Cyanogenic poisoning by spontaneous ingestion of star grass (Cynodon nlemfuensis var. nlemfuensis cv. 'Florico') in cattle / Intoxicação cianogênica pela ingestão espontânea de grama estrela (Cynodon nlemfuensis var. nlemfuensis cv. 'Florico') em bovinos

This study reports the epidemiological data and the clinical-pathological condition of five outbreaks of cyanogenic poisoning in cattle spontaneously ingesting star grass (Cynodon nlemfuensis Vanderyst var. nlemfuensis cv. 'Florico'). In all outbreaks, the areas where the plant was previously fertilized with high concentrations of nitrogen and the properties adopted the silvipastoral system. The first clinical signs appeared between 10 and 15 minutes after the first introduction of cattle and were characterized by muscular tremors, dyspnea, moderate tympanism, staggering gait, forced breathing with open mouth, sternal recumbency followed by death after 15 to 30 minutes and/or recovery in a few hours after the signs started. In total, 43 cows have become ill and 18 died. Two necropsies were performed and no significant changes were found except for the presence of the plant near the esophageal sphincter region. No histological lesions were seen through microscopy. Green leaves of the star grass were collected from all properties where the outbreaks occurred and the test of the picro-sodium paper was performed, revealing red-brick coloration in 20 minutes after maceration of the leaves.(AU)

Descrevem-se os dados epidemiológicos e quadro clínico-patológico de cinco surtos de intoxicação cianogênica em bovinos que ingeriram espontaneamente grama estrela (Cynodon nlemfuensis Vanderyst var. nlemfuensis cv. 'Florico'). Em todos os surtos, as áreas onde a planta se encontrava haviam sido previamente adubadas com altas concentrações de nitrogênio e as propriedades adotavam o sistema silvipastoril com Eucaliptus sp. Os primeiros sinais clínicos surgiram entre 10 e 15 minutos após a primeira introdução dos bovinos e caracterizou-se por tremores musculares, dispneia, timpanismo moderado, andar cambaleante, respiração forçada com a boca aberta, decúbito esternal seguido de morte após 15 a 30 minutos e/ou, recuperação em poucas horas após início dos sinais. No total, adoeceram 43 vacas e destas 18 morreram. Duas necropsias foram realizadas e não foram encontradas alterações significativas, exceto a presença da planta próxima a região do esfíncter esofágico. Através da microscopia não foram visualizadas lesões histológicas. Folhas verdes da grama estrela foram coletadas de todas as propriedades onde os surtos ocorreram e realizadas o teste do papel picro-sódico, o qual revelou coloração vermelho-tijolo em 20 minutos após maceração das folhas.(AU)

Smoke inhalation injury during enclosed-space fires: an update / Lesao por inalacao de fumaca em ambientes fechados: uma atualizacao

In view of the tragic fire at a nightclub in the city of Santa Maria, Brazil, which culminated in the sudden death of 232 young people, we decided to review the literature regarding smoke inhalation injury caused by enclosed-space fires, which can be divided into direct thermal damage, carbon monoxide poisoning, and cyanide poisoning. Such injuries often call for immediate orotracheal intubation, either due to acute airway obstruction or due to a reduced level of consciousness. The diagnosis and the severity of the thermal injury can be determined by fiberoptic bronchoscopy. The levels of gases and gas by-products in the bloodstream should be assessed as rapidly as possible, even while still at the scene of the incident. First responders can also treat carbon monoxide poisoning, with immediate administration of oxygen at 100%, as well as cyanide poisoning, with oxygen therapy and hydroxocobalamin injection.

Aproveita-se o trágico incêndio ocorrido em uma boate na cidade de Santa Maria, RS, que culminou na morte imediata de 232 jovens, para revisarmos a literatura com relação à lesão por inalação de fumaça em ambientes fechados, que pode ser dividida em dano térmico direito, intoxicação por monóxido de carbono e intoxicação por cianeto. Essas condições frequentemente levam à necessidade de intubação orotraqueal imediata, seja por obstrução aguda de vias aéreas, seja por depressão do nível de consciência. O diagnóstico e a gravidade da injúria térmica podem ser determinados pela fibrobroncoscopia. Quanto aos envenenamentos, a dosagem dos gases ou de seus subprodutos na corrente sanguínea é possível e deve ser realizada ainda na cena do incidente. Da mesma maneira, o tratamento da intoxicação por monóxido de carbono consiste na administração imediata de oxigênio a 100%, enquanto o da intoxicação por cianeto consiste em oxigenoterapia e hidroxicobalamina injetável como antídoto. .

Postmortem examination cases of cyanide poisoning A biological hazard.

Hydrocyanic acid and various cyanides are relatively common poisons both in suicide, accident and occasionally homicide. Acute poisoning with cyanide is most often self administered as the swift and sure action is generally known. Accidental poisoning from inhalation of vapours due to fires in buildings or by the free gas liberated from some commercial processes is also known to occur. The preparations are rarely used with homicidal intent. Whatever be the manner of poisoning, in medical settings the persons involved in postmortem examination of cases of death of cyanide poisoning are exposed to significant degree of cyanide remaining in the body cavities and tissues of the deceased. This risk is not only for the persons attending postmortem examination but also for the first respondents like police, rescue persons and also persons extending emergency care both outside and within hospital. Hydrocyanic acid is rapidly absorbed from all mucous surfaces and even from unabraded skin .Hence attending a case of cyanide poisoning involves a hazard of inhalation of cyanide gas from the victim The hazards involved in such situations are briefly reviewed.

Revisión de la toxicocinética y la toxicodinamia del ácido cianhídrico y los cianuros / Review of toxicokinetics and toxicodynamics of cyanides and hydrogen cyanide

El cianuro es uno de los tóxicos más peligrosos por su rápida y potente acción, muchas veces letal. Los diferentes tratamientos de la intoxicación tienen su base o explicación en el conocimiento de la toxicocinética y la toxicodinamia. La revisión de la toxicocinética del cianuro muestra que, si bien la vía de la tiosulfato-cianuro sulfotransferasa (rodanasa) es la principal vía metabólica, el complejo con albúmina sérica sería el primer proceso de detoxificación del cianuro en el metabolismo normal. El efecto protector de formadores de cianhidrinas en casos de intoxicación sigue siendo evaluado a nivel experimental. Los estudios actuales sobre la toxicodinamia del cianuro se enfocan en la afinidad de la unión del cianuro al centro binuclear hemo a3-CuB de la citocromo oxidasa en sus diferentes estados redox y enel mecanismo de inhibición de enzimas antioxidantes. Un mayor y mejor entendimiento de la detoxificación del cianuro así como de los mecanismos de acción tóxica podrían llevar al desarrollo de potenciales antídotos.

Cyanide is one of the most dangerous poisons because of its rapid and potent toxicity, most times with lethal outcomes. Different poisoning treatments are based on knowledge of cyanide’s toxicokinetic and toxicodynamic. The review of cyanide’s toxicokinetics shows that, although thiosulfate-cyanide sulfotransferase (rhodanese) is the major metabolic pathway, binding serum albumin would be the first process of detoxification of cyanide in normal metabolism. The protective effect of cyanohydrin formers in cases of poisoning remains experimentally evaluated. Cyanide’s binding affinity to the binuclear center heme a3-CuB of cytochrome oxidase within their different redox states and cyanide’s mechanism of inhibition of antioxidant enzymes are currently still being investigated. More and better understanding of cyanide’s detoxification pathways and/or mechanisms of toxic action could lead to the development of new potential antidotes.