MSD

MSD
MANUAL
MANUAL
Veterinary
Manual
IN THIS TOPIC

PROFESSIONAL VERSION

Cyanide Poisoning
in Animals
By Rhian B. Cope, BVSc, BSc, PhD, DABT, DABVT,
FACTRA, Australian Pesticides and Veterinary Medicines
Authority, Australian Government

Reviewed/Revised Apr 2021

Etiology | Clinical Findings | Diagnosis |

Treatment, Control, and Prevention |
Key Points | For More Information

Cyanide poisoning results from exposure to a source of

cyanide ions (CN-). 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

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 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. The
acute lethal dosage of hydrogen cyanide
(HCN) in most animal species is ~2 mg/kg.
Plant materials containing ≥200 ppm of
cyanogenic glycosides are dangerous.
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 cyanide and cyanide metabolite

(eg, 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

Although cyanide levels 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 stomach

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 contents. Feed analysis and neurohistopathology are
the gold-standard method of diagnosis of cyanide-
associated neuropathy toxidromes. Likewise, feed
analysis and fetal pathology are the gold-standard
methods of diagnosis of chronic cyanogenic glycoside-
associated teratogenic syndromes.

Etiology of Cyanide Poisoning

in Animals
Various chemical forms of cyanides are found in plants,
fumigants, soil sterilizers, fertilizers (eg, cyanamide),
pesticides/rodenticides (eg, calcium cyanomide), 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).

Cyanide preparations are still used as control agents for

vertebrate pests, such as feral pigs, fox, Australian
brush-tailed possums, and other pest or predator
species in a number of countries.

Cyanide salts are still used as killing agents in

entomology and (illegally) as a method of fishing and/or
collection of aquarium fish species (ie, cyanide fishing).
Various nitriles can be metabolized in such a way that
cyanide is released.

Combustion of common polyacrylonitriles (plastics),

wool, silk, keratin, polyurethane (insulation/upholstery),
melamine resins (household goods), and synthetic
rubber results in the release of cyanide gas.

Car fires are notorious sources of cyanide exposure,

and cyanide is also a notable component of internal

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 combustion engine exhaust and tobacco smoke.
Cyanide poisoning is thus a common component of
smoke inhalation toxidromes.

Toxicity can result from accidental, improper, or

malicious use or exposure. However, in livestock
species, the most frequent cause of acute and chronic
cyanide poisoning is 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 >3,000
different plant species distributed over ~110 different
families of ferns, gymnosperms, and angiosperms. Of
these plants, ~300 species are potential causes of acute
and chronic cyanogenic glycoside poisoning, and there
are ~75 different cyanogenic glycosides (all of which are
O-beta-glycosidic derivatives of alpha-hydroxynitriles).

Plant species of notable veterinary importance include

Sorghum spp (Johnson grass, Sudan grass, and S bicolor,
the common cereal grain crop referred to as "sorghum"
or the synonyms durra, jowari, milo), Acacia greggii
(guajillo), Amelanchier alnifolia (western service berry),
Linum spp (linseeds and flaxes), Sambucus nigra
(elderberry), Suckley suckleyana (poison suckleya),
Triglochin maritima and T palustris (marsh arrow
grasses), Mannihot esculentum (cassava), all members of
the Prunus genus until proved otherwise (apricot, peach,
chokecherry, pincherry, wild black cherry, ornamental
cherry, peaches, nectarines, apricots, almonds, bird
cherries, black thorn, cherry laurels [commercial
orchard species are often specifically bred for low
cyanide content; however, ornamental members of this
genus are often highly poisonous]), Nandina domestica
(heavenly or sacred bamboo), Phaseolus lunatus (lima

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 beans), members of the Vicia genus until proved
otherwise (vetches; often, pasture species have been
bred for low cyanogenesis), Lotus spp (bird's-foot
treefoils; often, pasture species have been bred for low
cyanogenesis), Trifolium sp (clovers; often, pasture
species have been bred for low cyanide content), Zea
mays (corn), Eucalyptus spp (gum trees), Hydrangea spp
(hydrangeas), Pteridium aquilinum (bracken fern), Bahia
oppositifolia (bahia), and Chaenomales spp (flowering
quince).

