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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 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 of 28 breaths per minute. Her blood Disease Control and Prevention.2 Carbon monoxide (CO), is 140/86 mm Hg, pulse is 92 beats per minute, an odorless, tasteless, and colorless gas, is the second most is 98.4-F, and saturation is 95% on common environmental pollutant after . 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 (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 . 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 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 was controlled with regular use of inhaled . 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 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 (HBO2) could be provided. . The body relies on oxygen to reach the cells to function, all body systems are affected by COP. Because EPIDEMIOLOGY organs such as the , brain, and 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: 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 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

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Elimination of CO from the blood follows an expo- nential relationship and depends on the rate of ventilation, inspired oxygen , and the amount of CO ex- posure.15 As the patients’ tissues are reoxygenated, there is a resultant reperfusion injury and peroxidation leading to reversible demyelination of the central nervous system .

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. symptoms without a history of these problems should be carefully assessed. Patients may present with 1 or more levels do not correlate with the severity of the clinical symptoms (Table 1). If cardiac, pulmonary, and or neu- effects. As the body tries to compensate for the rising rological comorbidities exist, presenting symptoms may COHb level, there are severe compensatory reactions include symptoms related to those systems suffering from that occur such as cerebral blood vessel dilation and an hypoxia.4,14 increase in coronary artery blood flow.12 Protein Binding Acute COP Carbon monoxide binds to other proteins. As the COHb Acute COP is defined as relatively brief exposure to high level increases, the protein binding increases, leading to levels of CO. The most common symptoms are headache, increased hypoxemia. As the binding to myoglobin, cy- nausea, and dizziness. Other common presenting symptoms tochrome, and guanylyl cyclase occurs, the body protein include vomiting, malaise, ataxia, seizures, loss of conscious- systems are rendered relatively inactive.13 Binding to myo- ness, and/or shortness of breath. Early clinical findings may globin reduces the oxygen available in the heart, and as a include increased blood pressure, heart rate, and respiratory 12,15,16 result, the individual will likely develop arrhythmias and rate. Clinical findings can progress to include con- decreased cardiac output. This may also contribute to di- fusion, loss of consciousness, hypotension, poor 1,11 rect skeletal muscle toxicity and rhabdomyolysis. The in- refill, cardiopulmonary arrest, coma, or death. hibition of cytochrome oxidase may impair adenosine 5’ triphosphate, which transports chemical energy within the Chronic COP cells for . The cellular deficit as well as the lack Chronic COP is defined as more lengthy exposure to low of oxygen available to the tissues results in generalized levels of CO. The clinical effects are related to a combi- systemic hypoxia, oxidative stress, cellular necrosis, apo- nation of the level of exposure as well as the duration, with ptosis, and the release of oxygen free radicals. The stim- presentations that can be delayed up to several months ulation of guanylyl cyclase increases cyclic guanosine or 2 to 3 years. Chronic COP has symptoms that are typ- monophospate and leads to cerebral vasodilation, which ically difficult to recognize because of their often non- has been associated with loss of consciousness. specific presentations and is oftentimes mistaken for a flulike illness.11 Weaver1 reports other symptoms such Increases in NO as chronic fatigue, memory deficits, difficulty working, Because of COP, the activities of NO and other oxygen free sleep disturbances, vertigo, neuropathy, paresthesias, re- radicals are increased, causing peripheral vasodilatation and infections, abdominal pain, and diarrhea. Chronic more free radical formation. High NO levels leads to cere- low-level CO exposure has been associated with cardio- bral vessel dilation and decreased cerebral blood flow, syn- megaly and polycythemia, presumably secondary to effects cope, and systemic hypotension. The free radical formation of chronic hypoxia.4 causes endothelial changes and oxidative damage to the When vague symptoms cannot be contributed to a brain, which may be responsible for the delayed neuro- more common cause, the critical care nurse should con- logical sequelae after CO exposure. Carbon monoxide is an sider chronic COP as a possible diagnosis. See Table 2 inflammatory mediator leading to increased tissue destruc- for signs and symptoms related to COHb levels as seen tion with increased capillary leakage and swelling.14 in the case studies.

