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Carbon Monoxide Poisoning Case Studies and Review

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Carbon Monoxide Poisoning Case Studies and Review Clinical DIMENSION Carbon Monoxide Poisoning Case Studies and Review Lisa A. Ruth-Sahd, DEd, RN, CCRN, CEN; Kristen Zulkosky, PhD, RN, CCRN; Mary E. Fetter, MSN, RN This article describes carbon monoxide poisoning. Using a case study approach, the article covers pathophysiology, epidemiology, clinical presentation, and complications. A nursing care plan is presented to guide the critical care nurse in the care of patients in this type of condition. Keywords: Carbon monoxide, Carbon monoxide poisoning, Case studies [DIMENS CRIT CARE NURS. 2011;30(6):303/314] Carbon monoxide poisoning (COP) results in approx- She denies hospitalization for asthma. She had no known imately 50 000 visits to the emergency department (ED) drug allergies. Physical examination in the ED revealed her annually in the United States1 and contributes to approx- to be slightly overweight and in mild respiratory distress, imately 2700 deaths annually, according to the Centers for with a respiratory rate of 28 breaths per minute. Her blood Disease Control and Prevention.2 Carbon monoxide (CO), pressure is 140/86 mm Hg, pulse is 92 beats per minute, an odorless, tasteless, and colorless gas, is the second most temperature is 98.4-F, and oxygen saturation is 95% on common environmental pollutant after carbon dioxide. room air. Breath sounds were clear bilaterally. The symptoms of COP are nonspecific and therefore The ED physician obtained laboratory work, which tend to be underrecognized in health care settings.3,4 It revealed the patient’s carboxyhemoglobin (COHb) level is crucial for the critical care nurse to rapidly identify and is 20%. Less than 10% is normal. Her other laboratory treat COP in order to avert deleterious patient complica- work was unremarkable including normal cardiac enzymes. tions and death. This article presents 2 case studies of pa- Her electrocardiogram showed normal sinus rhythm with tients who have had COP and discusses pathophysiology, no ST-T wave changes. Because of the patient’s complaints diagnosis, treatment, and nursing care. of headaches for the past 3 days after turning on the heat- ing system and intermittent shortness of breath that re- CASE STUDY 1 solves when she leaves the house, a diagnosis of COP was A 68-year-old white woman, Ms F., presented to the ED in made. It was requested to have her other family members November with complaints of throbbing headaches inter- come to the hospital to get tested as well. Ms F. denies mittently for the past 3 days. She reported taking ibuprofen having any family pets. every 8 hours for 2 days without relief. She also reported shortness of breath, dizziness, weakness, and intermittent CASE STUDY 2 chest pain. On the day prior to coming to the ED, she went A male patient, Mr S., presented to the ED having been shopping and ‘‘felt better.’’ Ms F. also admitted that her son driven there by his wife after she found him ‘‘barely breath- anddaughter-in-lawwholiveinthesecond-floorapartment ing in the garage with his car running.’’ She stated she was above her have also not been feeling well for the past few at work and came home to find him in his car ‘‘very days and have complained of headaches. They all denied groggy.’’ She reported, ‘‘he has been depressed for several recent travel or exposure to persons with infections. weeks after losing his job and consequently having finan- Ms F.’s medical history was significant for asthma that cial hardships.’’ Mr S. was in a state of respiratory arrest was controlled with regular use of inhaled bronchodilators. and was intubated shortly after being admitted to the ED DOI: 10.1097/DCC.0b013e31822fb017 November/December 2011 303 Copyright @ 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Carbon Monoxide Poisoning and placed on 100% oxygen. His pupils were dilated and propane-powered electric generator in their home for heat, very sluggish. As he was being intubated, he had a grand and all 4 were found dead the next morning because of COP. mal seizure. His medical history is significant for diabetes Patients at high risk for negative outcomes include children, mellitus and according to his wife ‘‘has been fairly well adults with cardiac disease, pregnant women, patients controlled until this past year.’’ He also had coronary artery with increased oxygen demand or decreased oxygen-carrying bypass surgery 2 years ago and is on blood pressure and capacity, or patients with chronic respiratory insufficiency. cholesterol medications. He is allergic to sulfa medica- tions. Physical examination in the ED revealed a pale man of 74 in who is unkempt and slightly overweight. He was Patients at high risk for negative very lethargic and disoriented. His blood pressure was outcomes include children, adults 166/102 mm Hg, pulse is 102 beats per minute, temper- ature is 96.4-F, and oxygen saturation is 92% on room with cardiac disease, pregnant air. His wife stated he is not a smoker. Breath sounds women, patients with increased were diminished, and his respiratory rate was 6 breaths oxygen demand or decreased per minute before being intubated. oxygen-carrying capacity, The ED physician obtained a venous blood sample, or patients with chronic which revealed the patient’s COHb level to be 49%, blood sugar of 185 mg/dL, and total cholesterol level respiratory insufficiency. of 260 mg/dL; cardiac enzymes and troponin T were within reference range. His electrocardiogram showed sinus tachycardia with no ST-T wave changes. An arterial PATHOPHYSIOLOGY blood gas was ordered, and plans were under way to trans- The pathophysiological cascade of COP is very complex; port Mr S. to a facility where hyperbaric oxygenation yet, despite this complexity, the end result is always tissue (HBO2) could be provided. hypoxia. The body relies on oxygen to reach the cells to function, all body systems are affected by COP. Because EPIDEMIOLOGY organs such as the heart, brain, and lungs require large The Centers for Disease Control and Prevention5 reports and continuous amounts of oxygen for functioning, they nonfatal, unintentional, nonYfire-related CO exposures to are the most susceptible to the effects of COP.4,11 The account for 15 200 hospital ED visits annually. In addition, pathophysiological effects of CO lead to problems in an estimated 480 people die each year of nonYfire-related 4 areas: hemoglobin binding, direct cellular toxicity, pro- COP.2,5 However, because the symptoms of COP may be tein binding, and increases in nitric oxide (NO). mild or incorrectly attributed to other diseases processes, the true incidence is unknown.6 Carbon monoxide poison- Hemoglobin-Binding Oxygen ingoccursmoreofteninthefallandwintermonths,with Hemoglobin-binding oxygen is transported throughout December and January having the highest numbers largely the body in the bloodstream via hemoglobin within the red because of gas furnaces and heaters.7,8 blood cell. Every 4-chain hemoglobin molecule (2 ! chains Children 4 years or younger have the highest nonfatal and 2 " chains) is able to transport 4 oxygen molecules. rate for CO exposure, whereas adults 65 years or older It is these oxyhemoglobin molecules that then release the accounted for 23.5% of COP deaths. Males and females oxygen into the tissues where the oxygen is needed for are equally affected; however, males are 2.3 times more cellular activities. Carbon monoxide diffuses rapidly across likely succumb to COP. Non-Hispanic whites and African the alveolar cell membrane and has a binding affinity for Americans have the highest death rate. The majority hemoglobin that is 200 times that of oxygen (Figure). (64%) of the nonfatal CO exposures happened in homes, Carboxyhemoglobin consequently has very little oxygen with the causes being due to a faulty furnace (18.5%) and to deliver to the tissues. Carbon monoxide also changes motor vehicles (9%).2,5,7,8 the structure of hemoglobin, which makes it more chal- Whereas suicide attempts were found to be the No. 1 lenging for the oxygen that is there to be released into the cause of COP in Taiwan,9 they were not the cause of tissues. Consequently, the toxicity related to the COP oc- COP in Turkey9 or in the United States.3,10 Gulati and col- curs in various systemic sites and leads to a leftward shift leagues3 report that acute unintentional COP has been in- in the oxyhemoglobin dissociation curve (Figure).11 creasing within immigrant populations after winter storms and other natural disasters because of the loss of electricity Direct Cellular Toxicity and the subsequent use of alternative forms of energy. Re- Studies are demonstrating a direct toxicity at the cellular cently, a group of 4 immigrant individuals were using a level that seems to explain why the CO-hemoglobin 304 Dimensions of Critical Care Nursing Vol. 30 / No. 6 Copyright @ 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Carbon Monoxide Poisoning Elimination of CO from the blood follows an expo- nential relationship and depends on the rate of ventilation, inspired oxygen partial pressure, and the amount of CO ex- posure.15 As the patients’ tissues are reoxygenated, there is a resultant reperfusion injury and lipid peroxidation leading to reversible demyelination of the central nervous system lipids. CLINICAL PRESENTATION The clinical symptoms of COP are highly variable, de- pending on the acuity and the length of exposure. Car- bon monoxide poisoning can be classified as acute and chronic. Because of the subtle nature of its presentation, Figure. Carbon monoxide binding to hemoglobin. Source: http:// it is important for the acute care nurse to maintain a high www.bing.com/images/search?q=carboxyhemoglobin&view= index of suspicion so rapid patient assessment can be ini- detail&id=72B6510D1FE89C7573E1212F1BBC10FE7E6651F0& tiated. Patients presenting with cardiac or neurological first=1&FORM=IDFRIR.
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