A number of insect species are also able to synthesize

hydrogen cyanide and/or sequester hydrogen cyanide
that is derived from the cyanogenic glycosides of their
plant hosts (notably the USA eastern tent caterpillar
Malacosoma americanum that is associated with mare
reproductive loss syndrome; however, cyanide is not the
cause of mare reproductive loss syndrome.
Invertebrates such as Burnet moths (Zygaena spp) that
feed on bird's-foot trefoils), as well as certain centipede
and millipedes, are potentially hazardous food sources
for exotic pet species.

Plant cyanogenesis in response to environmental

stressors is an important part of the etiology and risk of
acute cyanogenic glycoside poisoning. Within plants,
amino acids that are 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, and the presence of the detoxifying
enzyme beta-cyanoalanine synthase (which is
responsible for production of some of the cyanide
derivatives putatively involved in the chronic cyanide-
associated neurologic toxidromes). Even so-called
"acyanogenic" plants can become toxic under

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 appropriate environmental circumstances.

Environmental conditions that damage relevant plant

species, reduce protein synthesis, enhance the
conversion of nitrate to amino acids in the presence of
reduced protein synthesis, and/or inhibit beta-
cyanoalanine synthase potentially increase the risk of
cyanogenesis. Relevant environmental factors include
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, and various plant diseases. Herbicide
treatment of plants is important in that it may also
increase plant palatability.

Crushing and/or mastication of potentially cyanogenic

plants is important in development of the acute
toxidrome, because this releases cyanogenic glycosides
from plant cell vacuoles and exposes them to
catabolism by beta-glucosidase and hydroxynitrile lyase
present in the plant cell cytosol.

Young, rapidly growing areas of plants and areas of

regrowth after cutting often have high cyanogenic
glycoside content. As a rough approximation, rapidly
growing Sorghum spp are often hazardous until they
reach ~60 cm 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.
Plant seeds and leaves typically have higher cyanogenic
potential, whereas the fleshy parts of fruits generally
have low levels. Drying often increases the cyanogenic
potential of plants, whereas ensiling may reduce
cyanide content by ~50%.

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 Beta-glucosidase and hydroxynitrile lyase are also
present in the rumen microflora, and a rumen pH of
~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 (~4–6) reduces 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.

Under conditions of low-level exposure, mammals

detoxify ~80% of ingested cyanide to thiocyanate via
mitochondrial rhodanese. 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 hydroxycobalamin (vitamin
B12a) to yield cyanocobalamin (vitamin B12), 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 levels,
particularly under conditions of chronic, low level
exposure. Dietary sulfur and sulfur amino acid intake
are known to strongly affect the neurologic toxidromes
associated with chronic cyanide/cyanogenic glycoside
exposure in people.

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 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 reduced
iodination of tyrosine, reduced T3 synthesis, increased
blood TSH, goiter, and hypothyroidism. Similar effects
occur with some plant glucosinolates (goitrogenic
glycosides). Selenium deficiency appears to enhance
these effects.

Chronic, low-level cyanide/cyanogenic glycoside

exposure (often in combination with low dietary sulfur
and/or sulfur amino acid intake) is associated with
neuropathy syndromes in horses and ruminants.
Sorghum cystitis ataxia syndrome of horses is
associated with diffuse nerve fiber degeneration in the
lateral and ventral funiculi of the spinal cord and brain
stem. Similar syndromes have been described in
ruminants. Comparisons between these syndromes as
chronic cyanogenic glycoside–associated human
myeloneuropathies (such as Konzo and tropical ataxic
neuropathy) have been made; however, the precise
toxins and modes of action are yet to be fully defined.
All of these toxidromes appear to be related to a
combination of chronic cyanide/cyanogenic glycoside
exposure combined with low dietary sulfur and/or
sulfur amino acid intake and possibly other nutritional
deficiencies. Lathyrogenic plant cyanide metabolites
such as beta-cyanoalanine have been implicated as
causative or at least contributory agents.

Chronic, low-level cyanogenic glycoside exposure

(notably from Sorghum spp) has been associated with
musculoskeletal teratogenesis (ankyloses or
arthrogryposes) and abortion.

