Recognition

and Treatment of Acute

Cyanide Poisoning

C Y A N I D E S U P P L E M E N T

Author: Stephen W. Borron, MD, MS, San Antonio, Tex

Stephen W. Borron, Clinical Professor of Surgery, Division ofEmergency Medicine, University of Texas Health Science Center,San Antonio, Tex.

For correspondence, write: Stephen W. Borron, MD, MS, FACEP,FACMT, Division of Emergency Medicine (Surgery), MSC 7736,7703 Floyd Curl Drive, San Antonio, TX 78229; E-mail: borron@uthscsa.edu.

J Emerg Nurs 2006;32:S12-8.

0099-1767/$32.00

Copyright n 2006 by the Emergency Nurses Association.

doi: 10.1016/j.jen.2006.05.011

S12

recent publication describes the case of a teenager

Awho arrived at a community emergency room in

a hemodynamically unstable, apneic, and unre-

sponsive state and later died in a pediatric intensive care

unit.1 The cause of death, confirmed by laboratory results

available 2 days after the onset of symptoms, was cyanide

poisoning. The 17-year-old male was previously healthy,

was not taking medications, and had no history of drug

abuse. Toxicity was manifested suddenly and dramatically

by seizures and loss of consciousness while the boy was

visiting at a classmate’s house. Supportive care was ini-

tiated in the emergency room beginning shortly after the

onset of toxicity and continued in the intensive care unit;

however, the patient did not receive antidotal therapy until

cyanide poisoning was presumptively diagnosed approxi-

mately 4 hours after symptom onset—far too late, the au-

thors later concluded, to be effective, particularly given the

amount of cyanide to which the patient was exposed.1

This case illustrates many of the challenges in the

recognition and treatment of acute cyanide poisoning. Be-

cause cyanide poisoning can rapidly culminate in incapa-

citation and death, prompt recognition of cyanide toxicity

and early initiation of treatment are necessary for saving

lives and reducing morbidity.2-4 However, the nonspecific

nature of the signs and symptoms of cyanide poisoning

and the inability of most hospital laboratories to rapidly

confirm the presence of cyanide make diagnosis difficult.

These challenges notwithstanding, acute cyanide poisoning

can be successfully treated. As part of the first line of care

for the critically ill patient in the prehospital and hospital

settings, the emergency nurse can play an integral role in

the recognition and treatment of acute cyanide poisoning.

This article discusses the recognition and treatment of acute

JOURNAL OF EMERGENCY NURSING 32:4S August 2006

C Y A N I D E S U P P L E M E N T / B o r r o n

cyanide poisoning with emphasis on information that pre-

pares the emergency nurse to respond to a cyanide emergency.

Causes of Acute Cyanide Poisoning

A detailed discussion of the potential causes of acute cya-

nide poisoning—inhalation of fire smoke, accidental inges-

tion, occupational exposure, industrial incidents, homicide

or suicide attempts, terrorism, and ingestion of cyanogenic

substances—is presented by Schnepp elsewhere in this sup-

plement.5 In western countries, the most common cause of

cyanide poisoning is inhalation of smoke from structural

fires. As hydrogen cyanide is produced during combustion

of carbon- and nitrogen-based materials, it is generated in

nearly every fire.6 Modern structural fires, in particular, can

produce high concentrations of hydrogen cyanide because

of the abundance of substrates such as plastics and other

polymers, synthetic fibers, wool, and silk. In keeping with

the pervasiveness of cyanide in modern fires, cyanide is

found, often at toxic-to-lethal concentrations, in the blood

of most fire victims in which its presence is assessed.7 Tox-

icologic evidence suggests that cyanide is at least as im-

portant as carbon monoxide as cause of smoke-inhalation

morbidity and mortality in many fires.6-9 Besides fire smoke,

other causes of cyanide poisoning include occupational and

industrial incidents and use in suicide, murder, and terrorism.

