Cyanide poisoning is an acute and often fatal poisoning, most commonly observed in ruminant species. Although animals are often found deceased, clinical signs can include dyspnea, muscle fasciculations, and hyperemic mucous membranes. Diagnosis of poisoning includes testing of suspect material, GI content, and biological samples. A combination of sodium nitrite followed by sodium thiosulfate can be used to treat poisonings, but because of the rapid onset of clinical signs and death, treatment might not be possible or practical.
Cyanide poisoning (cyanide toxicosis) results from exposure to a source of cyanide ions (CN-). Four main syndromes associated with cyanide poisoning are recognized: acute cyanide poisoning, chronic cyanide poisoning-related hypothyroidism, chronic cyanide and cyanide metabolite-associated neuropathy toxidromes, and chronic cyanogenic glycoside exposure—associated musculoskeletal teratogenesis.
Acute cyanide poisoning is the most common syndrome. The chronic forms are rarely observed or have been induced only in research settings.
In acute cyanide poisoning, CN- binds to, and inhibits, the ferric (Fe3+) heme moiety form of mitochondrial cytochrome-c oxidase (synonyms: aa3, complex IV, cytochrome A3, EC 7.1.1.9). 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.
Cyanide also binds to other heme-containing enzymes, such as members of the cytochrome P450 family, and to myoglobin. However, these tissue cyanide "sinks" do not provide sufficient protection from histotoxic anoxia.
Under conditions of low-level exposure, mammals detoxify approximately 80% of ingested cyanide to thiocyanate via mitochondrial rhodanese (1). Thiocyanate is then largely excreted in urine. Often, the rate of the rhodanese pathway is limited by the availability of thiosulfate; also notably, dogs have lower overall rhodanese activity than other species.
Minor but toxicologically important pathways of detoxification in mammals include the combination of cyanide with hydroxocobalamin (vitamin B12a) to yield cyanocobalamin , and the nonenzymatic combination of cyanide with cysteine to form beta-thiocyanoalanine, which is converted to 2-iminothiazolidine-4-carboxylic acid and subsequently excreted. Small amounts of beta-thiocyanoalanine are also excreted in saliva.
Dietary levels of sulfur amino acids (L-cysteine and L-methionine) strongly influence the rate of detoxification of cyanide, and low dietary intakes are associated with higher blood cyanide concentrations, particularly under conditions of chronic low-level exposure. Dietary sulfur and sulfur amino acid intake are known to strongly affect the neurological toxidromes associated with chronic cyanide/cyanogenic glycoside exposure in humans.
Although cyanide poisoning can clinically resemble nitrate and nitrite poisoning, the mechanism of action of acute cyanide poisoning, involving iron and eventual hypoxia and anoxia does not include the formation of methemoglobin associated with nitrate and nitrite poisoning.
The acute lethal oral dosage of hydrogen cyanide (HCN) in most animal species is approximately 2 mg/kg (2, 3). Plant materials containing ≥ 200 ppm on a wet-weight (as-fed) basis of cyanogenic glycosides are dangerous (4).
Cyanide poisoning is often a component of smoke inhalation poisoning.
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 low-level cyanide/cyanogenic glycoside exposure is associated with increased exposure to the cyanide metabolite thiocyanate. Under conditions of thiocyanate overload, thiocyanate acts as a competitive inhibitor of thyroid follicular cell iodine uptake by the sodium-iodide symporter. This results in decreased iodination of tyrosine, decreased triiodothyronine (T3) synthesis, increased blood thyrotropin concentration, goiter, and hypothyroidism. Similar effects occur with some plant glucosinolates (goitrogenic glycosides). Selenium deficiency appears to enhance these effects.
Chronic cyanide and cyanide metabolite (eg, various glutamyl beta-cyanoalanines)–associated neuropathy toxidromes 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 involves ankyloses or arthrogryposes and abortion.
Etiology of Cyanide Poisoning
Cyanide is found in a variety of forms, such as hydrogen cyanide (HCN or prussic acid), potassium cyanide (KCN), and sodium cyanide (NaCN). Plants, industrial compounds, pesticides, and building fires all serve as potential sources of cyanide.
Plants in Etiology of Cyanide Poisoning
The most frequent cause of cyanide poisoning in livestock species is the ingestion of plants that either constitutively contain cyanogenic glycosides or are induced to produce cyanogenic glycosides and cyanolipids as a protective response to environmental conditions (plant cyanogenesis).