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 Clinical Findings of Cyanide
Poisoning in Animals
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; however, the ability to
detect this smell is genetically determined in people,
and anosmic people (a significant proportion of the
population) cannot detect it. Salivation, excess
lacrimation, and voiding of urine and feces 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. Serum ammonia and
neutral and aromatic amino acids are typically
increased. Cardiac arrhythmias are common due to
myocardial histotoxic hypoxia. Death occurs during
severe asphyxial convulsions. The heart may
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, so prognosis of
recovery without therapeutic intervention is grave: it
would take more than 4 days to eliminate >95% of the
cyanide present.

Chronic cyanide poisoning: Chronic cyanogenic glycoside

hypothyroidism will present as hypothyroidism with or

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 without goiter. Cystitis ataxia toxidromes are typically
associated with posterior ataxia or incoordination that
may progress to irreversible flaccid paralysis, cystitis
secondary to urinary incontinence, and hindlimb urine
scalding and alopecia. Death, although uncommon, is
often associated with pyelonephritis. Late-term abortion
and musculoskeletal teratogenesis may also occur.

Lesions
Acute cyanide poisoning: Necropsy personnel may
require appropriate personal protective equipment,
including respirators with suitable cartridges. Venous
blood is classically described as being "bright cherry
red"; however, this color rapidly fades after death or if
the blood is exposed to the atmosphere. Whole blood
clotting may be slow or not occur. Mucous membranes
may 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” may be
detected after opening. Rumen contents may provide a
positive sodium picrate paper test (or positive results on
other rapid cyanide test strip systems). Rumen gases
may provide positive results in cyanide Draeger tube
rapid test systems. Agonal hemorrhages of the heart
may be seen. Liver, serosal surfaces, tracheal mucosa,
and lungs may be congested or hemorrhagic; some
froth may be seen 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
may result in a generalized dark coloration of skeletal
muscle. Neither gross nor histologic lesions are
consistently seen.

Multiple foci of degeneration or necrosis may be seen in

the CNS of dogs chronically exposed to sublethal

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 amounts of cyanide. These lesions have not been
reported in livestock.

Chronic cyanide poisoning: Goiter may be present.

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
brain stem. Hindlimb urine scalding and alopecia may
be present.

Diagnosis of Cyanide
Poisoning in Animals
Determination of cyanide (and/or cyanide
glycoside and/or relevant cyanide
metabolite) concentrations in food and
stomach contents

For cyanide-associated neuropathy

syndromes: feed analysis and
neurohistopathology

For chronic cyanogenic glycoside-associated

teratogenic syndromes, Feed analysis and
fetal pathologies

Appropriate history, clinical signs, postmortem findings,

and demonstration of HCN in rumen (stomach)
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 may liberate cyanide gas
(eg, rumen contents and rumen gas cap).

A rapid qualitative and presumptive diagnosis can be

made by testing representative plant samples or
stomach contents using the picric acid paper test or by

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 collecting rumen gas cap samples by trocarization and
testing with a Draeger cyanide gas detection tube or
other cyanide gas detection system. Negative results
with such rapid presumptive tests do not completely
exclude the possibility of cyanide poisoning.

Suitable specimens for more sophisticated testing

include the suspected food source, rumen/stomach
contents, samples of the rumen gas cap, heparinized
whole blood, liver, and muscle. 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.

Measurement of the urinary metabolite of cyanide,

thiocyanate, may reveal increased concentrations after
cyanide poisoning.

Hay, green chop, silage, or growing plants containing

>220 ppm cyanide as HCN on a wet-weight (as is) basis
are very dangerous as animal feed. Forage containing <
100 ppm HCN, wet weight, is usually safe to pasture.
Analyses performed on a dry-weight basis have the
following criteria: >750 ppm HCN is hazardous, 500–750
ppm HCN is suspect, and < 500 ppm HCN is considered
safe.

Normally expected cyanide concentrations in blood of

most animal species are usually < 0.5 mcg/mL. Minimal

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 lethal blood concentrations are ~3 mcg/mL or less.
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 may be 4–5 times greater than serum
concentrations because of binding to ferric ions and
sequestration in RBCs.

