Paediatrics chapters
Diabetic ketoacidosis in children
The life-threatening acute complication of type 1 diabetes: how it develops, how to recognise and grade it, the steps of fluid, insulin and potassium treatment, and how to prevent and treat cerebral oedema.
- DKA is hyperglycaemia + acidosis + ketones: Nelson uses pH under 7.3, bicarbonate under 15 mEq/L with raised ketones; it is triggered by new-onset diabetes, missed insulin or infection.
- The child is dehydrated yet passing a lot of urine, with vomiting, abdominal pain, Kussmaul breathing, acetone breath and drowsiness; total-body potassium is low even when the serum level is normal or high.
- Treat with isotonic saline bolus 10 to 20 mL/kg, slow deficit replacement, IV insulin 0.1 U/kg/hour, potassium once urine flows, glucose added as sugar falls, no routine bicarbonate, and watch for cerebral oedema (treat with mannitol).
On this page
Overview
Diabetic ketoacidosis (DKA) is a common, life-threatening acute complication of type 1 diabetes and is often the way new diabetes first shows itself. It results from insulin deficiency plus a rise in counter-regulatory hormones (glucagon, cortisol, growth hormone, catecholamines). The child is dehydrated, acidotic and potassium-depleted. Treatment must correct these gradually, because the most feared complication, cerebral oedema, is linked to treatment itself.
Definition
| Source | Glucose | pH | Bicarbonate | Ketones |
|---|---|---|---|---|
| Nelson | High (usually 200 to over 1000 mg/dL) | Below 7.3 | Below 15 mEq/L | Raised in serum or urine |
| Akbar | Usually over 250 mg/dL | Below 7.25 | 15 mEq/L or less | Ketonaemia, ketonuria |
- Severe DKA (Akbar): pH 7.1 or less and bicarbonate 10 mEq/L or less.
- Akbar quotes mortality as high as 6 to 10% in his setting.
The two books use slightly different pH cut-offs (7.3 and 7.25). Learn both, but remember the core triad: hyperglycaemia, acidosis, ketosis.
Precipitating factors
- New-onset type 1 diabetes whose symptoms were not recognised in time.
- Omitted insulin doses in a known diabetic.
- Intercurrent illness or infection: insulin needs rise but are not met.
- Insulin pump failure (no depot insulin, so DKA can develop quickly).
- Other physiological stress that raises counter-regulatory hormones.
Pathophysiology
| Process | Result |
|---|---|
| No insulin → less glucose uptake, more gluconeogenesis and glycogenolysis | Hyperglycaemia |
| Glucose above renal threshold | Osmotic diuresis: water, sodium, potassium, phosphate lost → dehydration |
| Unopposed lipolysis → fatty acids oxidised in liver | Ketones (beta-hydroxybutyrate, acetoacetate, acetone) → high anion gap metabolic acidosis |
| Poor perfusion | Lactic acid adds to acidosis |
| Acidosis drives K+ out of cells in exchange for H+; kidneys then excrete it | Serum K normal or high at first, but total-body K depleted |
| Vomiting, fast breathing | More fluid loss |
Serum potassium may be high, normal or low at presentation, but total-body potassium is always depleted. A low serum potassium at presentation is an ominous sign.
Measured sodium is falsely low because high glucose (and lipids) draw water into the plasma.
Clinical features
- Polyuria, polydipsia, weight loss, bedwetting in the preceding days.
- Nausea, vomiting and abdominal pain (can mimic an acute abdomen; ileus).
- Dehydration: dry mouth, sunken eyes, tachycardia, poor perfusion, hypotension if severe.
- Kussmaul breathing: deep, sighing, rapid breaths (respiratory compensation).
- Fruity (acetone) smell on the breath.
- Altered consciousness: drowsiness, confusion, coma.
- Fever is unusual; if present, look for infection as the trigger.
A dehydrated, vomiting child who is still passing large volumes of urine has an osmotic diuresis: think DKA, not gastroenteritis.
"Dry but wet": dry mouth, wet nappy.
