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Ketoacidotic diabetic coma
Last reviewed: 04.07.2025

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Ketoacidotic diabetic coma is a condition that develops against the background of diabetes mellitus and is characterized by hyperglycemia and a high level of ketonemia. It is an acute and life-threatening complication of diabetes, developing mainly in patients with type 1 diabetes. This condition is accompanied by metabolic disorders, which are characterized by hyperglycemia, ketoacidosis and ketonuria.
Causes ketoacidotic diabetic coma.
Late diagnosis of type 1 diabetes mellitus, intercurrent diseases, surgical interventions, injuries, stressful situations; violations of the treatment regimen.
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Symptoms ketoacidotic diabetic coma.
Stage I of compensated diabetic ketoacidosis is characterized by thirst, polyuria, headache, dizziness, drowsiness, loss of appetite, nausea, and abdominal pain. A slight smell of acetone is felt in exhaled air. The level of beta-hydroxybutyrate reaches 3 mmol/l. Symptoms of dehydration develop.
In stage II of decompensated diabetic ketoacidosis, consciousness becomes soporous, pupillary response to light and tendon reflexes are reduced. Tachycardia develops. Blood pressure is low. Abdominal syndrome joins in with frequent vomiting, loose stools and pseudoperitonitis. Polyuria is replaced by oliguria.
Stage III - diabetic ketoacidotic coma - is characterized by loss of consciousness, depressed reflexes, narrow pupils with no reaction to light. The smell of acetone is felt in the room. Dehydration and hemodynamic disturbances are expressed. Kussmaul breathing. Hepatomegaly and anuria are determined. Hyperglycemia at the level of 20-30 mmol/l, the level of ketone bodies in the blood is 1.7-17 mmol/l. Plasma osmolality does not exceed 320 mOsm/kg. Ketonuria is determined.
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Treatment ketoacidotic diabetic coma.
Treatment of patients in ketoacidosis or ketoacidotic coma should be started immediately. In the first hour, 0.9% sodium chloride solution is administered intravenously by drip at a rate of 20 ml/(kg x h), in the first 12 hours - 50% of the total daily requirement. In the next 6 hours - 25% of the calculated dose; in the remaining 6 hours - the last 25% of the daily fluid volume (total 100-120 ml/kg). If glycemia is 12-12 mmol/l, 5% glucose solution is also administered (the insulin dose is the same), then 0.9% sodium chloride solution. Short-acting insulin is administered at a dose of 0.1 U/kg, then 0.1 U/kg x h) intravenously by drip until the pH is normalized. Glycemic control is performed hourly, acid-base balance parameters (pH, BE) are determined once every 1-2 hours. If there is no infusion pump, insulin is administered hourly at 0.1 U/kg intravenously by jet stream. If pH <7, 4% sodium bicarbonate solution is administered at a rate of no more than 5 ml/kg in the first 1-3 hours. The infusion is stopped when pH reaches 7. Gastric lavage and a cleansing enema with sodium bicarbonate are performed. Potassium chloride is administered to prevent hypokalemia. Oxygen therapy with 50% humidified O2 and installation of a catheter in the bladder are indicated.
To prevent cerebral edema, it is necessary to avoid a sharp decrease in hyperglycemia and the introduction of a large amount of hypotonic solutions in the first 6 hours from the start of treatment, maintaining glycemia at a level of 10-15 mmol/l. After normalization of pH, insulin is administered every 2 hours.