The 17-year-old described above was poisoned by intentional

adulteration of a beverage with 1.5 g potassium cyanide.1

Recognition of Acute Cyanide Poisoning

Clinical manifestations and laboratory findings in acute cya-

nide poisoning ref lect hypoxia caused by cyanide’s deac-

tivation of cellular oxygen-utilization mechanisms.10 Cyanide

inhibits the activity of mitochondrial cytochrome oxidase,

an enzyme necessary for the normal use of oxygen in cellular

metabolism, and thereby prevents cells from extracting and

using oxygen from arterial blood.

CLINICAL MANIFESTATIONS

Development of toxicity is generally rapid, at a rate de-

pendent on the form of cyanide and the amount and route

of exposure.11 Exposure to large doses, particularly by inha-

lation or ingestion, can produce marked symptoms nearly

immediately and can result in death in minutes. Less rapid

progression of symptoms with survival times of several

August 2006 32:4S

hours has also been reported, particularly in cases of ex-

posure by ingestion.12 The variability in absorption and

onset of toxicity can be explained by the presence or ab-

sence of food in the stomach, the solubility of the cyanide

salt involved, and other factors. In the case of ingestion of

nitriles, which release cyanide when they are metabolized,

onset of toxicity may be delayed for hours. These obser-

vations illustrate the existence of a window of time, albeit

narrow, for effective intervention.

JOUR

In western countries, the most commoncause of cyanide poisoning is inhalationof smoke from structural fires.

The clinical presentation in acute cyanide poisoning

can change quickly.13 Health care providers typically first

encounter patients after severe toxicity has developed. Se-

vere or advanced poisoning is manifested by hypotension,

seizures, coma, respiratory depression, cardiovascular col-

lapse, and cardiorespiratory arrest (Table 1).2-4,13,14 In a

series of 101 patients treated by the Paris Fire Brigade for

smoke inhalation-associated cyanide poisoning from 1995

to 2003, 37.6% were found in cardiac arrest, and 45.5%

were neurologically impaired.15 Respiratory depression is

generally not accompanied by cyanosis because of in-

creased venous oxygen saturation.10,11 Often very transi-

tory, early signs and symptoms include hypertension with

ref lex bradycardia; neurologic symptoms such as faint-

ness, confusion, headache, and anxiety; and tachypnea and

dyspnea.2-4,10,11,13,14 As these signs and symptoms illustrate,

the heart and the brain are especially vulnerable to cyanide

poisoning because of their high requirements for oxygen.

Other findings that can, but do not always, occur in

cyanide poisoning include bright-red retinal veins because

of elevated venous oxygen concentration; and a bitter-

almond odor of victims’ breath or gastric contents.11 As the

gene necessary for detecting the bitter-almond odor is ab-

sent in approximately half of the population, absence of the

bitter-almond odor does not necessarily ref lect the absence

of cyanide toxicity. The almond odor may be masked by

the odor of smoke in the case of smoke inhalation.

LABORATORY FINDINGS

Hallmark laboratory findings in acute cyanide poison-

ing are metabolic acidosis with markedly elevated plasma

NAL OF EMERGENCY NURSING S13

TABLE 1

Clinical manifestations and laboratory abnormalities

in acute cyanide poisoning2-4,13,14

Clinical manifestations

Early manifestations . Faintness

. Flushing

. Anxiety

. Excitement

. Drowsiness

. Vertigo

. Headache

. Dyspnea

. Perspiration

. Tachypnea

. Tachycardia

Later manifestations . Altered consciousness

. Tremulousness

. Seizure

. Respiratory depression

. Noncardiogenicpulmonary edema

. Respiratory arrest

. Cardiac arrhythmia

. Cardiovascular collapse

Laboratory abnormalities

Elevated plasma lactate Possibly indicative of cyanidepoisoning: z8 mmol/L inpure cyanide poisoning,N10 mmol/L in smokeinhalation