Plant cyanogenesis is a common process and has been documented in > 2,500 plant species distributed > 110 families of ferns, gymnosperms, and angiosperms. Of these plants, approximately 300 species are potential causes of acute and chronic cyanogenic glycoside poisoning, and there are approximately 75 cyanogenic glycosides (all of which are O-beta-glycosidic derivatives of alpha-hydroxynitriles) (5). See the table .
Cyanogenic Glycoside–Containing Plants of Veterinary Importance
Scientific Name | Common Name |
|---|---|
Sorghum spp | Johnson grass, Sudan grass, milo |
Acacia greggii | Guajillo |
Amelanchier alnifolia | Saskatoon serviceberry |
Linum spp | Linseed/flax |
Sambucus nigra | Elderberry |
Suckley suckleyana | Poison suckleya |
Triglochin maritima T palustris | Seaside arrowgrass Marsh arrowgrass |
Manihot esculenta | Cassava |
Prunus sppa | Apricot, peach, chokecherry, pin cherry, wild black cherry, ornamental cherry, peach, nectarine, almond, bird cherry, blackthorn, cherry laurel |
Nandina domestica | Heavenly bamboo |
Phaseolus lunatus | Lima bean |
Vicia sppa | Vetches |
Lotus sppa | Trefoils |
Trifolium sppa | Clovers |
Zea mays | Corn |
Eucalyptus spp | Gum trees |
Hydrangea spp | Hydrangeas |
Pteridium aquilinum | Bracken fern |
Bahia oppositifolia | Oppositeleaf bahia |
Chaenomeles spp | Flowering quinces |
a Commercial orchard or pasture species specifically bred for low cyanide content. | |
Plant cyanogenesis in response to environmental stressors is an important part of the etiological basis and risk of acute cyanogenic glycoside poisoning. Within plants, amino acids not used for protein synthesis can be metabolized to alpha-hydroxynitriles and then to cyanogenic glycosides. Plants are protected from the potential adverse effects of cyanogenic glycosides by two features:
Cyanogenic glycosides are largely found within cell vacuoles.
The detoxifying enzyme beta-cyanoalanine synthase is present (and is responsible for production of some of the cyanide derivatives putatively involved in chronic cyanide-associated neurological toxidromes).
Even so-called acyanogenic plants can become toxic under appropriate environmental circumstances. Environmental conditions that damage relevant plant species, decrease protein synthesis, enhance the conversion of nitrate to amino acids in the presence of decreased protein synthesis, and/or inhibit beta-cyanoalanine synthase potentially increase the risk of cyanogenesis. Relevant environmental factors include the following:
crushing
wilting
freezing
high environmental temperatures
herbicide treatment
water stress
cool and moist growing conditions
nitrate fertilization
high soil nitrogen:phosphorus ratios
soil phosphorus deficiency
low soil sulfur (decreases detoxification of cyanogenic glycosides to thiocyanates within plants)
insect attack
various plant diseases
Herbicide treatment of plants is important in that it may also increase plant palatability.
Crushing and mastication of potentially cyanogenic plants are important in development of the acute toxidrome, because these actions release cyanogenic glycosides from plant cell vacuoles and expose them to catabolism by beta-glucosidase and hydroxynitrile lyase present in the plant cell cytosol.
Aside from plant cyanogenesis, age and growth rate should also be taken into consideration. Young, rapidly growing areas of plants and regrowth after cutting often have high cyanogenic glycoside content. For example, rapidly growing Sorghum spp are often hazardous until they reach approximately 60 cm (24 inches) in height. However, this is no guarantee of safety, and if there is any doubt regarding cyanogenic potential, samples of potential forage should be tested.
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Plant seeds and leaves typically have higher cyanogenic potential, whereas the fleshy parts of fruits generally have low levels. Drying as a result of drought often increases the cyanogenic potential of plants, whereas drying over a period of time and ensiling decreases cyanide content by approximately 50% (6).
Because of their physiology, ruminants are particularly susceptible to cyanogenic plants. Beta-glucosidase and hydroxynitrile lyase are also present in rumen microbiota, and a rumen pH of approximately 6.5–7 favors conversion of cyanogenic glycosides to cyanide. Ruminants on high-energy grain rations are somewhat less susceptible because their lower rumen pH (approximately 4–6) decreases the formation of cyanide. Consumption of water before grazing on cyanogenic pastures appears to increase the risk.
