Monday, November 19, 2012



Initially called hyperosmolar non-ketotic (HONK) hyperglycaemia. The dominant clinical feature is dehydration. It mainly occurs in older subjects with type 2 diabetes mellitus. The cycle of hyperglycaemia, dehydration (occurring due to vomiting, polyuria, glycosuria osmotically takes more water in urine) and increased counter regulatory hormones (induced by acidosis and dehydration and hyperglycemia) is same in ketoacidosis but is more severe. There is hypernatremia caused by renal sodium resorption in response to hypovolaemia, together with osmotic diuresis causing persistent free water loss. 

Non-ketotic hyperosmolar state usually occurs during marginal insulin deficiency, and their insulinaemia has sufficient antilipolytic effect to prevent the lipolytic and ketotic problems seen in ketoacidosis. There is decrease in anion gap <20 mmol/L and bicarbonate is normal and pH >7.30. There is hypernatraemia and more severe water loss 18 L in typical adult.


During alcoholism and resulting poor diet is association with vomiting, this cause ketoacidosis and low, normal or elevated blood glucose. Ketosis is caused by lack of insulin action which results in mobilization of NEFAs and their conversion to ketone bodies as alternative fuel. This is potentiated by counter-regulatory hormones like glucagon, cortisol and catecholamines secreted in response both to hypoglycaemia and extracellular fluid volume contraction. 

In addition, alcohol metabolism depletes cellular NAD+ which by restricting pyruvate formation from lactate, causes accumulation of lactate and depletion of pyruvate, a gluconeogenic substrate. As is the case in DKA, alteration in mitochondrial redox state favors beta hydroxybutyrate over acetoacetate production. A complex acid-base disorder ensues from the combined effects of ketosis causing metabolic acidosis, and a combination of extracellular fluid contraction and vomiting causing metabolic alkalosis. 
Related Posts Plugin for WordPress, Blogger...