Clinical and Metabolic Characteristics of Hyperosmolar Nonketotic Coma

Abstract

Clinical and metabolic data of twenty patients with hyperosmolar nonketotic coma (HNC) and ten patients in ketoacidosis (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 diabetogenic 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 0.45 per cent saline and moderate amounts of insulin. DIABETES 20: 228-38, April, 1971. Hyperosmolar nonketotic coma is a syndrome characterized by severe hyperglycemia, hyperosmolarity and dehydration in the absence of ketoacidosis. Although first described by Frerichs 1 more than eighty years ago, this condition received little attention until the report of Sament and Schwartz 2 in 1957. Soon afterward additional reports appeared and by 1965 Schwartz and Apfelbaum 3 were able to review sixty-three cases collected from the world literature. Over two hundred case reports have now been published and available data 4 indicate that this syndrome is approximately one sixth as frequent a cause of coma as ketoacidosis. Despite increased recognition, the published mortality rate remains in the order of 40 per cent

The role of ?diabetogenic? hormones on carbohydrate and lipid metabolism following oral glucose loading in insulin dependent diabetics: Effects of acute hormone administration

“…The observations in severe derangements of diabetic control include elevated plasma levels of glucagon [3], cortisol [4], growth hormone [5,6], and catecholamines [7,8]. The hierachy of their pathogenetic significance, however, remains to be established.…”

Quantitative evolutionary design of nutrient processing: Glucose

“…That nonreabsorbed glucose remains in the urine, pulling along water and other solutes (especially salt) by the mechanism known as osmotic diuresis, resulting in large volumes of hypotonic urine, dehydration, increasingly hypertonic serum, and ultimately death. Both in humans and in our rats, the rise in serum glucose concentration accounts for only part of the rise in serum osmolality; it accounts for 57-63% of the rise in humans (30,32,33) and for 40-70% of the rise in our rats. The remainder of the rise in serum osmolality in humans represents the rise in serum concentrations of ions (especially sodium) and urea; the same solutes probably contribute in rats, along with a rise in amino acid concentrations, because of the amino acid content of the infused TPN.…”

Plasma Insulin and Glucagon and Their Release from Pancreatic Islet in Hyperosmolar Diabetic Rat.

“…In HYPEROSMOLAR nonketotic diabetic coma (HNKC) is generally found in the aged and untreated non-insulin dependent diabetics who have been treated with diuretics, glucocorticoids, mannitol or tube feeding in the case of cerebrocardiovascular disease or surgical operation [1][2][3], but its pathogenesis is still not fully clarified and the dehydration is considered to be one of the most important factors contributing to that state. The production of experimental hyperosmolar diabetic rat has already been reported [4,5].…”