High venous oxygenconcentration

Possibly indicative of cyanidepoisoning: arteriovenousoxygen saturation differenceb10 mm Hg

C Y A N I D E S U P P L E M E N T / B o r r o n

lactate and excessive venous oxygenation (Table 1).2,10,16

Elevations in plasma lactate are caused by the shift of

cyanide-poisoned cells from aerobic metabolism to anae-

robic metabolism, which generates lactate as a toxic by-

product. Plasma lactate concentration normally ranges from

0.5 to 2.2 mmol/L. A concentration z8 mmol/L suggests

the possibility of cyanide poisoning.2,10,16 However, ele-

vated plasma lactate is not specific to cyanide poisoning

and therefore does not definitively signify cyanide toxic-

ity. For example, plasma lactate concentration is also ele-

vated in cardiac arrest of any cause and in carbon monoxide

S14 J

poisoning,10 which, like cyanide poisoning, is common in

smoke-inhalation victims. The elevation of lactate observed

in pure carbon monoxide poisoning17 is generally less than

that in cyanide poisoning such that markedly elevated

plasma lactate in the setting of smoke inhalation is more

suggestive of cyanide.

OUR

Severe or advanced cyanide poisoningis manifested by hypotension,seizures, coma, respiratory depression,cardiovascular collapse, andcardiorespiratory arrest.

Based on the observation of a direct relationship be-

tween plasma lactate concentration and clinical indices of

cyanide toxicity, plasma lactate concentration has been sug-

gested as a marker of severity of cyanide toxicity both im-

mediately after poisoning and during recovery.9,16 Plasma

lactate may be inf luenced by factors other than cyanide

toxicity in the critically ill patient.11 Plasma lactate concen-

tration can be affected by seizures, apnea, cardiovascular

failure, and endogenous or administered catecholamines.10

In one study, for example, the specificity of a plasma lac-

tate concentration for a toxic blood cyanide concentration

(z1.0 mg/L) was affected by whether or not catechol-

amines (e.g., epinephrine, norepinephrine, dobutamine, do-

pamine) had been given.16 Specificity was 85% in patients

who had not been treated with catecholamines compared

with 70% in the overall sample, which included both pa-

tients who had received catecholamines and patients who

had not.

Hallmark laboratory findings in acutecyanide poisoning are metabolic acidosiswith markedly elevated plasma lactateand excessive venous oxygenation.

Excessive venous oxygenation, the second main labo-

ratory finding in acute cyanide poisoning, is ref lected in a

low (b10 mm Hg) arteriovenous oxygen saturation differ-

ence (Sa02-Sv02) on arterial and venous blood gas analysis.1

Excessive venous oxygenation is attributed to the inability

of cells to extract and use oxygen from arterial blood.

