RU2847535C1 - Method of treating hypoxic encephalopathy in the post-resuscitation period of acute severe methadone poisoning complicated by circulatory arrest - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention relates to medicine, namely to anaesthesiology-resuscitation and toxicology, and can be used for treating hypoxic encephalopathy in the post-resuscitation period in acute severe methadone poisoning complicated by circulatory arrest. After 24 hours from the beginning of the therapy, with stabilization of haemodynamic parameters, cytoflavinum is administered in dose of 0.86 ml/kg of body weight, dissolved in 10 % glucose solution, in amount of 21.42 ml/kg of body weight intravenously drop-by-drop at rate of 3 ml/min.

EFFECT: method provides higher clinical effectiveness in severe patients with acute methadone poisoning complicated by circulatory arrest, due to administration of cytoflavinum in dose of 0.86 ml/kg of body weight in 10 % glucose solution in amount of 21.42 ml/kg of body weight intravenously drop-by-drop at rate of 3 ml/min.

1 cl, 1 ex

Description

The invention relates to the field of medicine, in particular to anesthesiology-resuscitation and toxicology, and can be used to treat acute severe methadone poisoning complicated by circulatory arrest in the post-resuscitation period.

The closest to the claimed method is the treatment of hypoxic encephalopathy in acute opioid poisoning complicated by circulatory arrest (Cardiopulmonary and cerebral resuscitation. A teaching aid for students, residents, postgraduate students and doctors. Authors: V.V. Moroz, I.G. Bobrinskaya, V.Yu. Vasiliev, A.N. Kuzovlev, E.A. Spiridonova, E.A. Tishkov. Research Institute of Orthopedics, Russian Academy of Medical Sciences, Moscow State Medical University of the Russian Federation. Moscow, 2011. Page 44) by fractional intravenous or intramuscular administration of naloxone at a dose of 400 mcg intravenously or 800 mcg intramuscularly with further titration according to the effect to a total dose of 6-10 mg.

The main disadvantage of the method chosen as a prototype is the ineffective restoration of the brain, as well as the progression of edema-swelling of the brain with the development of a seizure syndrome, which leads to irreversible changes in the brain.

The objective of the invention is to increase the effectiveness of treatment of severely ill patients with acute methadone poisoning complicated by circulatory arrest through effective restoration of the brain in the post-resuscitation period.

The technical result of the stated task is achieved by a method for treating hypoxic encephalopathy in the post-resuscitation period in acute severe methadone poisoning complicated by circulatory arrest. This method involves administering Cytoflavin at a dose of 0.86 ml/kg of body weight 24 hours after the start of therapy, when hemodynamic parameters have stabilized. The drug is dissolved in a 10% glucose solution at a volume of 21.42 ml/kg of body weight, administered intravenously at a rate of 3 ml/min. This allows for the restoration of the body's enzymatic activity and the activation of energy-dependent processes. The active components of the drug (succinate, inosine, riboflavin, and nicotinamide) are utilized in all tissues and are not affected by the failure of any particular organ.

Thus, by providing a complex effect, the drug reduces the degree of hypoxic damage to the brain by more quickly normalizing energy supply, restoring the antioxidant system and reducing the activity of lipid peroxidation processes, which contributes to more effective restoration of the brain.

During the treatment of hypoxic brain injury, when circulatory arrest occurs, type B lactic acidosis must be corrected by eliminating the deficiency of pyruvate dehydrogenase complex cofactors. Cytoflavin, which contains riboflavin, nicotinamide, inosine, and sodium succinate, is the most effective treatment. Cytoflavin helps eliminate nicotinamide adenine dinucleotide (NAD) and flavin adenine dinucleotide (FAD) deficiencies. By delivering protons and electron pairs to the NAD dehydrogenase and FAD dehydrogenase enzyme complexes, they ensure the proper functioning of the electron chain on the inner mitochondrial membrane. Eliminating the deficiency of NAD+ and FAD+ molecules increases the activity of aerobic glycolysis and, thus, reduces the manifestations of lactic acidosis. Cytoflavin, which includes inosine, nicotinamide, and riboflavin, supports the enzyme systems involved in the synthesis of NAD and FAD molecules. In addition, cytoflavin has pronounced antioxidant properties and its use leads to an increase in antioxidant potential in the form of an increase in the level of reduced glutathione, thereby reducing the activity of lipid peroxidation processes.