Monogastric animals with low stomach pH are also somewhat less susceptible to cyanogenic glycoside poisoning. However, these factors do not guarantee immunity from poisoning.
Although not often reported, grazing of sorghum species for an extended duration presents a potential risk of chronic poisoning in horses, cattle, and sheep. Neurological and urinary signs predominantly occur in horses whereas teratogenic effects are more likely to be observed in cattle and sheep.
The suspected agents associated with sorghum intoxication include cyanogenic glycosides, hydrocyanic acid, lathyrogenic nitriles, and nitrate. Consumption of sorghum seeds is not known to produce clinical complications. Low dietary sulfur and/or sulfur amino acid intake and possibly other nutritional deficiencies may also play a role in sorghum-associated intoxication.
Insects and Invertebrates in Etiology of Cyanide Poisoning
A number of insect and invertebrate species are also able to synthesize hydrogen cyanide or sequester hydrogen cyanide derived from the cyanogenic glycosides of their plant hosts. These species are potentially hazardous food sources for exotic pets and include US eastern tent caterpillars (Malacosoma americanum); burnet moths (Zygaena spp), which feed on bird's-foot trefoils; and certain centipedes and millipedes.
Industrial Compounds and Pesticides in Etiology of Cyanide Poisoning
Fumigants, soil sterilizers, fertilizers (eg, cyanamide), and salts used in industrial processes (eg, for gold mining, metal cleaning, electroplating, and photographic processes) are all potential sources of cyanide poisoning. Such salts used in industry liberate cyanide gas in the presence of acids (eg, in the stomach).
Cyanide salt formulations are still used as insecticides. Such salt formulations have been implemented as an illegal method of fishing and/or collecting aquarium fish species (cyanide fishing).
A number of countries use cyanide preparations, such as NaCN, as control agents for pest and predator species. For example, cyanide fumigants may be used to kill rodents and insects in the holds of ships, storage warehouses, or railway cars; NaCN capsules are used in single-dose ejector devices to control wild canids that prey on livestock, which can result in exposure to nontarget species, including dogs (7). The use of cyanide as a pesticide agent depends on regulations in each country.
Fires and Combustibles in Etiology of Cyanide Poisoning
Fires and the combustion of various materials—including polyacrylonitriles (plastics), wool, silk, keratin, polyurethane (insulation/upholstery), melamine resins (household goods), and synthetic rubber—also serve as potential sources of poisoning from the release of cyanide gas. Because cyanide is a notable component of both engine exhaust and tobacco, poisoning is a common component of smoke inhalation toxidromes.
Clinical Findings of Cyanide Poisoning
Clinical signs of acute cyanide poisoning 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. Animals can initially display excitement and tachypnea, followed by dyspnea and tachycardia. The classic "bitter almond" breath smell might be present; however, not all people can detect this smell.
Salivation, excess lacrimation, and voiding of urine and feces can occur. Direct irritation of the GI tract can occur if cyanide salts are ingested. Vomiting can occur, especially in pigs.
Muscle fasciculation is common and progresses to generalized spasms and coma before death. Animals may stagger and struggle before collapse. Because of acute onset, clinical signs might not be observed, and animals are often found dead. Mucous membranes are bright red but can become cyanotic terminally. Serum ammonia and neutral and aromatic amino acid concentrations are typically increased.
Cardiac arrhythmias are common due to myocardial histotoxic hypoxia. Death occurs during severe asphyxial convulsions. The heart can continue to beat for several minutes after struggling, and breathing stops. The elimination half-life of cyanide in dogs is reported to be 19 hours (8), so the prognosis for recovery without therapeutic intervention is grave; it would take more than 4 days to eliminate > 95% of the cyanide present.
Because of natural elimination of cyanide at low doses, chronic cyanide poisoning resulting from accumulation of cyanide over an extended period of time is rare. Most reports of chronic cyanide poisoning involve research animals.
Hypothyroidism has been associated with chronic cyanogenic glycoside intoxication.
Cystitis ataxia toxidromes associated with chronic cyanide and cyanide metabolite ingestion are typically associated with posterior ataxia or incoordination that can progress to irreversible flaccid paralysis, urinary incontinence, hindlimb urine scalding, and alopecia. Late-term abortion and musculoskeletal teratogenesis can also occur but are rare. Cystitis ataxia toxidromes and reproductive complications have been associated with consumption of Sorghum spp.
Lesions in Cyanide Poisoning
In cases of acute cyanide poisoning, venous blood is classically described as bright cherry red; however, this color rapidly fades after death or on exposure to the atmosphere.
