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Neketone hyperosmolar syndrome
Last reviewed: 23.04.2024
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Neketone hyperosmolar syndrome is a metabolic complication of diabetes mellitus, characterized by hyperglycemia, pronounced dehydration, plasma hyperosmolarity, impaired consciousness.
It is most often observed in type 2 diabetes mellitus, often under conditions of physiological stress.
Causes of the non-ketone hyperosmolar syndrome
A neketone hyperosmolar syndrome, also called a hyperosmolar hyperglycemic condition, is a complication of Type 2 diabetes mellitus, with a mortality rate of 40%. It usually develops after a period of symptomatic hyperglycemia, in which fluid intake is insufficient to prevent severe dehydration due to osmotic diuresis caused by hyperglycemia.
Preceding factors may be concomitant acute infection, drugs that interfere with glucose tolerance (glucocorticoids) or increase fluid loss (diuretics), failure to comply with doctor's instructions or other medical conditions. Serum ketone bodies, plasma glucose levels and osmolality are typically much higher than in diabetic ketoacidosis (DKA):> 60 mg / dL (> 33 mmol / l) and> 320 mOsm / L, respectively.
Symptoms of the non-ketone hyperosmolar syndrome
The initial symptom is a violation of consciousness, ranging from confusion or disorientation to coma, usually as a result of severe dehydration with or without prerenal azotemia, hyperglycemia, hyperosmolarity. Unlike DKA, local or generalized convulsions and transient hemiplegia can be observed. Serum potassium levels are usually normal, but sodium levels can be low or high, depending on the fluid deficit. Urea of blood and serum creatinine level are increased. Usually, the arterial blood pH is more than 7.3, but sometimes a slight metabolic acidosis develops due to the accumulation of lactates.
The average fluid deficit is 10 liters, a frequent cause of death is acute circulatory failure. At autopsy, widespread thrombosis is often found, in some cases bleeding can occur as a result of disseminated intravascular coagulation. Other complications include aspiration pneumonia, acute renal failure, acute respiratory distress.
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Treatment of the non-ketone hyperosmolar syndrome
Neketone hyperosmolar syndrome is treated by intravenous injection of 1 liter of 0.9% saline for 30 minutes, then an infusion therapy with a speed of 1 l / h is necessary to increase blood pressure, improve circulation and urinary excretion. With the normalization of blood pressure, a glucose level of about 300 mg / dL, a 0.45% saline solution is possible. The rate of intravenous fluids should be adjusted depending on blood pressure, heart function, balance between fluid intake and elimination.
Insulin is administered intravenously at a dose of 0.45 IU / kg bolus, followed by administration at a rate of 0.1 MEDKhch) after infusion of the first liter of the solution. Hydration alone can sometimes reduce the plasma glucose level, hence, it may be necessary to reduce the dose of insulin; too rapid decrease in osmolality can lead to edema of the brain. Increased doses of insulin are required for some patients with type 2 diabetes mellitus with non-ketone hyperosmolar syndrome.
When the plasma glucose level reaches 200250 mg / dL, insulin administration should be reduced to basal levels (12 IU / h) until the patient's complete rehydration and recovery of the patient's ability to feed. To avoid hypoglycemia, it may be necessary to add an infusion of 5% dextrose. After relief of an acute episode and recovery, patients are usually transferred to adapted doses of subcutaneous insulin.
With the achievement of a stable condition, many patients can resume taking oral antihyperglycemic drugs.
Substitution of potassium is similar to DFA: 40 meq / h at a serum K level of <3.3 meq / L; 20 30 meq / h at K level of 3.34.9 meq / l; there is no need for an introduction at a level of 5 meq / L.