| Carbon Monoxide Poisoning | | Counselor, Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion of carbonaceous material. CO at sufficiently high concentrations can kill. Commonly overlooked or misdiagnosed, CO intoxication often presents a significant clinical challenge. Most fatalities result from fires, stoves, portable heaters, and automobile exhaust. These often are associated with malfunctioning or obstructed exhaust systems and suicide attempts. Other sources of CO include cigarette smoke, vented gas water heaters, kerosene space heaters, charcoal grills, hibachis, Sterno stoves, propane-fueled forklifts, gas-powered concrete saws, inhaling spray paint, indoor tractor pulls, and swimming behind a motorboat. Children riding in the back of enclosed pickup trucks seem to be at particularly high risk for CO exposure. Industrial workers at pulp mills, steel foundries, and plants producing formaldehyde are at risk for exposure, as are personnel at fire scenes and individuals working indoors with combustion engines or combustible gases. We value all your comments, so, if you have a suggestion for a newsletter subject but haven't submitted it yet, or if you have already submitted one but think of another, please take a minute to let us know by clicking on your "Reply" button and dropping us a note. To learn more about AMFS, Inc., the organization run by Physicians and Attorneys that provides medical experts and case review services nationwide, and has produced the following informational newsletter to aid you in understanding complex medical issues, please click here - www.medicalexperts.com. |
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| Pathophysiology: CO toxicity causes impaired oxygen delivery and utilization at the cellular level. CO affects several different sites within the body but has its most profound impact on the organs with the highest oxygen requirement (eg, brain, heart). Toxicity primarily results from cellular hypoxia caused by impedance of oxygen delivery. CO reversibly binds hemoglobin, resulting in relative anemia. Because it binds hemoglobin 230- 270 times more avidly than oxygen, even small concentrations can result in significant levels of carboxyhemoglobin (HbCO), and can rob tissue of essential oxygen. Symptoms typically begin with headaches at HbCO levels around 10%. Levels of 50-70% may result in seizure, coma, and death. |
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| Frequency/Mortality/Morbidity: Approximately 2 million death certificates are filed yearly in the US. During the 10-year period from 1979-1988, 56,133 death certificates contained codes addressing CO as a contributing cause; 25,889 (46%) were suicides, 15,523 (28%) involved burns or fires, 210 were deemed homicides, and 11,547 (21%) were categorized as unintentional. Heroin, the second leading cause of poisoning fatality, followed CO with 5948 deaths. In the same period, all other unintentional poisonings resulted in 40,424 deaths. Of unintentional fatalities, 57% were associated with automobile exhaust. The next leading identifiable causes are coal, wood, or kerosene stoves and fireplaces; combustion of natural gas from a pipeline; combustion of gasoline, acetylene, or utility gas; and industrial sources. Increasing evidence implicates ambient urban CO levels in rates of angina, arrhythmias, and cardiac arrest. Presuming that the evidence is quantifiable and depending on the true extent, this implies a significant underreporting of CO- associated deaths. |
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| | History: Misdiagnosis commonly occurs because of the vagueness and broad spectrum of complaints; symptoms often are attributed to a viral illness. Specifically inquiring about possible exposures when considering the diagnosis is important. Any of the following should alert suspicion in the winter months, especially in relation to the previously named sources and when more than one patient in a group or household presents with similar complaints. Symptoms may not correlate exactly with HbCO levels. Known acute poisoning, malaise, flulike symptoms, headache, drowsiness, dizziness, weakness, confusion, fatigue, dyspnea on exertion, chest pain, palpitations, lethargy, confusion, depression, distractibility, hallucination, agitation, nausea, vomiting, diarrhea, abdominal pain, visual disturbance, syncope, seizure, memory and gait disturbances, bizarre neurologic symptoms, and coma. |
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| | Physical: Physical examination is of limited value. Inhalation injury or burns should always alert the clinician to the possibility of CO exposure. However, some of the classical physical findings of CO toxicity include: cherry red skin, flame-shaped retinal hemorrhages, bright red retinal veins, papilledema, noncardiac pulmonary edema, amnesia, gait disturbances including dysequilibrium, stupor, and coma. |
