ACUTE CARBON MONOXIDE POISONING
Carbon monoxide (CO) is a colorless, odorless, tasteless gas that, physiologically, is
a chemical asphyxiant. When inhaled, it combines with hemoglobin more readily than
does oxygen, displacing oxygen from hemoglobin and thereby interfering with oxygen
transport by the blood. In other words, breathing carbon monoxide can lead to
asphyxiation - unconsciousness and even death.
ETIOLOGY
The majority of CO exposures occur in the winter months. The most common source
of residential CO-related poisoning is un-vented or faulty furnaces and heaters. Increased
risk occurs anytime these products are operated in enclosed areas with poor ventilation
1. Living poisoning Common sources of CO include car and boat exhaust fumes,
smoke from fire, defective or poorly ventilated furnaces, gas powered engine exhaust,
home water heaters, or wood stoves. Motor vehicle exhaust is the most common
source of fatal CO intoxication, with most deaths associated with stationary vehicles.
Deaths in garages frequently occur even with garage doors or windows open for
ventilation. Smoke from fire is the second leading cause of CO poisoning and is the
most common cause of death in building fires. Many cases of poisoning occur in the
winter months. Car exhausts may become blocked with snow and more nonelectric
heating and cooking devices are used in confined spaces, particularly during winter
power outages.
2. Occupational poisoning Exposure to methylene chloride, a common ingredient in
paint remover, can also cause CO poisoning. It is absorbed through inhalation,
ingestion, or dermal contact, and is converted to CO by the liver. Methylene chloride is
stored in body tissues and released gradually; the carbon monoxide elimination half
life in people exposed to methylene chloride is more than twice that of inhaled carbon
monoxide.
3. Accidental poisoning Nature gas explosion or coal gas leakage, inhalation gas in
fire, suicide or homicide with CO.
TOXIC MECHANISM
Carbon monoxide has a significant affinity to the iron (or copper) sites in hemoglobin,
the principal oxygen-carrying compound in blood. The affinity between carbon monoxide
and hemoglobin is 230~260 times stronger than the affinity between hemoglobin and
oxygen. CO binds to the hemoglobin, producing carboxyhemoglobin (COHb). An ambient
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CO level of 100 ppm produces an COHb of 16% at equilibration, which is enough to
produce clinical symptoms. Carbon monoxide is naturally found in the body as a product
of hemoglobin breakdown, therefore normal COHb concentrations can range from 1% to
2%. Smokers have a baseline COHb concentration of up to 3%~10% and otherwise
healthy heavy smokers can tolerate levels of COHb of up to 15%. COHb concentrations
greater than 10% indicate a recent exposure and the need for clinical intervention The
patients with COPD or CHD are sensitive to the increase of COHB concentration. Oxygen
blood content is actually increased in the case of CO poisoning; levels of oxygen available
for tissue use are decreased as CO shifting the oxygen dissociation curve to the left,
which causes all the oxygen is in the blood, none is being given to the tissues, and this
causes tissue hypoxic injury. A second mechanism involves CO also has a high affinity for
myoglobin and effects on the mitochondrial respiratory enzyme chain which is responsible
for effective tissue utilization of oxygen. After acute CO poisoning the organs most
sensitive to hypoxia will be most affected; i.e. the brain and the heart. Another mechanism,
(The delayed neurological effects may develop over days following the initial acute
poisoning) involves formed blood cells and chemical mediators which cause brain lipid
peroxidation. 50% COHb concentration can cause severe anoxia, heart and breathing will
stop and action of brain wave will vanish at the 60%~70% concentration of COHb.
CLINICAL PRESENTATION
CO poisoning causes acute symptoms such as headache, nausea, weakness,
angina, dyspnea, loss of consciousness, and coma. Neuropsychiatric symptoms may
develop weeks later.
1.
Acute poisoning
Table 1: Signs and Symptoms of Acute CO Poisoning
Severity
Mild
Moderate
Severe
COHB（%）
10%~20%
30%~40%
40%~60%
Symptoms
Asymptomatic
Headache
Nausea
Dizziness
Confusion
Chest pain
Dyspnea
Weakness
Blurred vision
Chest pain
Heart palpitations
Disorientation
Signs
Vomiting
Tachypnea
Tachycardia
Cognitive deficits
Ataxia
Myonecrosis
Coma
Seizures
Ventricular dysrhythmias
Hypotension
Myocardial ischemia
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2.
Delayed Neuropsychiatric Syndrome Neurologic injury following acute CO
poisoning may be delayed for several weeks to months after exposure. A wide
range of neurologic abnormalities has been reported (Table2).
Table 2
Neurologic impairments from acute CO poisoning
Parkinsonism
Persistent vegetative state
Akinetic mutism
Agnosia
Apraxia
Visual impairment
Amnestic/confabulatory state
Psychosis
Cognitive impairment
LABORATORY TEST
1. Percentage carboxyhaemoglobin (COHb) The percentage COHb as a measure of
CO poisoning is a specificity index, but it is limited because COHb levels are affected
by the removal from the source of CO for 8h and any oxygen treatment given before
measurement of it. It is also can be an index of severity of CO poisoning and reflex the
time of exposure,
2. Arterial Blood Gas In acute CO poisoning patients, PaO2 and SaO2 decrease,
PaCO2 is normal or decrease slightly. Metabolic acidosis always occurs at long time
poisoning patients, arterial pH and base excess(BE) decrease.
3. Electroencephalogram（EEG）An electroencephalogram reveals diffuse low slowing
waves. The manifests of EEG aren’t paralleled relationship to the patients’ condition.
4.
Neuroimaging
molecular
Abnormalities have been shown by computed tomography(CT),
resonance
imaging(MRI),
and
single-photon-emission
computed
tomography(SPECT). The regions most commonly involved include the globus
pallidus and the deep white matter
DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS
