Cyanide intoxication

Sodium nitroprusside 0.25-10 mcg/kg/minute as IV infusion11 Immediate 1-2 minutes Nausea, vomiting, muscle twitching, sweating, thiocyanate and cyanide intoxication Most hypertensive emergencies use with caution with high intracranial pressure or azotemia... 

Much of the toxicological interest in cyanide relating to mammals has focused on its rapid lethal action. However, its most widely distributed toxicologic problems are due to its toxicity from dietary, industrial, and environmental factors (Way 1981, 1984 Gee 1987 Marrs and Ballantyne 1987 Eisler 1991). Chronic exposure to cyanide is correlated with specific human diseases Nigerian nutritional neuropathy, Leber s optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill etal. 1978 Way 1981 Sprine etal. 1982 Beminger et al. 1989 Ukhun and Dibie 1989). The effects of chronic cyanide intoxication are confounded by various nutritional factors, such as dietary deficiencies of sulfur-containing amino acids, proteins, and water-soluble vitamins (Way 1981). 

Cyanide poisoning is associated with changes in various physiological and biochemical parameters. The earliest effect of cyanide intoxication in mice seems to be inhibition of hepatic rhodanese... 

Attempted suicide by 39-year-old male, unknown amount of NaCN Severe tremors and progressive loss of muscle tone — representing the first case of cyanide intoxication with delayed onset of symptoms 9... 

Buzaleh, A.M., E.S. Vazquez, and A.M.C. Batlle. 1989. Cyanide intoxication. I. An oral chronic animal model. 

Casadei, E., P. Jansen, A. Rodrigues, A. Molin, and H. Rosling. 1984. Mantakassa an epidemic of spastic paraparesis associated with chronic cyanide intoxication in a cassava staple area of Mozambique. 2. Nutritional factors and hydrocyanic acid content of cassava products. Bull. World Health Org. 62 485-492. 

Grandas, F., J. Artieda, and J.A. Obeso. 1989. Clinical and CT scan findings in a case of cyanide intoxication. Movement Disord. 4 188-193. 

Yamamoto, K., Y. Yamamoto, H. Hattori, and T. Samori. 1982. Effects of routes of administration on the cyanide concentration distribution in the various organs of cyanide-intoxicated rats. Tohuku Jour. Exper. Med. 137 73-78. 

Several studies of occupational exposures and one study with a human subject were located. In the occupational exposures (summarized in Table 5- 3), neurological symptoms consistent with cyanide intoxication were demonstrated, but the likelihood of concomitant exposure to other chemicals could not be ruled out. For example, cleaners and cutting oils, as well as sodium and copper cyanide, may be present in electroplating operations (ATSDR 1997). The experimental human study involved the exposure of a single subject and a dog to a high concentration for a short exposure period. 

Blanc, P., M.Hogan and M.Mallin. 1985. Cyanide intoxication among silver-reclaiming workers. J. Amer. Med. Assoc. 253 367-371. 

Ibrahim et al. 1963). Aiken and Braitman (1989) determined that cyanide has a direct effect on neurons not mediated by its inhibition of metabolism. Consistent with the view that cyanide toxicity is due to the inability of tissue to utilize oxygen is a report that in cyanide-intoxicated rats, arterial p02 levels rose, while carbon dioxide levels fell (Brierley et al. 1976). The authors suggested that the low levels of carbon dioxide may have led to vasoconstriction and reduction in brain blood flow therefore, brain damage may have been due to both histotoxic and anoxic effects. Partial remyelination after cessation of exposure has been reported, but it is apparent that this process, unlike that in the peripheral nervous system, is slow and incomplete (Hirano et al. 1968). The topographic selectivity of cyanide-induced encephalopathy may be related to the depth of acute intoxication and distribution of blood flow, which may result in selected regions of vascular insufficiency (Levine 1969). 

In addition to binding to cytochrome c oxidase, cyanide inhibits catalase, peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, and succinic dehydrogenase activities. These reactions may make contributions to the signs of cyanide toxicity (Ardelt et al. 1989 Rieders 1971). Signs of cyanide intoxication include an initial hyperpnea followed by dyspnea and then convulsions (Rieders 1971 Way 1984). These effects are due to initial stimulation of carotid and aortic bodies and effects on the central nervous system. Death is caused by respiratory collapse resulting from central nervous system toxicity. 

Ardelt BK, Borowitz JL, Isom GE. 1989. Brain lipid peroxidation and antioxidant protectant mechanisms following acute cyanide intoxication. Toxicology 56 147-154. 

Brierley JB, Brown AW, Calverley J. 1976. Cyanide intoxication in the rat Physiological and neuropathological aspects. J Neurol Neurosurg Psychiatry 39 129-140. 

Burrow GE, Liu DHW, Way JL. 1973. Effect of oxygen on cyanide intoxication V. physiologic effects. J Pharmocol Exp Ther 184 739-748. 

Cannon EP, Leung P, Hawkins A, et al. 1994. Antagonism of cyanide intoxication with murine carrier erythrocytes containing bovine rhodanese and sodium thiosulfate. J Toxicol Environ Health 41(3) 267-274. 

Hirano A, Levine S. Zimmerman HM. 1968. Remyelination in the central nervous system after cyanide intoxication. J Neuropathol Exp Neurol 27 234-245. 

Isom GE, Burrows GE, Way JL. 1982. Effect of oxygen on the antagonism of cyanide intoxication-cytochrome oxidase, in vivo. Toxicol Appl Pharmacol 65 250-256. 

Isom GE, Way JL. 1974a. Cyanide intoxication Protection with cobaltous chloride. Toxicol Appl Pharmacol 24 449-456. 

Isom GE, Way JL. 1974b. Effect of oxygen on cyanide intoxication. VI. Reactivation of cyanide-inhibited glucose metabolism. J Pharmacol Exp Ther 189 235-243. 

Johnson JD, Isom GE. 1987. Peroxidation of brain lipids following cyanide intoxication in mice. Toxicology 46 21-28. 

Moore SJ, Norris JD, Ho IK, et al. 1986. The efficacy of ketoglutaric acid in the antagonism of cyanide intoxication. Toxicol Appl Pharmacol 82 40-44. 

Osuntokun BO. 1980. A degenerative neuropathy with blindness and chronic cyanide intoxication of dietary origin The evidence in the Nigerians. In Smith RL and Bababunmi EA, eds. Toxicology in the tropics. London Taylor and Francis, 16-52. 

Owasoyo JO, Iramain CA. 1980. Acetylcholinesterase activity in rat brain Effect of acute cyanide intoxication. Toxicol Lett 6 1-3. 

Persson SA, Cassel G, Sellstrom A. 1985. Acute cyanide intoxication and central transmitter systems. Fund Appl Toxicol 5 5150-5159. 

Schwartz C, Morgan RL, Way LM, et al. 1979. Antagonism of cyanide intoxication with sodium pyruvate. Toxicol Appl Pharmacol 50 437-441. 

Smith, et al. 1963. Neuropathological changes in chronic cyanide intoxication. Nature 200 179-181. 

Way JL, Burrows G. 1976. Cyanide intoxication Protection with chlorpromazine. Toxicol Appl Pharmacol 36 93-97. 

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