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Common causes of Carbon Monoxide poisoning include:
PREVENTION: Smoke detectors and carbon monoxide detectors can make a difference in your home. But if such devices are not properly maintained they won’t make a difference.
One of the most serious situations for carbon monoxide poisoning is in space heaters in apartments or hotel rooms. Stand alone heating units also include on the wall heating systems that you find in a high percentage of hotel rooms.
When in a hotel room with an older type system check to see if there is a carbon monoxide detector in the room. Travelling with a portable carbon monoxide detector is a good plan as only a few states have a law requiring CO detectors in hotels, and none in all rooms. Hotels
WARNING: Older ski resorts have a poor safety record for carbon monoxide poisoning so be particularly cautious when staying at ski resorts.
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DIAGNOSIS AND THE DANGERS OF MISDIAGNOSIS OF CARBON MONOXIDE POISONING:
Carbon monoxide (CO) may be the cause of more than one-half of the fatal poisonings reported in many countries: fatal cases also are grossly under-reported or mis-diagnosed by medical professionals. Therefore, the precise number of individuals who have suffered from CO intoxication is not known. “A patient who presents from a house fire or after a suicide attempt with automobile exhaust may not represent a diagnostic dilemma. However, a family presenting with the symptoms of nausea and vomiting or a patient with a headache that is improving can easily be misdiagnosed and discharged back to the dangerous environment where they may subsequently suffer more serious exposures.” 1
Thus, it is critical that emergency rooms and other primary care sources screen those with winter flu symptoms for suspicions of carbon monoxide poisoning. Significant clues include:
The health effects associated with exposure to CO range from the more subtle cardiovascular and neuro-behavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO.
The primary test for CO poisoning is testing of carboxyhemoglobin (COHb) measured at the time of hospital admission. While this test doesn't’t always correlate with the symptoms, signs, and prognosis of acute CO poisoning correlate it remains a critical first look to identify CO poisoning. We believe the use of this test and all other tests discussed herein must be dramatically increased when the real world diagnostic clues point to the potential for CO poisoning. However, a normal (COHb) test result must not be the end of the inquiry. Other laboratory tests to consider as non-exclusive additions to the diagnostic effort include pulse oximetry, complete blood count, arterial blood gasmonitoring, electrolytes, cardiac markets, blood uera nitrogen, creatine, creatine phosphokinese, chest radiography and ECG.
MRI, neuropsychological (neuropsychometric) and neurobehavioral analysis may also be necessary. A triangulated diagnosis based upon potential for exposure, real world symptoms, including neurobehavioral changes and consideration of all scientific diagnostic tests, is necessary to prevent a mild case of exposure from becoming a tragic case of carbon monoxide death or severe disability. Each scientific test must be looked as an independent chance to find the answer, not an exclusive rule out tool. Since CO poisoning can poison any part of the body, simply testing blood or imaging the brain, is insufficient.
The early symptoms (headache, dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Low level chronic exposure can also cause long term consequences, especially in someone with a lower threshold for danger, particularly those with cardiac conditions.
Complications occur frequently in CO poisoning. Immediate death is most likely cardiac in origin because myocardial tissues are most sensitive to the hypoxic effects of CO. Severe poisoning results in marked hypotension, lethal aarhythmias, and electrocardiographic changes. Pulmonary edema may also occur.
Neurological manifestation of acute CO poisoning includes disorientation, confusion, and coma. Headache may be the first sign. Dizziness, instability can also be a marker of the exposure.
Perhaps the most insidious effect of CP poisoning is the development of delayed neuropsychiatric impairment within 2 – 40 days after poisoning and the slow resolution of neurobehavioral consequences.
Carbon monoxide poisoning during pregnancy results in high risk for the mother by increasing the short-term complication rate and for the fetus by causing fetal death, developmental disorders, and chronic cerebral lesions.
The most common test for carbon monoxide poisoning is the blood test for carboxyhemoglobin (COHb) measured at the time of hospital admission. However, this test is susceptible to false negatives. As with all other neurologic conditions, the soft signs will point to disability well before the laboratory evidence may indicate it.
