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sebagai referensi pribadi.

Cyanide poisoning occurs when a living organism is exposed to a compound that

produces cyanide ions (CN−) when dissolved in water. Common poisonous cyanide

compounds include hydrogen cyanide gas and the crystalline solidspotassium

cyanide and sodium cyanide. The cyanide ion halts cellular respiration by inhibiting

the enzyme cytochrome c oxidase found in the mitochondria.

Cyanide poisoning is a form of histotoxic hypoxia because the cells of an organism

are unable to use oxygen, primarily through the inhibition of cytochrome c oxidase.

Acute hydrogen cyanide poisoning can result from inhalation of fumes from burning

polymer products that use nitrile in their production, such as polyurethane, or vinyl.[1] It can also be caused by breakdown of nitroprusside into nitric oxide and cyanide

during treatment of hypertensive crisis.[specify]

If cyanide is inhaled it causes a coma with seizures, apnea, and cardiac arrest, with

death following in a matter of seconds. At lower doses, loss of consciousness may

be preceded by general weakness, giddiness, headaches, vertigo, confusion, and

perceived difficulty in breathing. At the first stages of unconsciousness, breathing is

often sufficient or even rapid, although the state of the victim progresses towards a

deep coma, sometimes accompanied by pulmonary edema, and finally cardiac

arrest. A cherry red skin color that changes to dark may be present as the result of

increased venous hemoglobin oxygen saturation. Cyanide does not directly

cause cyanosis. A fatal dose for humans can be as low as 1.5 mg/kg body weight.[2]

In addition to its uses as a pesticide and insecticide, cyanide is contained in tobacco

smoke and smoke from building fires, and is present in some foods such

asalmonds, apricot kernel, apple seeds, orange seeds, cassava (also known as yuca

or manioc), and bamboo shoots. Vitamin B12, in the form of hydroxocobalamin(also

spelled hydroxycobalamin), may reduce the negative effects of chronic exposure,

and a deficiency can lead to negative health effects following exposure. [3]

Exposure to lower levels of cyanide over a long period (e.g., after use of improperly

processed cassava roots as a primary food source in tropical Africa) results in

increased blood cyanide levels, which can result in weakness and a variety of

symptoms, including permanent paralysis, nervous lesions,[4][5][6]  hypothyroidism,[5

]and miscarriages.[7][8] Other effects include mild liver and kidney damage.[9][10]

Cyanide has the potential to be bioremediated. Among the enzyme families which

degrade cyanide are nitrogenases, rhodanese, and the nitrilases. Cyanide

hydratases, part of the lyase enzyme family that convert cyanide are present in

certain species of fungi hydrolyze cyanide to formamide, Cyanide dihydratases

convert it directly to formate and ammonia, end products that pose far less toxicity.[11]

The United States standard cyanide antidote kit first uses a small inhaled dose

of amyl nitrite, followed by intravenous sodium nitrite, followed by

intravenous sodium thiosulfate.[12] Hydroxocobalamin is newly approved in the US

and is available in Cyanokit antidote kits.[13] Sulfanegen TEA, which could be

delivered to the body through an intra-muscular (IM) injection, detoxifies cyanide and

converts the cyanide into thiocyanate, a less toxic substance.[14] Alternative methods

of treating cyanide intoxication are used in other countries.

Agent Description

Nitrites

The nitrites oxidize some of the hemoglobin's iron from

the ferrous state to the ferric state, converting the

hemoglobin into methemoglobin.

Cyanide binds avidly to methemoglobin, forming

cyanmethemoglobin, thus releasing cyanide from

cytochrome oxidase.[15] Treatment withnitrites is not

innocuous as methemoglobin cannot carry oxygen, and

severe methemoglobinemia may need to be treated in

turn withmethylene blue.[note 1]

Thiosulfate The evidence for sodium thiosulfate's use is based on

animal studies and case reports: the small quantities of

cyanide present in dietary sources and in cigarette

smoke are normally metabolized to relatively harmless

thiocyanate by the mitochondrial

enzyme rhodanese(thiosulfate cyanide

sulfurtransferase), which uses thiosulfate as a

substrate. However, this reaction occurs too slowly in

the body for thiosulfate to be adequate by itself in acute

cyanide poisoning. Thiosulfate must therefore be used

in combination with nitrites.[15]

Hydroxocobalamin

Hydroxocobalamin, a form (or vitamer) of vitamin

B12 made by bacteria, and sometimes denoted vitamin

B12a, is used to bind cyanide to form the

harmless cyanocobalamin form of vitamin B12.