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Whole blood clotting might be slow or not occur.
Mucous membranes can also be pink initially, then become cyanotic after respiration ceases.
The rumen may be distended with gas; in some cases the odor of bitter almonds might be detected after opening but is not detectable by all individuals.
Agonal hemorrhages of the heart may be evident. Liver, serosal surfaces, tracheal mucosa, and lungs can be congested or hemorrhagic; some froth might be present in respiratory passages. Cyanide also binds to iron (both Fe2+ and Fe3+) present in myoglobin (although this occurs more slowly than the binding to cytochrome-c oxidase and, hence, is not protective); this can result in a generalized dark coloration of skeletal muscle.
Neither gross nor histological lesions are consistently observed.
Goiter can be present in cases of chronic cyanide poisoning. Cystitis ataxia toxidromes are characterized by opportunistic bacterial cystitis with or without pyelonephritis and diffuse nerve fiber degeneration in the lateral and ventral funiculi of the spinal cord and brainstem. Hindlimb urine scalding and alopecia can be present. Death, although uncommon, is often associated with pyelonephritis.
Multiple foci of degeneration or necrosis, particularly of the white matter, may be observed in the CNS of dogs chronically exposed to sublethal amounts of cyanide. Such neurological lesions have not been reported in livestock. In addition, degeneration of renal epithelium and vacuolation of colloid of thyroid follicles can also be observed in dogs.
Diagnosis of Cyanide Poisoning
Cyanide concentration measurement
Feed analysis
Histological evaluation
Appropriate history, clinical signs, postmortem findings, and demonstration of cyanide (as CN-) in rumen/gastric contents or other diagnostic specimens support a diagnosis of cyanide poisoning.
Veterinarians should be aware of the possible need to use appropriate personal protective equipment, including a respirator, when collecting samples that could liberate cyanide gas (eg, rumen contents and rumen gas cap).
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Because of the rapidly fading color of "bright cherry" blood, appearance of blood alone should not be used to definitively diagnose cyanide poisoning.
A rapid qualitative and presumptive diagnosis can be made by testing representative plant samples or rumen/gastric contents using the picric acid paper test or by collecting rumen gas cap samples by trocarization and testing with a cyanide gas detection tube or other cyanide gas detection systems. Negative results with such rapid presumptive tests do not completely exclude the possibility of cyanide poisoning.
Although cyanide concentrations can be determined in various biological media from poisoned animals, often the most reliable method of diagnosis is determination of cyanide (and/or cyanide glycoside and/or relevant cyanide metabolite) concentrations in food and gastric contents. Suitable specimens include the suspected food source, rumen/gastric contents, samples of the rumen gas cap, heparinized whole blood, liver, and muscle. Communication with the laboratory should be considered to establish testing capabilities for cyanide or its metabolites.
Antemortem whole blood is preferred; other specimens should be collected as soon as possible after death, preferably within 4 hours. Specimens should be sealed in an airtight container, refrigerated or frozen, and submitted to the laboratory without delay. When cold storage is unavailable, immersion of specimens in 1–3% mercuric chloride has been satisfactory. The rationale for using liver as a diagnostic sample is that cyanide binds to the Fe3+ form of cytochrome P450 and other heme-containing metabolic enzymes. The rationale for using skeletal muscle is that cyanide will bind to the iron moiety in myoglobin. Cyanide can also be detected in fresh brain tissue (9).
Measurement of the metabolite of cyanide, thiocyanate, within serum may reveal increased concentrations after intoxication.
Hay, green chop, silage, or growing plants containing> 200 ppm cyanide as HCN on an as-fed basis are very dangerous as animal feed (4). Forage containing < 100 ppm HCN, wet weight, is usually safe to pasture. Analyses performed on a dry-weight basis have the following criteria: < 500 ppm HCN is considered safe, 500–750 ppm HCN is suspect, and> 750 ppm HCN is hazardous and should not be the only source of feed for animals (10).
Expected cyanide concentration in the blood of most animal species is usually < 0.5 mcg/mL (11). Minimal lethal blood concentration is approximately 3 mcg/mL or more. Cyanide concentrations in muscle are similar to those in blood, but concentrations in liver are generally lower than those in blood. In dogs, whole blood cyanide concentrations can be 4–5 times greater than serum concentrations because of binding to ferric ions and sequestration in RBCs. Cyanide concentrations > 1 ppm within tissues are considered to be clinically relevant (12).
