Clinical and metabolic characteristics of hyperosmolar nonketotic coma.

TLDR: It is suggested that dehydration and hyperosmolarity may play significant roles in the etiology of HNC, and that therapy should, therefore, be directed at restoration of normal osmolarity and correction of water deficits with 0.45 per cent saline and moderate amounts of insulin.

Abstract: Clinical and metabolic data of twenty patients with hyperosmolar nonketotic coma (HNC) and ten patients in keto-acidosis (DA) are compared HNC patients were older; fewer were previously known diabetics; more had multiple chronic diseases Common precipitating factors in HNC included infection, dehydration and administration of diabeto-genic drugs Blood glucose and urea nitrogen, plasma sodium, bicarbonate and osmolarity were significantly higher in HNC Plasma potassium and chloride levels were similar in both groups Patients with HNC had significantly lower plasma levels of free fatty acids, cortisol and growth hormone Plasma insulin levels in HNC were low and not significantly different from those observed in KA Patients with HNC required more fluids and less insulin therapy Mortality was 20 per cent in HNC, lower than that generally observed in this condition, but higher than that of KA, 0 per cent On the basis of the above findings, it is suggested that dehydration and hyperosmolarity may play significant roles in the etiology of HNC, and that therapy should, therefore, be directed at restoration of normal osmolarity and correction of water deficits with 045 per cent saline and moderate amounts of insulin