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within similar time frames. It is important to not assume TABLE 1 Long-term Neuropsychiatric Impairment Following Carbon flulike symptoms are indeed influenza if lacking key symp- Monoxide toms such as fever, myalgia, or cough, which are typically not present in COP. Diarrhea is also not typical of COP; Apathy/indifference therefore, one should not settle for a diagnosis of gastro- Apraxia enteritis when presented with vomiting in absence of di- 17 Ataxia arrhea. Another important question for the nurse to ask Confusion is whether any indoor pets are acting differently. Because pets do not eat the same food as humans or share viruses Dementia with humans, an ill pet in the same household at the same Depression time may indicate COP.14,19 Seizure disorder Vision and gait disturbance TABLE 2 Clinical Features of Carbon Monoxide Poisoning Choreathetosis Clinical Features Mutism Case 1 Case 2 Personality changes Pulmonary Urinary and fecal incontinence Arterial blood Increased Decreased Memory impairment gas changes, shortness respiratory rate respiratory rate of breath Respiratory depression, 28 breaths/min 6 breaths/min The critical care nurse must realize that the ‘‘cherry COHb levels (93% for red’’ discoloration often described as a hallmark nonsmokers and characteristic symptom of COP is actually very rarely 910% for smokers) 4,15,17 seen clinically. A significant number of patients may Central nervous system be totally asymptomatic but are brought to the hospital Headache, dizziness; Headache Decreased level of because of the environmental concerns.3 ataxia; alteration or dizzy consciousness loss of consciousness; DIAGNOSTIC TESTING AND EVALUATION seizures 3 15 Gulati and colleagues and Bledsoe and McEvoy report Cardiovascular the underdiagnosis in COP, stating that COP may not be QT interval changes; Intermittent No cardiac diagnosed in 30% to 50% of patients while seeking care hypertension or chest pain symptoms for other complaints. This is due to the fact that symptoms hypotension are often attributed to other causes. Therefore, obtaining a Cardiac enzymes: Negative thorough health history is vital to identifying COP, par- tropinin T, creatinine enzymes ticularly in patients with vague symptoms. The astute crit- kinase, creatinine ical care nurse must ask patients about heating systems or kinaseYMB other risk factors for COP. Determining specifically when No ST-segment and where the patient experiences symptoms may help iden- changes tify a CO source, whether in their home, work, or automo- Gastrointestinal bile, or during extracurricular activities (such as boating), or when using appliances, such as generators.4,18 When environ- Nausea, vomiting; Denies Denies mental exposure is suspected, local fire departments typically diarrhea; abdominal complaints complaints are summoned to assess the quality of atmospheric air.11,14 The critical care nurse must consider whether other Constitutional family members are ill with similar symptoms. In differ- General fatigue, Weakness Weakness entiating COP from a viral illness among a family, the personality changes, onset of symptoms for the various family members is sig- weakness nificant. Patients with viral illnesses typically develop symp- Malaise Very lethargic toms and seek treatment serially as one person passes on the illness to the next. In COP, patients develop symptoms Abbreviation: COHb, carboxyhemoglobin.