Feed analysis and histological evaluation of neural tissue are the gold standard methods of diagnosis of cyanide-associated neuropathy toxidromes. For chronic cyanogenic glycoside–associated teratogenic syndromes and hypothyroidism, relevant diagnostic modalities include feed analysis, postmortem evaluation of fetal remains, and histological evaluation of the thyroid.
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Differential diagnoses include poisonings by the following:
toxic gases (carbon monoxide and hydrogen sulfide)
toxic plants (yew and oleander)
infectious or noninfectious diseases and other toxidromes that cause sudden death
Treatment and Control of Cyanide Poisoning
Removal from source of exposure
Administration of sodium nitrite followed by sodium thiosulfate
Methylene blue if diagnosis is uncertain (ie, for nitrate poisoning)
Hydroxocobalamin and oxygen supplementation
In cases of acute cyanide poisoning, immediate treatment is necessary. However, given the acute nature of cyanide intoxications, treatment might not be possible or practical.
Animals should be removed from the source of exposure. Removal from the source of exposure is the main clinical priority in chronic cyanide-associated toxidromes.
Activated charcoal can be considered for decontamination of the GI tract but is not highly effective. However, because of cyanide's toxicity, one dose of activated charcoal could be beneficial in small, monogastric animals if administered quickly after oral exposure.
Hydroxocobalamin (vitamin B12a) is the gold standard antidote for cyanide because of its effectiveness and low toxicity. It does not further compromise tissue oxygenation (methemoglobin formation) or induce hypotension (profound vasodilation). Hydroxocobalamin detoxifies cyanide by binding to it and forming cyanocobalamin (ie, a decoy receptor approach), which is then excreted in urine. The suggested dosage is at least 70 mg/kg, infused IV over 15 minutes, repeated as necessary (13). In dogs, administration of hydroxocobalamin (75–150 mg/kg, IV over 7.5 minutes, once) with oxygen supplementation has been observed to improve survivability (14). In swine, administration of hydroxocobalamin can be attempted (65 mg/kg, IV, over 2–3 minutes) (15).
Hydroxocobalamin produces chromaturia (which can result in false urinalysis results), as well as infusion site reactions, GI upset, pruritus, and dysphagia. Hydroxocobalamin is costly, which might limit its use in herd and flock animals.
Dimethyl trisulfide (15% solution, 33.3–42.9 mg/kg, IM, once) in rabbits (16) and (40% solution, 82.5 mg/kg, IM, once) in swine (17) has been experimentally examined as an additional potential treatment for acute cyanide poisoning.
When available, oxygen should be used to supplement antidotal therapy, especially in small animals. Hyperbaric oxygen therapy (100% oxygen breathed intermittently at a pressure > 1 atmosphere absolute) causes an above-normal PaO2 and markedly increases the amount of oxygen dissolved in plasma. Oxygen-dependent cellular metabolic processes benefit from heightened oxygen tension in capillaries and enhanced oxygen diffusion from capillaries to critical tissues (18).
The older approach to the treatment of acute cyanide poisoning is to break the cyanide–cytochrome-c oxidase bond and reestablish the mitochondrial electron transport chain. One way to accomplish this is by inducing methemoglobinemia through the use of a nitrite compound such as amyl nitrite alone (0.3 mL vial, inhaled), or a slow IV infusion of a nitrite salt (typically sodium nitrite at 10 g/100 mL of distilled water or saline solution [0.9% NaCl]; 10–20 mg/kg, IV, over 7.5 minutes) followed by sodium thiosulfate (413 mg/kg, IV) (19). If using amyl nitrite, the number of vials needed may be dependent on animal size (20). Methemoglobin acts as a high-affinity decoy chemical receptor for cyanide and forms cyanmethemoglobin. Cyanmethemoglobin can then be detoxified by rhodanese to thiocyanate.
Because the rhodanese-mediated detoxification of cyanide to thiocyanate is usually capacity- and rate-limited by the availability of sulfur donors, the initial treatment with nitrites is usually followed up by a slow injection of sodium thiosulfate (20% w/v) at ≥ 413 mg/kg, IV, over 2.5 minutes (19). Sodium nitrite therapy may be carefully repeated at 10 mg/kg, IV, every 2–4 hours or as needed.
Ideally, decisions regarding repeated treatment with nitrites should consider the degree of methemoglobinemia present. Thiosulfate is generally well tolerated; however, vomiting and hypotension can occur. The thiosulfate injection can be repeated if necessary.
