Ketoacidotic diabetic coma
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Ketoacidotic diabetic coma is a condition that develops on 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, it develops mainly in patients with type 1 diabetes. This condition is accompanied by metabolic disorders, which are characterized by hyperglycemia, ketoacidosis and ketonuria.
Causes of the ketoacidotic diabetic coma
Late diagnosis of type 1 diabetes mellitus, intercurrent diseases, surgery, injuries, stressful situations; treatment regimens.
[9]
Symptoms of the ketoacidotic diabetic coma
Stage I of compensated diabetic ketoacidosis is characterized by thirst, polyuria, headache, dizziness, drowsiness, loss of appetite, nausea, and abdominal pain. In the exhaled air there is a slight smell of acetone. The level of beta-hydroxybutyrate reaches 3 mmol / l. Symptoms of dehydration develop.
At stage II of decompensated diabetic ketoacidosis, consciousness becomes soporous, pupils respond to light and tendon reflexes are reduced. Tachycardia develops. Blood pressure is low. Abdominal syndrome is associated with frequent vomiting, loose stools and symptoms of pseudoperitonitis. Polyuria is replaced by oliguria.
Stage III - diabetic ketoacidotic coma - is characterized by loss of consciousness, depression of reflexes, narrow pupils with no response to light. The smell of acetone is felt in the room. The phenomena of dehydration and impaired hemodynamics are expressed. Breath Kussmaul. Determine hepatomegaly, anuria. 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.
What's bothering you?
What do need to examine?
How to examine?
What tests are needed?
Who to contact?
Treatment of the ketoacidotic diabetic coma
Treatment of patients with ketoacidosis or ketoacid coma should be started immediately. In the first hour, a 0.9% solution of sodium chloride is injected intravenously at a rate of 20 ml / (kgkhch), in the first 12 hours - 50% of the total daily requirement. In the next 6h - 25% of the calculated dose; in the remaining 6 hours - the last 25% of the daily volume of liquid (only 100-120 ml / kg). In case of glycemia 12–12 mmol / l, a 5% glucose solution is also injected (the insulin dose is the same), then a 0.9% solution of sodium chloride. Insulin of short action is administered in a dose of 0.1 U / kg, then - 0.1 U / kgkh) intravenously until the pH is normalized. Glycemia control is carried out hourly, the determination of the parameters of CBS (pH, BE) 1 time in 1-2 hours. In the absence of infusion, insulin is administered hourly 0.1 U / kg intravenously. If the pH is <7, a 4% solution of sodium bicarbonate is injected at a rate of no more than 5 ml / kg in the first 1-3 hours. The infusion is stopped when the pH is reached 7. A gastric lavage and a cleaning enema with sodium bicarbonate is performed. To prevent hypokalemia injected potassium chloride. Showing oxygen therapy 50% moistened O 2, installing a catheter in the bladder.
For the prevention of cerebral edema in the first 6 hours after the start of treatment, it is necessary to avoid a sharp decrease in hyperglycemia and the introduction of a large number of hypotonic solutions, while maintaining glycemia at the level of 10-15 mmol / l. After pH has normalized, insulin is administered every 2 hours.