Diabetic Ketoacidosis in Children

The biochemical criteria for the diagnosis of DKA are: 

• hyperglycaemia (blood glucose >11mmol/L) 
• venous pH < 7.10, HCO3 < 5mmol/L
• ketonaemia / ketonuria and glycosuria.

DKA is categorised by the severity of the acidosis: 

• Mild: pH 7.25 - 7.30, HCO3 10-15mmol/L 
• Moderate: pH 7.10 - 7.25, HCO3 5-10mmol/L 
• Severe: pH < 7.10, HCO3 < 5mmol/L

Sodium

• volume expansion to restore peripheral circulation should begin immediately with 0.9% sodium chloride (depends on the circulatory status)
• If shocked give 10ml/kg of 0.9% sodium chloride over 10-20minutes, this may be repeated if necessary but should not exceed 30ml/kg.
• Subsequent fluid management should begin with 0.9% sodium chloride with added KCl (for at least the first 4-6 hours), at a rate to replace the fluid deficit over 48 hours
• If hypernatraemia (corrected Na >150mmol/L) fluid management should also begin with 0.9% sodium chloride and correction of fluid and electrolyte deficit should be over 48-72 hours
• Calculate and monitor corrected sodium throughout therapy 
• Corrected Na = Measured Na + 2 x [(glucose – 5.5) ÷ 5.5] mmol/L 
• As the plasma glucose concentration falls, measured and corrected sodium should rise steadily 
• A fall in serum sodium is one of the few biochemical correlates of impending cerebral oedema

Potassium

• Potassium replacement is always required in DKA, as total body potassium is depleted
• hypokalaemia at presentation represents a significant total body potassium deficit, whereas hyperkalaemia implies reduced renal function
• Insulin administration and the correction of acidosis will drive potassium back into the cells, decreasing serum levels. Therefore, potassium replacement should always precede insulin therapy, unless hyperkalaemia or anuria is present. 

serum K+ (mmol/L)	Plan
< 2.5	·      discuss with Intensivist on call for advice as cardiac monitoring will be required
2.5 - 3.5	·      administer 40-60mmol KCl per litre of IV fluids and monitor K+ hourly
3.5-5.0	·      administer 30-40mmol KCl per litre of IV fluids to maintain K+ at 3.5-5.0 mmol/L
>5	·      do not give IV KCL. Monitor K hourly until K+ < 5.0mmol/L, then administer 30- 40mmol KCl per litre of IV fluids to maintain serum K+ at 3.5-5.0 mmol/L

• The maximum recommended rate of intravenous potassium replacement is 0.5mmol/kg/hour

Insulin

• to normalise blood glucose concentration and suppress lipolysis and ketone production. 
• should not be started until the circulating volume has been restored, the serum potassium is known and appropriate potassium replacement has commenced.
• Insulin Dose: 0.1units/kg/hr (50units soluble insulin (Actrapid, Humulin R) diluted in 50mls of 0.9%Saline, 1unit = 1ml) 
• 0.05u/kg/hr should be considered in children < 5 years of age /  known diabetes who have a lower blood glucose due to partial insulin treatment prior to presentation / severe DKA (pH <7, bicarbonate 5mmol/l)
• During the first 60-90 minutes of rehydration, the blood glucose may fall substantially even without insulin therapy
• After resuscitation, the desired rate of fall in blood glucose is 4-5 mmol/hour 
• When the BGL falls to 12-15 mmol/L, add 5% Dextrose to the IV fluids to keep blood glucose in the desired range of 8-12mmol/L. If necessary more dextrose may be added to the IV fluids
• insulin infusion should not be stopped or reduced below 0.05u/kg/hr until the acidosis has resolved
• If the biochemical parameters of DKA (pH, HCO3 and Anion Gap) do not improve, reassess the patient, recalculate the IV fluid replacement, review the insulin therapy (delivery and dose) and consider possible causes of impaired response to insulin (e.g. infection, errors in insulin preparation)
• insulin infusion should be replaced every 24 hours to avoid inactivation of insulin
• In unusual circumstances where IV administration is not possible, the use of hourly IM or SC injections of short or ultra short acting insulin (0.1units/kg/hour) has been shown to be effective

Phosphate

• There is a depletion of intracellular phosphate in DKA and insulin administration results in a fall in plasma phosphate as phosphate re-enters the cells 
• no evidence of any clinical benefit in DKA. 
• Administration of phosphate may induce hypocalcaemia 
• KPO4 may be used as an alternative to or in combination with KCl to avoid hyperchloraemia, provided careful monitoring for hypocalcaemia is performed

Acidosis

• Even severe acidosis is reversible by fluid and insulin replacement
• The use of large amounts of 0.9% Saline has been associated with the development of a hyperchloraemic metabolic acidosis after the clinical status has improved and ketosis has resolved. Treatment with NaHCO3 may be considered.

References:

1. http://www.bsped.org.uk/clinical/docs/DKAguideline
2. Management of Diabetic Ketoacidosis (DKA) in Children. SA Child Health Clinical Network