Diabetic ketoacidosis (DKA) is defined by the biochemical triad of ketonaemia, hyperglycaemia and acidaemia (1).
DKA may result from:
- absolute deficiency of circulating insulin e.g. -
- previously undiagnosed type 1 diabetes mellitus
- patients who do not take insulin deliberately or inadvertently (especially the long acting component of a basal-bolus regimen)
- relative deficiency
- caused by increased levels of the counter regulatory hormones: catecholamines, glucagon, cortisol and growth hormone as a response to tress in conditions such as sepsis, trauma, or gastrointestinal illness with diarrhea and vomiting etc. despite taking the usual recommended dose of insulin (2)
DKA is thought to be indicative, or even diagnostic, of type 1 diabetes, but increasingly there are cases of ketone-prone type 2 diabetes being recognised (3).
- patients with type 2 diabetes who have ketosis-prone diabetes represents 20 to 50 % of persons with DKA (these patients have impaired insulin secretion)
It should be regarded a medical emergency; its rapid recognition and accurate treatment are essential to prevent morbidity and mortality.
It should be noted that there are subtle differences in the management in children and in adults.
- (1) Savage MW et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med. 2011;28(5):508-15
- (2) Wolfsdorf JI et al. Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2014;15 Suppl 20:154-79.
- (3) Joint British Diabetes Societies (JBDS) 2013. Inpatient Care Group. The management of diabetic ketoacidosis in adults.