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Determining Degree of Severity and Carbon monoxide poisoning is often classified as mild, Carboxyhemoglobin levels are typically measured with moderate, and severe. The main cause of mildly elevated blood gas analysis, either venous or arterial. Correlation COHb levels in cigarette smokers is the cigarette smoke15; between venous and arterial samples for COHb levels and therefore, exposure is defined by a COHb level greater pH is excellent; therefore, venous samples are typically than 2% to 3% in nonsmokers or greater than 9% to preferable.17 Venous blood gases will typically reveal an 1,20-22 10% in smokers. In mild and moderate COP, the elevated PO2 level of 30 to 50 mm Hg (normally around patient may or may not have symptoms as described in 25 mm Hg) in significant CO exposure, whereas arterial 11 Table 2 but does have elevations in the COHb levels. In PO2 results may be low or normal. Arterial measurement mild COP, the level is less than 30%, whereas in moderate of PO2 reflects the amount of oxygen in the plasma not COP, it is greater than 30% to 40%. Severe is identified bound to hemoglobin and therefore will not be affected by when the patient is unconscious and has a COHb level COP.14 Although venous COHb is adequate for diagnosis, greater than 40%.11,17 Regardless of measured COHb arterial blood gas measurement is done if clinically indi- levels, severity of symptoms can also be affected by indi- cated and provides additional data regarding gas exchange, vidual variations such as hemoglobin level, age, physical degree of acidosis, and level of COHb.1 Presence of met- activity, metabolic rate, concomitant cardiovascular and/ abolic acidosis correlates with exposure duration, severity or systemic disease, and degree and duration of exposure.9 of symptoms, or risk of adverse sequelae. Lactate levels Hampson and Hauff23studied the correlation between may also be helpful as a marker for severe poisoning.4 COHb levels and clinical symptoms and found correla- tions to loss of consciousness, reduced arterial pH, and Additional Considerations death within 30 days with elevated COHb levels. Danger- If intentional exposure is suspected, further laboratory ous levels are considered to be greater than 25%, with studies are indicated to evaluate for presence of alcohol, death associated with levels greater than 50%. Because benzodiazepines, narcotics, amphetamines, or other drugs. there is no direct connection between clinical effects or treat- The acute care nurse plays a vital role in advocating for ment response with COHb levels, these numbers should be and connecting the patient to mental health resources.1 used only as a guide to help determine exposure levels.11 These patients are at increased risk for future suicide completion or death from high-risk behavior and should Methods of COHb Evaluation have psychological or psychiatric evaluation, as well as Carboxyhemoglobin levels can be measured by various appropriate follow-up and involvement of family to assist methods. The acute care nurse must realize that pulse ox- with compliance.22,23 imetry is of no value because it does not distinguish COHb from oxyhemoglobin and will give a falsely elevated oxygen PROGNOSIS saturation level.17 Levels of COHb can be measured via pulse Hampson and Hauff24 assessed the prognosis of 38 pa- CO oximetry, which uses multiple wavelengths of light to tients who had COP to determine the mortality rate for measure the percentage of COHb present (SpCO). The mon- medically treated patients. They found that patients who itoring probe is applied to the finger in a similar fashion as had severe and needed endotracheal a common pulse oximeter used for SpO2 monitoring. Pulse intubation had a higher mortality rate. In a follow-up CO oximetry results correlate well with venous COHb study by Hampson et al,22 1073 adult patients surviving levels, and its use is helpful in quickly differentiating COP acute COP were treated with hyperbaric oxygen. Results from cyanide poisoning. In addition, its use in prehospital showed that the patients were at increased risk for long- care has led to the ability to exclude COP as a diagnosis and term mortality and required close follow-up after discharge. avoid unnecessary transport of patients and subsequent The increased mortality was felt to be from concomitant overloading of ED resources during CO emergencies.15 disease processes such as psychiatric illnesses and behaviors.

TREATMENT CONSIDERATIONS The acute care nurse must realize that pulse oximetry is of no value Initial Treatment because it does not distinguish Emergency personnel must first evaluate the patient while COHb from oxyhemoglobin and considering the patient’s safety as well as their own safety. will give a falsely elevated The second intervention is the administration of normo- baric oxygen via a nonrebreather reservoir face mask with oxygen saturation level. high-flow 100% oxygen until the COHb is less than 5%.1 Because 100% oxygen delivery is difficult to achieve

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Copyright @ 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Carbon Monoxide Poisoning outside the operating room,18 first responders must con- have a COHb level of 25% or greater, are exposed for sider whether to endotracheally intubate the patient based 24 hours or more, are 36 years or older, or are diagnosed on level of consciousness and degree of respiratory dis- with serious COP, as manifested by transient or prolonged tress. is indicated regardless of pulse ox- unconsciousness, abnormal neurological signs, cardiovas- imetry or arterial pressure of oxygen.8 cular dysfunction, or severe acidosis.1,3,23 Goldstein11 spe- Treatment of mild symptoms typically consists of ad- cifically notes altered mental status, syncope, seizures, and ministration of high-flow oxygen for 4 hours with frequent hypotension as indications for HBO2 therapy. Other re- reevaluation of symptoms12 in the ED with subsequent lative indications may include persistent symptoms that discharge to home. Before discharge however, the source do not resolve after 4 hours of high-flow oxygen therapy of CO must be identified, and other potentially affected via nonrebreather mask, concurrent burns, or pregnancy individuals evaluated.4 with any amount of exposure.12 (Refer to Table 3 for

