Key aspects of diagnosis and sedation of patients with acute alcohol-related psychosis in the intensive care unit
Background. The problem of acute alcohol-related psychosis continues to be in the limelight of domestic and foreign researchers. In Ukraine, the problem of effective treatment for severe forms of acute alcohol-related psychosis, namely delirium, remains largely unresolved today, in particular, in the aspect of achieving adequate and effective sedation of patients. This is primarily due to the fact that insufficient level of sedation makes medical personnel use additional methods of forced fixation (chest, lower extremities) of such patients with the purpose of creating a certain “control” of staying in the department; on the other hand, excessive sedative therapy requires careful monitoring of vital functions, first of all, external breathing. An increase in the dose of drugs for sedation and the use of additional drugs with a depressing effect on the central nervous system leads to a negative impact on the function of organs performing detoxification, including the already provoked and alcohol-damaged liver, which, in turn, not only influence the length of patients’ stay in the intensive care unit (ICU) and the result of treatment, but also increases its cost. The main purpose of our work was to analyze the effect of using various sedation regimens on the rate and frequency of achieving effective sedation, the need for additional control and duration of stay in the ICU of patients with severe alcohol-related delirium diagnosed according to the criteria of Delirium Detection Score (DDS). Materials and methods. In 2016–2017, at the premises of ICU of Cherkassy Regional Psychiatric Hospital, 36 patients with severe alcohol-related psychosis (males aged 35 to 50 (42.5 ± 7.5) years) and a long history of alcohol abuse — from 6 to 12 (9 ± 3) years were examined and treated. Alcohol delirium was diagnosed with DDS, and a preliminary survey according to the Alcohol Use Disorders Identification Test was conducted. All patients received intensive care: pharmacological correction of psychomotor agitation syndrome, detoxification and correction of violations of water-electrolyte balance (infusion of balanced saline solutions — 40–50 ml/kg in the first day of treatment followed by correction of infusion rate according to the calculation of daily requirement and pathological costs in the following days), correction of magnesium deficiency with 25% MgSO4 solution 30–40 ml per day, sodium thiosulfate with intravenous bolus (30 % of solution in a dose of 20–30 ml per day for the entire period of treatment), correction of cerebral metabolism disorders (vitamins: B1 5% 12 ml/day, B6 5% 8 ml/day, PP 4–6 ml/day, inosine (riboxinum) 20 ml intravenous, alpha-lipoic acid (berlithion) 600 mg/day). Depending on the use of the sedation scheme, patients were divided into two groups: group A (n = 18) received diazepam (diazepex) 0.5% 4 ml intramuscularly (i.m.) every 8 hours and sodium oxybutyrate 20% — 10 ml as constant infusion of 0.9% NaCl solution 400 ml during 4 hours twice daily; group B (n = 18) received diazepam (diazepex) 0.5% 4 ml i.m. every 8 hours and phenobarbital 200 mg per os 2 times a day. The target was to achieve a level of sedation from –2 to 0 on the Richmond scale throughout the period of administration of sedative medications (3–4 days) without the use of auxiliary methods of compulsory fixation and other pharmacological adjuvants. Results. The results of our studies indicate that infusion of sodium oxybutyrate combined with the basic use of benzodiazepine preparations had significant advantages in achieving the target sedation level in patients with severe alcohol-related delirium, as compared to phenobarbital. Moreover, the duration of stay of patients receiving phenobarbital in the ICU increased by 1.5 day. Conclusions. This result may be explained by the fact that when benzodiazepines are combined with sodium oxybutyrate, a summation of the sedative effect due to the impact on the gamma-aminobutyric acid receptors associated with the Cl-ion channel occurs first, resulting in compensatory accumulation of glutamate, therefore, the patient wakes up faster after drug withdrawal.
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