4-Dimethylaminophenol

4-Dimethylaminophenol (4-DMAP) has been

proposed[by whom?] in Germany as a more rapid antidote

than nitrites with (reportedly) lower toxicity. 4-DMAP is

used currently by the German military and by the

civilian population. In humans, intravenous injection of

3 mg/kg of 4-DMAP produces 35 percent

methemoglobin levels within 1 minute. Reportedly, 4-

DMAP is part of the US Cyanokit, while it is not part of

the German Cyanokit due to side effects (e.

g. hemolysis).

Dicobalt edetate Cobalt ions, being chemically similar to iron ions, can

also bind cyanide. One current cobalt-based antidote

available in Europe is dicobalt edetate or dicobalt-

EDTA, sold as Kelocyanor. This agent chelates cyanide

as the cobalticyanide. This drug provides an antidote

effect more quickly than formation of methemoglobin,

but a clear superiority to methemoglobin formation has

not been demonstrated. Cobaltcomplexes are quite

toxic, and there have been accidents reported in the UK

where patients have been given dicobalt-EDTA by

mistake based on a false diagnosis of cyanide

poisoning. Because of its side effects, it should be

reserved only for patients with the most severe degree

of exposure to cyanide; otherwise, nitrite/thiosulfate is

preferred.[18]

Glucose

Evidence from animal experiments suggests that

coadministration of glucose protects against cobalt

toxicity associated with the antidote agent dicobalt

edetate. For this reason, glucose is often administered

alongside this agent (e.g. in the formulation

'Kelocyanor').

It has also been anecdotally suggested that glucose is

itself an effective counteragent to cyanide, reacting with

it to form less toxic compounds that can be eliminated

by the body. One theory on the apparent immunity

of Grigory Rasputin to cyanide was that his killers put

the poison in sweet pastries and madeira wine, both of

which are rich in sugar; thus, Rasputin would have

been administered the poison together with massive

quantities of antidote. One study found a reduction in

cyanide toxicity in mice when the cyanide was first

mixed with glucose.[19] However, as yet glucose on its

own is not an officially acknowledged antidote to

cyanide poisoning.

3-

Mercaptopyruvateprodrugs

The most widely studied cyanide-metabolizing pathway

involves utilization of thiosulfate by the

enzyme rhodanese, as stated above. In humans,

however, rhodanese is concentrated in the kidneys

(0.96 units/mg protein) and liver (0.15 u/mg), with

concentrations in lung, brain, muscle and stomach not

exceeding 0.03 U/ml.[20] In all these tissues, it is found in

the mitochondrial matrix, a site of low accessibility for

ionized, inorganic species, such as thiosulfate. This

compartmentalization of rhodanese in mammalian

tissues leaves major targets of cyanide lethality,

namely, the heart and central nervous system,

unprotected. (Rhodanese is also found in red blood

cells, but its relative importance has not been clarified.[21][22])

A different cyanide-metabolizing pathway, 3-

mercaptopyruvate sulfurtransferase (3-

MPST, EC 2.8.1.2), which is more widely distributed in

mammalian tissues than rhodanese, is being explored.

3-MPST converts cyanide to thiocyanate, using the

cysteine catabolite, 3-mercaptopyruvate (3-MP).

However, 3-MP is extremely unstable chemically.

Therefore, a prodrug, sulfanegen sodium (2, 5-

dihydroxy-1,4-dithiane-2,5-dicarboxylic acid disodium

salt), which hydrolyzes into 2 molecules of 3-MP after

being administered orally or parenterally, is being

evaluated in animal models.[23][24]

Oxygen therapy

Oxygen therapy is not a cure in its own right. However,

the human liver is capable of metabolizing cyanide

quickly in low doses (smokers breathe in hydrogen

cyanide, but it is such a small amount and metabolized

so fast that it does not accumulate).

