13.1 Pediatric Diabetic Ketoacidosis (DKA): Fluids, Insulin and Cerebral Injury
Key Takeaways
Diagnose DKA using hyperglycemia, acidosis and ketosis. Use the more severe category reached by venous pH or bicarbonate. Consider HHS or mixed DKA/HHS when marked hyperosmolality accompanies the hyperglycemia.
Restore perfusion with isotonic fluid. In a volume-depleted child without shock, ISPAD starts 0.9% saline at 10–20 mL/kg over 20–30 minutes. Choose subsequent fluid composition and deficit replacement using the pediatric protocol and serial findings.
Begin IV regular insulin at 0.05–0.1 units/kg/hour at least one hour after fluids start and after assessing potassium safety. Avoid a loading bolus. Add dextrose as glucose falls and use ketone and acid–base trends to decide when IV insulin can stop.
Calculate corrected sodium and effective osmolality separately. Use measured sodium in the osmolality equation. Reassess unexpected values with the fluid prescription, perfusion and neurologic exam.
New neurologic deterioration can signal DKA-related cerebral injury. Give IV mannitol or 3% saline promptly, protect cerebral perfusion and defer imaging until treatment is underway.
Pediatric Diabetic Ketoacidosis: Fluids, Insulin and Cerebral Injury
Quick Answer: Diagnose DKA from hyperglycemia, acidosis and ketosis. Restore perfusion with isotonic fluid, review potassium before insulin, and add dextrose as glucose falls so insulin can continue clearing ketones. Follow measured and corrected sodium, effective osmolality and neurologic status together. Treat suspected cerebral injury immediately without waiting for imaging.
Diagnosis and Severity
Insulin deficiency and counter-regulatory hormones increase hepatic glucose production and ketone formation. Hyperglycemia causes osmotic diuresis with water and electrolyte losses. Accumulating ketoacids lower bicarbonate and cause a high-anion-gap metabolic acidosis, often with compensatory Kussmaul breathing.
The 2022 ISPAD biochemical criteria for typical DKA are glucose above approximately 200 mg/dL, venous pH below 7.30 or bicarbonate below 18 mmol/L, and blood beta-hydroxybutyrate (BOHB) at least 3 mmol/L or moderate to large ketonuria. Prefer blood BOHB when available. DKA can occur in type 1 or type 2 diabetes. Significant ketosis and acidosis can also occur without marked hyperglycemia, for example after partial treatment. Evaluate the clinical context.
| ISPAD severity threshold | Venous pH | Serum bicarbonate |
|---|---|---|
| Mild | Below 7.30 | Below 18 mmol/L |
| Moderate | Below 7.20 | Below 10 mmol/L |
| Severe | Below 7.10 | Below 5 mmol/L |
The thresholds are nested. Use the most severe category reached by either measure. Acidosis grades biochemical severity. Perfusion, mental status, age, electrolyte instability and local monitoring capability also determine the level of care.
Hyperglycemic hyperosmolar state (HHS) typically has glucose above 600 mg/dL and effective osmolality above 320 mOsm/kg, with little ketosis, venous pH above 7.25 and bicarbonate above 15 mmol/L. A child with DKA and marked hyperosmolality can have a mixed crisis. Recognize it early and obtain expert management because fluid, electrolyte and insulin needs differ from standard DKA. ISPAD guideline
Initial Fluid and Ongoing Replacement
For a volume-depleted child without shock, ISPAD starts 0.9% saline at 10–20 mL/kg over 20–30 minutes and uses the higher initial volume when tissue perfusion is poor. In shock, ISPAD uses rapid 20 mL/kg boluses of 0.9% saline with reassessment after each. Persistent shock also calls for evaluation of other causes. Obtain weight, establish access and monitor perfusion, neurologic status, glucose, electrolytes and acid–base status.
After initial expansion, use the pediatric protocol for maintenance plus estimated deficit replacement. ISPAD allows replacement over 24–48 hours, with subsequent fluid selection based on hydration, sodium and osmolality. For this phase ISPAD allows 0.45%–0.9% saline or a balanced crystalloid. Track fluid already received, including at the referring facility. In the PECARN FLUID randomized trial, neither of the tested replacement rates nor sodium chloride concentrations significantly altered neurologic outcomes. This finding applies to the regimens studied and supports timely restoration of perfusion.