Investigations
| Test | Typical finding |
|---|---|
| Blood glucose | High (often over 300 mg/dL) |
| Blood gas | pH low, bicarbonate low, low PCO2 (compensation) |
| Ketones | High in blood and urine |
| Urine | Glycosuria, ketonuria |
| Sodium | Normal, low or high; falsely lowered by hyperglycaemia |
| Potassium | High, normal or low (total body depleted) |
| Urea and creatinine | Raised (prerenal) |
| Blood count | Leucocytosis with left shift, even without infection; raised haemoglobin and haematocrit from dehydration |
| Phosphate, calcium, magnesium | Phosphate depleted |
| Cultures, chest X-ray, urine culture | If infection is suspected |
Na 130, Cl 98, HCO3 8 (mEq/L)
Anion gap = 130 − (98 + 8) = 24 → raised (ketoacids)
Treatment
Goals: restore circulation, replace water and salt slowly, stop ketone production with insulin, replace potassium, and avoid rapid shifts in osmolality.
1. Resuscitation and first fluid
- Assess airway, breathing and circulation; nil by mouth (Akbar); weigh the child, since a recent weight lets the deficit be calculated.
- Bolus 10 to 20 mL/kg of 0.9% saline or Ringer lactate (no glucose) over the first hour; may be repeated if still shocked.
- The bolus is part of the total fluid, not extra.
2. Rehydration
- Assume about 10% dehydration in severe DKA (most are 5 to 10%); deficit = 10% × weight (kg) × 1000 = 100 mL/kg.
- Total fluid = deficit + maintenance − bolus already given.
- Nelson: replace the remaining deficit plus maintenance slowly over 36 to 48 hours; use 0.9% saline for the first 4 to 6 hours, then 0.45% saline. Ongoing urine losses are not usually replaced.
- Akbar's protocol: after the first-hour bolus, give 0.45% saline with potassium, at a rate of (85 mL/kg + maintenance − bolus) spread over the next 23 hours.
- Maintenance per 24 hours: 100 mL/kg up to 10 kg body weight, plus 50 mL/kg for each kg between 10 and 20, plus a smaller amount for each kg above 20 (Akbar's DKA table uses 25 mL/kg).
Bolus (first hour): 10 mL/kg × 30 = 300 mL of 0.9% saline
Maintenance per 24 h: 1000 + 500 + (10 × 25) = 1750 mL
Next 23 hours: (85 × 30) + 1750 − 300 = 2550 + 1750 − 300 = 4000 mL
Rate: 4000 ÷ 23 ≈ 174 mL/hour of 0.45% saline with potassium
20 kg child, 10% dehydrated: deficit = 0.10 × 20 × 1000 = 2000 mL
Maintenance: 1000 + (10 × 50) = 1500 mL/24 h → 3000 mL over 48 h
Bolus given: 10 mL/kg = 200 mL
Remaining over 48 h: 2000 − 200 + 3000 = 4800 mL → 4800 ÷ 48 = 100 mL/hou
Fluids are given slowly in DKA (over 24 to 48 hours), unlike gastroenteritis. Rapid shifts in serum osmolality are linked to cerebral oedema.
3. Insulin
- Regular (soluble) insulin by continuous IV infusion at 0.1 U/kg/hour (Akbar's table allows 0.05 to 0.1 U/kg/hour). Neither book uses a loading bolus.
- Run it on a separate line so its rate can be changed independently; count its volume in the total fluid.
- Aim for glucose to fall no faster than 100 mg/dL per hour.
- When glucose falls to about 250 to 300 mg/dL, add 5% dextrose to the IV fluid (increase to 10% if needed) and keep the insulin running.
- If glucose drops below 200 mg/dL before acidosis clears, increase the dextrose; do not cut insulin by more than half, and never stop it until acidosis resolves.
Insulin, not fluid or bicarbonate, switches off ketone production. Give dextrose to protect glucose rather than stopping insulin.
4. Potassium
- Start potassium once urine output is confirmed, whatever the initial level (it will fall as insulin and correction of acidosis move K+ into cells).
- 20 to 40 mEq/L in the IV fluid; Nelson suggests half as potassium chloride, half as potassium phosphate (gives phosphate without excess, which could cause hypocalcaemia).
- Withhold potassium if serum K is above 6 mEq/L until it falls.
5. Bicarbonate
- Avoid routinely (Nelson). Risks: paradoxical CNS acidosis, tissue hypoxia (shift of the oxygen dissociation curve), osmotic shifts and more cerebral oedema.
- Akbar reserves it for severe acidosis (pH under 7.0 to 7.1) with cardiac or respiratory compromise.
6. Treat the trigger
Look for and treat infection with appropriate antibiotics.
