Cyanide Poisoning

Vogel, Stephen N; Sultan, Thomas R.; Eyck, Raymond P. Ten

doi:10.3109/15563658108990043

Cited by 130 publications

(67 citation statements)

References 44 publications

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“…Cyanide inhibits many metabolic processes but, the most commonly recognised mechanism of toxicity is its binding to and inhibition of cytochrome c oxidase, leading to: a cessation of cellular respiration; a shift to anaerobic metabolism; and a reduction in cellular ATP levels [21,[38][39][40]. This is invariably associated with cytotoxic hypoxia and lactic acidosis [41]. Cyanide at the concentrations found in the present study would be expected to inhibit cellular respiration in the local environment of the CF lung, including in airway epithelial cells and alveolar macrophages, as well as in other invading microbes.…”

Section: Discussionmentioning

confidence: 99%

Pseudomonas aeruginosa, cyanide accumulation and lung function in CF and non-CF bronchiectasis patients

Ryall¹,

Davies²,

Wilson³

et al. 2008

Eur Respir J

104

102

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In patients with cystic fibrosis (CF) and non-CF bronchiectasis, Pseudomonas aeruginosa is the most important respiratory pathogen. It is able to synthesise hydrogen cyanide, a potent inhibitor of cellular respiration.The present study investigated whether cyanide is present in the sputum of CF and non-CF bronchiectasis patients infected with P. aeruginosa, and whether the detection of cyanide affected lung function. Cyanide was measured in sputum using a cyanide ion selective electrode.Cyanide was detected in sputum from 15 out of 25 CF and non-CF bronchiectasis patients with current P. aeruginosa infection; however, it was not detected in any of the 10 patients without this organism. Maximum levels were 130 mM (mean¡SE 72¡6.6 mM). Concurrent lung function data were available on all 21 P. aeruginosa-infected CF patients; the group with measurable sputum cyanide (n511) was not different from those without (n510) on the basis of age or sex. However, those with detectable cyanide had significantly poorer lung function than those without (forced expiratory volume in one second (% predicted) 26.8¡3.8 versus 46.0¡6.7%; forced vital capacity (% pred) 44.4¡4.9 versus 60.1¡7.7%).Cyanide is detectable in sputum from cystic fibrosis and non-cystic fibrosis bronchiectasis patients infected with Pseudomonas aeruginosa, and is also associated with impaired lung function.

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Section: Discussionmentioning

confidence: 99%

Pseudomonas aeruginosa, cyanide accumulation and lung function in CF and non-CF bronchiectasis patients

Ryall¹,

Davies²,

Wilson³

et al. 2008

Eur Respir J

104

102

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“…Nos bovinos intoxicados experimentalmente pelo tifton 68 observa-se que a respiração alterou-se pouco em termos de frequência, porém foi mais profunda e intensa. Isto pode ser explicado pela incapacidade das células em captar o oxigênio das hemá-cias, em razão da inibição da respiração celular aeróbica, conforme comentam Vogel et al (1981).…”

Section: Discussão E Conclusõesunclassified

Intoxicação espontânea e experimental por tifton 68 (Cynodon nlemfuensis Vanderyst) em bovinos

et al. 2017

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RESUMO: Tifton 68 (Cynodon nlemfuensis Vanderyst) é uma gramínea cultivada na região sul do Brasil, responsável por manifestações clínicas superagudas de dispneia, dificuldade de deglutição, tremores musculares, timpanismo e decúbito em bovinos. A morte ocorre rapidamente após o início dos primeiros sinais e não são encontradas alterações macro e microscópicas significativas. O presente estudo descreve os aspectos epidemiológicos, clínicos e lesionais da intoxicação espontânea por tifton 68 que ocorreu nos municípios de Rio do Sul, Pouso Redondo, Taió e Rio do Campo, estado de Santa Catarina, Brasil, nos anos de 1996, 1997, 1998 e 2010, respectivamente. Experimentalmente foram avaliadas a presença de ácido cianídrico nas folhas verdes e secas desta planta, através do teste do papel picrossódico e a reversão da intoxicação pela utilização de uma solução antídoto específica de tiossulfato de sódio e nitrito de sódio. A reprodução experimental consistiu na administração de folhas verdes de tifton 68 para dois bovinos com doses a partir de 10,3g/kg. O quadro de intoxicação cianogênica foi confirmado pela imediata resposta ao tratamento intravenoso com a solução antídoto. As amostras da planta verde forneceram resposta positiva ao teste do papel picrossódico. O feno de tifton 68 não demonstrou qualquer toxicidade, mesmo em altas doses (18 e 27g/kg), sendo seguro para a alimentação de bovinos.