Worked fluid calculation: For a 20-kg child with a protocol-estimated 7% deficit, 0.07 × 20 kg × 1,000 mL/kg gives 1,400 mL. After a 400-mL initial bolus counted toward the deficit, 1,000 mL remains. If the selected replacement interval is 48 hours, deficit replacement adds about 20.8 mL/hour. Using the ISPAD daily maintenance method, the first 10 kg contributes 1,000 mL/day and the next 10 kg contributes 500 mL/day. Total maintenance is 62.5 mL/hour, giving a starting combined estimate of about 83.3 mL/hour. Use the protocol and serial findings to adjust the prescription. ISPAD fluid recommendations · PECARN FLUID trial
Insulin and Dextrose
Begin IV regular insulin at least one hour after fluids start, once potassium is safe for insulin under the pediatric protocol. Use 0.05–0.1 units/kg/hour and avoid an IV loading bolus. The lower dose can be appropriate in less severe DKA. Follow the ketone and acid–base response. If improvement stalls, check insulin delivery, dose, perfusion and other causes such as infection.
Add 5% dextrose around 250–300 mg/dL, or sooner if glucose is falling rapidly after initial expansion. Adjust dextrose to avoid hypoglycemia while continuing insulin for ketone clearance. Some children need 10% or 12.5% dextrose. A two-bag system keeps the prescribed combined flow rate constant and varies the mix of two otherwise identical solutions. With D0 and D10 bags, equal flow produces D5 and a D10 share of 75% produces D7.5. Persistent rapid glucose decline despite dextrose, or refractory hypokalemia, may require an insulin rate adjustment with specialist guidance. ISPAD insulin recommendations · Pediatric two-bag example
Potassium, Phosphate and Bicarbonate
| Finding | Action |
|---|---|
| Low potassium at presentation | Begin monitored replacement before insulin. Follow the local hold threshold and infusion limits. ISPAD's executive summary specifies below 3.0 mmol/L, while its detailed section specifies below 3.5 mmol/L and a maximum IV replacement rate usually 0.5 mmol/kg/hour. The Canadian pediatric guideline withholds insulin at 3.0 mmol/L or below. Check the local pathway in borderline cases. |
| Normal or high serum potassium | Total body potassium is usually depleted. Insulin and correction of acidosis can lower serum potassium quickly. Add potassium after volume expansion when appropriate. ISPAD commonly starts at 40 mmol/L in the infusate. In initial hyperkalemia, defer supplementation, recheck frequently and begin when urine output is documented and potassium is below 5.5 mmol/L under the ISPAD approach. Consider renal function. |
| Phosphate depletion | Monitor phosphate. ISPAD recommends prompt treatment below 1 mg/dL (about 0.32 mmol/L), even without symptoms. Some protocols treat at higher levels when there is organ dysfunction. Use the local replacement protocol and follow calcium, magnesium and potassium. Phosphate can be part of the potassium replacement mixture, which is chosen for current labs and available formulations. |
| Persistent acidosis | Treat DKA with fluids and insulin. Avoid routine bicarbonate. ISPAD reserves it for unusual circumstances such as life-threatening hyperkalemia or venous pH below 6.9 with compromised cardiac contractility. |
ISPAD electrolyte recommendations · Canadian pediatric DKA recommendations
Sodium and Effective Osmolality
Hyperglycemia pulls water into extracellular fluid and can lower the measured sodium. Corrected sodium estimates the value attributable to water and sodium balance after accounting for the glucose effect. Use the ISPAD formula with glucose in mg/dL.
Calculate effective osmolality with measured sodium. Glucose is converted to mmol/L by dividing the mg/dL value by 18. Urea is omitted because it does not contribute appreciably to effective tonicity.
Worked trend: With measured sodium 128 mEq/L and glucose 650 mg/dL, corrected sodium is 136.8 mEq/L and effective osmolality about 292.1 mOsm/kg. Four hours later, sodium 125 and glucose 350 give corrected sodium 129.0 and effective osmolality about 269.4. Review the unexpectedly low repeat values, fluid sodium concentration and delivery, perfusion and neurologic exam, and repeat labs as needed. The chart shows measured and corrected sodium on the same scale. ISPAD does not require a routine rise in measured sodium. If sodium needs correction, adjust the sodium concentration of the infusate. In severe dehydration or circulatory compromise, ISPAD advises increasing the infusate sodium when measured sodium is low and fails to rise appropriately. The trend alone cannot diagnose cerebral injury or justify cutting perfusion-supporting fluids. ISPAD sodium guidance · PECARN sodium and mental status analysis
Recognize and Treat Cerebral Injury
Clinical cerebral injury can occur before or during therapy. Severe acidosis, higher initial BUN, marked hypocapnia and younger age raise concern. Recheck neurologic status frequently. New or worsening headache, unexpected bradycardia, altered consciousness, incontinence, cranial nerve signs or abnormal breathing warrant immediate assessment.