Admission criteria include unresolved symptoms, diag- a summary of indications for HBO2 therapy in COP.) nostic findings consistent with severe poisoning, or other Timing of treatment is variable; however, studies report medical or psychosocial causes for increased observa- a correlation between increase in mortality and duration 8 13 tion. The critical care nurse should anticipate possible after exposure before treatment with HBO2. Critical care intubation and admission to the intensive care unit for nurses should anticipate rapid preparation for HBO2 treat- cardiopulmonary monitoring and support, neurological ment when the previously mentioned criteria are noted. evaluation, and the possibility of hyperbaric oxygen ther- Pregnancy does not elevate a woman’s risks related to apy in cases of moderate to severe COP11 (Table 4). CO toxicity; however, in cases of severe COP, fetal mor- tality may exceed 50%.1 Because fetal hemoglobin has a HBO2 Therapy Overview greater affinity for CO binding than adult hemoglobin, Hyperbaric oxygen therapy is a long-standing, yet con- and fetal blood requires a longer period to eliminate CO troversial, treatment. In HBO2, compressed 100% oxygen in comparison to adult blood, HBO2 therapy is more is delivered at 2 to 3 times the normal atmos- strongly recommended for pregnant women, particularly pheric pressure. Typical treatment duration is 90 minutes, if fetal distress is suspected. Carboxyhemoglobin levels although regimens may vary in the number and duration greater than 15% in pregnant women represent severe of treatments. Although delivery of 100% oxygen can poisoning.11 reduce the removal rate of CO from COHb in 80 minutes Disadvantages of HBO2 therapy include patient as compared with 4 to 6 hours in room air conditions, the and ruptured tympanic membrane or sinus . Less removal of CO is further hastened to approximately 20 commonly seen risks include hyperoxic seizures, oxidative 12,15,16,18 to 30 minutes with the use of HBO2 therapy. In stress, , hemorrhage, and decompres- 1,4 addition, HBO2 therapy increases the amount of oxygen sion sickness. Pneumothorax or mediastinal emphysema dissolved in the blood,8,24,25 induces cerebral vasoconstric- is rarely seen.13 One must also consider the risks associ- tion (reducing intracranial pressure and cerebral edema), ated with transportation to a treatment center that pro- 1,14 1,26 and reduces the risk of oxidative injury after COP. vides HBO2 therapy. An untreated pneumothorax is 1 Studies performed in animals suggest HBO2 therapy may the only absolute contraindication to HBO2 therapy. reduce morbidity and mortality and limit direct cellular toxicity, thereby decreasing the incidence of delayed Controversial Issues With HBO2 Therapy neuropsychiatric sequelae.14,15,17 According to Beppu and colleagues,27 neurological symp- toms can be completely resolved for most patients with inhaled oxygen and/or hyperbaric oxygen therapy; how- Hyperbaric oxygen therapy ever, Weaver and colleagues25,26 have cited its use as con- is a long-standing, yet troversial. Weaver and colleagues conducted double-blind, randomized clinical trials comparing the rate of cognitive controversial, treatment. sequelae in patients with COP treated with HBO2 with those treated with normobaric oxygen. Their findings de- monstrated a significant decrease in the rate of cognitive

sequelae at 6 weeks for patients treated with HBO2. Indications for HBO2 Therapy Interestingly, patients in this study had nearly normal No widespread agreement exists among practitioners COHb levels just before their first treatment session. 25,26 as to clear standards for patient selection for HBO2 Weaver et al recommend consideration of HBO2 ther- therapy in COP.4 The Undersea and Hyperbaric Med- apy for patients with acute poisoning. Kao and Nanagas4 ical Society recommends HBO2 therapy for patients who recommend consideration of a risk-benefit analysis for each