The International Programme on Chemical

Safety issued a survey (IPCS/CEC Evaluation of

Antidotes Series) that lists the following antidotal agents

and their effects: oxygen, sodium thiosulfate, amyl

nitrite, sodium nitrite, 4-dimethylaminophenol,

hydroxocobalamin, and dicobalt edetate ('Kelocyanor'),

as well as several others.[25] Other commonly-

recommended antidotes are 'solutions A and B' (a

solution offerrous sulfate in aqueous citric acid, and

aqueous sodium carbonate, respectively) and amyl

nitrite.

The UK Health and Safety Executive (HSE) has

recommended against the use of solutions A and B

because of their limited shelf life, potential to cause iron

poisoning, and limited applicability (effective only in

cases of cyanide ingestion, whereas the main modes of

poisoning are inhalation and skin contact). The HSE

has also questioned the usefulness of amyl nitrite due

to storage/availability problems, risk of abuse, and lack

of evidence of significant benefits. It also states that the

availability of Kelocyanor at the workplace may mislead

doctors into treating a patient for cyanide poisoning

when this is an erroneous diagnosis. The HSE no

longer recommends a particular cyanide antidote.[26] Qualified UK first aiders are now only permitted to

apply oxygen therapy using a bag valve mask,

providing they have been trained in its usage.

1. Jump up^ Methylene blue has historically been used as an antidote to

cyanide poisoning,[16] but is not a preferred therapy due to its theoretical risk

of worsening of cyanide symptoms by displacement of cyanide from

methemoglobin, allowing the toxin to bind to tissue electron transport chains.[17]

2. On December 5, 2009, a fire in the night club Lame Horse (Khromaya

Loshad) in the Russian city of Perm took the lives of 156 people. 111 people

died on the spot and 45 later in hospitals. One of the main causes of death

was poisoning from cyanide and other toxic gases released by the burning of

plastic andpolystyrene foam used in the construction of club interiors. Taking

into account the number of deaths, this was the largest fire in post-Soviet

Russia.[citation needed][when?]

3. On January 27, 2013, a fire at the Kiss nightclub in the city of Santa Maria, in

the south of Brazil, caused the poisoning of hundreds of young people by

cyanide released by the combustion of soundproofing foam made

with polyurethane. By March 2013, 241 fatalities were confirmed.[27][28]

4. Hydrogen cyanide in the form of Zyklon B was used in German extermination

camps during World War II, and especially from March 1942 onwards, when it

was first used experimentally to murder Russian prisoners of war

at Auschwitz. Use of the poison was scaled up rapidly until custom-built gas

chambers (holding up to about 2000 victims) were constructed as part of the

new crematoria complex at Auschwitz-Birkenau. There was also a large

undressing room next to the gas chamber, and the victims were told to

undress and leave their clothes on a numbered peg for collection later. They

were told that they would receive a hot shower, and false shower heads were

fitted in the ceilings of the gas chambers, so as to maintain the deception. The

gas chambers were sealed hermetically to prevent gas leakage. The Zyklon B

pellets were then dropped into the chamber via small openings in the roof.

When the pellets were exposed to moisture and human heat (as in a closed

chamber), they gave off gaseous HCN, which then killed the victims. Workers

in theSonderkommando were employed to remove the corpses from the gas

chamber and strip them of any valuables, such as gold teeth, before the

bodies were cremated. The gas was used mainly at Auschwitz and Majdanek,

but theextermination camps such as Treblinka built earlier used engine

exhaust gas, in which carbon monoxide was the toxic component. The gas

chambers were either mobile lorries as at Chelmno or specially built

chambers as at Sobibor andBelzec. The victims included prisoners of

war, Jews from across Europe, Romani gypsies, Poles, ill and disabled

peopleof all nationalities, as well as political

prisoners, homosexuals, Jehovah's witnesses and anyone who opposed the

Nazis.