The Muir bedside criteria organize signs occurring during treatment. Diagnostic signs include an abnormal response to pain, posturing, cranial nerve palsy or a neurogenic breathing pattern. Major signs include altered mentation, a sustained fall in heart rate of more than 20 beats/min unrelated to sleep or improved perfusion, and age-inappropriate incontinence. Minor signs include vomiting, headache, lethargy, diastolic pressure above 90 mmHg and age under five. The studied rule uses one diagnostic sign, two major signs, or one major and two minor signs. Use it as an aid. Treat when clinically suspected. Muir bedside criteria study · Pediatric cerebral injury risk study
Caution
Give hyperosmolar therapy immediately and call critical care. ISPAD lists mannitol 0.5–1 g/kg IV or 3% saline 2.5–5 mL/kg IV, each over 10–15 minutes. Elevate the head with midline positioning when feasible and maintain blood pressure and perfusion. Adjust isotonic fluid under the local protocol. Defer imaging until treatment is underway and the child is stable enough. If airway protection or ventilation requires intubation, preserve compensation appropriate to the metabolic acidosis with pediatric critical care support. An automatic PaCO₂ target of 35–40 mmHg can abruptly worsen acidemia. Avoid additional hypocapnia beyond expected compensation unless directed for overt intracranial hypertension. ISPAD cerebral injury guidance
Resolution and Transition
Assess vitals, mental status, glucose and intake and output at least hourly. Repeat electrolytes, venous gases and BOHB every 2–4 hours or sooner if indicated. Recheck potassium more frequently when abnormal. Use clinical recovery and biochemical resolution before transitioning. BOHB below 1 mmol/L or closure of the anion gap can help document resolution. Calculate the gap as measured sodium minus the sum of chloride and bicarbonate and interpret it with the local reference interval and albumin. ISPAD also lists pH above 7.30 or bicarbonate above 18 mmol/L as biochemical indicators. Hyperchloremic acidosis can persist after ketone clearance. Urine ketones can remain positive as BOHB is converted to acetoacetate. Glucose normalization alone is insufficient.
When DKA has resolved and the child can tolerate intake, coordinate subcutaneous insulin with the diabetes team. Give rapid-acting insulin about 15–30 minutes before stopping IV insulin under ISPAD guidance, with a longer overlap for long-acting insulin according to the regimen. Investigate triggers such as a missed insulin dose, pump delivery failure or intercurrent illness. Before discharge, confirm access to insulin and supplies, review glucose and ketone checks and sick-day instructions, and arrange follow-up. ISPAD monitoring and transition guidance
A 9-year-old with polyuria and deep respirations has glucose 480 mg/dL, venous pH 7.16, bicarbonate 8 mmol/L, blood beta-hydroxybutyrate 5.4 mmol/L and potassium 4.2 mmol/L. The child is alert and volume depleted without shock. Which initial sequence follows ISPAD guidance?
Begin 0.9% saline at 10–20 mL/kg over 20–30 minutes. Reassess perfusion and potassium and start IV regular insulin without a loading bolus at least one hour after fluids begin.
Start a regular insulin IV loading bolus before fluid, then give the first volume expansion with dextrose in 0.45% saline.
Use dextrose in water with added potassium for initial volume expansion and start insulin when the glucose reaches 250 mg/dL.
Give bicarbonate to raise the pH above 7.20 before starting isotonic fluid and insulin.
During pediatric DKA treatment, glucose falls from 650 to 350 mg/dL over four hours and measured sodium falls from 128 to 125 mEq/L. The child remains alert with stable perfusion. Which interpretation and next step are appropriate?
Corrected sodium rises from 128 to 130 mEq/L. Continue the current prescription without reassessing the results.
Corrected sodium falls from 136.8 to 129.0 mEq/L and effective osmolality falls from about 292 to 269 mOsm/kg. Reassess the results, IV fluid composition, perfusion and neurologic status.
Effective osmolality falls from about 310 to 277 mOsm/kg using corrected sodium. Diagnose cerebral injury and give mannitol based on that change.
Measured sodium must rise during treatment. Halve the IV fluid rate based on this sodium result alone.
Three hours after starting DKA treatment, a previously alert 6-year-old develops a severe headache, confusion and a sustained fall in heart rate from 132 to 94 beats/min despite stable perfusion and wakefulness. Blood pressure is 122/84 mmHg. What is the immediate priority?
Obtain a head CT and give hyperosmolar therapy only after edema is visible.
Give sodium bicarbonate and stop insulin to bring the pH and glucose into range before evaluating the neurologic change.
Give IV mannitol 0.5–1 g/kg or 3% saline 2.5–5 mL/kg over 10–15 minutes. Support perfusion and call pediatric critical care.
Continue the current regimen and wait for diastolic pressure to exceed 90 mmHg before treating.
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