Differential diagnoses include poisonings by:

nitrate or nitrite

urea

organophosphates

carbamates

chlorinated hydrocarbon pesticides

toxic gases (carbon monoxide and

hydrogen sulfide)

as well as infectious or noninfectious

diseases and other toxidromes that cause
sudden death

Treatment, Control, and

Prevention of Cyanide
Poisoning in Animals
Immediate treatment with
hydroxocobalamin and oxygen

Methylene blue if diagnosis is in doubt

(signs are similar to those of nitrate
poisoning)

Removal from the source of exposure

In cases of acute cyanide poisoning, immediate

treatment is necessary. Activated charcoal is ineffective,
and its use is not recommended. Hydroxocobalamin
(vitamin B12a ) is the gold-standard antidote for cyanide

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 because of its effectiveness and low toxicity. It has a
great advantage of not further compromising tissue
oxygenation and not inducing hypotension.
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 70 mg/kg, infused IV over 15
minutes, repeated as necessary. Hydroxocobalamin
produces chromaturia (which may result in false
urinalysis results), as well as infusion site reactions, GI
upset, pruritus, and dysphagia. Hydroxocobalamin is
costly, which may limit its use in herd and flock animals.

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 partial pressure of oxygen
(pO2) in arterial blood 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.

The older (and less expensive—making it likely more

practical for grazing animals) 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 using Fe3+ in hemoglobin (ie,
inducing methemoglobinemia), which then acts as a
high-affinity decoy chemical receptor for cyanide and
forms cyanmethemoglobin. 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. Cyanide bound to

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 methemoglobin 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, treatment with nitrites is usually followed up by
injection of sodium thiosulfate. 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 may reduce any ongoing
production of cyanide in the rumen/stomach
environments.

If possible, 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.
Thiosulfate is generally well tolerated; however,
vomiting and hypotension can occur. The thiosulfate
injection can be repeated if necessary. Oral
administration of thiosulfate can also be considered in
an attempt to convert any cyanide in the
stomach/rumen into thiocyanate. Sodium nitrite
therapy may be carefully repeated at 10 mg/kg, every 2–
4 hours or as needed. Ideally, decisions regarding
repeated treatment with nitrites should consider the
degree of methemoglobinemia present.

Notably, thiosulfate treatment alone (sodium thiosulfate

at ≥500 mg/kg, IV, plus 30 g/cow orally for ruminants,
with the objective of facilitating the detoxification of any
remaining HCN in the rumen) has been successful in
some cases. However, thiosulfate treatment should
ideally be preceded by nitrite induction of

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 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 best preventive step is to test suspect feed and/or

pastures before allowing consumption. Pasture and
forage sorghums (eg, Sudan grass and sorghum-Sudan
grass hybrids) should not be grazed until they are >60
cm tall or have been proved by testing to have
acceptable cyanide levels, to reduce danger from
prussic acid poisoning. Animals should be fed before
first turning out to pasture; hungry animals may
consume forage too rapidly to detoxify HCN released in
the rumen. Animals should be turned out to new
pasture later in the day; potential for prussic acid
release is reported to be highest during early morning
hours. Free-choice salt and mineral with added sulfur
may help protect against prussic acid 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.

Green chop forces livestock to eat both stems and

leaves, thereby reducing problems caused by selective
grazing. Cutting height can be raised to minimize
inclusion of regrowth.

Sorghum hay and silage usually lose ≥50% of prussic

acid content during curing and ensiling processes. Free
cyanide is released by enzyme activity and escapes as a
gas. Although a rare occurrence, hazardous
concentrations of prussic acid may still remain in the
final product, especially if the forage had an extremely
high cyanide content before cutting. Hay has been dried

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 at oven temperatures for up to 4 days with no
significant loss of cyanide potential. These feeds 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. At least in theory,
the risk of chronic cyanide poisoning syndromes may be
reduced by iodine supplementation in the case of
hypothyroidism and by sulfur-containing amino acids in
the case of chronic neurologic toxidromes. Great care
must be taken when providing supplemental elemental
sulfur sources in ruminants because of the possible risk
of polioencephalomalacia.

Key Points

Manage grazing and feed conditions

for environmental stress to minimize
risk, and analyze feed before allowing
consumption.

Hydroxocobalamin plus 100% oxygen

should be administered as soon as
possible after suspected cyanide
poisoning.

Treatment should not be delayed for

diagnostic confirmation.

Removal from the source of exposure

is the main clinical priority in chronic
cyanide-associated toxidromes.

Prognosis for cases of chronic cyanide

poisoning other than those associated
with thyroid syndromes is guarded.

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 For More Information
Also see pet health content regarding
cyanide poisoning.

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