NAL OF EMERGENCY NURSING 32:4S August 2006

C Y A N I D E S U P P L E M E N T / B o r r o n

Blood cyanide concentrations currently have only a

confirmatory role in the initial management of acute cya-

nide poisoning because the results of standard assays are

generally not available within the time required to initiate

intervention.2 Although blood cyanide concentrations are

not practical in initial management, they are used to con-

firm toxicity. Cyanide should be measured in whole blood

because red blood cells concentrate cyanide more than other

constituents of blood do.11 The usefulness of blood cyanide

concentrations depends on early sampling and careful stor-

age and analysis because of the rapid metabolism of cya-

nide, its instability in blood samples, and the vulnerability

of cyanide assays to multiple sources of interference.11,18

For cyanide in whole blood, the toxicity threshold for cya-

nide alone ranges from 0.5 to 1.0 mg/L, and the lethal

threshold ranges from 2.5 to 3.0 mg/L.2,7,9,10

DIAGNOSIS OF ACUTE CYANIDE POISONING

Given the absence of a point-of-care blood cyanide test

that can rapidly confirm poisoning, acute cyanide poison-

ing is presumptively diagnosed based on index of suspicion

and clinical presentation.11 Rapid loss of consciousness or

development of coma and cardiovascular instability in the

presence of elevated (N8 mmol/L) plasma lactate suggest

the possibility of acute cyanide poisoning.2,10,16

Contextual clues to cyanide poisoning can provide piv-

otal diagnostic information when considered in conjunc-

tion with the clinical presentation.18 Information useful for

assessing the possibility of cyanide poisoning includes the

patient’s occupation, the patient’s mental status before

poisoning, and the location and circumstances of the poi-

soning. Occupations with potential exposure to cyanide

include laboratory scientists and technicians, metal workers

and miners, aircraft workers, firefighters, exterminators,

and fumigators. Exposure to fire smoke, in particular, in-

creases the clinical suspicion of cyanide poisoning. Acute

cyanide poisoning should be suspected in anyone who

inhales smoke in a closed-space fire, particularly in the

presence of soot in the mouth, altered mental status, and

hypotension.2,6,19 Smoke-inhalation victims are likely to

suffer concurrent cyanide and carbon monoxide poisoning.7

Although contextual clues such as exposure to fire

smoke can be critical in diagnosing acute cyanide poison-

ing, the apparent absence of such clues does not exclude a

August 2006 32:4S

diagnosis. The relative ease of obtaining cyanide can facil-

itate concealment of contextual clues in cases of intentional

poisonings such as suicide, murder, and terrorism. In re-

cent poisonings, such as the March 5, 2006, suicide of a

Minnesota State University student,20 individuals other-

wise unlikely to be in a position to procure cyanide ordered

it over the Internet. In the case of the 17-year-old described

above,1 contextual clues available at the time of poisoning

did not lead to suspicion of cyanide toxicity. The pre-

viously healthy victim with no history of depression was

visiting a classmate’s house when he complained of feel-

ing unwell and lost consciousness. Only after the window

of opportunity for effective intervention had passed did

investigators learn that the patient was poisoned by inten-

tional adulteration of a beverage with potassium cyanide

that the perpetrator had purchased via the Internet.

JOUR

Acute cyanide poisoning is presumptivelydiagnosed based on index of suspicionand clinical presentation. Rapid loss ofconsciousness or development of comaand cardiovascular instability in thepresence of elevated ( N8 mmol/L)plasma lactate suggest the possibility ofacute cyanide poisoning.

The challenges in recognizing acute cyanide poison-

ing could be heightened in multiple-victim events such as

industrial accidents and terrorist attacks. A diagnosis could

be missed if the nonspecific early symptoms of toxicity

such as dizziness, weakness, diaphoresis, and hyperpnea

are misconstrued as anxiety or mass hysteria, which are

observed commonly in multiple-victim incidents.11 Con-

versely, manifestations of anxiety or panic could be mis-

interpreted as signs and symptoms of cyanide exposure.13

Symptoms of respiratory distress and other nonspecific find-

ings in a possible mass-exposure incident should educe a

search for other physical signs, such as mydriasis, altered

mental status, or hemodynamic instability to increase

confidence in the diagnosis. Point-of-care measurement of

lactate might also help in eliminating panic as the etiology

NAL OF EMERGENCY NURSING S15

TABLE 2

Management of acute cyanide poisoning2,14

Measure Action

Termination of exposure . For inhalation exposure, removal of victim from site of exposure, using appropriate personalprotective equipment

. For exposure by ingestion, gastric lavage and activated charcoal unless contraindicated

. For dermal exposure, decontamination of skin with soap and water

Supportive care Basic Life Support. 100% oxygen

. Cardiopulmonary support or resuscitation

Advanced Life Support. Sodium bicarbonate for metabolic acidosis

. Anticonvulsants for seizures

. Epinephrine for cardiovascular collapse

Antidotal treatment . Cyanide Antidote Kit (amyl nitrite + sodium nitrite + thiosulfate) (not generally recommendedin smoke-inhalation victims)

. Hydroxocobalamin (proposed antidote in the United States; can be used regardless of suspectedcyanide source, including fire smoke)

C Y A N I D E S U P P L E M E N T / B o r r o n

although this diagnostic tool is unlikely to be available at the

incident scene.

