scholarly journals On the importance of nonionic osmotically active substances of the blood for the pathogenesis of severe alcoholic delirium

Author(s):  
Volodymyr Zadorozhnyi

The main non-ionic osmotically active substances in blood serum are glucose and urea. The aim of the study was to study the changes in the water-osmotic state caused by non-ionic (organic) substances in patients with delirium tremens (DT) and in a state of alcohol withdrawal, and to assess their influence on the blood leukocyte composition and the clinical manifestations of the disease. A total of 747 men were examined in a state of alcohol withdrawal; of these, 450 people had manifestations of severe DT (F10.43), 213 — “classic” DT (F10.4), 84 patients had signs of alcohol withdrawal with somatic and vegetative manifestations (F10.3). To quantitatively describe the composition of leukocytes, an index equal to the neutrophil to lymphocyte ratio (NL-R) was used. We were able to mathematically describe a previously unknown quantitative relationship between the osmolarity level due to non-ionic osmotically active substances in blood serum and the NL-R values. It is expressed by the following formula: G + U = 1 mmol/L (log2 NL-R + 9.5), where G — concentration of glucose in blood serum, mmol/l; U is the concentration of urea in the blood serum, mmol/l; NL-R — neutrophil-lymphocyte index, units; 1 mmol/l — coefficient providing the required dimension of the result; log2 — logarithm with base 2; 9.5 is a constant whose size depends on the selected system of units. It was found that regular changes in blood osmolarity in patients with alcohol withdrawal and DT, both at the stage of initiation of psychosis and during the progression of the disease and the formation of severe DT, occur mainly, and maybe completely, due to non-ionic osmotically active substances. Glucose and urea have their unique role in the formation of homeostasis disorders during the development of the disease in individuals with uncomplicated alcohol withdrawal, as well as DT of varying severity.

2008 ◽  
Vol 42 (11) ◽  
pp. 1703-1705 ◽  
Author(s):  
Jamil Darrouj ◽  
Nitin Puri ◽  
Erin Prince ◽  
Anthony Lomonaco ◽  
Antoinette Spevetz ◽  
...  

Objective: To report a case of alcohol withdrawal and delirium tremens successfully treated with adjunctive dexmedetomidine. Case Summary: A 30–year-old man with a history of alcohol abuse was admitted to the general medical unit because of altered mental status and agitation. He was initially treated for alcohol withdrawal with benzodiazepines; his condition then deteriorated and he was transferred to the intensive care unit. Because of the patient's poor response to benzodiazepines (oxazepam and lorazepam, with midazolam the last one used), intravenous dexmedetomidine was started at an initial dose of 0.2 µg/kg/h and titrated to 0.7 µg/kg/h to the patient's comfort. Midazolam was subsequently tapered to discontinuation due to excessive sedation. In the intensive care unit, the patient's symptoms remained controlled with use of dexmedetomidine alone. He remained in the intensive care unit for 40 hours; dexmedetomidine was then tapered to discontinuation and the patient was transferred back to the general medical unit on oral oxazepam and thiamine, which had been started in the emergency department. He was discharged after 5 days. Discussion: A review of the PubMed database (1989-2007} failed to identify any other instances of dexmedetomidine having been used as the principal agent to treat alcohol withdrawal. The use of sedative to treat delirium tremens Is well documented, with benzodiazepines being the agents of choice. The clinical utility of benzodiazepines is limited by their stimulation of the γ-aminobutyric acid receptors, an effect not shared by dexmedetomidine, a central α2-receptor agonist that induces a state of cooperative sedation and does not suppress respiratory drive. Conclusions: In patients with delirium tremens, dexmedetomidine should be considered as an option for primary treatment. This case illustrates the need for further studies to investigate other potential uses for dexmedetomidine.


2021 ◽  
Vol 15 (3) ◽  
pp. 57-61
Author(s):  
R. M. Balabanova ◽  
E. V. Ilyinykh ◽  
M. V. Podryadnova ◽  
S. I. Glukhova ◽  
M. M. Urumova

Over the past decades, there has been an increase in the incidence of asymptomatic hyperuricemia (AHU), which includes an increased level (>360 μmol/L) of uric acid (UA) in the blood serum of patients with no clinical manifestations of gout. AHU is reported in various rheumatic diseases, mainly in osteoarthritis, in which AHU is one of the manifestations of the metabolic syndrome. There is relationship between AHU and pulmonary hypertension in systemic sclerosis, arterial hypertension (AH) in men with seronegative rheumatoid arthritis, extensive cutaneous psoriasis and metabolic disorders in psoriatic arthritis. There are almost no data on AHU in ankylosing spondylitis (AS), which served objective for this work.Objective: to assess the association of AHU with AS duration and activity and the presence of comorbid diseases.Patients and methods. A retrospective analysis of 48 medical histories of patients with diagnosed AS, who were treated in V.A. Nasonova Research Institute of Rheumatology from 2015 to 2019 years, whose serum UA level was >360 μmol/L.Results and discussion. More than half of patients with AS and AHU were overweight, 21% were obese. AH was diagnosed in 43.7% of patients. Stage II–III chronic kidney disease was detected in 16.7% of patients, urolithiasis – in 18.8%. 4 (8.3%) patients had diabetes mellitus. The serum UA level in patients with AS was 422.0 ± 61.6 μmol/L. In patients with AS, an association between AHU and age, duration and disease activity was noted. There was no statistically significant rela- tionship between HG and blood glucose, cholesterol, creatinine levels, body mass index. Correlation analysis revealed a statistically significant relationship between the glomerular filtration rate (GFR) and the age of patients (r=-0.54, p<0.001), the duration of the disease (r=-0.40, p<0.05), cholesterol level (r=-0.48, p=0.01), UA level (r=-0.45, p=0.03) and blood pressure (r=-0.54, p<0.001). There was no association between disease activity and GFR (p>0.05).Conclusion. In AS, an association between an increased level of UA in the blood serum and the duration and activity of the disease, and patient's age, was established.


