Biomedical Engineering Reference
In-Depth Information
the cessation of aerobic respiration and cellular
hypoxia. The central nervous system, particularly
the respiratory center, is especially susceptible to
this effect and respiratory failure is the usual cause
of death. Tissues with the highest oxygen require-
ments are also susceptible to cyanide toxicity:
brain, liver, heart [15].
exposure to low concentration, diagnosis, elimi-
nating further exposure and successful treatment
are possible.
6.3.4.2 Severe cyanide exposure
In high concentrations there is a transient increase
in the depth and rate of respiration within a few
seconds. This stimulation may be so powerful that
a casualty cannot voluntarily hold his or her breath.
Violent convulsions occur after 20-30 s with cessa-
tion of respiration within 1-2 minutes. Cardiac
failure follows 3-4 minutes later.
6.3.4 Signs, Symptoms and Severity of
Exposure
The more rapidly the tissue cyanide levels build
up, the more acute the signs and symptoms of
poisoning and the smaller the total absorbed dose
required to produce a given effect. Hydrogen
cyanide causes no distinguishable external effects
because it is colorless and a non-irritant. Because
cyanogen chloride causes irritation of mucous
membranes it produces similar effects as riot-
control, mustard and nerve agents with irritation
of the eyes, nose, and airways, as well as marked
lacrimation, rhinorrhea, and bronchosecretions.
6.3.5 Medical Management
Successful treatment for acute cyanide poisoning
depends upon removal of the casualty from cyanide
exposure and rapid fixation of the cyanide ion,
either by methemoglobin (metHB) formation or
by fixation with cobalt compounds. Management
of cyanide gas poisoning begins with removal
of the patient to fresh air. Dermal decontamina-
tion is unnecessary if exposure has been only to
vapor, but wet clothing should be removed and
the underlying skin should be washed with soap
and water or water alone if liquid on the skin is
a possibility. Since cyanide is rapidly detoxified
by the body, any casualty who is fully conscious
and breathing normally more than 5 minutes after
presumed exposure has ceased will likely recover
spontaneously and will not require treatment. Arti-
ficial resuscitation, though possible, is not likely
to be helpful in the absence of drug treatment.
Attention to the basics of intensive supportive
care is critical and includes mechanical ventilation
as needed, circulatory support with crystalloids and
vasopressors, correction of metabolic acidosis with
IV sodium bicarbonate, and seizure control with
benzodiazepine administration. Because cyanide
reversibly inhibits cellular utilization of oxygen the
administration of 100% oxygen has been found
empirically to exert a beneficial effect and should
be a part of general supportive care for every
cyanide-poisoned patient.
Severe exposure and those that are symptomatic
after cessation of exposure may further benefit
from specific antidotal therapy. This is provided
6.3.4.1 Minimal to mild cyanide exposure
The onset and progression of signs and symp-
toms after ingestion of cyanide or after inhalation
of a low concentration of vapor are slow. The
first effects may not occur until several minutes
after exposure, and the time course of these effects
depends on the amount absorbed and the rate of
absorption. With exposure to low concentrations,
after an initial transient hyperpnea, the early symp-
toms are weakness of the legs, vertigo, nausea
and headache for several hours before complete
recovery. Later, consciousness is lost, respira-
tion decreases in rate and depth, and convulsions,
apnea, and cardiac dysrhythmias and cardiac arrest
follows. If exposure is terminated before death it
may still be followed by convulsions and coma
which may last for hours or days depending on
the duration of exposure to the agent. If coma is
prolonged, recovery may disclose residual damage
to the central nervous system manifested by irra-
tionality, altered reflexes and unsteady gait which
may last for several weeks or longer. Permanent
deafness (neural damage) has also been described.
Because this cascade of events is prolonged with
