The non-ketotic hyperosmolar syndrome (NKHS) is a metabolic complication of diabetes mellitus (DM), which is characterized by hyperglycemia, extreme dehydration, hyperosmolar plasma and changes in consciousness in the absence of relevant ketosis. It occurs in a diabetes type 2, often in the context of physiological stress on. NKHS is diagnosed by severe hyperglycemia and plasma Hyperosmolality and the absence of significant ketosis. Treatment consists of i.v. Administration of saline and insulin. The complications include coma, seizures and death.
The non-ketotic hyperosmolar syndrome (NKHS) is a metabolic complication of diabetes mellitus (DM), which is characterized by hyperglycemia, extreme dehydration, hyperosmolar plasma and changes in consciousness in the absence of relevant ketosis. It occurs in a diabetes type 2, often in the context of physiological stress on. NKHS is diagnosed by severe hyperglycemia and plasma Hyperosmolality and the absence of significant ketosis. Treatment consists of i.v. Administration of saline and insulin. The complications include coma, seizures and death.
(Hyperosmolar hyperglycemic state) does not ketotic hyperosmolar syndrome (NKHS) is a metabolic complication of diabetes mellitus (DM), which is characterized by hyperglycemia, extreme dehydration, hyperosmolar plasma and changes in consciousness in the absence of relevant ketosis. It occurs in a diabetes type 2, often in the context of physiological stress on. NKHS is diagnosed by severe hyperglycemia and plasma Hyperosmolality and the absence of significant ketosis. Treatment consists of i.v. Administration of saline and insulin. The complications include coma, seizures and death. The NKHS is a complication of diabetes type 2 and has a mortality rate of up to 40%. It usually occurs after a period of symptomatic hyperglycemia during which the fluid intake to avoid a strong dehydration that can occur during a hyperglycemic induced osmotic diuresis, was not sufficient. Triggering factors include: Acute infections and other medical conditions drugs that impair glucose tolerance (glucocorticoids) or fluid loss increase (diuretics) Error in observance of Diabetestherapiplans serum ketones are not present, since the amounts of insulin in most patients with diabetes type-2 suppress ketogenesis sufficient. Since the symptoms of acidosis missing, most patients endure a significantly longer osmotic dehydration prior to the presentation to the doctor, which is why the plasma glucose (> 600 mg / dL [> 33.3 mmol / L]) and osmolality (> 320 mOsm / L) is usually much higher than in diabetic ketoacidosis (DKA). Symptoms and complaints The primary symptom of a NKHS is an altered state of consciousness, which can range from confusion about disorientation to coma. Usually this is the basis of an extreme dehydration with or without pre-renal azotemia, hyperglycemia and hyperosmolarity. In contrast to DKA focal or generalized seizures, and transient hemiplegia may occur. Diagnostic blood sugar levels serum osmolarity Generally NKHS is presumed if significantly elevated glucose values ??in a fingertip sample as part of a clarification of an altered mental status has been made. As long as no measurements were taken, the measurement of serum electrolytes, urea nitrogen, creatinine, glucose, ketones and plasma osmolality should be. The urine should be tested for ketones. Serum potassium levels are usually normal, but the values ??for sodium can be high or low depending on the volume deficit. The Harnstofstickstoff and serum creatinine are significantly increased. The arterial pH is usually> 7.3, but occasionally occurs a slight metabolic acidosis due to an accumulation of lactate. The average fluid deficit is 10 l and acute cardiovascular failure is a common cause of death. An extensive thrombosis is often found at autopsy. In some cases, it can cause bleeding also because of intravascular disseminated coagulation. Other complications include aspiration pneumonia, acute renal failure and acute respiratory distress syndrome. Intravenous treatment 0.9% saline correction of hypokalemia intravenous insulin (as long as the serum potassium is 3.3 mmol / l at ?) The treatment consists in the administration of 1 l 0.9% saline solution for 30 minutes, followed by a continuous infusion at a sweep rate of 1 l / h so as to raise blood pressure and improve circulation and kidney function. If the blood pressure reached normal values ??and 300 mg / dl approach the mirror for plasma glucose (16.7 mmol / l), a 0.45% saline solution should be used. The infusion rate should be adjusted to blood pressure, heart function and the fluid balance. After the first liter of brine was added, insulin is administered as a bolus at a dose of 0.1 units / kg i.v. administered. Then followed by a continuous infusion at a dose of 0.1 units / kg body weight / h. The rehydration alone can lower the plasma glucose levels significantly occasionally even so the insulin dose may need to be reduced. Too rapid reduction of osmolality can lead to cerebral edema. Occasionally need insulinesistente type 2 diabetics with a NKHS higher insulin doses. When the plasma glucose levels at 300 mg / dl (16.7 mmol / l) are, insulin infusion should at basal levels (1-2 units / h) are reduced, namely until rehydration is complete and the patient eat again can. The target value for glucose is between 250 and 300 mg / dL (13.9 to 16.7 mmol / l). The addition of 5% dextrose in the infusion is sometimes necessary to avoid hypoglycemia. After recovering from the acute phase, patients should a corresponding s.c. Administration of insulin to be changed. Most patients can, if their condition is stable once again, to continue the therapy with oral hypoglycemic agents. The potassium substitution is quite similar to DKA 40 mEq / h in serum potassium <3.3 mEq / l, 20 to 30 mEq / hour at serum potassium from 3.3 to 4.9 mEq / l and no substitution at serum potassium ? 5 mEq / l. Summary infections, poor compliance with the treatment plan and certain medications can make glucose levels rise significantly, leading to dehydration and impairment of consciousness in patients with diabetes type-2. Patients have enough insulin to prevent ketoacidosis. The average fluid deficit is 10 l; the treatment is administered i.v. in 0.9% saline plus insulin infusion after the first liter of liquid. The target value for plasma glucose in acute treatment is between 250 and 300 mg / dL (13.9 to 16.7 mmol / l). Potassium supplements depending on serum potassium levels.