No standard definition, but typically glucose >11mmol/L, with pH <7.3 and/or bicarb <15. Associated with glycosuria and ketonuria, and blood ketones >3mmol/l. It is unusual but possible to present with near normal glucose values. May be how a patient with diabetes presents for the first time, if not diagnosed in time, else usual triggers are inadequate insulin, and/or intercurrent illness.
Abdominal pain and vomiting are a key feature. Can sometimes be misdiagnosed as acute abdomen eg appendicitis. As acidosis increases, Kussmaul breathing develops (deep +/- fast), sometimes misdiagnosed as pneumonia. Thirst is pronounced, and the child often looks gaunt. The child is pale, tachycardic and appears shocked. Eventually the child loses consciousness. The most feared complication, cerebral oedema, often does not develop until after rehydration begins. Many of the details of management are aimed at avoiding rapid fluid shifts that might provoked cerebral oedema.
BSPED 2009 guidelines incorporate international guidelines from ESPE (2004) and International Society for Pediatric and Adoles diabetes (2007).
Mild cases, where the child is not vomiting, can be managed with sick day doses of insulin given subcutaneously. If in doubt, however, intravenous fluids and insulin should be used until there is clear improvement.
If consciousness is reduced, consider airway management and a NG tube (aspiration is a significant risk). Coma may be related purely to degree of acidosis, but monitor for signs of raised intracranial pressure that would suggest cerebral oedema.
Shock manifest as hypotension or poor peripheral pulses should be treated with 10ml/kg boluses of normal saline, up to a maximum of 30ml/kg. Do not give fluid boluses for tachycardia or poor perfusion alone.
Consider PICU for:
Assess degree of dehydration. Never estimate more than 8%.
Include resuscitation boluses in volume calculations. Aim to correct dehydration over 48 hours. Use normal saline with 40mmol/l (20mmol per bag) unless high suspicion of anuria (always a degree of renal impairment on U&Es).
Blood glucose levels start falling with fluid resuscitation alone. Postpone insulin therapy for at least 1 hour after initiating fluid resuscitation. There is certainly no need for a bolus of insulin.
Give short acting insulin by continuous infusion via Y connector (not added to bag) using a 1 unit/ml solution (eg 50 units soluble insulin to 49.5 ml of 0.9% saline) starting at 0.1 units/kg/hr. Some people prefer 0.05. The aim is to reduce the blood glucose steadily but gradually.
Some people recommend reducing the rate of insulin if the glucose falls by more than 5-8 mmol/l per hour but no evidence for this.
Most DKA have subclinical (ie CT abnormal) cerebral oedema! But mostly asymptomatic. Presents typically 4-12 hours after initiation of treatment! May start with headache but then progressive neurological deterioration esp drowsiness, confusion, irritability. Focal signs incl pupil abnormalities and posturing are very worrying. Preterminal is Cushing's triad: bradycardia, hypertension, irregular respiration. Restlessness may be due to a full bladder!
Young & Asian more at risk. Acidosis more important than glucose level in predicting. Increased risk if insulin given in first 60 mins hence policy to delay. Mechanism? Neurones adapt to dehydration by retaining fluid then challenged by fluid therapy. Change in vascular permeability (seen on MRI - would explain cases presenting before therapy).
One warning sign is said to be a static or falling corrected sodium despite rehydration. Expect a Na rise of 2mmol/l per 5.5 fall in glucose.
Management: (see Emergencies)
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