Nonketotic hyperglycemia-hyperosmolar coma

Non-ketotic hyperglycemia - introduction of hyperosmolar coma Non-ketotic hyperglycemia-hyperosmolar coma (NKHHC) is a complication of type 2 diabetes with a mortality rate of more than 50%, often occurring after symptomatic hyperglycemia for a period of time, and fluid intake is insufficient to prevent hyperglycemia-induced infiltration. Severe dehydration caused by sexual diuresis. This syndrome is characterized by hyperglycemia, severe dehydration, high blood permeability causing disturbance of consciousness, sometimes accompanied by epilepsy, and the cause may be accompanied by acute infection or other conditions (such as elderly people living alone). basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious complication:

Nonketotic hyperglycemia - the cause of hyperosmolar coma

The disease often occurs after symptomatic hyperglycemia for a period of time, and fluid intake is insufficient to prevent severe dehydration caused by hyperglycemia-induced osmotic diuresis, which may be accompanied by an acute infection or other condition.

Non-ketotic hyperglycemia - hyperosmolar coma prevention

1 Removal of the cause: the infected person applied antibiotics. 2 correction of shock: shock after rehydration has not been corrected, can be transferred to plasma. 3 due to hyperosmosis, increased blood viscosity, prevention and treatment of arteriovenous thrombosis and disseminated intravascular coagulation (DIC), the corresponding anticoagulant therapy. 4 to prevent brain edema during treatment.

Nonketotic hyperglycemia - hyperosmolar coma complications Complication

Common complications of this disease:

1. Severe hyperglycemia, hyperosmotic state of plasma;

2. Mental disorder;

3. Failure to rescue in time can endanger life.

Non-ketotic hyperglycemia - hyperosmolar coma symptoms common symptoms coma fatigue pulse fast and weak cold sweat loss water polyuria

Central nervous system changes, extreme hyperglycemia, dehydration, high osmotic pressure, mild metabolic acidosis without significant hyperketosis, prerenal azotemia (or previous chronic renal failure), at the time of presentation The state of consciousness is from ambiguity to coma. Unlike ketoacidosis (DKA), there may be localized or systemic epilepsy, which may have a partial hemiplegia. Blood glucose is often close to 1000 mg/dl (55.5 mmol/L), which is significantly higher than most DKA. The patient's plasma osmotic pressure on admission was about 385 mOsm/kg, while the normal value was about 290 mOsm/kg. At the beginning, plasma bicarbonate was slightly reduced (17-22 mmol/L), and plasma ketone bodies often had no strong positive reaction. Serum sodium Potassium is normal, but serum urea nitrogen (BUN) and serum creatinine are significantly elevated.

Non-ketotic hyperglycemia - examination of hyperosmolar coma

1, blood sugar and blood glucose increased significantly, more than 33.3mmol / L (600mg / dL), and even as high as 83.3-266.6mmol / L (1500-4800mg / dL), due to dehydration and renal function disorders, renal sugar threshold increased.

2. Plasma osmotic pressure Plasma osmotic pressure (mmol/L) = 2 × (sodium + potassium) (mmol / L) + blood glucose (mmol / L) + blood urea nitrogen (mmol / L) or plasma osmotic pressure (mmol / L ) = 2 × (potassium + sodium) mEd / L + blood glucose (mg / dL) / 18 + blood urea nitrogen (mg / dL) / 2.8

3, blood biochemistry: due to severe dehydration and intracellular fluid escape, blood potassium, sodium concentration is normal and high, but the body's total potassium and sodium are significantly lost, such as the body's potassium deficiency can reach 40-100mmol.

Non-ketotic hyperglycemia-hyperosmolar coma diagnosis

Differentiation from hyperosmotic conditions caused by other causes, such as dialysis therapy, dehydration therapy, high-dose corticosteroid therapy, etc. can lead to hyperosmolar state, patients with dysthymia are easily misdiagnosed as cerebrovascular accidents and delay treatment, cerebrovascular accident Commonly used drugs are harmful to the disease, such as mannitol, hypertonic sugar, corticosteroids, etc., all of which increase hypertonic state; phenytoin can not stop convulsions and seizures caused by hypertonic state, and can inhibit insulin secretion and high blood sugar Further deterioration, so differential diagnosis is very important.

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