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COP. General findings may include focal areas of ische- TABLE 3 Indications for Use of Hyperbaric Oxygen Therapy in COP mia or cerebral edema. The most common findings on these studies are lesions in the globus pallidus of the basal Commonly accepted indications ganglia and the cerebral white matter.4,27 Ischemia or ne- & Neurological findings crosis in the globus pallidus is particularly related to severe 28 a. Altered mental status COP. Patients with abnormal findings on imaging stud- ies of the brain are more likely to have poorer outcomes, b. Coma including persistent neurological impairment or death.4 c. Focal neurological deficits Carbon monoxide poisoning effects on the nervous d. Seizures system can be organized on a continuum of impairment & Pregnancy with COHb levels 915% from early to delayed. Early clinical manifestations in- clude dizziness, headache, mild confusion, and nausea & History of loss of consciousness and vomiting. In severe cases, patients may have an Other considerations altered mental status, syncope, seizures, or acute stroke- & Cardiovascular compromise (hypotension, ischemia, infarction, like syndromes and become comatose. Hypotension can dysrhythmia) also be attributed to the severity of central nervous sys- 4,29 & Metabolic acidosis tem structural damage. Long-term nonspecific and 4 & Extremes of age neurocognitive and neuropsychological sequelae may develop a month or even later after exposure and can & Elevated COHb level (925%) persist for a year or longer.4,30 & Abnormal neuropsychometric testing results Delayed neuropsychiatric sequelae occur after an & Concurrent burns apparent recovery from acute symptoms with a latency 30 & Persistent symptoms despite normobaric oxygen period lasting 2 to 40 days. Delayed neuropsychiatric sequela may appear as any neurological and/or psychi- Abbreviations: COHb, carboxyhemoglobin; COP, carbon monoxide poisoning. atric symptom such as memory loss, confusion, ataxia, Adapted from Kao and Nanagas4 with added information from Goldstein.11 seizures, urinary and fecal incontinence, emotional labil- ity, disorientation, hallucinations, parkinsonism, delirium, individual patient, including discussion with the patient amnesia, mutism, cortical blindness, psychosis, gait, and and family, when making treatment decisions regarding other motor disturbances. The incidence of delayed neu- the use of HBO2 therapy. ropsychiatric sequelae for COP patients is estimated to be 1% to 47%.4,27 Jiang and colleagues20 note that stem COMPLICATIONS cell therapy may improve recovery of brain structure and There are many complications related to COP for which function in rats after severe COP and may be beneficial for the acute care nurse must vigilantly assess the patient. severe COP and delayed neurological sequelae. Long-term Maintaining the patient on bed rest is essential to reduce neuropsychiatric impairment following COP can be found tissue oxygen demand and reduce the likelihood of or- in Table 1. gan ischemia.14,28 As the exposure to CO increases, the entire body is affected. Because the brain and heart are Cardiac the most oxygen-dependent organs, they are the most The cardiac effects of COP are due to hypoxia and result sensitive to the effects of COP.4 in decreased myocardial function. The decreased oxygen delivery to, and consumption of oxygen by the myocar- Neurological dium causes the patient to have hypotension, dysrhyth- Patients should have an initial comprehensive baseline mias, tachycardia, chest pain, ischemia, infarction, and neurological examination, including evaluation of cerebel- sometimes cardiac arrest.14,31 Death from COP may be lar function and neuropsychological testing with the Mini- due to the ventricular dysrhythmias. Yelken et al31 suggest Mental Status Examination.4,6 Testing to rule out other assessing ST-segment depression and changes in QT, causes of neurological changes may also be helpful, in- corrected QT, and corrected QT dispersion as well as car- cluding glucose levels, serum ethyl alcohol levels, and/or diac enzymes, particularly in patients with increased risk of urine toxicology screen.14 Computed tomography or mag- cardiac disability.14 The critical care nurse must use cau- netic resonance imaging studies may be performed as part tion in administering medications known to prolong QT in- of a diagnostic workup to rule out other causes of neu- tervals.31 Echocardiogram findings may reveal patterns of rological symptoms or to evaluate declining neurological myocardial injury ranging from transient global left ven- status and assess for brain damage following diagnosis of tricular dysfunction consistent with stunned myocardium