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| | Lab Studies: HbCO analysis is the key to the diagnosis. Four special caveats should be noted: Individuals who chronically smoke may have mildly elevated CO levels as high as 10%; presence of fetal hemoglobin, as high as 30% at 3 months, may be read as an elevation of HbCO level to 7%; patients with preexisting disease can experience increased exertional angina with HbCO levels of just 5-10%, if cyanide toxicity is suspected (eg, industrial fire), cyanide exposure can be suggested by an unexplained metabolic acidosis. Other basic labs should be obtained as well as an electrocardiogram. |
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| | Imaging Studies: Chest x-ray and head CT scan are the main studies to obtain. Chest x-ray changes such as ground glass appearance, perihilar haze, peribronchial cuffing, and intra-alveolar edema imply a worse prognosis than normal findings. CT of the head is important because studies have indicated that CO may cause brain lipid peroxidation and leukocyte-mediated inflammatory changes in the brain. Following severe intoxication, patients display central nervous system (CNS) pathology, including white matter demyelination. This leads to edema and focal areas of necrosis, typically of the bilateral globus pallidus. A CT scan will diagnosis this pathology. |
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| | Emergency Room Treatment: Pulse oximetry readings do not accurately reflect oxygenation level since the machines cannot distinguish oxyhemoglobin from carboxyhemoglobin. The patient should be placed on a cardiac monitor and given 100% oxygen by face mask until their carboxyhemoglobin levels are well below 10%, and preferably below 2-3% in those who are cardiac or pulmonary compromised. Patients should be admitted to a monitored setting if HbCO levels are 30-40% or above 25% with associated symptoms. Patients with HbCO levels greater than 40%, or those with cardiovascular or neurologic impairment should be transferred to a hyperbaric oxygen facility. Also, persistent impairment after 4 hours of normobaric oxygen therapy necessitates transfer to a hyperbaric center. Serial neurologic examinations, including funduscopy, CT scans, and, possibly, MRI, are important in detecting the development of cerebral edema. Cerebral edema requires intracranial pressure (ICP) and invasive blood pressure monitoring to further guide therapy. Head elevation, mannitol, and moderate hyperventilation to 28-30 mm Hg PCO2 are indicated in the initial absence of ICP monitoring. Glucocorticoids have not been proven efficacious, yet the negative aspects of their use in severe cases are limited. In patients who fail to improve clinically, consider other toxic inhalants or thermal inhalation injury. Be aware that the nitrites used in cyanide kits cause methemoglobinemia, shifting the dissociation curve leftward and further inhibiting oxygen delivery at the tissue level. Combined intoxications of cyanide and CO may be treated with sodium thiosulfate 12.5 g intravenously to prevent the leftward shift. |
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| | Hyperbaric Oxygen: HBO at 3 ATM (atmospheres) raises the amount of oxygen dissolved in the serum to 6.8%, enough to sustain cerebral metabolism. Elimination half-life is reduced to 15-23 minutes. Chambers are either small monoplace hulls, allowing space for a single supine patient who can be viewed through a window at the head, or they are acrylic walled and allow full visualization. Many of these monoplace chambers allow for care of the critically ill, including IV lines, arterial lines, and ventilator. Others are large multiplace chambers that permit ventilation equipment and allow medical teams to accompany the patient. Treatment regimens usually involve 100% oxygen at 3 ATM for 90-120 minutes. The nearest hyperbaric oxygen center can be located by contacting the Divers Alert Network (DAN) at Duke University at (919) 684-2948. |
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| | Prognosis: Cardiac arrest, coma, metabolic acidosis, and high HbCO levels are associated with poor outcome. Abnormal findings on CT scan are associated with persistent neurologic impairment. Neuropsychiatric testing may have prognostic efficacy in determining delayed sequelae. |
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| | Medical/Legal Concerns: Failure to accurately diagnose is the principle concern. Patients with cardiovascular disease and pregnant patients must be treated aggressively and quickly. Anticipating and mitigating against the possibility of delayed neurologic sequelae is also very important. Failure to transfer a person to a HBO facility when it is indicated can result in a poor outcome, and may lead to litigation. Also, failure to contact all parties who still may be at risk from exposure could allow for further CO toxicity, and an additional litigation risk. |
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