5. Hydrogen cyanide gas has also been used for judicial execution in some

states of the United States, where cyanide was generated by reaction

between potassium cyanide (or sodium cyanide[29][30]) dropped into a

compartment containingsulfuric acid, directly below the chair in the gas

chamber.[31]

Cyanide was stockpiled in chemical weapons arsenals in both the Soviet Union and

the United States in the 1950s and 1960s.[citation needed] However, as a military agent,

hydrogen cyanide was not considered very effective, since it is lighter than air and

needs a significant dose to incapacitate or kill.

Cyanide salts are sometimes used as fast-acting suicide devices. Cyanide reacts at

a higher level with high stomach acidity.

In February 1937, the Uruguayan short story writer Horacio Quiroga committed

suicide by drinking cyanide in a hospital at Buenos Aires.

In 1937, polymer chemist Wallace Carothers committed suicide by cyanide.

In the 1943 Operation Gunnerside to destroy the Vemork Heavy Water Plant in

World War II (an attempt to stop or slow German atomic bomb progress), the

commandos were given cyanide tablets (cyanide enclosed in rubber) kept in the

mouth and were instructed to bite into them in case of German capture. The

tablets ensured death within three minutes.[32]

Cyanide, in the form of pure liquid prussic acid (a historical name for hydrogen

cyanide), was the favored suicide agent of the Third Reich. It was used to commit

suicide by Erwin Rommel (1944), after being accused of conspiring against

Hitler; Adolf Hitler's wife, Eva Braun (1945); and by Nazi leaders Heinrich

Himmler(1945), possibly Martin Bormann (1945), and Hermann Göring (1946).

It is speculated that, in 1954, Alan Turing used an apple that had been injected

with a solution of cyanide to commit suicide after being convicted of having a

homosexual relationship—illegal at the time in the UK—and forced to undergo

hormonal castration.

Members of the Sri Lankan LTTE (Liberation Tigers of Tamil Eelam,

whose insurgency lasted from 1983 to 2009), used to wear cyanide vials around

their necks with the intention of committing suicide if captured by the government

forces.

On June 6, 1985, serial killer Leonard Lake died in custody after having ingested

cyanide pills he had sewn into his clothes.

On June 28, 2012, Wall Street trader Michael Marin ingested a cyanide pill

seconds after a guilty verdict was read in his arson trial in Phoenix, AZ; he died

minutes after.[33]

In 2000, a spill at Baia Mare, Romania resulted in the worst environmental

disaster in Europe since Chernobyl.[34]

In 2000, Allen Elias,[35] CEO of Evergreen Resources was convicted of

knowing endangerment for his role in the cyanide poisoning of employee

Scott Dominguez.[36][37] This was one of the first successful criminal

prosecutions of a corporate executive by the Environmental Protection

Agency.

John Tawell, a murderer who in 1845 became the first person to be arrested

as the result of telecommunications technology

Grigori Rasputin (1916; attempted, later killed by gunshot)

Goebbels children (1945)

Chicago Tylenol murders (1982)

Ronald Clark O'Bryan (1944–1984)

Richard Kuklinski (1935–2006)

Jonestown, Guyana, was the site of a large mass murder-suicide,[38] in which

over 900 members of the Peoples Temple drank potassium cyanide–

laced Flavor Aid in 1978.

In 1995, a device was discovered in a restroom in the Kayabacho Tokyo

subway station, consisting of bags of sodium cyanide and sulfuric acid with a

remote controlled motor to rupture them in what was believed to be an

attempt by the Aum Shinrikyo cult to produce toxic amounts of hydrogen

cyanide gas.[39]

In 2003, Al Qaeda reportedly planned to release cyanide gas into the New

York City Subway system. The attack was supposedly aborted because there

would not be enough casualties.[40]

Homicide[edit]

The Detective Conan manga/anime series has a large number of cases in which

the victims are killed by cyanide, with all or most mentioning an 'almond scent' to

describe it.

Raymond Chandler uses "a little potassium hydrocyanide" against private

detective Philip Marlowe in The Little Sister – "merely relaxing".

In Agatha Christie's And Then There Were None, the first death occurs from

cyanide poisoning.

