Гіперосмолярний гіперглікемічний стан (ГГС)

The primary symptom of hyperosmolar hyperglycemic state is altered consciousness varying from confusion or disorientation to coma, usually as a result of extreme dehydration with or without prerenal azotemia, hyperglycemia, and hyperosmolality. In contrast to diabetic ketoacidosis, focal or generalized seizures and transient hemiplegia may occur.

• Blood glucose level

• Serum osmolarity

Hyperosmolar hyperglycemic state is initially suspected when a markedly elevated glucose level is found in a fingerstick specimen obtained in the course of a workup of altered mental status. If measurements have not already been obtained, urine should be tested for ketones and the following should be measured in a blood sample:

• Serum electrolytes

• Blood urea nitrogen (BUN)

• Creatinine

• Glucose

• Ketones

• Plasma osmolality

Serum potassium levels are usually normal, but sodium may be low or high depending on volume deficits. Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1.6 mEq/L (1.6 mmol/L) for each 100 mg/dL (5.6 mmol/L) elevation of serum glucose over 100 mg/dL (5.6 mmol/L). BUN and serum creatinine levels are markedly increased. Arterial pH is usually > 7.3, but occasionally mild metabolic acidosis develops due to lactate accumulation.

The fluid deficit can exceed 10 L and acute circulatory collapse is a common cause of death. Widespread thrombosis is a frequent finding on autopsy and in some cases bleeding may occur as a consequence of disseminated intravascular coagulation. Other complications include aspiration pneumonia, acute renal failure, and acute respiratory distress syndrome.

• IV 0.9% saline

• Correction of any hypokalemia

• IV insulin (as long as serum potassium is ≥ 3.3 mEq/L [≥ 3.3 mmol/L])

Treatment consists of IV saline, correction of hypokalemia, and IV insulin (1, 2).

Treatment is 0.9% (isotonic) saline solution; 1000 mL is given in the first hour. Smaller boluses (500 mL) can be given if there is risk for exacerbation of heart failure or volume overload. Additional boluses may be needed for hypotensive patients. After the first hour, intravenous fluids should be adjusted based on hemodynamic and electrolyte status but should generally be continued at a rate of 250 to 500 mL/hour. A corrected sodium should be calculated. If the corrected sodium is < 135 mEq/L (< 135 mmol/L), then isotonic saline can be continued. If the corrected sodium is normal or elevated, then 0.45% saline (half normal) should be used.

Dextrose should be added once the glucose level reaches 250 to 300 mg/dL (13.9 to 16.7 mmol/L). The rate of infusion of IV fluids should be adjusted depending on blood pressure, cardiac status, and the balance between fluid input and output.

Insulin is given at 0.1 unit/kg IV bolus followed by a 0.1 unit/kg/hour infusion after the first liter of saline has been infused and hypokalemia has been corrected. Hydration alone can sometimes precipitously decrease plasma glucose, so insulin dose may need to be reduced. A too-quick reduction in osmolality can lead to cerebral edema. Occasional patients with insulin-resistant type 2 diabetes with hyperosmolar hyperglycemic state require larger insulin doses. Once plasma glucose reaches 300 mg/dL (16.7 mmol/L), insulin infusion should be reduced to basal levels (1 to 2 units/hour) until rehydration is complete and the patient is able to eat.

Target plasma glucose is between 250 and 300 mg/dL (13.9 to 16.7 mmol/L). After recovery from the acute episode, patients are usually switched to adjusted doses of subcutaneous insulin.

Potassium replacement is similar to that in diabetic ketoacidosis: 40 mEq/hour for serum potassium < 3.3 mEq/L (< 3.3 mmol/L); 20 to 30 mEq/hour for serum potassium between 3.3 and 4.9 mEq/L (3.3 and 4.9 mmol/L); and none for serum potassium ≥ 5 mEq/L (≥ 5 mmol/L).