7. Monitoring
| What | How often |
|---|---|
| Blood glucose | Every hour |
| Electrolytes and blood gas | Every 2 to 3 hours (Akbar: 2 to 4 hours in the first 24 h) |
| Calcium, phosphate, magnesium | Every 4 to 6 hours |
| Neurological status, vital signs, fluid balance | Frequently (hourly) |
- Urine ketones may seem to rise as treatment works (beta-hydroxybutyrate is converted to acetoacetate, which the strip detects), so they are not a guide to progress.
8. Changing to subcutaneous insulin
- When acidosis has resolved, the child is conscious and eating, and the trigger is treated (Akbar adds glucose around 180 to 240 mg/dL).
- Give the first subcutaneous dose 30 to 45 minutes before stopping the IV infusion, to avoid a gap in insulin.
Complications
Cerebral oedema
- Clinically evident in 1 to 5% of DKA episodes; mortality 20 to 80%; the most serious complication of DKA and its treatment.
- Typically 6 to 12 hours after starting treatment, often after initial improvement.
- Risk factors: high initial urea, low initial PCO2, sodium failing to rise as glucose falls, and bicarbonate therapy.
- Warning signs: headache, vomiting, falling consciousness, irritability, bradycardia with rising blood pressure, apnoea, dilated or unequal pupils, ophthalmoplegia, papilloedema, seizures.
- Treatment: act at once with IV mannitol, then intubation and ventilation if needed; Akbar advises keeping mannitol ready at the bedside from the start.
"Headache + slow pulse + high BP in DKA = brain swelling."
Other complications
- Hypokalaemia (arrhythmias) and hypophosphataemia.
- Hypoglycaemia (if dextrose not added).
- Intracranial thrombosis or infarction.
- Acute kidney injury (acute tubular necrosis).
- Pancreatitis, pulmonary oedema, bowel ischaemia.
- Peripheral oedema 24 to 48 hours into treatment.
Prevention
- Early recognition of diabetes symptoms (thirst, polyuria, weight loss, bedwetting).
- Sick-day rules: never omit insulin; check ketones when glucose is high or the child is unwell; seek help early.
Expect: the triad of hyperglycaemia, acidosis and ketosis with pH under 7.3 (Akbar 7.25) and bicarbonate under 15; severe DKA at pH 7.1 or less; triggers of new diabetes, missed insulin and infection; polyuria despite dehydration, Kussmaul breathing, acetone breath and abdominal pain; falsely low sodium and depleted total-body potassium; leucocytosis without infection; 10 to 20 mL/kg isotonic bolus; assumed 10% deficit replaced slowly; insulin infusion 0.1 U/kg/hour without bolus; dextrose added at 250 to 300 mg/dL; potassium after urine output; no routine bicarbonate; cerebral oedema at 6 to 12 hours with headache, bradycardia and hypertension, treated with mannitol; switching to subcutaneous insulin 30 minutes before stopping the drip.
Quick revision
- Triad: glucose high, pH under 7.3 (Akbar 7.25), HCO3 under 15, ketones.
- Severe: pH 7.1 or less, HCO3 10 or less.
- Triggers: new diabetes, missed insulin, infection.
- Polyuria with dehydration, vomiting, abdominal pain, Kussmaul, acetone breath.
- K+ total-body low; Na falsely low; WBC high without infection.
- Bolus 10 to 20 mL/kg 0.9% saline; deficit about 100 mL/kg, replaced slowly.
- Insulin 0.1 U/kg/hour IV, no bolus; fall in glucose no more than 100 mg/dL/hour.
- Add dextrose at 250 to 300; never stop insulin before acidosis clears.
- K+ 20 to 40 mEq/L after urine flows; none if K above 6.
- No routine bicarbonate; cerebral oedema 6 to 12 h; mannitol.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Why is insulin not stopped when blood glucose falls in DKA?
Insulin is needed to switch off ketone production and clear the acidosis; glucose is protected by adding dextrose to the drip instead, and the infusion is never stopped before acidosis resolves.
Why is potassium given even when the serum level is normal?
Total-body potassium is depleted, and insulin and correction of acidosis push potassium back into cells, so serum levels fall quickly once treatment starts.
Why are fluids given slowly in DKA?
Rapid shifts in osmolality are linked to cerebral oedema, the commonest cause of death in childhood DKA, so the deficit is replaced over 24 to 48 hours after the initial bolus.
When does cerebral oedema usually occur and how is it treated?
Usually 6 to 12 hours after treatment begins, often after early improvement; it is treated urgently with IV mannitol and, if needed, intubation and ventilation.