In Agatha Christie's Sparkling Cyanide (also entitled Remembered Death), based

upon her Hercule Poirot short story entitled "Yellow Iris", Rosemary and George

Barton are poisoned by cyanide crystals.

In Ngaio Marsh's Death At The Bar, Luke Watchman, a top London barrister and

King's Counsel dies of potassium cyanide poisoning after a freak dart throwing

accident whilst holidaying in Devon.

In Hit Man: A Technical Manual for Independent Contractors by "Rex Feral", the

use of cyanide to poison a mark is explained in detail.

In the Joseph Kesselring play Arsenic and Old Lace, two old ladies mix wine

with arsenic, cyanide and strychnine to use to kill old men.

In Roald Dahl's short story "The Landlady", a landlady poisons a young boy

named Billy Weaver staying in her Bed and Breakfast with tea that was said to

taste suspiciously like cyanide (described as tasting like "bitter almonds"),

presumably to stuff him.

In the film "The Little Girl Who Lives Down the Lane", Rynn Jacobs (Jodie Foster)

poisons Frank Hallet (Martin Sheen) with cyanide-tainted tea, serving him

almond cookies to mask the taste.

Bishop Lilliman was killed by 'V', forcing the bishop to swallow a communion

wafer poisoned with cyanide in Alan Moore and David Lloyd's comic book

series, V for Vendetta.

In the manga Battle Royale, Yuko Sakaki's assigned weapon is hydrocyanic acid.

She uses it to poison food intended for Shuuya Nanahara, but it ends up being

ingested by Yuka Nakagawa.

In Phoenix Wright: Ace Attorney: Trials and Tribulations game, the third case

solved by the player involves a programmer who is murdered when potassium

cyanide is slipped into his coffee at a restaurant.

In the game Hitman: Contracts, the player can assassinate people using cyanide.

In the 1999 Midsomer Murders episode "Judgement Day", the second murder

victim is poisoned by cyanide mixed in a glass of wine.

In the 2008 Doctor Who episode "The Unicorn and the Wasp", the Doctor is

nearly poisoned by cyanide, but manages to metabolize it and detoxify himself

using a combination of proteins, salt, and a shock, plus the advantage of his non-

human physiology.

In the Assassin's Creed video game series, Alan Turing was revealed to have

been killed by Templars who laced an apple (which he would later eat) with

cyanide in an attempt to make it look as if he had committed suicide.

In the film Irrational Man, cyanide is used to kill a judge.

In Agatha Christie's novel The Hollow, a woman called Gerda Christow kills

herself when she gets caught by murder of her husband.

In Agatha Christie's novel The Secret Adversary, the villain "Mr Brown"

commits suicide using cyanide concealed in a signet ring.

In Robert Louis Stevenson's Strange Case of Dr Jekyll and Mr Hyde, Dr.

Jekyll kills himself with cyanide, deduced as the smell of kernels (almonds) is

evident.

In Ian Fleming's James Bond stories and the movies based on them, 00

agents are issued cyanide capsules for use in the event of capture by the

enemy. James Bond is described as having thrown his away.

Gabriel García Márquez's novel Love in the Time of Cholera begins with

Jeremiah de Saint-Amour's suicide by cyanide poisoning.

Australian author Nevil Shute's 1957 novel about life after nuclear war, On the

Beach, gives the scenario of the Australian government giving survivors free

cyanide tablets to commit suicide rather than face death from radiation

poisoning.

In the James Bond film Dr. No (1962), James Bond believes that his cab

driver is an enemy agent, and after a fight scene, begins to interrogate the

driver, who proceeds to poison and kill himself with cyanide embedded in a

cigarette.

In William Styron's 1979 novel Sophie's Choice and the movie based on the

book, Sophie and Nathan commit suicide by ingesting a cyanide pill.

In Ford Maddox Ford's novel The Good Soldier one of the main characters,

Florence, commits suicide by drinking her phial of "prussic acid" after learning

that her lover is having an affair with another woman.

In Japanese author Koushun Takami's 1999 novel Battle Royale and the

film Battle Royale based on the book, Yuko Sakaki is given a small bottle

of potassium cyanide (KCN) as a "special bonus" in addition to the weapon

provided in her day pack.

