9% normal saline at 10-20 mL/kg over the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour (without an initial bolus), while aggressively monitoring and replacing potassium to prevent life-threatening complications, particularly cerebral edema. 1, 2
Initial Assessment and Diagnostic Confirmation
Obtain STAT laboratory studies including venous blood gases, complete metabolic panel, complete blood count, urinalysis, and direct measurement of β-hydroxybutyrate (not urine ketones) 3, 4, 2. DKA is confirmed when blood glucose >250 mg/dL, venous pH <7.3, serum bicarbonate <15 mEq/L, and moderate ketonuria or ketonemia are present 4, 2.
Calculate corrected sodium by adding 1.6 mEq/L for each 100 mg/dL glucose above 100 mg/dL 3, 1. This corrected value determines subsequent fluid choice and helps assess true sodium status 1.
Critical pitfall: Never rely on urine ketones or nitroprusside-based tests for monitoring treatment response—these only measure acetoacetate and acetone, completely missing β-hydroxybutyrate (the predominant ketoacid), and paradoxically appear to worsen as the patient improves 3, 4.
Fluid Resuscitation Protocol
Initial Phase (First Hour)
Administer 0.9% normal saline at 10-20 mL/kg over the first hour to restore intravascular volume and renal perfusion 1, 2. Never exceed 50 mL/kg total fluid volume in the first 4 hours—this is the single most critical threshold for preventing cerebral edema in children 1.
Subsequent Fluid Management (After First Hour)
- If corrected sodium is normal or elevated: switch to 0.45% NaCl at 4-14 mL/kg/hour 1
- If corrected sodium is low: continue 0.9% NaCl at reduced rates of 4-14 mL/kg/hour 1
- Alternatively, use 1.5 times the 24-hour maintenance requirements (approximately 5 mL/kg/hour) to accomplish smooth rehydration, never exceeding two times maintenance 3
The induced change in serum osmolality must never exceed 3 mOsm/kg/hour to prevent cerebral edema 1. Monitor serum electrolytes, glucose, and osmolality every 2-4 hours throughout treatment 3, 1, 2.
When serum glucose reaches 250 mg/dL, add 5% dextrose to IV fluids while continuing insulin infusion to clear ketones 3, 4.
Insulin Therapy
Do NOT give an IV bolus of insulin in pediatric patients—this differs critically from adult protocols 3, 1, 2. Start continuous IV regular insulin infusion at 0.1 units/kg/hour only after initial fluid resuscitation has begun, delaying insulin by 1-2 hours after starting fluids 3, 2, 5.
Target a glucose reduction of 50-75 mg/dL per hour 3. If plasma glucose does not fall by 50 mg/dL in the first hour, verify adequate hydration status, then double the insulin infusion rate hourly until steady decline is achieved 3.
Continue insulin infusion until ketoacidosis resolves (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L), not just until glucose normalizes, as ketonemia takes longer to clear than hyperglycemia 3, 4, 2.
Potassium Replacement (Critical for Preventing Fatal Arrhythmias)
If initial serum potassium is <3.3 mEq/L, delay insulin therapy and aggressively replace potassium first—insulin will drive potassium intracellularly and precipitate life-threatening cardiac arrhythmias 1, 4.
Once serum potassium falls below 5.5 mEq/L and adequate urine output is confirmed, add 20-30 mEq/L potassium to IV fluids using a mixture of 2/3 KCl and 1/3 KPO₄ 3, 1, 2. Maintain serum potassium between 4-5 mEq/L throughout treatment 4, 2.
Monitoring Protocol
- Vital signs and neurological status: continuously, with hourly neurological checks to detect early signs of cerebral edema 1, 2
- Blood glucose: every 1-2 hours until stable 2
- Serum electrolytes, BUN, creatinine, osmolality, venous pH: every 2-4 hours 3, 1, 2
- β-hydroxybutyrate: every 2-4 hours to monitor ketosis resolution 4
After initial diagnosis, repeat arterial blood gases are unnecessary—venous pH (typically 0.03 units lower than arterial) and anion gap adequately monitor acidosis resolution 3, 4.
Cerebral Edema Prevention and Recognition
Cerebral edema is the leading cause of death during DKA treatment in children 5, 6. Risk factors include severity of acidosis, greater hypocapnia (after adjusting for acidosis), higher BUN at presentation, and bicarbonate treatment 6.
Never use hypotonic fluids initially, as this accelerates osmotic shifts and increases cerebral edema risk 1. Avoid fluid overload and excessively rapid correction of osmolality 3, 1.
Monitor mental status continuously to rapidly identify changes suggesting cerebral edema 3. If cerebral edema is suspected, immediately administer mannitol or hypertonic saline 5.
Transition to Subcutaneous Insulin
When DKA resolves (glucose <200 mg/dL, bicarbonate ≥18 mEq/L, pH >7.3, anion gap ≤12 mEq/L), start subcutaneous insulin 2-4 hours before discontinuing IV insulin 4, 2. Continue IV insulin for 1-2 hours after starting subcutaneous insulin to prevent recurrence of ketoacidosis 2.
Special Considerations
Never administer bicarbonate therapy—it is contraindicated in pediatric DKA management except in extreme circumstances (pH <6.9) 4. Bicarbonate increases cerebral edema risk 6.
Identify and treat the precipitating cause (infection, insulin omission, new-onset diabetes) to prevent recurrence 4, 2. Recurrent DKA is almost always due to insulin omission and requires comprehensive education and psychosocial support 2, 5.