2000 ◽  
Vol 57 (4) ◽  
pp. 257-260 ◽  
Author(s):  
Croissant ◽  
Mann

Wenn Alkoholabhängige die Alkoholzufuhr abrupt vermindern oder unterbrechen, kommt es in der Regel zur Ausbildung eines Alkoholentzugssyndroms. In den meisten Fällen entwickelt sich ein vegetatives Syndrom mit Störungen des Magen-Darm-Traktes, des Kreislaufes, der Atmung und des ZNS. In der Regel klingen die Hauptsymptome des Entzugssyndroms nach vier bis sieben Tagen ab, längere Verläufe sind selten. Eine medikamentöse Behandlung ist bei rund einem Drittel der Patienten erforderlich. Hierfür wurde eine Fülle von Pharmaka vorgeschlagen. In den ersten Stunden nach dem Alkoholentzug ist die Sensibilität der Noradrenalinrezeptoren erniedrigt, steigt dann aber erheblich an. Die Zahl der NMDA-Rezeptoren nimmt durch chronische Intoxikation mit Ethanol zu. Der Standard der Therapie basiert vorwiegend auf der oralen Monotherapie mit Clomethiazol und alternativ mit Benzodiazepinen. Die Höhe der Dosis orientiert sich an der Ausprägung der Symptomatik. Bei schwerer Entzugssymptomatik kann die Behandlung auf einer Intensivstation mit Infusionstherapie notwendig werden, z.B. im Rahmen eines Delirium tremens, welches einen lebensbedrohlichen Zustand darstellt. Hier haben sich neben Clomethiazol auch Benzodiazepine bewährt.


2009 ◽  
Vol 20 ◽  
pp. S81
Author(s):  
Rafael Monte ◽  
Ramón Rabuñal ◽  
Milagros Peña ◽  
Hugo López ◽  
Ana Pazos ◽  
...  

Author(s):  
Satish Keshav ◽  
Palak Trivedi

Alcohol intoxication occurs when the quantity of alcohol (ethanol) consumed exceeds one’s tolerance for the substance, with consequent impairment of the individual’s mental and physical functional status. Alcohol abuse is a broad term for general ill health (mental, social, and/or physical) resulting from the repetitive, compulsive, and uncontrolled consumption of alcoholic beverages. Manifestations of alcohol abuse include a failure to fulfil one’s responsibilities, resulting in loss of employment, personal relationships, or finances. Alcohol dependence is a condition which arises as a result of alcohol abuse and occurs when an individual continually uses alcohol despite significant areas of dysfunction, with evidence of physical dependence.Alcohol withdrawal syndrome is the set of symptoms and physical signs observed when an individual reduces or abruptly stops alcohol consumption after prolonged periods of excessive intake; it is largely due to the development of a ‘hyperexcitable’ central nervous system. Delirium tremens is the most severe form of alcohol withdrawal; it manifests as altered mental status, hallucinations, and sympathetic overdrive, which may progress to cardiovascular collapse if left untreated.


2016 ◽  
Vol 36 (1) ◽  
pp. 28-38 ◽  
Author(s):  
Lynsey J. Sutton ◽  
Annemarie Jutel

Management of alcohol withdrawal in critically ill patients is a challenge. The alcohol consumption histories of intensive care patients are often incomplete, limiting identification of patients with alcohol use disorders. Abrupt cessation of alcohol places these patients at risk for alcohol withdrawal syndrome. Typically benzodiazepines are used as first-line therapy to manage alcohol withdrawal. However, if patients progress to more severe withdrawal or delirium tremens, extra adjunctive medications in addition to benzodiazepines may be required. Sedation and mechanical ventilation may also be necessary. Withdrawal assessment scales such as the Clinical Institute of Withdrawal Assessment are of limited use in these patients. Instead, general sedation-agitation scales and delirium detection tools have been used. The important facets of care are the rapid identification of at-risk patients through histories of alcohol consumption, management with combination therapies, and ongoing diligent assessment and evaluation. (Critical Care Nurse. 2016;36[1]:28–39)


2002 ◽  
Vol 23 (2) ◽  
pp. 83-94 ◽  
Author(s):  
David A. Fiellin ◽  
Patrick G. O'Connor ◽  
Eric S. Holmboe ◽  
Ralph I. Horwitz

2015 ◽  
Vol 33 (5) ◽  
pp. 701-704 ◽  
Author(s):  
Dong Wook Kim ◽  
Hyun Kyung Kim ◽  
Eun-Kee Bae ◽  
So-Hee Park ◽  
Kwang Ki Kim

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