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TABLE 4 Nursing Care Plan for Patients With Carbon Monoxide Poisoning33

Diagnosis Desired Outcome Interventions Rationale for Interventions

Impaired gas exchange related to Maintain a pulse oximetry 1. Monitor respiratory rate, depth, 1. Increased respiratory rate and use ventilation imbalance reading 995% or patients and effort of accessory muscles indicate secondary to COP baseline hypoxia

Arterial blood gas within 2. Utilize oxygen to maintain Pao2 2. Airway is unable to compensate reference range 990 mm Hg and monitor oxygen without oxygen for patient saturation continuously. Notify the pulmonologist if G90% CO levels will return to 3. Auscultate sounds every 1-3 h 3. Presence of crackles or wheezes reference range may alert the nurse to changing in respiratory status. 4. Monitor for changes in mental 4. These findings may indicate the status, restlessness, agitation, and presence of hypoxia confusion 5. Position the patient in semiYFowler 5. Upright position and ‘‘proning’’ position, with an upright posture of enhance oxygenation, and turning is 45 degrees and turn the patient important to prevent complications of every 2 h; may consider using prone immobility and decrease the positioning development of atelectasis 6. Prepare patient for placement on 6. May be necessary to maintain as warranted oxygenation and acid-base balance 7. Assess CO levels every day until the 7. As oxygen levels increase, the CO level is G10 level should exponentially decrease 8. Instruct patient/family regarding the 8. Hypoxia and hypoxemia may possible use of mechanical ventilation necessitate supportive oxygenation. Knowledge of this will decrease apprehension of the patient and family

9. Consider HBO2 therapy 9. Collaborate with pulmonologist to

determine if HBO2 is indicated Ineffective airway clearance Clear airway of secretions. 1. Auscultate lung fields every 1-3 h 1. Presence of crackles or wheezes may related to smoke inhalation alert the nurse to changing in and/or CO inhalation. respiratory status Maintain a patent airway 2. Monitor respiratory rate, depth, 2. Increased respiratory rate and use of and effort accessory muscles indicate hypoxia Clear breath sounds 3. Monitor blood gas values and pulse 3. Oxygen saturation G90% or a partial oxygen saturation levels pressure of oxygen G80% indicates significant oxygenation concerns 4. Encourage the patient to use a 4. This prevents the glottis from closing forced expiratory cough or ‘‘huff and helps to clear secretions from cough’’ central airways 5. Observe color and amount of sputum 5. Normal sputum is clear or gray 6. Assess for bronchophony 6. Bronchophony is present with increased lung consolidation Risk for acute confusion related to Demonstrate restoration of 1. Assess the patient’s behavior and 1. Assessing frequently will alert the decreased oxygen supply cognitive status to baseline cognition throughout the day and night nurse to subtle changes 2. Monitor mental status examinations 2. Noting changes quickly may lead to noting behavior, mood and affect, early intervention insight and judgment, cognition, and level of attention

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TABLE 4 Nursing Care Plan for Patients With Carbon Monoxide Poisoning,33 continued

