Salt Lake City Office
963 Folsom Avenue
Salt Lake City, UT 84104-1130
Phone: (801) 355-4433
Making a diagnosis of CO poisoning is crucial, as acute high level CO poisoning can be fatal in just a few minutes. The symptoms are usually multiple, many are non-specific, and some are vague. They can involve many of the body systems. Please be aware that the symptom list below is not complete and that they often do not follow this rank ordering at presentation. Moreover, many of the more severe symptoms (eg. below ataxia) are only seen with acute high level CO exposure.
* Dizziness on exertion
* Fatigue, weakness
* Nausea, vomiting
* Dyspnea on exertion
* Cutaneous vessel dilation
* Mental Confusion, difficulty with thinking
* Fine manual dexterity abnormal
* Visual disturbances
* Hallucinations, confusion
* Retinal hemorrhages
* Syncope, collapse
* Tachypnea (increased ventilation), further tachycardia
* Lactic acidosis
* Cheyne Stokes ventilation
* Coma, convulsions
* Cardiac and ventilatory depression
* Cardiorespiratory failure (death)
Making a diagnosis of CO poisoning is crucial, since the condition can be fatal in just a few minutes. The symptoms are widely varied, many are non-specific, and can involve many body systems.
Victims often believe, or are led to believe, that they are have the “flu”, gastroenteritis, etc. CO poisoning is very often misdiagnosed clinically as:
* Psychiatric illness
* Heart disease
* Food poisoning
There are clues that signal the likelihood of CO poisoning:
* If everyone in the family suddenly becomes ill with some of the above symptoms.
* If the victim is in a situation where he or she may be exposed to high CO levels.
* If symptoms are relieved when the victim moves to a different location / into fresh air.
As a noted emergency room physician has said, “the standard of care for carbon monoxide poisoning may well be misdiagnosis”
The following is a list of symptoms which have been applied mainly to acute CO poisoning. Many sources suggest they can be closely related to blood COHb level. Please note that in practice, severity of symptoms DO NOT correlate well with COHb level. Thus, any conclusions about COHb from symptoms, or vice versa, should be drawn with the greatest caution!
* No obvious symptoms
* Decreased tolerance for exercise in persons with existing pulmonary disease
* Decreased angina threshold
* Decreased threshold for visual stimuli
* Decreased visual acuity
* Severe headache
* Increased respiration
* Impaired judgement
* Visual disturbance
* Decreased awareness
* Cardiac irregularities
* Muscle weakness
* Usually death in a few minutes
70% -and up
* Immediately fatal
Acute- Cerebral edema and hemorrhages
Chronic- Necrotic lesions in basal ganglia and demyelination
Acute- Myocardial necrosis
Chronic- Myocardial infarcts
Primary- Pulmonary edema
Secondary- Aspiration pneumonia in comatose patients
Lobar necrosis with chronic repeated exposure
Parenchymatous degeneration leading to necrosis
Intramuscular hemorrhages, swelling, and rhabdomyolysis
Marrow hypertrophy in chronic CO-hypoxia
Erythema, blisters, and gangrene
Clinical Degree of Intoxication – Symptoms
I – Mild Headache, vomiting, tachycardia, no disturbances of consciousness
II – Moderate Disturbances or loss of consciousness without other neurological symptoms, tachycardia, nocioceptive reflexes still intact
III – Severe Loss of consciousness, intense muscular tonus, pathological neurological symptoms, tachycardia and tachypnea, circulatory and respiratory disturbances not observed
IV – Very Severe Loss of consciousness, clinical signs of central nervous system damage, circulatory and respiratory disturbances
Comment: Many many different classifications of severity of CO poisoning are in existence. Just as COHb level does not correlate well with short-term symptomatology or with the longterm effects, the symptoms and effects of CO poisoning do not fit easily into discrete classes as the above suggests. This table is presented as just one possible approach to classification of the effects of CO poisoning, but not necessarily one embraced by the website writer.
* Carboxyhemoglobin Saturation
* other Arterial blood gases and pH
* Complete blood count
* Serum glucose and lactic acid concentration
* Serum electrolytes, and urea nitrogen and creatinine concentrations
* Urine analysis
* Electrocardiogram and echocardiogram
* Chest X-ray
* Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities
* Serum aspartate and alanine transferase (SGOT, SGPT) activities
* Serum myoglobin concentration
* Neuropsychologic screening test
* Drug screening
* Cerebral computed tomography
Note: With the exception of neuropsychologic evaluation, most of the above tests are usually only of value in acute, higher-level CO poisoning. In such instances, the first eight tests should be done as quickly as possible after presentation.
In the early days of mining, caged canaries were hung in the tunnels. The birds, being so small, were especially susceptible to poisonous gases because of their high metabolism and ventilation rate. If the bird died, it was an alarm telling the miners get out of the mine. Now electronic CO detectors are available for the home.
It is best to avoid exposure to sources of CO
* Make sure fuel-burning equipment is working correctly and is properly exhausted. This includes furnaces, hot water heaters, and propane and gasoline powered vehicles used indoors.
* Stop smoking.
* Don’t leave your car running in the garage, especially if it is attached to your house. It could poison you in the car, and CO could get into the house and afflict others.
* If you are in heavy traffic, keep your windows rolled up. This is especially true if you are caught in traffic in an enclosed space like a tunnel.
Management of CO Poisoning – Quick Points
* Remove victim from the site of CO exposure
* oxygen immediately – If possible take a blood sample for COHb before this is done
* Use endotracheal intubation in comatose patients to facilitate ventilation
* Remove the patient to a hyperbaric facility when indicated (if at all possible)
* Keep the patient calm and avoid physical exertion by the patient
* Manage complications: e.g. electrolyte imbalance, brain edema, cardiac arrhythmias
Guidelines for Management
* Remove patient from the site of CO exposure
* Immediately administer high-flow, 100% oxygen through a tight-fitting mask
* If possible take a blood sample for COHb before O2 is given
* Consider endotracheal intubation to facilitate ventilation in comatose patients
* In cases of severe poisoning, or in presence of unconsciousness or neurological signs, treat with hyperbaric oxygen
* Keep patient calm to reduce metabolic rate and oxygen consumption and avoid physical exertion by the patient; insulate body and warm, if hypothermic
* Look for signs of cardiovascular and neuropsychiatric dysfunction
* Manage complications: e.g. electrolyte imbalance, cardiac arrhythmias
* Consider supporting cardiovascular function with inotropes, antiarrhythmics, etc.
* Consider treating cerebral edema with hyperosmotics such as mannitol, and with steroids, to lower intracranial pressure and restore brain blood flow
* Treat pregnant patients more aggressively, even those with moderate CO poisoning
* Comatose patients who survive may show immediate or delayed neuropsychiatric deficits; hyperbaric oxygen therapy decreases the incidence of both types of sequelae
* Survivors should avoid exertion for 3-6 weeks after severe poisoning