Carbon Monoxide Poisoning and CO Poisoning Complicated by Cyanide Poisoning

Carbon monoxide (CO) poisoning is the most common form of poisoning in the industrialized world and the most common cause of death by poisoning.  Thousands of Americans die of carbon monoxide poisoning every year.  More than 10,000 people miss at least a day of work because of CO exposure.  A survey of death certificates in the U.S. between 1978 and 1988 showed that CO exposure contributed to the deaths of more than 56,000 people.

Carbon monoxide results from of inhaling CO from any fossil fuel burning source.  This includes gasoline, diesel, propane, natural gas, charcoal and charcoal briquettes, etc.  Inhaling methylene chloride, a common ingredient in floor and paint stripping agents, will cause it to metabolize into carbon monoxide.  Cyanide is another chemical that metabolically poisons the cells.48 It is also produced by factories and during fires and mining accidents.

CO is one of most insidious toxins because often people have no idea that they’re being poisoned. Carbon monoxide can actually produce a kind of euphoria and resultant lack of judgment. In the winter months it has been estimated that a high percentage of emergency room patients with complaints of headache, and/or symptoms of flu are, in fact, suffering from CO poisoning.  This is a result of the exhaust of furnaces, heaters and generators, as well as coal and wood burning stoves, without adequate ventilation. Also, sitting in a car or boat for an extended period of time with the motor idling can result in CO poisoning. During power outages many people use gas-powered generators for heat, cooking, and lights. This often results in cases of CO poisoning.

Some people are exposed to chronic low-level carbon monoxide poisoning, such as smokers and toll collectors that constantly breathe exhaust fumes.  The damage done by chronic exposure is cumulative and can result in dementia and other psychiatric disorders.

HBOT delivered at the time of toxic poisoning has dramatic results.  This is also true for hydrogen sulfide and cyanide.  The diagnosis cannot be made unless exposure is suspected.  Further, the percentage of CO bound to the hemoglobin does not correlate with the prognosis and often does not correspond to the clinical condition caused by tissue toxicity.  HBOT is indicated in the presence of almost any sign or symptom and the sooner it is initiated, the better the outcome.  The mortality rate in severe cases is 30 % when started after six hours of exposure, but only 13.5% if started less than six hours after exposure.

Clinicians are using HBOT for the secondary deterioration in patients that can occur within days to six weeks after the initial poisoning when emergency treatment was not obtained.  This is an “off-label” use of HBOT.  Symptoms can recur weeks or months after an acute poisoning.49 Neurological and psychiatric abnormalities can also occur after patients have been treated for acute poisoning and seem to have recovered.  These symptoms can occur from two to 40 days after CO exposure and manifestations include disorientation, apathy, bradykinesia (slowed movement as in Parkinson’s disease), gait disturbances, aphasia (language impairment), apraxia (inability to carry out learned tasks), incontinence, personality changes, and rarely, seizures and coma.  The incidence is 35.8% for those patients treated with either ambient pressure oxygen or with HBOT at more than six hours.  The incidence of this syndrome among patients treated with HBOT in less than six hours was only 7%.

Carbon monoxide is preferentially taken up by hemoglobin—the oxygen-carrying portion of the red blood cell.  Hemoglobin is 240 times likelier to bind with carbon monoxide than with oxygen.50 In CO poisoning the body is starved of oxygen, and a cascade of events takes place—without oxygen the cells cannot produce energy, cell function decreases, and the cells are poisoned by their own waste products.  Lack of oxygen often leads to swelling, in the brain especially, which causes more tissue destruction.  The brain is particularly affected by CO poisoning, the symptoms of which are drowsiness and other mental effects.

The heart is also impacted because it, like the brain, needs a lot of oxygen.  The heart is especially vulnerable because the gas binds three times more strongly to the heart muscle than other muscle tissue.  For this reason, people with heart disease are more susceptible to CO poisoning.

HBOT puts so much extra oxygen into the bloodstream that the body’s hemoglobin is forced to bind to oxygen instead of carbon monoxide.  The blood plasma is also supersaturated with oxygen and puts more into the starved tissues.  HBOT reduces swelling and counteracts the breakdown of brain cells.

The use of HBOT can reduce the time it takes for CO to leave the body.  The half-life (the length of time it takes for half of the CO to clear the body) of CO in the bloodstream is 5.3 hours when breathing regular air at sea level.  With HBOT at 3 ATA the half-life is 23 minutes.51

In 1942, Dr. Edgar End and Dr. C.W. Long were the first to show that high-pressure oxygen was more effective than normal-pressure oxygen in treating CO poisoning. Human beings were first treated by HBOT for CO poisoning in 1960.  It is a life-saving treatment even if there is a delay between exposure and HBOT.

Children, pregnant women and the elderly are more susceptible to CO poisoning.  The fetus is especially effected by CO poisoning, even more so than the mother. A 1989 report showed that carbon monoxide poisoning is responsible for more than 50% of the approximately 12,000 fire-associated deaths that occur each year.52

Neubauer thinks that proper treatment of smoke inhalation should include the use of HBOT.  But usually firefighters are given normal-pressure oxygen at the scene.  Lab tests given them show how much carbon monoxide is in the blood, but not within the body’s tissues.  If the blood test shows a normal reading, often no further treatment is given.  As a result, some firefighters continue to have ongoing heart and brain problems from smoke inhalation.

Neubauer thinks that treatment should be continued until the patient’s SPECT scans are normal.  This may take up to three or four weeks.  A 1989 report by Dr. S.R. Thom showed no residual damage among 500 patients treated with HBOT.  The incidence of brain damage was 12% in those treated with only normal oxygen.53

His protocol is that the first treatment be given as soon as possible after exposure at 3 ATA for one hour and the second at 2.5 ATA for one hour, given within 4-6 hours after the first treatment if the patient is in a coma or stupor.  The third treatment should be at 2.0 followed by ten treatments at 1.5. The total number of treatments will vary with each patient.

Many doctors believe that one session of HBOT is sufficient for CO poisoning.  The use of multiple treatments is not standard practice in the U.S. However, it is allowed in mainland China where the incidence of CO poisoning is very high due to the burning of coal inside the home.

The physiological benefits of HBOT are improvement of oxygenation and hastened CO and hemoglobin dissociation, restoration of mitochondrial function, and inhibition of adherence of white blood cells to the capillary walls.

Notes
48Harch, 43.
49Neubauer, 108.
50Ibid., 109.
51Ibid., 111.
52Ibid, 112.
53Ibid.