Diagnosis Desired Outcome Interventions Rationale for Interventions

3. Treat the underlying COP that is the 3. Working and collaborating with cause of the confusion in collaboration the health care team improve with the health care team patient outcomes 4. Use clear communication techniques 4. This may help confused patients and provide simple examples to to care for themselves the patient 5. Decrease sensory exposure and 5. Patients with confusion may ensure a calm environment become agitated especially if there is sensory overload 6. Teach the patient’s significant 6. It is helpful for significant others others why the patient is confused to understand the rationale as to why their loved one is confused Activity intolerance related to Be able to tolerate 1. Measure oxygen saturation during 1. Patient may require supplemental imbalance between oxygen periods of activity activity oxygen when performing activities supply and demand of daily living secondary to COP 2. Monitor response to activity by 2. May all indicate hypoxia checking for use of accessory muscles or skin color changes 3. Instruct patient to use purse-lip 3. This helps to slow down the rate of breathing 4. Collaborate with pulmonary 4. Pulmonary rehabilitation has been rehabilitation shown to relieve dyspnea and fatigue Anxiety related to change in health Identify and verbalize 1. Assess the patient’s level of anxiety 1. Anxiety may cause deleterious status secondary to COP symptoms of anxiety and physiological reactions to anxiety effects on patient recovery (eg, tachycardia, tachypnea, nonverbal expressions of anxiety) 2. Explore previously used coping skills 2. Successful coping skills used in the past may help again 3. When possible, remove sources of 3. Explaining to and teaching the anxiety patient may reduce anxiety 4. Use therapeutic touch and provide 4. Decreases anxiety back rubs and massage Readiness for effective therapeutic Report an understanding of 1. Use open-ended questions to explore 1. This approach is necessary to help regimen management related to the need for smoke and the patients’ uncertainties the patient begin to plan for functioning smoke detectors and CO detectors and escape self-management CO detectors in the home and routes as well as proper plan for escape routes worked ventilation if alternative out and reviewed modes of heat are used 2. Teach about smoke detectors and CO 2. Education can help prevent future detectors in the home and plan for accidental COP escape routes worked out and reviewed 3. If suicide attempt, collaborate with 3. Some COP is intentional, so psychiatric services and plan to identifying the reason for COP is coordinate treatment in psychiatric important to coordinate the facility appropriate type of referrals and follow-up treatment

Abbreviations: CO, carbon monoxide; COP, carbon monoxide poisoning; HBO2, hyperbaric oxygen.

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TABLE 5 Prevention Guidelines for COP18 CO monitor & Install a CO alarm (listed by an independent testing laboratory) near the sleeping areas and on every level of the home & Know the difference between the sound of the smoke alarms and the sound of the CO alarms & Call the local fire department’s nonemergency telephone number to find out what number to call if the CO monitor alarms & Check or replace the battery when you change the time on your clocks each spring and fall & If the detector sounds, leave your home immediately and call 911 & Do not remove smoke detectors Heating systems & Having heating system & When purchasing new heating and cooking equipment Fireplace & Open the flue for adequate ventilation & Have chimney and flue checked for blockages, corrosion, and partial and complete disconnections Kerosene or gas heaters & Open a window slightly whenever using a kerosene or gas heater (kerosene heaters are illegal in many states) Gas oven & Never use a gas oven to heat your home Home purchase & Have a qualified technician evaluate the integrity of the heating and cooking systems, as well as the sealed spaces between the garage and house Camping & Use battery-powered heaters and flashlights in tents, trailers, and motor homes Barbecue grills & Never use them in the home or garage Automobile safety & Never leave a car running near an attached garage or in a garage even if the door is open Generator, charcoal grill, camp stove, or & Never use inside home, basement, or garage even with open doors and windows other gasoline or charcoal-burning device

Abbreviations: CO, carbon monoxide; COP, carbon monoxide poisoning. Sources: http://healthandenergy.com/carbon_monoxide_poisoning.htm; http://www.cdc.gov/co/guidelines.htm; http://www.cpsc.gov/CPSCPUB/PUBS/466.html. or regional wall motion abnormalities suggesting under- become hypoxic and convert to anaerobic metabolism, lying coronary disease that is potentially brought to the lactic acid is produced and released into the system, which surface from the tissue hypoxia related to COP.32 could lead to . If acidosis is present, it is not Carbon monoxide poisoning exacerbates underlying recommended to treat pH levels greater than 7.15 with cardiovascular disease, making patients with COP more intravenous sodium . Doing so may actually susceptible to cardiac effects.4,6,17 Even in patients with further increase carbon dioxide levels, as carbon dioxide is normal coronaries, CO exposure has been found to a byproduct of sodium bicarbonate metabolism. If it is cause angina, nonspecific electrocardiogram changes, indicated to be administered because of lack of improve- and myocardial infarction.1,4,17 The critical care nurse ment, mechanical ventilation may be necessary to assist should educate patients regarding the importance of with elimination of excess carbon dioxide and prevention close cardiovascular follow-up. of .14

