Normal levels can be up to 10 jgml while lethal levels range from 50 to 200 jgml Management and treatment of cyanide poisoning

Once cyanide poisoning is diagnosed, the main goals of treatment are preventing cellular anoxia as well as inactivating and removing the cyanide. This is accomplished by aggressive cardiorespiratory support with 100 per cent oxygen and, if symptoms are severe, administration of antidote (e.g. Eli Lilly Cyanide Antidote Kit). Health care providers should not inhale the victim's expired air nor perform mouth to mouth resuscitation. The victim's clothes and skin can be contaminated; thus proper clothes removal and washing of the skin must occur.

Mechanical ventilation may be necessary for initial management. Oxygen increases the rate of conversion of reduced cytochrome oxidase to the oxidized form, allowing the electron transport chain to function again (S§j.kowskLan.d..Penney 1994). The use of hyperbaric oxygen is controversial, but may be beneficial (GosseL

and Bricker 1990), particularly with concomitant CO poisoning. Sodium bicarbonate should be administered if the pH is below 7.16. Anticonvulsants are used to treat any seizures that may develop. In addition, antiarrhythmics and vasopressors may be necessary for corresponding arrhythmias or hypotension. Gastric lavage with activated charcoal may be beneficial if administered shortly after oral ingestion of cyanide. Emesis induction is contraindicated because of the possibility of rapidly induced unconsciousness, coma, or aspiration.

Cyanide antidotes (T§..b]e.,.2) include amyl nitrite, sodium nitrite, and sodium sulfate. Nitrites act by inducing the formation of methemoglobin, which has a stronger affinity for cyanide than cytochrome oxidase. This reaction forms cyanomethemoglobin which protects from further cyanide toxicity. It is believed that nitrites may have an additional protective mechanism. It is suggested that methemoglobin be kept between 25 and 40 per cent ( Rindone...,a.D.d Sloan® 1992) to prevent adverse effects, such as cyanosis. These levels should be followed serially to prevent toxicity. If severe methemoglobin toxicity develops, the treatment of choice is 1 to 2 mg/kg of methylene blue. It must be used with extreme caution because of its potential to release cyanide. A serious adverse effect associated with nitrite usage is the production of severe hypotension with rapid infusion and subsequent cardiovascular collapse.

1. fiF)1WH pii'i ¿JB :'Lr>"+ri anI rtufed lor i :•"]!] E- aw*


2. Wen 'V j«>fM a ftaJate HT|< M soi/s MKI SCIF^W HOTIMS*, Hifotii (iimwi^iwi thtHi ff&xt ^«hsmgfetwwM ¿i tw ¿m^Ma 27V LMI

1 Safin kJULs. a lulif Am. ¿ ¿i- fse-« si lí IV

4. t in Zh fyrwpi reappear et pens. t art 3 are upiaM


Table 2 Administration of the Eli Lilly Cyanide Antidote Kit

Sodium thiosulfate donates sulfur which enhances rhodanase activity by increasing the rate of conversion of cyanide to sodium thiocyanate ( Rindonejod Slo.a.Q,e

1.9.92). The coadministration of chlorpromazine or colbaltous chloride potentiates the effectiveness of sodium thiosulfate ( and Sodium thiocyanate toxicity resembles cyanide toxicity of the central nervous system. Symptoms include muscle weakness, nausea, vomiting, hallucinations, twitching, coma, and death. Sodium thiocyanate is mildly neurotoxic (e.g. tinnitus, miosis, hyper-reflexia) at 1 mmol/l and may be life threatening at levels three to four times higher. Prolonged exposure may produce reversible hypothyroidism because of competition with iodine.

Other cyanide poisoning treatments are available. With hydroxocobalamin (vitamin B 12a), cyanide replaces the hydroxy group to form cyanocobalamin (vitamin B12) which is subsequently eliminated via the kidney. At therapeutic doses (20-70 mg/kg), vitamin B 12a does not change mean blood pressure, left ventricular end-diastolic pressure, or the PR or QT intervals of the ECG. Hydroxocobalamin is a safe, rapid, and powerful antidote for cyanide poisoning which is recommended during the prehospital stage; however, its routine use is impractical and expensive, particularly for long-term use for nitroprusside prophylaxis ( Rindone and Sioane.1992).

Hydroxocobalamin is not yet available in the United States (

A variety of drugs remain experimental or are not approved for use in the United States. In Germany, 4-dimethylaminophenol hydrochloride (4-DMAP) is used; its action is similar to that of nitrites. Although the production of methemoglobin is faster than with sodium nitrite, efficacy is no better than with nitrites. 4-DMAP does not produce the same profound hypotension as nitrites, but has been associated with renal failure in animals. Hydroxylamine is also a rapid methemoglobin former, but it is less toxic than 4-DMAP and provides anticonvulsive action by augmenting g-aminobutyric acids in the brain, which may be decreased in cyanide poisoning.

Cobalt EDTA, a very effective treatment used in the United Kingdom, can cause severe side-effects, particularly when cyanide poisoning does not exist. Metabolic acidosis, hypotension, massive edema, and ventricular tachycardia have been found in animal and human studies. Because of cobalt's side-effects (diaphoresis, angina, and vomiting), cobalt EDTA should be reserved only for severe cyanide poisoning.

Administration of a-ketoglutarate in two doses of 50 mg/kg 20 min apart has been demonstrated to increase the 50 per cent lethal dose (LD 50) for nitroprusside 1.7 times and to decrease cyanide by 30 per cent. Sodium thiosulfate 1 g/kg alone increased LD 5C 5.5 times with an 88 per cent reduction in cyanide. The coadministration of a-ketoglutarate and sodium thiosulfate increased the LD 50 by 6.9, i.e. an overall cyanide reduction of 98 per cent. Cyanide and a-ketoglutarate form a-ketoglutaric-cyanhydrin, which is subsequently excreted through the kidneys. Pyruvate slightly potentiates the antidotal effect of thiosulfate, but not that of nitrites.

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