Administration of Cytoflavin at a dose of less than 0.86 ml/kg body weight is ineffective. Increasing the dose of Cytoflavin above 0.86 ml/kg increases the risk of metabolic desynchronization, i.e., a mismatch between oxygen delivery and increased metabolic needs. Cytoflavin at a dose of 0.86 ml/kg body weight is dissolved in a 10% glucose solution in a volume of 21.42 ml/kg body weight and administered intravenously by drip at a rate of 3 ml/min, since the theoretical osmolarity of a 10% glucose solution is 555 mOsm/L (from 541 to 662 mOsm/L), which is one of the factors reducing cerebral edema-swelling. At a dose of the solution less than 0.86 ml/kg body weight, there is a risk of ineffectiveness of the method; increasing the dose above 0.86 ml/kg increases the risk of metabolic desynchronization. The rate of administration is selected in such a way as to increase the effectiveness of treatment and eliminate unfavorable results (with a decrease in the rate of administration, the risk of ineffectiveness of the method increases; with an increase in the rate of administration, there is a risk of developing hyperglycemia and hypervolemia). It is important to administer maximum volumes within the recommended doses within 24 hours to avoid hemodilution and hypervolemia.

The method is as follows. The patient receives inotropic and infusion therapy during the post-resuscitation period. After hemodynamic deterioration has been controlled, Cytoflavin at a dose of 0.86 ml/kg of body weight is dissolved in a 10% glucose solution at a volume of 21.42 ml/kg of body weight and administered intravenously at a rate of 3 ml/min.

Example. Patient T., 37 years old, was admitted to the State Budgetary Institution "St. Petersburg Research Institute for Emergency Medicine named after I.I. Dzhanelidze" on January 3, 2023 with a diagnosis of: Acute methadone poisoning, severe. Mixed encephalopathy (toxic, dysmetabolic). Complications: Acute cerebral failure. Acute respiratory failure. Acute circulatory failure. Condition after clinical death on January 3, 2023. Concomitant symptoms: Severe hypothermia.

Upon admission, the patient's general condition was considered extremely critical. The severity of his condition was due to the post-clinical death state, despite successful resuscitation efforts, and toxic-hypoxic encephalopathy. Twenty-four hours after the start of therapy, hemodynamic parameters stabilized, and treatment was administered as described. After 12 hours, positive changes were noted with the therapy, including a recovery of consciousness to a Glasgow Coma Scale score of 9 (stupor). Twenty-four hours after the start of therapy, the level of consciousness was 14 (mild obtundation). On the third day, the patient regained consciousness and began breathing spontaneously. He was discharged from the hospital five days later.

The proposed method improves the effectiveness of treatment for patients with acute methadone poisoning complicated by circulatory arrest, reduces the risk of irreversible hypoxic-ischemic brain damage, the likelihood of profound patient disability, and death. With the use of Cytoflavin, after stabilization of hemodynamic parameters, a more rapid recovery of consciousness and the regulatory function of the central nervous system, in particular the restoration of spontaneous breathing, occurs.

Claims (1)

A method for treating hypoxic encephalopathy in the post-resuscitation period in acute severe methadone poisoning complicated by circulatory arrest, characterized by the fact that 24 hours after the start of therapy, when hemodynamic parameters are stabilized, cytoflavin is administered at a dose of 0.86 ml/kg of body weight, dissolved in a 10% glucose solution, in a volume of 21.42 ml/kg of body weight intravenously by drip at a rate of 3 ml/min.