Non-ketotic hyperglycemic coma is a metabolic derangement in which there is an abnormally high serum glucose level without ketoacidosis. It can occur as a complication of diabetes mellitus type 2 (known or unknown). In 30–40% of cases, it is the patient's initial presentation of diabetes. It also occurs in pancreatic disorders that interfere with the production of insulin, and in conditions marked by an excess of steroids, as in steroid therapy or acute stress conditions (such as infection, stroke, etc.). Hyperosmolality, resulting from the extremely high concentration of sugar in the blood, causes a shift of water from the intracellular fluid (the less concentrated solution) into the blood (the higher concentrated solution). This results in cellular dehydration. Another symptom of HHNK, polyuria, occurs because the high plasma osmolality prevents the normal osmotic return of water to the blood by the renal tubules osmotic diuresis, and it is excreted in the urine. This leads to a decreased blood volume, which severely hampers the kidney's excretion of glucose and a vicious cycle is begun.[1]
The difference between diabetic ketoacidosis (DKA) and non-ketotic hyperglycemic coma is the fact that in non-ketotic hyperglycemic coma, the body still continues to release enough insulin to not enter a state of starvation. In DKA, the body cannot use the sugar in the blood, and must begin to metabolize fat and muscle tissue for sustainance, producing acids and ketones as byproducts. In non-ketotic hyperglycemic coma, the pH of the blood is not affected to the same degree as with a patient in DKA.
emedicine.medscape.com/article/766804 Hyperosmolar Hyperglycemic State (HHS) [also known as Hyperosmolar Hyperglycemic Nonketotic coma]