New-Onset Paediatric DKA in a District Hospital at 03:00
A 6-year-old boy, previously well, weighing 20 kg, is brought at 03:00 with three days of vomiting, abdominal pain and polyuria. He is drowsy but rousable, GCS 14 (E4 V4 M6), with deep sighing respirations at 34/min. Capillary refill is 3 seconds, extremities are cool, mucous membranes dry and skin turgor reduced. Heart rate 136/min, BP 96/58 mmHg, temperature 37.8°C, SpO2 98% on air. Bedside glucose is 32 mmol/L and blood ketones 5.4 mmol/L. Venous gas: pH 7.06, pCO2 22 mmHg, bicarbonate 7 mmol/L, base excess -24. Sodium 129 mmol/L, potassium 5.1 mmol/L, chloride 98 mmol/L, urea 14 mmol/L, creatinine 88 µmol/L; corrected sodium 136 mmol/L. There is no family history of diabetes. The paediatric retrieval team is 2 hours away and the nearest paediatric intensive care bed is 60 minutes away by ambulance.
1. Write your fluid plan for the first hour for this 20 kg child, with volumes and rates, and explain what you would deliberately not do.
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First hour: 200 mL of 0.9% sodium chloride over 30 minutes, then reassess.
That is 10 mL/kg. He has delayed capillary refill and cool peripheries but is not in hypotensive shock, so a single modest 10 mL/kg bolus is appropriate; if perfusion is still poor after it, a second 10 mL/kg over 30 minutes is reasonable, but repeated large boluses are avoided because rapid osmotic shifts are associated with cerebral oedema.
After resuscitation, calculate the ongoing prescription:
- Deficit: assume 5-10% dehydration; at 7% that is 70 mL/kg = 1400 mL.
- Maintenance by the 4-2-1 rule for 20 kg = 60 mL/h.
- Replace the deficit over 48 hours = about 29 mL/h.
- Total roughly 85-90 mL/h of 0.9% saline with 40 mmol/L potassium chloride added (his potassium is 5.1 mmol/L but with insulin it will fall; potassium is added once the level is below 5.5 mmol/L and urine output is confirmed).
Deliberately avoided:
- Hypotonic fluid (0.45% saline): it worsens the risk of cerebral oedema; isotonic fluid is used throughout.
- An insulin bolus, and insulin started before fluids: insulin is begun at least an hour after fluid resuscitation has started.
- Sodium bicarbonate: the acidosis corrects with insulin and fluids; bicarbonate risks paradoxical CSF acidosis, hypokalaemia and cerebral oedema. It is reserved for pH <6.9 with circulatory collapse, and even then is contentious.
- Rapid correction: the plan is to lower glucose by no more than about 5 mmol/L per hour.
Hourly glucose, 2-hourly potassium and hourly neurological observations are mandatory.
2. When and how do you start insulin, how do you manage potassium and glucose over the next 12 hours, and what defines resolution of the ketoacidosis?
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Insulin: start a continuous infusion of 0.05-0.1 units/kg/hour (1-2 units/hour for 20 kg) once fluids have been running for at least an hour and potassium is at least 3.5 mmol/L. No bolus. Soluble insulin should not be given subcutaneously in a child with cool peripheries and possible dehydration because absorption is unpredictable.
Glucose handling: add 5% dextrose to the maintenance fluid when glucose falls below about 15 mmol/L, or use a two-bag system so the dextrose can be titrated without stopping insulin. Insulin must keep running at the same rate while dextrose is increased; stopping insulin to control glucose will let ketogenesis continue.
Potassium: check hourly at first. As insulin drives potassium intracellularly, hypokalaemia is predictable; if potassium drops below 3.5 mmol/L, increase replacement and slow the insulin rate, and if it falls below 3.0 mmol/L hold insulin briefly and give IV potassium with cardiac monitoring.
Monitoring: hourly capillary glucose and ketones, 2-hourly electrolytes and venous gas, strict fluid balance with urine output, hourly GCS and pupil checks, and look at the corrected sodium - a falling corrected sodium while glucose falls suggests excessive free water and a rising cerebral oedema risk.
Resolution (all three): pH above 7.30, bicarbonate above 15 mmol/L, and blood ketones below 0.6 mmol/L. Only then transition to subcutaneous insulin, overlapping the infusion by 30-60 minutes to avoid rebound ketosis. Do not discharge on the basis of a normal glucose alone.
3. At hour 8 he complains of headache, becomes irritable, and his heart rate falls from 132 to 88/min with BP 122/78 mmHg and GCS 12. What is happening and what do you do, in order?
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This is cerebral oedema until proven otherwise. Headache, irritability, rising blood pressure with bradycardia, and a falling level of consciousness in a child being treated for DKA is the classic triad; it typically occurs 4-12 hours into treatment and is the leading cause of death in paediatric DKA.
Immediate actions:
- Stop the fluid bolus; reduce the maintenance infusion by one third.
- Give hyperosmolar therapy now, without waiting for imaging: 3% saline 2.5-5 mL/kg (50-100 mL over 10-15 minutes) aiming for a sodium rise of 3-5 mmol/L, or mannitol 0.5-1 g/kg (10-20 g) over 15-30 minutes if 3% saline is unavailable. Do not give both simultaneously; the choice depends on what is on the shelf and on the sodium level.
- Head of bed up 30 degrees, head midline, oxygen, treat fever, keep normocapnia and avoid hypotension.
- Airway and ventilation if GCS is 8 or falling; ventilate to a normal pCO2 because hyperventilation reduces cerebral perfusion and is only used briefly as a bridge if there are signs of herniation.
- Urgent CT head to exclude haemorrhage, infarction or thrombosis, but do not delay treatment for it.
- Call the retrieval team and the paediatric intensive care unit - this child needs a critical care bed.
Also check glucose, sodium and osmolality: a rapidly falling serum sodium or a very rapid glucose fall supports the diagnosis. Reassess the insulin rate; do not stop insulin entirely if ketones remain high, but slow it. Mortality is significant even with correct treatment, so escalate early and document the timeline.