childhood ketoacidosis differential diagnosis treatment of childhood ketoacidosis
The primary cause of diabetic ketoacidosis (DKA) is insufficient effective insulin. The deficiency of this powerful anabolic hormone impairs glucose utilisation by tissues, and leaves the catabolic actions of counterregulatory hormones (e.g. glucagon, growth hormone, and catecholamines) unopposed. Thus inappropriate gluconeogenesis occurs compounding the hyperglycaemia, which causes hyperosmolarity and ensuing polyuria, dehydration and loss of electrolytes.
Secondly lipolysis of adipose tissue leads to increased free fatty acid circulation, which on hepatic oxidation produces the ketone bodies (acetoacetic acid and ?-hydroxybutyric acid) that cause the metabolic acidosis.
The biochemical criteria required for a diagnosis of DKA to be made is the presence of ketones in urine (urine dipsticks only detect the acetoacetic acid and not acetone or ?-hydroxybutyrate), blood glucose > 11 mmol/L together with a venous pH of <7.3 and/or bicarbonate <15mmol/L. In young children, or partially treated children DKA may also occur in association with near normal glucose levels.1
Epidemiology. The incidence of DKA at diagnosis in children with type 1 diabetes mellitus (T1DM) in Europe is approximately 1 per 10,000 children. DKA is more commonly found at diagnosis of T1DM in children aged <4 years old, children from families with low socioeconomic standing and children with no first degree relative with T1DM.2 In children with established T1DM the risk of an episode of DKA is in the region of 1-10% per child per year and many of these will occur as a result of poor adherence to a therapeutic regime.