DKA in an adolescent: deteriorating consciousness during treatment
A 12-year-old boy with a 3-week history of polyuria and weight loss is brought in drowsy. He weighs 38 kg. Capillary glucose 31 mmol/L, blood ketones 6.1 mmol/L, venous pH 7.06, bicarbonate 5 mmol/L, sodium 132 mmol/L, potassium 4.8 mmol/L, chloride 98 mmol/L, urea 9 mmol/L, creatinine 88 micromol/L. He receives 380 mL of 0.9% sodium chloride over 45 minutes, then 0.9% saline with 40 mmol/L potassium at maintenance plus deficit over 48 hours, and an insulin infusion at 0.05 units/kg/hour. Two hours later his glucose is 21 mmol/L and ketones 4.0; the fluid rate is reduced and 10% dextrose added when glucose reaches 14 mmol/L. At 8 hours he complains of headache and vomits; he is drowsy with GCS 13, heart rate 56, blood pressure 138/86, and pupils are equal and reactive. Glucose is 11 mmol/L, sodium 136 mmol/L.
1. What is your diagnosis and immediate management?
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This is cerebral oedema complicating diabetic ketoacidosis. The warning signs are headache, vomiting, drowsiness with a falling GCS, hypertension, and bradycardia. The pupils are still equal and reactive, which is reassuring, but deterioration can be rapid. Immediate management: call for senior and intensive care support, protect the airway, and give hypertonic saline 3% at 3-5 mL/kg over 10-15 minutes, or mannitol 0.5-1 g/kg over 10-15 minutes if hypertonic saline is unavailable. Reduce the fluid infusion rate by about one-third, keep the insulin infusion running, and avoid a bolus of hypotonic fluid. Elevate the head of the bed, maintain oxygenation and circulation, and monitor neurological status, pupils, heart rate and blood pressure every 15 minutes. Recheck glucose, sodium and ketones. If there is no improvement, repeat hypertonic saline. Do not delay treatment for imaging; CT is only to exclude other causes if the diagnosis is uncertain or after stabilisation.
2. Critique the fluid and insulin prescription he received.
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The initial 10 mL/kg 0.9% saline bolus is appropriate for shock or poor perfusion. The subsequent plan is problematic: maintenance plus deficit over 48 hours, using 0.9% saline, may deliver too much fluid, especially if the deficit was overestimated. Current guidance is to calculate maintenance plus a 5-10% deficit and replace evenly over 48 hours, but many centres use a simpler regimen of maintenance with a modest deficit and avoid rapid correction. The insulin infusion at 0.05 units/kg/hour is acceptable, but adding dextrose when glucose reaches 14 mmol/L is early; many protocols add dextrose at 14-17 mmol/L, so this is reasonable, but it must be paired with continued insulin to clear ketones.
The key error may be the total fluid rate and the lack of frequent neurological checks. Rapid or excessive fluid, a rapid fall in osmolality, and bicarbonate use are risk factors for cerebral oedema. I would review the hourly fluid balance, use isotonic fluid, avoid hypotonic fluid, and ensure the sodium is not falling too quickly. The measured sodium of 132 mmol/L is falsely low because of hyperglycaemia; the corrected sodium is about 140 mmol/L. I would not give bicarbonate unless pH is <6.9 with impaired cardiac function.
3. How would you adjust management over the next 12 hours?
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After hypertonic saline, reassess GCS, pupils and vital signs every 15 minutes and repeat hypertonic saline if there is no improvement. Keep the insulin infusion at 0.05-0.1 units/kg/hour until ketones are <0.6 mmol/L and pH >7.3, not just until glucose falls. Continue isotonic fluid at a reduced rate, aiming for a slow fall in glucose of 4-6 mmol/L/hour and a gradual rise in bicarbonate. Add dextrose 5-10% when glucose is 14-17 mmol/L to allow continued insulin. Monitor sodium, potassium, phosphate and magnesium; potassium may fall as insulin drives it intracellularly.
Once stable, arrange CT head only if there is no response or focal signs. Transfer to a paediatric intensive care unit. After recovery, debrief the family and the team, review the fluid prescription, and document the event. At follow-up, screen for psychosocial factors, provide diabetes education, and ensure sick-day rules are understood. Cerebral oedema can cause long-term neurological sequelae, so arrange developmental and neurological follow-up.