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Nonketone hyperosmolar syndrome.
Last reviewed: 04.07.2025
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Nonketotic hyperosmolar syndrome is a metabolic complication of diabetes mellitus, characterized by hyperglycemia, severe dehydration, plasma hyperosmolarity, and impaired consciousness.
Most commonly observed in type 2 diabetes mellitus, often under conditions of physiological stress.
Causes of non-ketone hyperosmolar syndrome.
Nonketotic hyperosmolar syndrome, also called hyperosmolar hyperglycemic state, is a complication of type 2 diabetes mellitus with a mortality rate of up to 40%. It typically develops after a period of symptomatic hyperglycemia in which fluid intake is insufficient to prevent severe dehydration due to osmotic diuresis caused by hyperglycemia.
Precipitating factors may include concomitant acute infection, drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics), noncompliance with physician instructions, or other medical conditions. Serum ketone bodies are not detectable, and plasma glucose and osmolarity are typically much higher than in diabetic ketoacidosis (DKA): > 600 mg/dL (> 33 mmol/L) and > 320 mOsm/L, respectively.
[ Symptoms of non-ketone hyperosmolar syndrome.
The initial symptom is altered consciousness, ranging from confusion or disorientation to coma, usually as a result of severe dehydration with or without prerenal azotemia, hyperglycemia, and hyperosmolarity. In contrast to DKA, focal or generalized seizures and transient hemiplegia may be present. Serum potassium levels are usually normal, but sodium levels may be low or high depending on the fluid deficit. Blood urea and serum creatinine are increased. Arterial pH is usually greater than 7.3, but mild metabolic acidosis due to lactate accumulation occasionally develops.
The average fluid deficit is 10 L, and acute circulatory failure is a common cause of death. Autopsy often reveals widespread thrombosis, and in some cases bleeding may occur as a result of disseminated intravascular coagulation. Other complications include aspiration pneumonia, acute renal failure, and acute respiratory distress syndrome.
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Treatment of non-ketone hyperosmolar syndrome.
Nonketone hyperosmolar syndrome is treated with intravenous fluids of 1 liter of 0.9% saline over 30 minutes, followed by infusion therapy at a rate of 1 L/h to increase blood pressure, improve circulation and urine output. When blood pressure and glucose levels are normalized to about 300 mg/dL, replacement with 0.45% saline is possible. The rate of intravenous fluid administration should be adjusted depending on blood pressure, cardiac function, and the balance between fluid intake and output.
Insulin is given intravenously at a dose of 0.45 IU/kg as a bolus followed by a dose of 0.1 IU/kg h after infusion of the first liter of solution. Hydration itself can sometimes decrease plasma glucose levels, so a reduction in insulin dose may be necessary; too rapid a reduction in osmolarity can lead to cerebral edema. Some patients with type 2 diabetes mellitus with nonketotic hyperosmolar syndrome require increased insulin doses.
When plasma glucose levels reach 200–250 mg/dL, insulin administration should be reduced to basal levels (12 IU/h) until the patient is fully rehydrated and able to eat. Supplementation with 5% dextrose infusion may be necessary to avoid hypoglycemia. After the acute episode has been controlled and patients have recovered, they are usually transferred to adapted doses of subcutaneous insulin.
Once stable, many patients can resume oral antihyperglycemic medications.
Potassium replacement is similar to DKA: 40 mEq/h for serum K < 3.3 mEq/L; 20-30 mEq/h for K 3.3-4.9 mEq/L; no need for administration for K 5 mEq/L.