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“…Many patients poisoned with cyanide do not manifest hypotension despite having a depressed level of consciousness or coma [63,[68][69][70][71][72][73][74][75][76]. However, hypotension generally occurs in more severely poisoned patients and appears to correlate with a lower serum pH [64-66, 70, 74-79].…”

Section: Wouldn't Cyanide Poisoning Associated With Severementioning

confidence: 99%

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

Villano

O'Connell

et al. 2015

J. Med. Toxicol.

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A 28-year-old man was brought to the Emergency Department (ED) for evaluation of a depressed level of consciousness that developed while in jail. Sixteen hours previously, he had been arrested on charges of murder. The patient's mental status was reported as normal at the time of arrest, and it had remained so during several hours of interrogation and during the booking process at jail. Following interrogation, the patient was placed into a cell with no other inmates. During the jail intake process, the patient had not reported any history of medical problems nor was he prescribed with any medications. Paramedics arrived to find him unresponsive, but maintaining airway reflexes and hemodynamically stable. They measured a blood glucose of 300 mg/dL and noted one episode of blood-tinged emesis during transport to the ED. No seizure activity was witnessed.On arrival to the ED, vital signs were: heart rate 132/min, blood pressure 129/74 mmHg, temperature 35.3°C (95.5°F), respiratory rate 24/min, and 100 % oxygen saturation on 15 l/ min of oxygen delivered by non-rebreather face mask.Physical examination was notable for a depressed level of consciousness. His eyes remained closed to pain, he withdrew all extremities equally to pain, and he was non-verbal. He had no signs of trauma, and his pupils were normal in size and reactive. Rapid sequence tracheal intubation was performed for airway protection. An electrocardiogram was normal except for sinus tachycardia at a rate of 111/min. An initial peripherally drawn arterial blood gas obtained immediately after intubation revealed: pH 6.97, pCO 2 40 mmHg, pO 2 215 mmHg. A computed tomography scan of the brain was normal. Initial blood chemistry panel was significant for a serum bicarbonate of 7 mEq/L, glucose of 362 mg/dL, and a normal potassium, blood urea nitrogen (BUN), creatinine, and calcium. The initial serum anion gap was 34 mEq/L. Measured serum osmolality was 320 mOsm/kg, yielding an osmol gap of 9 mOsm/kg (using formula of [2(Na)+BUN/2.8+glu-cose/18] for calculated serum osmolarity). Initial lactate was 156.5 mg/dL (normal reference range 4.5-19.8 mg/dL) and beta-hydroxybutyrate (βHB) 2.9 mg/dL (normal reference range 0.0-2.8 mg/dL). Initial liver panel included an aspartate aminotransferase (AST) of 64 U/L, alanine aminotransferase (ALT) of 27 U/L, and bilirubin of 0.4 mg/dL. Prothrombin time was 13.1 s (reference range 9.7-12.5), and lipase was normal at 25 U/L. Initial creatinine phosphokinase (CK) was slightly elevated at 373 U/L (0-175). Urinalysis was positive for small ketones and crystals were not present. Measurements of acetone and acetoacetate were not performed. Serum ethanol and salicylate levels were undetectable, and a urine drug of abuse panel by immunoassay was negative for amphetamines as a class, barbiturates as a class, benzodiazepines as a class, benzoylecgonine (cocaine metabolite), methadone, opiates as class, oxycodone, phencyclidine, and tetrahydrocannabinoids. Iron concentration was normal at 87 mcg/dL.Over the first hour of management,...

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Cyanide Poisoning

Cited by 130 publications

References 44 publications

Pseudomonas aeruginosa, cyanide accumulation and lung function in CF and non-CF bronchiectasis patients

Pseudomonas aeruginosa, cyanide accumulation and lung function in CF and non-CF bronchiectasis patients

Intoxicação espontânea e experimental por tifton 68 (Cynodon nlemfuensis Vanderyst) em bovinos

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

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