Think of this analogy: early onset of Alzheimer's appears years before disease has progressed to the point that neuroimaging can see the lesions. Yet, there is no doubt of a cognitive or neurobehavioral decline. The difference is that with Alzheimer's, the laboratory results will eventually catch up with the symptoms because of the progressive nature of the disease and the age of the patient makes the diagnosis one which the average practitioner is comfortable making without so called “scientific proof.”
Being late on the diagnosis of carbon monoxide is far more serious than being late on diagnosis of Alzheimer's. First, in a chronic exposure situation, you may be sending the patient back into a toxic environment, where the exposure could continue or worsen. Second, the Delayed Neurological Sequalae may result in severe disability.
Other laboratory tests to consider as non-exclusive additions to the diagnostic effort include:
Neuroimaging. Both CT and MRI have do have increasing capacity of diagnosing CO poisoning, with MRI being the far more sensitive technique. As the resolution of MRI’s continues to improve, it will become even more sensitive. This can be particularly important in cases for late diagnosis, where the initial medical treatment was superficial and did not even consider CO poisoning as a cause. But no neurological syndrome should ever be ruled out based on normal neuroimaging. The most common neurologic diagnosis, migraine, has virtually no neuroimaging to support the overwhelming majority of diagnosis, upon which a multi-billion dollar migraine drug industry is based. The irony of neurologic diagnosis is that if there is no “cure” which involves active treatment or therapies, far too many neurologists have little or no experience with the diagnosis. Almost all neurologist will understand MS or Alzheimer’s disease, almost none the diagnostic criteria for concussion. Not considering the full diagnostic scheme can have catastrophic consequences in a carbon monoxide exposure case.
Neuropsychological Testing. Neuropsychological testing is a highly sensitive measure for determining neurologic, particularly cognitive, dysfunction. While it is sometimes criticized as a stand alone diagnostic tool, much of that criticism is unwarranted,2 provided the diagnostician looks at the context of the change in the function, not just “history” or current dysfunction. Further, incorporating reports of changes in neurobehavioral symptoms, adds considerably to both the sensitivity and the specificity of the diagnosis. What simple neuropsychological tools could add to the equation in any case of suspected ongoing CO exposure is raise the index of suspicion, to the get to the bottom of the source of the toxin. As so often is the focus of the TV show House, taking enough time in the diagnostic process to consider the environment, not just the overt explanation of the patients symptoms, can save lives and prevent disability. Inquiries into the cognitive and neurobehavioral changes that a patient may have experienced in the days or hours before hospitalization could provide a roadmap to discovering the CO exposure.
The Undiagnosed Fatalities. While there is no empirical research to support this, we believe that the fatalities from CO poisoning are far greater than reported, especially in the cardiac population. If a person with a known cardiac condition has a heart attack, stroke or arrest as a result of CO poisoning, we believe that in most such cases, unless other family members get sick at the same time, no analysis of CO poisoning will ever be made. We believe the CDC or research university should undertake a large scale surveillance study of cardiac events in the winter “flu” season, to determine how much more prevalent a CO exposure event plays a part.
1 Kao, L, Nanagas, K, Toxity Clin Lab Med 26 (2006) 99-125 Louise W.Kao, M.D., Department of Emergency Medicine, Indiana School of Medicine, Indianapolis, IN, Kristine A. Nanagas, M.D., Medical Toxocology of Indiana, Indiana Poison Center, Indianapolis, IN
2 A significant proportion of revisionism in classic neuropsychological diagnostic measures is fueled by research funded by the insurance industry, both to reduce the cost of neurologic treatment and to limit damages in personal injury cases. Terms like malingering, conversion disorder and somatoform disorder, which have little practical relevance in real world treatment, are making up much of the focus of current neuropsychological (also called neuropsychometric) research. Malingering would have virtually no place in a CO diagnosis equation; Conversion disorder is a fantasy of psychiatrists, left over from the days of Freud and somatoform disorder occurring after age 35, is only valid when the diagnosis has been made previously in a patients lifetime and is just an additive diagnosis in almost all cases, a bizarre way of describing the fact that emotional people suffer emotional challenges when faced with injury and disability.
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