|
|
|
|
|
|
|
|
|
|
|
|
||||||||
|
|
|
|
|
|
|
|
||
|
|
||||||||
| Newsletters and Reviews Anticoagulant Rodenticides Carbon Monoxide Celexa Chemical Warfare Dangers of the Sun Ethylene Glycol Fertilizers Herbals Hydrofluoric Acid Insect Repellents Methanol Poison Ivy Rabies Raves and Club Drugs Tox Update 2007 Winter Hazards Download Newsletters Order Bulk Material |
Carbon Monoxide Revised 10/09 In the In the year 2007, the American Association of Poison Control Centers answered 15,769 calls regarding carbon monoxide exposures. Of these, 65% were mild exposures and managed in the home. The others (approximately 5,500) were managed in a healthcare setting with the majority being treated and released. While this data reflects poison control center data, it is estimated that the majority of CO exposures nationwide are not reported to poison centers. Background and mechanism of toxicity Carbon monoxide binds to hemoglobin with an affinity 250 times greater than oxygen. It also causes the hemoglobin to hold onto carbon monoxide, thus preventing delivery and release of oxygen to the tissues. The end result is tissue hypoxia. CO has a high affinity for myoglobin. The areas most affected are those which have high oxygen demands, especially the brain and the heart. Hypoxia does not explain all of the toxicity associated with CO. Carbon monoxide also diffuses into cells and binds to cytochromes in the oxidative phosphorylation system. This inhibits the generation of energy. When exposed to CO, white blood cells adhere to the vascular endothelium. When these white blood cells are later re-exposed to oxygen, they release cytokines which cause lipid peroxidation of cell membranes. This lipid peroxidation has been shown in animals to be responsible for the permanent and delayed effects of CO on the central nervous system. Cerebral hypoperfusion may contribute to delayed neurologic signs and symptoms. Other possible mechanisms contributing to CO toxicity include alternation in neurotransmitter release, carboxyhemoglobin formation, CO binding to cyp P450 interfering with enzymatic function, and interaction with platelets mediating vascular damage. Symptoms The clinical symptoms of CO poisoning are highly variable and there is very poor correlation between CO blood levels and the patient’s symptoms. Mild symptoms are often mistaken for other processes, such as viral illness, the flu, gastroenteritis, or food poisoning. Symptoms of a mild CO intoxication include headache and nausea. Moderate exposures result in more severe headaches, nausea, vomiting, difficulty thinking, confusion, lethargy, weakness. More severe symptoms include chest pain, EKG changes, syncope, seizures, obtundation or loss of consciousness, cardiac dysrhythmias or cardiac arrest, respiratory distress, or cyanosis. Any condition that increases the body’s oxygen demands, such as exertion, trauma, burns, MI, CVA or concurrent drug ingestions, will produce more severe symptoms. It is also important to recognize secondary complications associated with CO toxicity. These can include cardiomyopathy, rhabdomyolysis, non-cardiogenic pulmonary edema, multiorgan failure, disseminated intravascular coagulation (DIC), persistent neurologic sequlae, and delayed neurologic sequlae. The neurologic sequlae may present from 2 to 28 days from time of exposure and may occur in as many as 15 percent of severely poisoned patients. Evaluation of Carboxyhemoglobin and Ambient CO levels and Laboratory Studies The following laboratory studies should be preformed on patients with CO exposures: (a) carboxyhemoglobin level, (b) serum chemistries to look for acidosis, (c) a complete blood count to look for anemia (patients with anemia are at a higher risk for tissue hypoxia), and (d) an arterial blood gas if the patient is having respiratory problems or there is concern about the patient’s oxygenation status. Most patients should have an EKG checked unless they are at very low risk for cardiac ischemia. In the setting of intentional CO poisoning and blood alcohol level should also be considered. If the patient was involved in a fire, the possibility of cyanide exposure from burning plastics should be considered, and if suspicion is high enough, treat for cyanide intoxication also. While any patient with mental status changes should receive an appropriate neurological evaluation, an MRI or PET scan can be considered to evaluation for CNS sequelae. Special Populations A special population that is important to recognize are pregnant patients. The fetus can be greatly affected by CO exposure because fetal hemoglobin has an even higher affinity for CO than adult hemoglobin.Pregnant females should be treated very aggressively for CO exposure and early referral for hyperbaric oxygen should be considered. Treatment The patient should immediately be removed from the source of carbon monoxide. After removal from the source, high concentrations of oxygen should be given to the patient since oxygen is the antidote to CO toxicity. The half life of COHb, while breathing room air, is approximately 5.3hr. With administration of 100% oxygen, the half-life is decreased to about 60 minutes. The addition of hyperbaric oxygen (100% oxygen at 2.8 times the normal atmospheric pressure) lowers the half-life to 23 minutes. Patients with mild to moderate symptoms can be treated with oxygen and observation for 3 to 6 hours, and if symptoms are resolved, they can be discharged to home. If there are severe symptoms, or if there is no improvement with normobaric oxygen, hyperbaric oxygen should be considered. Generally accepted indications for HBO include any signs of serious toxicity, such as altered mental status, history of loss of consciousness, focal neurological deficits, seizures, syncope, ischemic chest pain, EKG changes, new dysrhythmias, hypotension, or shock. COHb levels are generally not as helpful in the decision to use HBO as clinical signs, but most hyperbaric chambers have some guidelines. References Tintinelli et al. Chapter 198 Carbon Monoxide Poisoning. Keith W. Van Meter. Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill pp 1302-5, 2000. Ernst and Zibrak. Carbon Monoxide Poisoning. Hardy and Thom. Pathophysiology and Treatment of Carbon Monoxide Poisoning. Clinical Toxicology. 32(6) pp 613-29, 1994. Juurlink, Stanbrook, and McGuigan. Hyperbaric Oxygen for Carbon Monoxide Poisoning. Cochrane Database of Systematic Reviews. Issue 2, 2001. Piantadosi, Claude A. Carbon Monoxide Poisoning. Shochat and Lucchesi. Toxicity, Carbon Monoxide. eMedicine Journal. 2(5) May 2001. http://www.emedicine.com/EMERG/topic817.htm Weaver et al. Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning. 2007 Annual Report of the American Association of Poison Control Centers National Poisoning and Exposure Database. Clin Tox46:927-1057, 2008
|
