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Carbon Monoxide Poisoning CARBON MONOXIDE POISONING DANA BARTLETT, BSN, MSN, MA, CSPI Dana Bartlett is a professional nurse and author. His clinical experience includes 16 years of ICU and ER experience and over 20 years of as a poison control center information specialist. Dana has published numerous CE and journal articles, written NCLEX material, written textbook chapters, and done editing and reviewing for publishers such as Elsevire, Lippincott, and Thieme. He has written widely on the subject of toxicology and was recently named a contributing editor, toxicology section, for Critical Care Nurse journal. He is currently employed at the Connecticut Poison Control Center and is actively involved in lecturing and mentoring nurses, emergency medical residents and pharmacy students. ABSTRACT Known as the silent killer, carbon monoxide poisoning in individuals can present in various ways and the medical literature continues to contain areas of uncertainty and controversy. Symptoms of carbon monoxide poisoning tend to be nonspecific in mild and severe cases. Delayed neuropsychiatric effects can occur, which are considered a serious complication. Diagnosis of carbon monoxide poisoning is based upon the patient history and physical examination as well as an elevated carboxyhemoglobin level. The etiology, clinical presentation and treatment are discussed, including those for children and special cases such as during pregnancy. 1 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Policy Statement This activity has been planned and implemented in accordance with the policies of NurseCe4Less.com and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses. It is the policy of NurseCe4Less.com to ensure objectivity, transparency, and best practice in clinical education for all continuing nursing education (CNE) activities. Continuing Education Credit Designation This educational activity is credited for 3 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity. Statement of Learning Need Carbon monoxide poisoning is a common and potentially fatal event with nonspecific clinical findings. Clinicians knowledgeable in the identification and treatment of carbon monoxide poisoning can help to initiate neuroprotective interventions and improve patient outcomes. Course Purpose This course will help clinicians identify carbon monoxide exposures and the standard treatments for carbon monoxide poisoning. 2 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Target Audience Advanced Practice Registered Nurses and Registered Nurses (Interdisciplinary Health Team Members, including Vocational Nurses and Medical Assistants may obtain a Certificate of Completion) Course Author & Planning Team Conflict of Interest Disclosures Dana Bartlett, RN, MA, MSN, CSPI, William S. Cook, PhD, Douglas Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures Acknowledgement of Commercial Support There is no commercial support for this course. Please take time to complete a self-assessment of knowledge, on page 4, sample questions before reading the article. Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course. 3 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1. Carbon monoxide (CO) is a gas that is a. colorless. b. smells similar to car exhaust. c. taste similar to ammonia. d. All of the above 2. Carbon monoxide (CO) can be produced by a. toluene b. methylene chloride c. cyanide d. cadmium 3. One of the basic ways carbon monoxide (CO) causes harm is a. it decreases production of hemoglobin. b. it produces abnormal hemoglobin. c. it causes tissue hypoxia. d. it causes pulmonary or coronary vasoconstriction. 4. Carbon monoxide (CO) can cause a. pulmonary capillary vasoconstriction. b. production of methemoglobin. c. hemolysis. d. direct cellular toxicity. 5. Two organs particularly vulnerable to CO poisoning are a. the brain and the heart. b. the kidneys and the pancreas. c. the thyroid gland and the small bowel. d. the lungs and the liver. 