1.
Diagnosis Exposure to carbon monoxide is measured either directly from blood
samples and expressed as a percentage of COHb or indirectly using the carbon
monoxide in expired breath. Percentage COHb is the most frequently used biomarker
of carbon monoxide exposure. Although the diagnosis of carbon monoxide poisoning
can be confirmed by detecting elevated levels of blood COHb levels, the presence of
clinical signs and symptoms after known exposure to carbon monoxide should not be
ignored.
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2. Differential diagnosis overdose hypnagogue、cerebrovascular accident、diabetes
mellitus ketoacidosis
TREATMENT
1.
Stop inhaling CO
First step is to remove victim from the source of carbon
monoxide. Removal to fresh air is essential.
2. Oxygen therapy
Supplemental oxygen is the most important treatment for CO
poisoning.CO elimination is related to minute ventilation, duration of exposure, and the
fraction of inspired oxygen (FIO2).The half-life of COHb is 4–6 hours when the patient
is breathing room air, 40–80 minutes when the patient is breathing 100% oxygen, and
only 15–30 minutes when the patient is breathing hyperbaric oxygen.
2.1. Face mask oxygen therapy
High-flow oxygen by nonrebreather face mask or
endotracheal tube for several hours should immediately be provided to patients.
Treatment decisions should not be made based solely on COHb concentrations, since
they do not reliably correlate with degree of injury. Patients should be closely
observed and treated with 100% oxygen and high-flow 10L/min until all symptoms
resolve and the COHb concentration is below 5%.Usually COHb levels decreased
until below 15% will take 2 days
2.2. Hyperbaric Oxygen
CO removal can be speeded up by raising the oxygen
concentration, as with bottled gas containing greater fractions of oxygen, or by placing
the victim in a pressure chamber where he/she can be treated at 3 normal
atmospheres pressure with oxygen partial pressures of over 1600 mmHg for 30-120
minutes, called hyperbaric oxygen therapy (HBO). Several factors are considered
when treating carbon monoxide poisoning. Tests are done to determine the amount of
carbon monoxide in the blood. Infants, small children, older adults, or people with
health problems are more severely affected by carbon monoxide in the blood.
Treatment usually includes oxygen therapy to treat severe symptoms and lower
carbon monoxide levels in the blood as quickly as possible. If a pregnant woman has
carbon monoxide poisoning, treatment must be continued even after carbon
monoxide is no longer found in her blood, because there still may be carbon monoxide
in the blood of the fetus.
Table 4 Indications for Hyperbaric Oxygen Treatment
-Loss of conciousness
-Seizures
-Coma
-Altered mental status
-Neurologic symptoms not resolving after several hours of oxygen treatment
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-Pregnancy
-Presistent cardiac ischemia
-Age > 50 years and COHb > 25%
3. Mechanical ventilation
Mechanical ventilation is required with 100% oxygen
therapy until the COHb concentration is below 5%., and this entails having a tube
inserted in to the windpipe. Sometimes, plasmapheresis is used in severe patients to
remove high concentration COHb in blood.
4.
Prevention and cure of encephaledema
Encephaledema (cerebral edema) is
also a common result of severe carbon monoxide poisoning. This life threatening
condition entails the destruction of brain cells by compressing them into themselves
within the cranial compartment. Encephaledema occurs at 24～48h after serious CO
poisoning. Dehydrant is used to prevent it, such as 20％Mannitol and furosemide.
Convulsion can be treat with diazapam and phenytoin sodium.
5.
Promote functional recovery of brain cell
Triphosadenine, Coenzyme A,
high-dose cytochrome C.
PROGNOSIS
The prognosis is related to the level of carbon monoxide that a person is exposed to,
the duration of exposure, and the presence of underlying risk factors. A poor outcome is
predicted by lengthy carbon monoxide exposure, loss of consciousness, and advancing
age. The prognosis for people resuscitated after experiencing cardiac arrest with carbon
monoxide poisoning is poor. Therefore, in addition to the acute neurological sequelae
leading to loss of consciousness, coma and death, neurological sequelae such as poor
concentration and memory problems may be apparent in people recovering from carbon
monoxide poisoning (persistent neurological sequelae) or develop after a period of
apparent normality (delayed neurological sequelae). Delayed neurological sequelae
develop between 2 days to 240 days after exposure and are reported to affect 10–32% of
people recovering from carbon monoxide poisoning. Symptoms include cognitive changes,
personality changes, incontinence, psychosis, and Parkinsonism. Fortunately 50–75% of
people recover within 1 year.
PREVENTION
CO poisoning is largely preventable. Table 5 lists some recommendations from the
CDC for preventing CO exposure.

Have your furnace and fireplace cleaned and inspected before each heating
season. Have other fuel burning appliances checked regularly.
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
Use non-electrical space heaters only in well-ventilated areas.

Do not start or idle gas lawn mowers, cars, trucks, or other vehicles in an enclosed
area, even with the garage doors open.

Vent fuel-burning appliances outside whenever possible.

Do not ever use a charcoal grill inside your home, garage, tent, or camper.

Do not use portable heaters or lanterns while sleeping in enclosed areas such as
tents, campers, and other vehicles. This is especially important at high altitudes,
where the risk of CO poisoning is increased.

Read and follow manufacturer instructions and precautions that come with any
fuel-burning device.

Do not ever use a gas oven for heat inside your home.

Use an approved carbon monoxide detector with an audible alarm inside your
home
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