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With the introduction of large doses of insulin, there is a tendency to hypoglycemia and hypokalemia, a greater increase in growth hormone and more. slowing down lactate levels (Alberti et al.). Artificial B cells are only available for a small number of institutions, so their use has no practical significance.
Preference is given to small doses of insulin. The question of whether to inject them intramuscularly or intravenously is still under discussion (Alberti et al., Hayton et al., Soler et al.).
Depending on the technical equipment, the following method is practically recommended:
- without the introduction of infusion solutions: first 12–16–20 U of simple insulin intravenously and / or intramuscularly, then 8 U of simple insulin every 30 min or hourly intramuscularly, or especially with resistant at the beginning or increasing hyperglycemia, as well as poor blood circulation intravenous (Clumeck et al.). If the level of sugar reaches 300 mg / dl, then an infusion solution of glucose 50 and a small amount of insulin are administered [4–8–12 IU with 2–4-hour intervals subcutaneously depending on the level of sugar in the blood (Alberti ,. Menzel, Bigergeil, Mohnike et al.)].
It is necessary to remember about the half-cycle of the assimilation of simple insulin: when administered intravenously about 4-5 minutes (Turner et al.), And the duration of action is about 60 minutes (Clumeck et al.); with intramuscular injection - about 2 hours (Winder), with subcutaneous administration - about 4 hours (Binder). It is more correct to inject insulin at first intramuscularly, but not subcutaneously!
- when administered with infusion solutions: 6–8–12 U of simple insulin per hour in an electrolyte infusion solution 153 with human albumin 0.1–0.2 g added to prevent insulin from adsorbing to the infusion system, see 22.214.171.124) as long infusion (Genuth, Page et al., Kidson et al., Sempe et al.). If the blood sugar drops to 300 ml / dl, then infusion of glucose 50 and insulin are administered, as mentioned above.
To use fructose, sorbitol, xylitol as carriers of calories is not necessary, since there is a sufficient amount of glucose.
A decrease in blood sugar does not depend on the severity of ketosis or the already-administered insulin treatment, but on concomitant infectious processes (Alberti).
In order to replace water and electrolytes, it is necessary to begin the introduction of fluid before obtaining data on the sugar content in the blood!
Hyperosmolar acidotic coma: only with extremely pronounced hyperosmolarity (sodium level in plasma is above 150 meq / l) can hypotonic solutions be used (electrolyte infusion solution 70, electrolyte infusion solution 105) .105 meq Na +, 51 meq C1 - 54 meq HCO3 - on 1 d
Introduction of potassium
Potassium loss reaches 200-700 meq (Alberti). With the beginning of the introduction of fluid and insulin, the fluid begins to flow into the intracellular space, with the flow of potassium into the cells ahead of the flow of glucose. Even in the early stage of coma treatment, more than 50% of the injected potassium is excreted through the kidneys. Despite the fact that with the increase in the oxidation of ketonic acids, potassium can again enter into an exchange, simultaneously with the reverse development of acidosis, hypokalemia increases.
The introduction of potassium, if there are no contraindications to it - hyperkalemia (ECG, potassium content in plasma), anuria or oliguria, should be started under the control of the monitor. The dosage is adjusted individually (20–40 mEq / h, sometimes up to 80–100 mEq / h - Alberti, Ritz et al.). The optimal dose is 250-350 mEq / 24 h.
Acidosis is a consequence of insulin deficiency. Insulin therapy, along with reimbursement of volume, is given the most importance in the fight against acidosis. An hour after the start of treatment, the first positive changes in the acid-base state are detected, even without bicarbonate therapy. After 24 hours, there are still minor deviations (King et al.). Therapy with bicarbonate is currently carried out only when cardiovascular diseases require urgent elimination of acidosis (Assal et al., Alberti, Kind et al.).
Hasty compensation of acidosis is fraught with consequences (Alberti, Freirich): a sharp drop in the pH of the cerebrospinal fluid due to the increased influx of CO2 into the cells (Alberti, Assal et al.); a slow fall in the osmolality of the cerebrospinal fluid; hypokalemia; reduced CO2 dissociation due to the shift of the O2 dissociation curve with alkalosis appearing later and difficult to correct.
Excessive buffer therapy should be refrained (Richter, Heine!)
If alkalization therapy is carried out, then you should not strive for pH values below 7.1 (Alberti, French)!
Treatment of disorders of the cardiovascular system
As a rule, 1/4 mg of strophanthin is prescribed per day. In case of heart failure, the dose should be greater. If renal function is impaired, then digoxin is used instead of strophanthin. If during the treatment of coma the blood pressure suddenly drops (the systolic pressure becomes lower than 110 mm Hg), then levarterenol (norepinephrine hydrochloride) 5 mg / 100 ml is administered. However, it is necessary to exclude hypovolemia!
Antibiotics; with vomiting, nausea or atony of the stomach, prolonged aspiration of gastric contents; warming the patient.
Phosphate injections: As coma is treated with insulin and liquids for 24 hours, plasma phosphate concentrations fall below 1 mg / dl and only on the following days their level returns to normal. To improve the dissociation of O2 and at the same time improve the supply of oxygen to the tissues during coma therapy, the early introduction of phosphate is recommended (Ditzel, Ditzel, Standl). When phosphate deficiency decreases 2,3-diphospho-glycerate (2,3-DFG), which facilitates the transfer of oxygen to the tissue (Ditzel, Ditzel, Standl).
If extrarenal renal failure is excluded (hypovolemia!), Then comatose patients with anuria, high creatinine and a poor prognostic index can perform hemodialysis (Schneider, Ziegelasch). It is necessary to remember about errors when determining creatinine associated with the presence of ketone bodies in plasma (1 meq of acetoacetate gives a false increase in creatinine up to 2 mg / dl, according to Kattermann).
Dangerous complications of coma therapy
- Belated start of treatment. Immediate administration of insulin is necessary even before blood sugar levels are obtained.
- Hypoglycemia. With the introduction of small doses of insulin with artificial b-cells or infusion solutions, it can be avoided.
- Hypokalemia. Potassium is administered from the very beginning, if there are no contraindications: oliguria, hyperkalemia (plasma potassium control, monitoring observation).
- Edema of the brain - the so-called secondary shock - disquilibrium syndrome. It develops with a rapid drop in plasma osmolality (hyponatremia below 125 meq! - Duck et al.) Due to the preservation of hyperosmolarity in the cerebrospinal fluid and brain cells. Edema of the brain can be avoided with a gradual decrease in osmolality, the use of isotonic solutions, careful use of hypotonic solutions.
- Forced alkalization therapy.
- A sharp decrease in the concentration of sugar in the blood: you should only gradually eliminate metabolic disorders.
In a diabetic coma, the patient cannot be operated on, since surgery and anesthesia exacerbate the hopelessness of the situation (disturbances associated with surgery are added to metabolic disorders as a result of insulin deficiency!). The exception is the opening of abscesses in the unconscious state of the patient without anesthesia. If, in a bad state of metabolism, there are vital indications for an operation, then before the operation it is necessary to bring the metabolism to a satisfactory condition as quickly as possible with diabetic coma treatment.
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Metabolism decompensation (ketoacidosis, diabetic coma hyperosmolar acidotic or non-acidotic, lactic acidosis)