DIABETIC EMERGENCIES: DIABETIC KETOACIDOSIS (DKA)

DIABETIC KETOACIDOSIS

Approximately 30% of patient with type 1 diabetes present with ketoacidosis with clinical features of dehydration, shock, vomiting, abdominal pain, acidosis and cerebral impairment. There are four mechanisms of ketoacidosis: insulin deficiency, counter-regulatory hormone excess, fasting and dehydration. The most important is insulin deficiency. Hyperglycaemia and excess lipolysis cause dehydration and high circulating concentrations of NEFAs. Due to this hyperglycemia, ketosis and dehydration there is increase release in of counter-regulatory hormones which induce further hyperglycemia and lipolysis along with insulin resistance.

Biochemical features of ketoacidosis include hyperglycaemia, ketosis, metabolic acidosis and uremia. The characteristic ketosis is the consequence of increased lipolysis and decreased fat synthesis. Excess acetyl-CoA derived from beta oxidation of fatty acid is converted to the ketone bodies, acetoacetate and beta hydroxybutyrate with some acetone. Plasma beta hydroxybutyrate are 3 times more than acetoacetate.

Hyponatremia results from osmotic movement of intracellular water to interstitial and intravascular compartments drawn towards the hyperglycaemic plasma. Lipaemic serum (due to hypertriglyceridaemia) also gives false low sodium value.

Whole body potassium depletion is universal in DKA. Administration of insulin can also cause hypokalemia as insulin cause intracellular flux of potassium.

Cerebral oedema is one of the most feared complications of ketoacidosis mostly occurring in children.