In the second season of the US TV series 24, several of the terrorists keep

cyanide pills immediately on their person so they can swallow them

immediately to avoid capture.

In the Kannada film Cyanide (2006), which is about the incidents that

occurred in the peripheries of Bangalore after the assassination of the former

Indian Prime Minister Rajiv Gandhi, the killers of the Prime Minister use

cyanide vials to commit suicide to avoid being captured by the police.

In the film Unknown (2011), Jürgen commits suicide by emptying a bag of

sodium cyanide into his coffee, disguised as a packet of sugar.

In the film Captain America: The First Avenger (2011), Heinz Kruger commits

suicide by cyanide tablet upon being caught.

In the James Bond film Skyfall (2012), Javier Bardem's character, Silva,

discusses his failed attempt to commit suicide using a hydrogen cyanide

capsule whilst under interrogation. Rather than kill him, the hydrogen cyanide

burned his body internally, forcing him to wear a prosthetic face plate to hide

his disfigurement.

In the song To The End by My Chemical Romance, the bride in the album's

story drinks cyanide on her wedding day.

Cyanide poisoning can be difficult to detect. The effects of cyanide ingestion are very

similar to the effects of suffocation; because cyanide stops the cells of the body from

being able to use oxygen, which all cells need to survive. The symptoms of cyanide

poisoning are similar to those experienced when hiking or climbing at high altitudes.

General weakness, confusion, bizarre behavior, excessive sleepiness, coma,

shortness of breath, headache,dizziness, and seizures can all present with

cyanide poisoning.

Typically, an acute ingestion will have a dramatic, rapid onset, immediately

affecting the heart and causing sudden collapse. It can also immediately affect

the brain and cause a seizure or coma.

Chronic poisoning (over a long period of time) from ingestion or environmental

poisoning will have a more gradual onset.

The skin of a cyanide-poisoned person can sometimes be unusually pink or

cherry-red because oxygen will stay in the blood and not get into the cells. The

person may also breathe very fast and have either a very fast or very slow

heartbeat. Sometimes the person's breath can smell like bitter almonds, though

this can be difficult to detect.

Perhaps most important is the setting, rather than the signs or symptoms.

o A person who works in a laboratory or plastics factory has a higher risk of

cyanide poisoning.

o Home, RV, boat, or building fires always include the additional concern of

cyanide exposure.

o If you know someone has been depressed or has substance abuse problems

and you find him or her with any of the signs or symptoms of cyanide

poisoning, then a suicide attempt is possible.

Cyanide toxicity is generally considered to be a rare form of poisoning. However,

cyanide exposure occurs relatively frequently in patients with smoke inhalation from

residential or industrial fires. In addition, intensive treatment with sodium

nitroprusside or long-term consumption of cyanide-containing foods is a possible

source of cyanide poisoning. Historically, cyanide has been used as a chemical

warfare agent, and it could potentially be an agent for a terrorist attack. [1, 2]

Cyanide exists in gaseous, liquid, and solid forms. Hydrogen cyanide (HCN, also

known as prussic acid) is a volatile liquid that boils at 25.6° C (78.1° F). Potassium

and sodium cyanide salts are water soluble, whereas mercury, copper, gold, and

silver cyanide salts are poorly water soluble.

In addition, a number of cyanide-containing compounds, known as cyanogens, may

release cyanide during metabolism. These include, but are not limited to, cyanogen

chloride and cyanogen bromide (gases with potent pulmonary irritant effects), nitriles

(R-CN), and the vasodilator nitroprusside sodium, which may produce iatrogenic

cyanide poisoning during prolonged or high-dose intravenous (IV) therapy (>10

mcg/kg/min). (See Etiology.)

Industry widely uses nitriles as solvents and in the manufacturing of plastics. Nitriles

may release HCN during burning or when metabolized after absorption by the skin or

gastrointestinal tract. A number of synthesized and natural compounds produce HCN

when burned. These combustion gases likely contribute to the morbidity and

mortality from smoke inhalation. Finally, long-term consumption of cyanide-

containing foods, such as cassava root or apricot seeds, [3] may lead to cyanide

poisoning.

