27/01/2023
HCN poising
Causes:
• Cyanide poisoning results from exposure to a source of cyanide ions (CN-). Cyanides are found in plants, fumigants, soil fertilizers and rodenticides ( eg calcium cyanomide ) ,soil sterilizers, and salts used in industrial processes, such as gold mining, metal cleaning and electroplating, photographic processes, and others. Hydrogen cyanide is also known as prussic acid, and cyanide salts liberate cyanide gas in the presence of acids (eg, in the stomach).
• Toxicity can result from improper or malicious use ,but in the case of livestock,the most frequent cause is ingestion of plants that contain cyanogenic glycosides .These Include Triglochin maritime( arrow grass)
,sorghum spp (Sudan grass, common sorghum ),Prunus spp ( apricot,peach) ,apple ( Pyrus malus ) Zea mays ( corn) and Linum spp (flax).
• The acute lethal dosage of hydrogen cyanide (HCN) in most animal species is ~2 mg/kg of body weight. Plant materials containing ≥200 ppm of cyanogenic glycosides are dangerous. Cyanide poisoning is often a component of smoke inhalation poisoning.
There are four main syndromes in animals:
• Classical acute cyanide poisoning is when CN- binds to, and inhibits, the ferric (Fe3+) heme moeity form of mitochondrial cytochrome c oxidase (synonyms: aa3, complex IV, cytochrome A3, EC 1.9.3.1). This blocks the fourth step in the mitochondrial electron transport chain (reduction of O2 to H2O), resulting in the arrest of aerobic metabolism, systemic hypoxia, and death from histotoxic anoxia. Tissues that heavily depend on aerobic metabolism such as the heart and brain are particularly susceptible to these effects.
• Chronic cyanide poisoning-related hypothyroidism is due to disruption of iodide uptake by the follicular thyroid cell sodium-iodide symporter by thiocyanate, a metabolite in the detoxification of cyanide.
• Chronic cyanide and cyanide metabolite (e.g, various glutamyl beta-cyanoalanines)-associated neuropathy toxidromes, which include diseases such as sorghum cystitis ataxia syndrome in horses, as well as various cystitis ataxia syndromes in cattle, sheep, and goats
• Chronic cyanogenic glycoside exposure (notably from Sorghum spp) -associated musculoskeletal teratogenesis (ankyloses or arthrogryposes) and abortion.
Clinical Findings:
• In acute cyanide poisoning Signs generally occur within 15–20 minutes to a few hours after animals consume toxic forage, and survival after onset of clinical signs is rarely >2 hours.
• Excitement can be displayed initially, accompanied by rapid respiration rate. .
• Dyspnea follows shortly, with tachycardia.
• The classic “bitter almond” breath smell may be present.
• Sudden development of bloat(rumen distension).
• Salivation, excess lacrimation, and voiding of urine and f***s may occur. Vomiting may occur, especially in pigs..
• Muscle fasciculation is common and progresses to generalized spasms and coma before death.
• Animals may stagger and struggle before collapse. In other cases, sudden unexpected death may ensue.
• Mucous membranes are bright red but may become cyanotic terminally. Venous blood is classically described as “cherry red” because of the presence of high venous blood pO2; however, this color rapidly changes after death.
• Cardiac arrhythmias are common due to myocardial histotoxic hypoxia. Death occurs during severe asphyxial convulsions.
Differential Diagnosis:
• Nitrate or nitrite
• Urea
• Organophosphates
• Carbamates
• Chlorinated hydrocarbon pesticides
• Toxic gases (carbon monoxide and hydrogen sulfide)
• Enterotoxemia (over eating disease)
• As well as infectious or noninfectious diseases and other toxidromes that cause sudden death
Treatment:
• Immediate treatment with oxygen and Hydroxocobalamin (vitamin B12a ) is the gold-standard antidote for cyanide because of its effectiveness and low toxicity. Suggested dosage is 70 mg/kg, infused IV over 15 minutes, repeated as necessary.
• Methylene blue if diagnosis is in doubt (signs are similar to those of nitrate poisoning)
• Removal from the source of exposure
• Classically, various nitrites have been used for this purpose; eg, inhaled amyl nitrite followed by IV injection of a nitrite salt (typically sodium nitrite) has been used to rapidly induce methemoglobinemia.
• The contents of one 0.3-mL vial of amyl nitrite should be inhaled by the animal as soon as possible after exposure, followed by an IV infusion of sodium nitrite (10 g/100 mL of distilled water or isotonic saline; 20 mg/kg body weight) over 3–4 minutes. Nitrite treatment is then followed by a slow IV injection of sodium thiosulfate (20% w/w) at ≥500 mg/kg.
• Sodium nitrite therapy may be carefully repeated at 10 mg/kg, every 2–4 hours or as needed.