Oral dosing with sodium thiosulfate into the rumen and/or stomach has also been suggested because the reaction between thiosulfate and cyanide can also occur nonenzymatically, and this can decrease any ongoing production of cyanide in the rumen/stomach environments. Notably, thiosulfate treatment alone (sodium thiosulfate at ≥ 500 mg/kg, IV, plus 30 g/cow, PO, with the objective of facilitating the detoxification of any remaining HCN in the rumen) has been successful in some cases (10). Thiosulfate treatment should ideally be preceded by nitrite induction of methemoglobinemia in cases of confirmed cyanide poisoning; however, because thiosulfate is generally well tolerated, it is often administered alone in situations when cyanide exposure is likely but unconfirmed (eg, smoke inhalation or exposure to fires).
The combination of hydroxocobalamin (150 mg/kg, IV) and sodium thiosulfate (413 mg/kg, IV) could work as another potential treatment (19, 21).
Administration of thiosulfate alone (> 500 mg/kg, PO) has been reported to increase survival of cyanide poisoning in swine (22). The combination of orally administered sodium thiosulfate and glycine has been found to improve survival outcomes and physiological parameters in experimentally induced cyanide poisoning in pigs (23). Sodium tetrathionate (2 mol/L solution, 18 mg/kg, IM, once) in swine has also been observed to improve survivability (24). Although experimentally successful, practical application of dimethyl trisulfide and sodium tetrathionate is limited by availability.
Because cyanide and nitrate/nitrite poisoning appear similar in nature, methylene blue may be used (4 mg/kg, IV) if the diagnosis is unclear so as to prevent exacerbating a potential nitrate poisoning through additional nitrite administration (25, 26). Methylene blue can also be used if other treatment options are limited or unavailable (27).
Prevention of Cyanide Poisoning
To prevent cyanide poisoning, the best step is to test suspect feed and pastures before allowing consumption. Cyanide concentration in sorghum decreases as the plant grows taller and matures. Therefore, to decrease danger from HCN poisoning, pasture and forage sorghums (eg, Sudan grass and sorghum-Sudan grass hybrids) should not be grazed until they are > 60 cm (24 inches) tall or testing has confirmed cyanide concentrations within acceptable limits (28).
To prevent gorging and rapid consumption of HCN that overwhelms excretion mechanisms, animals should be fed before first turning out to pasture. Animals should be turned out to new pasture later in the day; potential for HCN release is reported to be highest during early morning hours.
Free-choice salt and mineral with added sulfur might help protect against HCN toxicity.
Grazing should be monitored closely during periods of environmental stress (eg, drought or frost).
Abundant regrowth of sorghum can be dangerous; these shoots should be frozen and wilted before grazing. In the author's experience, grazing of sorghum species during animal movement between environments should also be avoided. Consumption of sorghum hybrids with low cyanogenic potential or restriction of access to sorghum grasses may limit the incidence of cyanide poisoning. Alternative feed sources, rotational grazing, and feeding of fully cured sorghum feeds will decrease cyanide exposure.
Green chop forces livestock to eat both stems and leaves, thereby decreasing problems caused by selective grazing. However, feeding of green chop also carries the risk of cyanide poisoning. Cutting height can be raised to minimize inclusion of regrowth.
Sorghum hay and silage usually lose ≥ 50% of HCN content during curing and ensiling processes (28). Free cyanide is released by enzyme activity and escapes as a gas. Rarely, hazardous concentrations of HCN can remain in the final product, especially if the forage had an extremely high cyanide content before cutting. Hay has been dried at oven temperatures for up to 4 days with no noteworthy loss of cyanide potential. Hay and silage should be analyzed before use whenever high prussic acid concentrations are suspected. Potentially toxic feed should be diluted or mixed with grain or forage that is low in prussic acid content to achieve safe concentrations in the final product.
Key Points
Manage grazing and feed conditions for environmental stress to minimize risk, and analyze feed before allowing consumption.
Hydroxocobalamin plus 100% oxygen supplementation should be administered as soon as possible after suspected cyanide poisoning.
Treatment should not be delayed for diagnostic confirmation.
Preventing exposure to potential sources of cyanide is critical and may be more feasible than treatment.
The prognosis for cases of chronic cyanide poisoning other than those associated with thyroid syndromes is guarded.
For More Information
Also see pet owner content regarding cyanide poisoning.
References
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