Depending on its form, cyanide may cause toxicity through inhalation, ingestion,

dermal absorption, or parenteral administration. Clinical manifestations vary widely,

depending on the dose and route of exposure, and may range from minor upper

airway irritation to cardiovascular collapse and death within minutes. (See Clinical

Presentation.) In severe cases, rapid, aggressive therapy consisting of supportive

care and antidote administration can be lifesaving. (See Treatment andMedication.)

Cyanide as a chemical weapon

HCN (North Atlantic Treaty Organization [NATO] designation AC) is one of two

cyanide chemical warfare agents[4, 5, 6] ; the other is cyanogen chloride (NATO

designation CK). Cyanide is a rapidly lethal agent when used in enclosed spaces

where high concentrations can be achieved easily. [7, 8, 9, 10] In addition, because of the

extensive use of cyanide in industry in the United States, this agent presents a

credible threat for terrorist use.[5]

Cyanide was first used as a chemical weapon in the form of gaseous HCN in World

War I. Starting in 1915, the French military used approximately 4000 tons of cyanide,

without notable success. The failure of this measure was probably attributable to the

high volatility of cyanide and the inability of the 1- to 2-lb munitions used to deliver

the amounts of chemical required for biologic effects.[5, 6]

The introduction of cyanogen chloride by the French in 1916 made available a

compound that, being both more toxic and less volatile, was a more effective

chemical agent. Other alleged military uses of cyanide include Japanese attacks on

China before and during World War II and Iraqi attacks on Kurds in the 1980s.

Administer a cyanide antidote if the diagnosis of cyanide toxicity is strongly

suspected, without waiting for laboratory confirmation. Available antidotes are

hydroxocobalamin (Cyanokit) and sodium thiosulfate and sodium nitrite (Nithiodote).

Both are given intravenously.

Patients who present with more than minimal symptoms that resolve without

treatment should be admitted for observation and supportive care. In patients with

acute poisoning from hydrogen cyanide (HCN) gas or soluble salts, the principal

acute care concerns are hemodynamic instability and cerebral edema. The

continuous cardiac monitoring, respiratory and cardiovascular support, and frequent

neurologic evaluation these patients require is generally best provided in an

intensive care unit.

Conversely, acute poisoning from cyanogens (nitriles) or poorly soluble salts may not

manifest or become life-threatening for several hours after exposure. These patients

require a 24-hour observation period.[23, 24]

Oxygenation should be optimized and continuous cardiac monitoring provided.

Depending on the severity of symptoms, endotracheal intubation may be necessary

to optimize oxygen delivery and protect the airway. Serum lactate concentrations,

chemistries, and arterial or venous blood gases should be monitored.

Patients should be reevaluated 7-10 days after discharge from the hospital.[25]Delayed onset of Parkinson-like syndrome or neuropsychiatric sequelae may be

noted on followup.

Special concerns in pregnancy

Fetal demise is possible in cyanide poisoning. Aggressive support and antidotal

treatment of the mother is paramount. An obstetric evaluation following stabilization

of the mother is essential. Therapeutic abortion may be indicated in the presence of

fetal demise.

Murder mysteries and spy novels often feature cyanide as a fast-acting poison, but

you can be exposed to this toxin from everyday chemicals and even common foods.

Have you ever wondered how cyanide poisons and kills people, how much it takes

before it's toxic, and whether there is a cure? Here's what you need to know.

What Is Cyanide?

The term "cyanide" refers to any chemical containing a carbon-nitrogen (CN) bond.

Many substances contain cyanide, but not all of them are deadly poisons. Sodium

cyanide (NaCN), potassium cyanide (KCN), hydrogen cyanide (HCN), and cyanogen

chloride (CNCl) are lethal, but thousands of compounds called nitriles contain the

cyanide group yet aren't as toxic. In fact, you can find cyanide in nitriles used as

pharmaceuticals, such as citalopram (celexa) and cimetidine (Tagamet). Nitriles

aren't as dangerous because they don't readily release the CN- ion, which is the

group that acts as a metabolic poison.

