HCN cyanide toxicity Flashcards
Hydrogen cyanide (HCN) and cyanide salts are used in
For most species, the lethal dose of HCN is
Exposure to cyanide can occur via
Cyanide disrupts the ability
Clinical signs include
best indicators of both the presence and severity of cyanide poisoning
common industrial processes.
2 mg/kg.
inhalation, ingestion, or dermal exposure.
cells to use oxygen (O2) in oxidative phosphorylation. = histotoxic tissue hypoxia.
vomiting, hyperpnea, tachycardia and cardiac arrhythmias, seizures, coma, and apnea.
Plasma lactate levels and increased anion gap values
Whole-blood cyanide levels are available in many human laboratories. It may take time to obtain the results, so these tests are often of little use in emergency situations.
Treatment consists of
The classic bitter almond smell and cherry red blood are rarely seen outside of textbooks
Differential diagnoses
removing the animal from the source of exposure supportive measures (100% O2 and intravenous fluids) if exposure is certain, administering antidotal therapy
Recently, hydroxocobalamin has been employed as a cyanide antidote in humans and has been shown to reverse cyanide toxicity and reduce mortality in a canine model.
The classic bitter almond smell and cherry red blood are rarely seen outside of textbooks.
carbon monoxide
acute solvent inhalation
heart disease
cerebral disease
sources:
Fires
Gold mines
Fumigation
Electroplating and jewelry manufacturing
Photographic chemicals
Manufacture of plastics, rubber, and synthetic fiber
Pesticides (rodenticides, insecticides) - sodium cyanide baits into the mouths of the animals (i.e., “coyote-getters”)
Burning rubber
Certain drugs - prussic acid, and the nitroprussides are used as hypotensive drugs
Ingestion of certain plants - Naturally occurring cyanogenic glycosides, such as amygdalin, are found in numerous plants. Seeds of apples, plums, cherries, apricots, and the jetberry bush all release cyanide on digestion and are dangerous if the seed capsule is broken. As few as 5 to 25 seeds can cause intoxication. Natural oil of bitter almonds contains 4% HCN. In addition, some species of lima bean contain notable amounts of HCN. The dried root of cassava (i.e., tapioca) contains fairly large amounts of cyanide and can cause poisoning when eaten in large amounts or if it is improperly cooked
Terrorist attack
humans = intentional - involve drinking Na cyanide–containing insecticide
-second most common is smoke inhalation
MoA: -
via binding w
results in shift to anaerobic metabolism occurs,
cells cannot use O2 in oxidative phosphorylation
ferric (Fe+3) iron of the mitochondrial cytochrome oxidase system
lactic acid production
anion gap metabolic acidosis
histotoxic tissue hypoxia
4-5 bc concentrates in erythrocytes
19 hours
minutes
direct toxic action on cellular membranes, resulting in their necrosis
CS
primary manifestations of HCN:
inhalation onset:
ingestion onset:
nitroprussides/amygdalin onset:
- rapid tachypnea, hypotension, convulsions, coma
- acute cyanide poisoning progresses rapidly from convulsions to coma to shock to respiratory failure to death
- enclosed spaces may lose consciousness after few breaths, and death follows rapidly within 1 to 15 minutes
- 30 min to 1 hr after exposure in animals ingesting amounts large enough to be fatal
- as late as 12 hours occurs
cassava is reported to cause
Chronic ingestion of cyanide-containing cassava is reported to cause tropical ataxic neuropathy in people
smell of bitter almonds
cyanosis
noncardiogenic pulmonary edema
been reported often, but to detect this odor is genetically determined, and many people cannot do so
late sign that may not be present until agonal
may occur, even after ingestion alone
explain classic “cherry red” color:
stomach contents may produce a:
blood is normally oxygenated. However, the tissue is unable to extract or use the oxygen bc of the cyanide
=greater than normal O2 on venous side and the classic
bitter almond smell
Dx: PaO2 SpO2 lacate AG definitive dx
normal/high normal/high high = best indicator high = best indicator if no ABG Whole-blood cyanide levels are available in many human laboratories, but the results may take time = cannot be relied on to direct therapy inER
contribute to the documentation of the diagnosis
tx -
safety
Rescuers, must not enter w.out proper respirators or self-contained breathing apparatus. Mouth-to-mouth breathing should be avoided
tx mild CS - animals with only anxiety and hyperventilation
All cyanide antidotes are
charcoal?
Amyl nitrite antidotal therapy?
supportive measures alone without antidotal therapy
All cyanide antidotes are toxic, and therapy may be not only unnecessary but also dangerous
orig questioned but one dose is recommended
Amyl nitrite antidotal therapy, which is prominently used in human treatment, is not recommended in animals.
Methemoglobin formers
Sodium thiosulfate
Cobalt-EDTA
Hydroxocobalamin
+ve Potent
-ve Impairment of O2 delivery to tissue
+ve Efficient, Safe
-ve Delayed action
+ve very pontent, immediate
-ve numerous side effects
+ve Less potent, Immediate action, Safe
-ve expensive, red discoloration of skin and urine
tx
diagnosis of cyanide poisoning is certain
-sodium nitrite should be given ASAP
Sodium nitrite has potentially significant toxicity. This nitrite forms methemoglobin, which combines with cyanide to form cyanmethemoglobin
potent vasodilator, and rapid administration may result in hypotension
tx
Na thiosulphate:
=rhodanese enzyme in the liver converts
cyanide - thiocyanate - excreted in the urine
- toxic ingestion overwhelmes and needs more sulphur donors
- sodium thiosulphate acts as this donor
sodium nitrite forms methaemoglobinaemia
= then cyanide binds avidly to metHB
= cyanmethemoglobin
= releasing cyanide from cytochrome oxidase
-downside is now you have an additional hypoxic state in your patient
