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It is a carbamate ester marketed under the trade name Temik<span class="elsevierStyleSup">®</span>.</p><p id="par0015" class="elsevierStylePara elsevierViewall">It is a solid substance in the form of granules and blackish coloration used in agriculture as insecticide and nematicide. It induces the accumulation of acetylcholine in the nicotinic and muscarinic receptors of the nervous system by inhibiting cholinesterase in a reversible manner.</p><p id="par0020" class="elsevierStylePara elsevierViewall">A 30-year-old male farmer with no history of interest who was brought by the emergency healthcare team due to muscle spasms at home. This symptomatology began 15<span class="elsevierStyleHsp" style=""></span>min after the ingestion of 2 tablespoons of a substance called Temik<span class="elsevierStyleSup">®</span> as a suicide attempt after a family argument.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Physical examination showed generalized myoclonus, being more important in limbs (additional material, video 1) and in thorax. Blood pressure 100/50<span class="elsevierStyleHsp" style=""></span>mmHg, bilateral miosis, profuse sweating and bradycardia.</p><p id="par0030" class="elsevierStylePara elsevierViewall">We contacted the national toxicology center which reported the non-existence of specific treatment, and recommended to manage the complications arising from the ingestion of the toxin. Following these guidelines along with the information reported in the data sheet, the emergency healthcare team had proceeded to a nasogastric intubation to drain the stomach's content and administrate activated charcoal. Once in the ward for critically ill patients, the patients were monitored and 2<span class="elsevierStyleHsp" style=""></span>mg of atropine IV were used to reverse the bradycardia of 35<span class="elsevierStyleHsp" style=""></span>bpm. In order to control the muscle spasms, the patient was administered 10<span class="elsevierStyleHsp" style=""></span>mg IV diazepam.</p><p id="par0035" class="elsevierStylePara elsevierViewall">After 48<span class="elsevierStyleHsp" style=""></span>h having remained stable in this ward, plus the disappearance of fasciculations and bradycardia, the patient was discharged and referred to the mental health services for assessment.</p><p id="par0040" class="elsevierStylePara elsevierViewall">The diagnosis of aldicarb poisoning is essentially clinical. This is a syndrome consisting of muscarinic symptoms such as miosis, sweating, diarrhea, vomiting or hypersalivation; and nicotinic symptoms such as fasciculations or hypotonia. In severe cases there may be changes in the cardiac conduction, bradycardia, seizures or even coma.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">These symptoms together with a compatible sociocultural or work history, and in case of no reported contact with the substance, are key to the diagnosis. This is due to the fact that some of the cases reported have been involuntary poisoning (contact or intake of contaminated food) and some other cases have been a voluntary suicide attempt.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Aldicarb cannot be determined in plasma. Therefore, measuring the activity of plasma cholinesterase is a very useful and well defined analytical parameter that can help in the diagnosis (but not as an indicator of poisoning severity).</p><p id="par0055" class="elsevierStylePara elsevierViewall">Carbamates are considered to be less poisoning than organophosphates. On the one hand, they bind reversibly to acetylcholinesterase and on the other, they have great difficulty in crossing the blood–brain barrier.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> Therefore, the treatment is mainly supportive therapy, with monitoring and continuous cardiorespiratory monitoring.</p><p id="par0060" class="elsevierStylePara elsevierViewall">In the first moments after ingestion, the treatment should be supportive therapy and reducing absorption. In cases with evidence suggesting severe poisoning, we should start, ASAP, treatment with IV atropine (for adults, 2<span class="elsevierStyleHsp" style=""></span>mg IV every 5–10<span class="elsevierStyleHsp" style=""></span>min if necessary, until reduction of bronchial secretion, then continuous infusion of 0.02–0.08<span class="elsevierStyleHsp" style=""></span>mg/kg/h) might be required.</p><p id="par0065" class="elsevierStylePara elsevierViewall">The action of atropine is explained by the competitive antagonism of acetylcholine at the muscarinic receptors, even considering the decrease of certain symptoms as an additional diagnostic criterion. Atropine has no action on nicotinic receptors, therefore, in situations where symptoms arising from their stimulation prevail, the use of pralidoxime is recommended. Effectiveness has been proven for organophosphates being controversial for carbamates.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Its use is not unanimously recommended. However, it is recommended in severe carbamate poisoning refractory to atropine, organophosphate and carbamate poisoning as well as any pesticide poisoning that reduces the cholinesterase activity and conditions severe cholinergic symptomatology.</p><p id="par0075" class="elsevierStylePara elsevierViewall">Our case report is an example of healthcare through support and administration of atropine. This is sufficient in the severe poisoning with aldicarb, with the use of pralidoxime not being necessary.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a></p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Poyato Borrego M, Rufo Tejeiro O, Villarrasa Clemente FM. Mioclonías generalizadas tras la ingesta de aldicarb como intento de autolisis. Med Clin (Barc). 2019;152:329–330.</p>" ] ] "apendice" => array:1 [ 0 => array:1 [ "seccion" => array:1 [ 0 => array:4 [ "apendice" => "<p id="par0085" class="elsevierStylePara elsevierViewall">The following are the supplementary data to this article:<elsevierMultimedia ident="upi0005"></elsevierMultimedia></p>" "etiqueta" => "Appendix A" "titulo" => "Supplementary data" "identificador" => "sec0010" ] ] ] ] "multimedia" => array:1 [ 0 => array:5 [ "identificador" => "upi0005" "tipo" => "MULTIMEDIAECOMPONENTE" "mostrarFloat" => false "mostrarDisplay" => true "Ecomponente" => array:3 [ "fichero" => "mmc1.mp4" "ficheroTamanyo" => 8671828 "Video" => array:2 [ "mp4" => array:5 [ "fichero" => "mmc1.m4v" "poster" => "mmc1.jpg" "tiempo" => 0 "alto" => 0 "ancho" => 0 ] "flv" => array:5 [ "fichero" => "mmc1.flv" "poster" => "mmc1.jpg" "tiempo" => 0 "alto" => 0 "ancho" => 0 ] ] ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0030" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Self poisoning with pesticides" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "M. 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Kintz" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1191/096032700672133218" "Revista" => array:6 [ "tituloSerie" => "Hum Exp Toxicol" "fecha" => "2000" "volumen" => "19" "paginaInicial" => "657" "paginaFinal" => "662" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/11291736" "web" => "Medline" ] ] ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0050" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The pharmacokinetics and pharmacodynamics of severe aldicarb toxicity after overdose" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "A.P. Michel" 1 => "A. Mostafa" 2 => "J. Cooper" 3 => "J. Grice" 4 => "M.S. Roberts" 5 => "G.K. Isbister" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Clin Toxicol (Phila)" "fecha" => "2015" "volumen" => "53" "paginaInicial" => "6335" "paginaFinal" => "6635" ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000015200000008/v1_201904100623/S2387020619300932/v1_201904100623/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000015200000008/v1_201904100623/S2387020619300932/v1_201904100623/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020619300932?idApp=UINPBA00004N" ]
