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      Acute toluene intoxication–clinical presentation, management and prognosis: a prospective observational study

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          Abstract

          Background

          Toluene is one of the most widely abused inhaled drugs due to its acute neurologic effects including euphoria and subsequent depression. However, dangerous metabolic abnormalities are associated to acute toluene intoxication. It has been previously reported that rhabdomyolysis and acute hepatorenal injury could be hallmarks of the condition, and could constitute risk factors for poor outcomes. The objective was to describe the clinical presentation, to characterize the renal and liver abnormalities, the management and prognosis associated to acute toluene intoxication.

          Methods

          We prospectively assessed 20 patients that were admitted to a single center’s emergency department from September 2012 to June 2014 with clinical and metabolic alterations due to acute toluene intoxication.

          Results

          The main clinical presentation consisted of weakness associated to severe hypokalemia and acidosis. Renal glomerular injury (proteinuria) is ubiquitous. Biliary tract injury (alkaline phosphatase and gamma-glutamyl transpeptidase elevations) disproportional to hepatocellular injury is common. Rhabdomyolysis occurred in 80 % of patients, probably due to hypokalemia and hypophosphatemia. There were three deaths, all female, and all associated with altered mental status, severe acidosis, hypokalemia and acute oliguric renal failure. The cause of death was in all cases due to cardiac rhythm abnormalities.

          Conclusion

          The hallmarks of acute toluene intoxication are hypokalemic paralysis and metabolic acidosis. Liver injury and rhabdomyolysis are common. On admission, altered mental status, renal failure, severe acidemia and female gender (not significant in our study, but present in all three deaths) could be associated with a poor outcome, and patients with these characteristics should be considered to be treated in an intensive care unit.

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          Most cited references46

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          Hypokalemia.

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            Industrial solvents and liver toxicity: risk assessment, risk factors and mechanisms.

            Organic solvents utilized in various industrial processes may be associated with hepatotoxicity. The hepatotoxicity of some of the solvents was recognized as early as 1887, 1889 and 1904. Factors contributing to the hepatotoxicity of solvents include 1) species differences, 2) liver blood flow, 3) protein binding, 4) point of binding intracellularly, 5) genetic factors, 6) different cellular enzymatic degradation, 7) age, 8) nutritional condition, 9) interaction with alcohol, and 10) interaction with medications of use and abuse. The hepatotoxicity of solvents in general and of carbon tetrachloride, trichloroethylene, tetrachloroethylene, toluene, and 1,1,1-trichloroethene are discussed. Experimental animal data, human data, and in vitro studies are explored. Suggested mechanisms of direct toxicity, indirect toxicity and autoimmune mechanisms are elaborated. The most important message from this review is that laboratory testing that is commonly used by clinicians to detect liver toxicity may not be sensitive enough to detect early liver hepatotoxicity from industrial solvents and new methodologies are being encouraged and utilized in the early recognition and diagnosis of hepatotoxicity for solvents. The final clinical assessment of hepatotoxicity and industrial solvents must take into account synergism with medications, drugs of use and abuse, alcohol, age, and nutrition. Early recognition and reporting will be helpful in further understanding the incidence, cofactors and possible mechanisms.
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              Pathophysiology and management of hypokalemia: a clinical perspective.

              Potassium (K(+)) ions are the predominant intracellular cations. K(+) homeostasis depends on external balance (dietary intake [typically 100 mmol per day] versus excretion [95% via the kidney; 5% via the colon]) and internal balance (the distribution of K(+) between intracellular and extracellular fluid compartments). The uneven distribution of K(+) across cell membranes means that a mere 1% shift in its distribution can cause a 50% change in plasma K(+) concentration. Hormonal mechanisms (involving insulin, β-adrenergic agonists and aldosterone) modulate K(+) distribution by promoting rapid transfer of K(+) across the plasma membrane. Extrarenal K(+) losses from the body are usually small, but can be marked in individuals with chronic diarrhea, severe burns or prolonged sweating. Under normal circumstances, the kidney's distal nephron secretes K(+) and determines final urinary excretion. In patients with hypokalemia (plasma K(+) concentration <3.5 mmol/l), after the exclusion of extrarenal causes, alterations in sodium ion delivery to the distal nephron, mineralocorticoid status, or a specific inherited or acquired defect in distal nephron function (each of which affects distal nephron K(+) secretion), should be considered. Clinical management of hypokalemia should establish the underlying cause and alleviate the primary disorder. This Review aims to inform clinicians about the pathophysiology and appropriate treatment for hypokalemia.
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                Author and article information

                Contributors
                ccamara83@hotmail.com
                +521 811 4749 146 , renerodriguez@investigacion-meduanl.com , rodriguezgutierrez.rene@mayo.edu
                roberto_monreal@hotmail.com
                jgonzalezg@investigacion-meduanl.com
                Journal
                BMC Emerg Med
                BMC Emerg Med
                BMC Emergency Medicine
                BioMed Central (London )
                1471-227X
                18 August 2015
                18 August 2015
                2015
                : 15
                : 19
                Affiliations
                [ ]Servicio de Neurología, Hospital Universitario “Dr. José E. González”, Universidad Autónoma de Nuevo León, Monterrey, N.L. México, Madero y Gonzalitos S/N, Monterrey, NL 64460 Mexico
                [ ]Departamento de Medicina Interna, Servicio de Endocrinología, Hospital Universitario “Dr. José E. González”, Universidad Autónoma de Nuevo León, Monterrey, N.L. México, Madero y Gonzalitos S/N, Monterrey, NL 64460 Mexico
                [ ]Knowledge and Evaluation Research Unit, Division of Endocrinology, Diabetes, Metabolism and Nutrition, Department of Medicine, Mayo Clinic, Rochester, MN 55905 USA
                [ ]Departamento de Medicina Interna, Hospital Universitario “Dr. José E. González”, Universidad Autónoma de Nuevo León, Monterrey, N.L. México, Madero y Gonzalitos S/N, Monterrey, NL 64460 México
                Article
                39
                10.1186/s12873-015-0039-0
                4539858
                26282250
                b4016b70-071e-4690-824d-736fff96b299
                © Camara-Lemarroy et al. 2015

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 3 August 2014
                : 29 June 2015
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2015

                Emergency medicine & Trauma
                toluene,toxicity,rhabdomyolysis,renal tubular acidosis,hypokalemia
                Emergency medicine & Trauma
                toluene, toxicity, rhabdomyolysis, renal tubular acidosis, hypokalemia

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