Review article: Management of cyanide poisoning

Abstract

Cyanide poisoning is uncommon, but generates interest because of the presumed utility of an antidote immediately available in those areas with a high risk of cyanide exposure. As part of its regular review of guidelines, the Australian Resuscitation Council conducted a systematic review of the human evidence for the use of various proposed cyanide antidotes, and a narrative review of the relevant pharmacological and animal studies. There have been no relevant comparative or placebo-controlled human trials. Nine case series were identified. Treatment with hydroxocobalamin was reported in a total of 361 cases. No serious adverse effects of hydroxocobalamin were reported, and many patients with otherwise presumably fatal poisoning survived. Sodium thiosulphate use was reported in two case series, similarly with no adverse effects. Treatment with a combination of sodium nitrite, amyl nitrite and sodium thiosulphate was reported in 74 patients, with results indistinguishable from those of hydroxocobalamin and sodium thiosulphate. No case series using dicobalt edetate or 4-dimethylaminophenol were identified, but successful use in single cases has been reported. Hydroxocobalamin and sodium thiosulphate differ from alternatives in having negligible adverse effects, and on the basis of current evidence are the antidotes of choice. The indications for the use of an antidote, the requirements for supportive care and a recommended approach for workplaces where there is a risk of cyanide poisoning are presented.

Disulfiram inhibition of cyanide formation after acetonitrile poisoning

“…11,12 The same combination has been used successfully in a patient after severe poisoning with propionitrile, another cyanogenic compound. 13 The duration of antidote treatment should be sufficiently long because of the slow elimination of acetonitrile.…”

Efficacy of First-Line Sodium Thiosulfate Administration in a Case of Potassium Cyanide Poisoning

“…Cyanide exerts its toxicity by binding to cytochrome c oxidase a3, causing a cytotoxic hypoxia [2][3][4]7]. As a result the aerobic respiration is paralyzed with a buildup of lactate in mitochondria and rapid impairment of vital functions [2][3][4]7].…”

“…As a result the aerobic respiration is paralyzed with a buildup of lactate in mitochondria and rapid impairment of vital functions [2][3][4]7]. Clinical features include loss of consciousness, respiratory abnormalities, cardiovascular dysfunction, and severe hypotension progressing rapidly to cardio-respiratory arrest [2,[5][6][7]. In this frame, diagnosis of cyanide poisoning requires a careful correlation of the patient medical history, physical examination, and laboratory findings as severe lactate acidosis with increased anion gap [6].…”

“…Cyanide is a potent and fast acting poison, available in gaseous forms, poorly water-soluble salts and water-soluble potassium or sodium cyanide salts [1][2][3][4]. Cyanide exposure may occur following accidental enclosed fire-smoke inhalation or ingestion of salts.…”

“…Cyanide exposure may occur following accidental enclosed fire-smoke inhalation or ingestion of salts. Cyanide ingestion is mainly related to accidental events, deliberate self-harm or attempted homicides [1][2][3][4]. The ingestion of a minimal amount of potassium cyanide salts (200-300 mg) may cause death within minutes [1,5].…”