4 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Introduction Carbon monoxide is sometimes called the silent killer, and aptly so. It is a gas that is produced by incomplete combustion of carbon- containing material, it is colorless, odorless, and tasteless, and carbon monoxide (CO) can be lethal. Despite large-scale public education and prevention programs, CO exposure is still a serious public health problem. The pathophysiology, clinical effects, and the best methods for treating CO poisoning have been intensively studied, but there are still areas of uncertainty and controversy. Epidemiology Of Carbon Monoxide Poisoning Carbon monoxide poisoning is still very common, and is a leading cause of morbidity and mortality in the United States.1 Each year a minimum of 50,000 people who have been exposed to CO present to hospital emergency rooms and the estimated number of visits because of CO poisoning is much higher;2,3 in 2014 there were 1319 deaths caused by CO;4 and, large-scale CO caused by environmental factors are relatively common.5,6 Exposures to CO can happen at any time of the year but are more common in the winter. If temperatures are very cold and/or there is a power outage, people may attempt to heat their homes in unsafe ways. In late October of 2011 in Connecticut, a heavy snowstorm caused widespread power outages, and ambient temperatures at the time were unusually low. Emergency rooms in the state were inundated with cases of carbon monoxide poisoning caused by indoor use of gasoline generators and charcoal burning grills.6 5 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Carbon monoxide is produced when carbon-containing materials such as coal, oil, tobacco, or wood are burned. Common sources of CO exposures that can cause poisoning are automobile exhaust fumes, fumes from any gasoline powered engine, natural gas, and wood fires. It is important to remember that CO poisonings happen because of the production of CO that occurs when the source material is burned and when these combustion fumes are not properly ventilated. Two other exogenous sources of carbon monoxide are methylene chloride and methylene iodide. Methylene chloride is a chemical that is a common component of commercially available paint strippers. Inhaled methylene chloride vapors or methylene chloride that is ingested or dermally absorbed is converted in vivo to CO. Because it is stored in fat tissues and the metabolizing enzymes are quickly saturated, peak CO levels produced by methylene chloride inhalation, ingestion, or dermal absorption are seen 8 hours or longer after exposure.7 Methylene iodide is used by jewelers to examine gems and, like methylene chloride, it is converted in vivo to CO.8 Carbon monoxide poisoning caused by either of these is very uncommon; there has only been thirteen reported cases of methylene iodide poisoning.9,10 Carbon monoxide is also an endogenous compound. It is produced by the breakdown of hemoglobin, lipid peroxidation, and the metabolism of xenobiotics (substances foreign to the body), and it functions as an intrinsic signaling molecule that influences cell functioning proximally and distally.11,12 The normal level of carbon monoxide in the blood, which is carboxyhemoglobin (COHb) is 0.1%-1.0%, although it may be higher (carboxyhemoglobin levels are discussed later in this course). 6 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Although the concept is in the experimental stages, in vitro and animal research suggests that carbon monoxide may have therapeutic value.13,14 Carbon Monoxide Poisoning: Pathophysiology The mechanism by which CO was traditionally thought to cause poisoning was by its binding to hemoglobin. This is certainly one of the ways that CO causes harm, as will be discussed in detail later in this section. But research has shown that CO poisoning is much more complex and there are multiple, dynamic pathologic processes involved in CO poisoning. As Tomaszewski wrote: “CO toxicity cannot be attributed solely to COHb-mediated hypoxia. Neither the clinical effects nor the phenomena of delayed neurologic deficits can be completely predicted by the extent of binding between hemoglobin and CO.”1 The pathophysiologic mechanisms of CO poisoning are briefly reviewed below.1,2,15-21 Some of these are well outlined and their role in CO poisoning is known while others are more theoretical in nature, and many are interdependent but they are discussed separately for ease of understanding. Hemoglobin Binding and Oxygen Transfer Effects Carbon monoxide binds avidly to hemoglobin. It has an affinity for hemoglobin that is 200-250 times greater than that of oxygen. When CO displaces oxygen from hemoglobin and CO occupies the binding sites for oxygen on hemoglobin, this results in CO and hemoglobin combining to form carboxyhemoglobin (COHb). Carboxyhemoglobin 7 nursece4less.com nursece4less.com nursece4less.com nursece4less.com does not bind with oxygen, so most of the hemoglobin is rendered functionally useless. The oxyhemoglobin dissociation curve indicates how saturated hemoglobin is at any level of oxygen tension of the blood. (Oxygen tension refers to the partial pressure of oxygen, which said another way, is the pressure of oxygen in a mixture of gases). The oxyhemoglobin dissociation curve also indicates how
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