In the treatment of DKA there are four directions
- insulin therapy;
- recovery of lost fluid;
- correction of mineral and electrolyte metabolism;
- treatment of coma-provoking diseases and complications of ketoacidosis.
Insulin replacement therapy is the only etiological treatment for DKA. Only this hormone with anabolic properties can stop the severe generalized catabolic processes caused by its lack. To achieve an optimally active serum insulin level, its continuous infusion is required at 4-12 units / h. This concentration of insulin in the blood inhibits the breakdown of fats and ketogenesis, promotes the synthesis of glycogen and inhibits the production of glucose by the liver, thereby eliminating the two most important links in the pathogenesis of DKA. A regimen of insulin therapy using such dosages is called a “low dose regimen”. Earlier, much higher doses of insulin were used. However, it has been proven that insulin therapy in the low-dose regimen is accompanied by a significantly lower risk of complications than in the high-dose regimen.
A low dose regimen is recommended for the treatment of DKA, because:
- large doses of insulin (≥ 20 units at a time) can too sharply reduce blood glucose levels, which may be accompanied by hypoglycemia, cerebral edema, and a number of other complications;
- a sharp decrease in glucose concentration is accompanied by a no less rapid drop in serum potassium concentration, therefore, when using large doses of insulin, the risk of hypokalemia increases sharply.
It should be emphasized that in the treatment of a patient in the state of DKA, only short-acting insulins should be used, while medium and long-acting insulins are contraindicated before the patient is taken out of the state of ketoacidosis. The most effective are human insulins, however, in the treatment of patients in a comatose or precomatous state, the determining factor dictating the need for the introduction of any type of insulin is precisely the duration of its action, not its appearance. The introduction of insulin in a dose of 10-16 units is recommended. intravenously, by stream or intramuscularly, then by intravenous drip of 0.1 units / kg / h or 5-10 units / h. Typically, glycemia decreases at a rate of 4.2-5.6 mmol / l / h. If within 2-4 hours the level of hyperglycemia does not decrease, the dose of insulin administered increases; with a decrease in glycemia to 14 mmol / l, the rate of its administration decreases to 1-4 units / h. The decisive factor in choosing the speed and dose of insulin is the constant monitoring of blood glucose. It is advisable to conduct a blood test every 30-60 minutes using express glucose analyzers. However, it should be remembered that today many rapid glucose analyzers used for self-monitoring can show incorrect glycemia values at high blood sugar. After restoration of consciousness, the patient should not be given infusion therapy for several days. As soon as the patient’s condition has improved, and glycemia is stable at a level of ≤ 11-12 mmol / l, he should again start eating foods that are necessarily rich in carbohydrates (mashed potatoes, liquid cereals, bread), and the sooner he can be transferred to subcutaneous insulin therapy , all the better. Subcutaneously, short-acting insulin is first prescribed fractionally, 10-14 units. every 4 hours, adjusting the dose depending on the level of glycemia, and then switch to the use of simple insulin in combination with that of prolonged action. Acetonuria can persist for some time and with good rates of carbohydrate metabolism. For its complete elimination, sometimes it takes another 2-3 days, and to administer large doses of insulin for this purpose or do not need to give additional carbohydrates.
The state of DKA is characterized by pronounced resistance of peripheral target tissues to insulin, in connection with this, the dose required to remove the patient from a coma may turn out to be high, significantly exceeding usually the dose required by the patient before or after ketoacidosis. Only after complete correction of hyperglycemia and relief of DKA can a patient be prescribed insulin of medium duration of action subcutaneously as the so-called basic therapy. Immediately after removing the patient from the state of ketoacidosis, the sensitivity of tissues to insulin increases sharply, therefore control and adjustment of its dose is necessary in order to prevent hypoglycemic reactions.
Given the characteristic dehydration resulting from osmotic diuresis due to hyperglycemia, the restoration of fluid volume is a necessary element in the treatment of patients with DKA. Typically, patients have a fluid deficit of 3-5 liters, which should be completely replaced. For this purpose, it is recommended the introduction of 2-3 l of 0.9% saline during the first 1-3 hours, or at the rate of 5-10 ml / kg / h. Then (usually with an increase in plasma sodium concentration> 150 mmol / L), an intravenous administration of a 0.45% sodium solution is prescribed at a rate of 150-300 ml / h in order to correct hyperchloremia. In order to avoid excessively fast rehydration, the volume of saline injected per hour, with initially sharply expressed dehydration, should not exceed hourly diuresis by more than 500, maximum 1,000 ml. You can also use the rule: the total amount of fluid introduced in the first 12 hours of therapy should not exceed 10% of body weight. With systolic blood pressure is persistently <80 mm RT. Art. to prevent circulatory failure, in addition to an isotonic sodium chloride solution, a transfusion of plasma or plasma substitutes is indicated.