Treatment of Acute Cyanide Poisoning

Acute cyanide poisoning is treated by terminating exposure

and administering supportive care and antidotal therapy

(Table 2).2,14 These aspects of care are discussed further

in this supplement in Koschel’s article, Management of the

Cyanide-Poisoned Patient.21

DECONTAMINATION

Termination of cyanide exposure can entail removal of the

patient from the contaminated environment in the case

of inhalation exposure, removal of contaminated clothing

and rinsing of the skin in the case of dermal exposure, and

gastric lavage and administration of activated charcoal in

the case of ingestion unless contraindicated.22

SUPPORTIVE CARE

Initial supportive care involves the basic life support air-

way, breathing, and circulation (ABC) triad.2,11 Administra-

tion of 100% oxygen is viewed as an important component

of supportive care despite the fact that cyanide poisoning

involves deficient oxygen utilization rather than deficient

oxygen availability.11 It is hypothesized that increased oxy-

gen delivery could increase respiratory excretion of cyanide,

S16 J

reactivate mitochondrial enzymes inhibited by cyanide, and

activate oxidative systems other than mitochondrial cy-

tochrome oxidase.10,11 Administration of 100% oxygen is

essential to effective treatment of concurrent carbon mon-

oxide exposure. Advanced life support for acute cyanide

poisoning includes endotracheal intubation for comatose

patients, epinephrine infusion for cardiovascular collapse, so-

dium bicarbonate for metabolic acidosis and anticonvulsants

for seizures.10

ANTIDOTAL THERAPY

Several cyanide antidotes are available in one or more coun-

tries around the world, but the Cyanide Antidote Kit (CAK)

is the only one currently available in the United States.23

The CAK is composed of amyl nitrite, sodium nitrite, and

sodium thiosulfate. Amyl nitrite, available as perles, is given

by inhalation, sometimes via a mechanical ventilation de-

vice to initiate methemoglobin formation before intrave-

nous administration of sodium nitrite and sodium thiosulfate.