How Cyanide Poisons

In a nutshell, cyanide prevents cells from using oxygen to make energy molecules.

The cyanide ion, CN-, binds to the iron atom in cytochrome C oxidase in the

mitochondria of cells. It acts as an irreversible enzyme inhibitor, preventing

cytochrome C oxidase from doing its job, which is to transport electrons to oxygen in

the electron transport chain of aerobic cellular respiration. Without the ability to use

oxygen, mitochondria can't produce the energy carrier adenosine triphosphate

(ATP). Tissues that require this form of energy, such as heart muscle cells and nerve

cells, quickly expend all their energy and start to die. When a large enough number

of critical cells die, you die.

Exposure To Cyanide

Cyanide can be used as a poison or chemical warfare agent, but most people are

exposed to it unintentionally. Some ways to be exposed to cyanide include:

eating cassava, lima beans, yucca, or almonds

eating apple seeds , cherry stones, apricot pits, or peach pits

smoking cigarettes

burning plastic

burning coal

inhaling smoke from a house fire

ingesting acetonitrile-based products are used to remove artificial nails

drinking water, eating food, touching soil, or inhaling air that has been contaminated

exposure to rodenticide or other cyanide-containing pesticide

Many industrial processes involve compounds that contain cyanide or can react with

water or air to produce it. Paper, textile, photochemical, plastics, mining, and

metallurgy industries all may deal with cyanide. Some people report an odor of bitter

almonds associated with cyanide, but not all toxic compounds produce the scent and

not all people can smell it. Cyanide gas is less dense than air, so it will rise.

Symptoms of Cyanide Poisoning

Inhaling a high dose of cyanide gas rapidly causes unconsciousness and often

death. Lower doses may be survivable, especially if immediate aid is provided. The

symptoms of cyanide poisoning are similar to those displayed by other conditions or

exposure to any of a number of chemicals, so don't assume cyanide is the cause. Do

remove yourself from the cause of exposure and seek immediate medical attention!

Immediate Symptoms headache

dizziness

weakness

confusion

fatigue

lack of coordination

Symptoms from Larger Doses or Longer Exposure

low blood pressure

unconsciousness

convulsions

slow heart rate

lung damage

respiratory failure

coma

Death from poisoning usually results from respiratory failure or heart failure. A

person exposed to cyanide may have cherry-red skin from high oxygen levels or a

dark or blue coloring, from Prussian blue (iron binding to the cyanide ion). Also, skin

and body fluids may give off an odor of almonds.

How Much Cyanide Is Lethal?

How much cyanide is too much depends on the route of exposure, the dose, and

duration of exposure. Inhaled cyanide presents a greater risk than ingested cyanide.

Skin contact is not as much of a concern (unless it has been mixed with DMSO),

except touching the compound could lead to accidentally swallowing some of it. As a

rough estimate, since lethal dose depends on the exact compound and several other

factors, about half a gram of ingested cyanide will kill a 160-lb adult.

Unconsciousness, followed by death, could occur within several seconds of inhaling

a high dose of cyanide, but lower doses and ingested cyanide may allow a few hours

to a couple of days for treatment. Emergency medical attention is critical.

Is there a Treatment for Cyanide Poisoning?

Because it's a relatively common toxin in the environment, the body can detoxify a

small amount of cyanide. For example, you can eat the seeds of an apple or

withstand cyanide from cigarette smoke without dying.

When cyanide is used as a poison or a chemical weapon, treatment depends on the

dose. A high dose of inhaled cyanide is lethal too quickly for any treatment to take

effect. Initial first aid for inhaled cyanide is getting the victim to fresh air. Ingested

cyanide or lower doses of inhaled cyanide may be countered by administering

antidotes that detoxify cyanide or bind to it. For example, natural vitamin

B12, hydroxocobalamin, reacts with cyanide to form cyanocobalamin, which is

excreted in urine.

Inhalation of amyl nitrite may aid breathing in victims of cyanide and also carbon

monoxide poisoning, although few first aid kits contain these ampules anymore.

Depending on the conditions, complete recovery may be possible, although

paralysis, liver damage, kidney damage, and hypothyroidism are possible.