With a decrease in blood glucose to 15-16 mmol / l (250 mg / dl), infusion of a 5% glucose solution is necessary to prevent hypoglycemia and ensure the delivery of glucose to tissues, along with a 0.45% sodium chloride solution at a speed of 100-200 ml / h . It should be remembered that the achievement of persistent normoglycemia is not the immediate goal of treating patients in the state of DKA at the first stage. If dehydration persists with a decrease in glycemia, glucose is administered in parallel with saline. Substitution of fluid volume, along with a stabilizing hemodynamic effect, helps to reduce glycemia (even without insulin) by reducing the content of catecholamines and cortisol in blood plasma, the release of which occurs in response to a decrease in bcc.
Correction of the content of minerals and electrolytes lost due to osmotic diuresis is necessary. Also important is the correction of potassium in the blood plasma, whose reserves in the body are small. During the treatment of DKA, as glycemia decreases, potassium in large quantities will enter the cell, and also continue to be excreted in the urine. Therefore, if the initial level of potassium was within normal limits, a significant drop can be expected during therapy (usually 3-4 hours after its start). If diuresis is preserved, from the very beginning of insulin therapy, even with a normal level of serum potassium, continuous infusion begins, aiming to maintain potassium within 4-5 mmol / l. The simplified recommendations for its administration without taking into account the blood pH look like this: at a serum potassium level <3 mmol / l – potassium chloride at 3 g / h, at a level of 3-4 mmol / l – 2 g / h, at a level of 4- 5 mmol / l – 1.5 g / h, at a level of 5-5.9 mmol / l – 1 g / h; at a level of ≥ 6 mmol / l, administration is stopped. After removal from DKA, potassium preparations are prescribed orally for 5-7 days. It is also possible to prescribe potassium phosphate depending on the content of calcium and phosphorus in the blood plasma; too intense administration of potassium phosphate can cause hypocalcemia. The content of phosphates in the blood plasma should be corrected by introducing 10-20 mmol / h of potassium phosphate, up to a maximum of 40-60 mmol.
When correcting acidosis, it should be remembered that metabolic (diabetic) acidosis develops due to the increased intake of ketone bodies in the blood due to insulin deficiency, therefore, insulin replacement therapy is the etiological treatment of this type of acidosis, which in most cases helps to eliminate it. The introduction of sodium bicarbonate, so widely used earlier, is associated with an extremely high risk of complications:
- intracellular acidosis (although blood pH may increase);
- paradoxical cerebrospinal fluid acidosis, which can contribute to cerebral edema.
That is why recently the indications for the use of sodium bicarbonate in DKA have been significantly narrowed, and its routine use is strongly discouraged. Sodium bicarbonate can only be administered at a blood pH of <7.0 or a standard bicarbonate level of <5 mmol / L. If it is not possible to determine these indicators, then the risk of introducing alkali “blindly” far exceeds the potential benefit. Recently, a solution of drinking soda is not prescribed to patients either orally or rectally, which has been widely practiced previously.
Important directions in the treatment of DKA are the identification and treatment of concomitant diseases that could cause the development of ketoacidosis, as well as worsen its course. So, it is necessary to carefully examine the patient in order to diagnose and treat infectious diseases, especially urinary tract infections. In case of suspected infection, it is advisable to prescribe broad-spectrum antibiotics. Given the characteristic impairment of consciousness in patients, the diagnosis of meningitis, stroke, myocardial infarction may be of some difficulty. With a drop in blood pressure, despite the introduction of fluid, transfusion of whole blood or plasma-replacing solutions is possible.
Complications of DKA: deep vein thrombosis, pulmonary embolism, arterial thrombosis (myocardial infarction, stroke), aspiration pneumonia, cerebral edema, pulmonary edema, infection, rarely gastrointestinal bleeding and ischemic colitis, erosive gastritis, late hypoglycemia. Severe respiratory failure, oliguria and renal failure are noted. Complications of therapy: cerebral edema, pulmonary edema, hypoglycemia, hypokalemia, hyponatremia, hypophosphatemia.
In conclusion, it should be noted that DKA is by no means an integral sign of the course of diabetes. Given the education of patients with diabetes, the use of intensified insulin therapy, daily self-monitoring of metabolism and self-adaptation of the dose of insulin, the frequency of DKA can be reduced to almost zero.