The nitrites reduce blood cyanide concentrations by form-

ing methemoglobin, to which cyanide binds with higher

affinity than it binds cytochrome oxidase.10 Binding of cya-

nide to methemoglobin liberates cytochrome oxidase, which

is necessary for aerobic cellular respiration. Another mecha-

nism of action of nitrite therapy is generation of nitric

oxide, which is also involved in cellular respiration.24 Sodium

OURNAL OF EMERGENCY NURSING 32:4S August 2006

C Y A N I D E S U P P L E M E N T / B o r r o n

thiosulfate enhances transformation of cyanide to less toxic

thiocyanates, which are renally excreted.10

The potential for toxicity caused by the CAK is sig-

nificant. At antidotal doses, sodium nitrite can cause pro-

found vasodilation associated with syncope, hypotension,

tachycardia, dizziness, and nausea and vomiting.25 Nitrite-

induced methemoglobinemia, one therapeutic mechanism

of amyl nitrite and sodium nitrite, reduces the ability of

blood to transport oxygen to the cells.26,27 Nitrite-induced

methemoglobinemia may be particularly dangerous for

smoke-inhalation victims, who likely also have carboxyhe-

moglobinemia secondary to concomitant carbon monoxide

poisoning.27-29 Like methemoglobinemia, carboxyhemo-

globinemia reduces the ability of blood to transport oxygen

to the cells. Nitrite-induced methemoglobinemia super-

imposed on carboxyhemoglobinemia from carbon mon-

oxide exposure could lead to potentially fatal reduction in

the oxygen-carrying capacity of the blood. Because of the

potential for dangerous disruption of oxygen transport to

the cells, the CAK is generally considered unsuitable for

prehospital use in victims of smoke inhalation, the most

common cause of cyanide poisoning.3,6,18

The Clinical Dilemma: to Treat or Not to Treat in the

Context of an Uncertain Diagnosis

Successful treatment of acute cyanide poisoning is greatly

enhanced by antidotal treatment. Supportive care alone im-

pacts signs and symptoms but does not affect the body’s

cyanide burden or the time course of cyanide in the body.10

In cases of suspected cyanide poisoning, the need for rapid

administration of an antidote in the context of an uncertain

diagnosis creates a predicament for the clinician deciding

whether or not to administer the CAK. Use of the CAK

entails the risk of causing harm to nonpoisoned patients if

the presumptive diagnosis is incorrect. However, the conse-

quences of failure to use the CAK because of an uncertain

diagnosis include death if cyanide toxicity is present.

In an attempt to improve the risk:benefit ratio in

the antidotal treatment of cyanide poisoning, the vitamin

B12 precursor hydroxocobalamin has been proposed for

introduction in the United States. Hydroxocobalamin de-

toxifies cyanide by binding it to form vitamin B12, which

is excreted in urine.10 First licensed as an antidote in

France in 1996, hydroxocobalamin has been used safely

August 2006 32:4S

and effectively in both prehospital and hospital settings

to treat acute cyanide poisoning associated with smoke in-

halation, industrial exposure to cyanide gas, and ingestion

of cyanide salts.12,15,30,31

Hydroxocobalamin has a favorable tolerability pro-

file.12,15,30,31 It does not impair blood oxygenation and

seems to generally improve hemodynamic stability victims of

cyanide poisoning. The most common side effects are caused

by the red color of the compound: hydroxocobalamin is

associated with transient pink discoloration of the urine and

mucous membranes and may interfere with some colori-

metric laboratory tests.12,15,30-33 These effects have limited

clinical impact and typically resolve within a few days of

administration of hydroxocobalamin. Transient elevations

in blood pressure rarely requiring treatment may also oc-

cur after treatment with hydroxocobalamin.34 Hydroxo-

cobalamin, like all medications, has been associated with

occasional allergic reactions, primarily with long-term, low-

dose use for applications other than cyanide poisoning.35,36

The apparently low risk of introducing significant harm

with hydroxocobalamin could allow for more confident

empiric treatment of acute cyanide poisoning than is cur-

rently possible in the United States and could enhance the

feasibility of early prehospital treatment of suspected cya-

nide poisoning from all causes including smoke inhalation.

Conclusions

Acute cyanide poisoning constitutes a formidable clinical

challenge. The need for early intervention and the lack

of a point-of-care test for confirming cyanide toxicity

necessitate administration of antidotal therapy based on

a presumptive diagnosis. Rapid presumptive diagnosis is

difficult because of the relatively nonspecific nature of

signs and symptoms. The differential diagnosis is broad.

Cyanide poisoning should be considered in any individual

with rapid loss of consciousness or development of coma

and cardiovascular instability in the presence of elevated

(N8 mmol/L) plasma lactate—especially in the presence of

a recent history consistent with possible exposure. Altered

mental status or hemodynamic instability after exposure

to smoke in a structural fire, suggests the probability of

cyanide poisoning. When cyanide poisoning is strongly

suspected, rapid administration of an antidote is required.

JOURNAL OF EMERGENCY NURSING S17

C Y A N I D E S U P P L E M E N T / B o r r o n

The decision to administer an antidote for presumptive

cyanide poisoning involves consideration of the risk of

antidote-induced toxicity as well as the risk of withhold-

ing treatment if cyanide poisoning is present. The intro-

duction of hydroxocobalamin may help to improve the

risk:benefit ratio in the antidotal treatment of cyanide poi-

soning in the United States.

Acknowledgment

The author acknowledges the assistance of Jane Saiers, PhD, in writ-ing this manuscript. Dr. Saiers’ and the author’s work on thismanuscript was funded by EMD Pharmaceuticals.

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