Pulmonary Renal Pulmonary edema occurs in ‘‘10% to 30% of acute COP Renal failure and rhabdomyolysis occur because of the cases because of the direct effect on the alveolar mem- direct toxic effect of CO on skeletal muscle.4,14 branes, left ventricular failure, aspiration, or neurogenic pulmonary edema.’’21 Collaboration with pulmonary Fetal and Pediatric Considerations medicine often affords the patient the best opportunity of Carbon monoxide poisoning affects infants more severely survival. than adults because CO binds more closely to fetal hemo- globin than adult hemoglobin. Occult COP may be more Metabolic life-threatening with infants. Even with the older pediatric Respiratory is possible in mild cases, whereas patient, COP may be lethal because of their higher meta- metabolic acidosis is common in severe cases.6 As tissues bolic rate and oxygen uptake4 (Table 4).

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PATIENT EDUCATION AND PREVENTION 15. Bledsoe B, McEvoy M. Where there’s CO, there’s not always fire. How pulse CO-oximetry serves as an important assess- Unintentional COP may be partially preventable through ment & triage tool. J Am Med Serv. 2009;34(3):5-8. public education and prevention programs and/or govern- 16. Lakhani R, Bleach N. Carbon monoxide poisoning: an unusual mental regulations. Educational initiatives to teach about cause of dizziness. J Laryngol Otol. 2010;124(10):1-3. 17. Khandelwal S, Kaide C, Marshall B, Rund D. Carbon monoxide: the dangers of charcoal (grills, hibachis, or buckets) and know your enemy. Emerg Med. 2009;39(1):32-38. liquid fuels (gasoline or propane-powered generators) as 18. Iqbal S, Clower J, Boehmer T, Yip F, Garbe P. Carbon monoxide- alternative sources of heat without the appropriate ventila- related hospitalizations in the U.S.: evaluation of a web-based query system for public health surveillance. Public Health Rep. tion must be presented. In addition, patients need to know 2010;125:423-432. that faulty furnaces, motor vehicles, stoves, gas ranges, 19. Sahjian M, Frakes M. Where there is smokeI inhalation and vented gas heaters are frequent causes of COP. Ad- injuries, carbon monoxide, and cyanide poisoning. Adv Emerg Nurs J. 2008;30(2):180-187. ditional prevention topics are found in Table 5. 20. Jiang G, Gao J, Xu Y, Ma Y, Jiang G, Yan W. Structural and functional improvement of injured brain after severe acute carbon monoxide poisoning by stem cell-based therapy in rats. SUMMARY Crit Care Med. 2009;37(4):1416-1422. Carbon monoxide poisoning is a potentially lethal patient 21. Bledsoe B, Nowicki K, Creel J, Carrison D, Severance H. Use of pulse co-oximetry as a screening and monitoring tool in mass carbon condition that may be misdiagnosed or not diagnosed at monoxide poisoning. Prehosp Emerg Care. 2010;14(1):131-133. all. The critical care nurse must maintain a high index of 22. Hampson N, Rudd R, Hauff N. Increased long-term mortality suspicion so the patient may have the best chance of sur- among survivors of acute carbon monoxide poisoning. Crit Care Med. 2009;37(6):1941-1947. vival. Collaboration with pulmonary medicine often af- 23. Hampson N, Hauff NM. Carboxyhemoglobin levels in carbon fords the patient the best opportunity of survival. Patient monoxide poisoning: do they correlate with the clinical picture? education and must also be part of the Am J Emerg Med. 2008;26:665-669. 24. Hampson NB, Hauff NM. Risk factors for short-term mortal- critical care nurses’ repertoire of intervention. ity from carbon monoxide poisoning treated with hyperbaric oxygen. Crit Care Med. 2008;36(9):2523-2527. 25. Weaver L, Hopkins R, Chan K, et al. Hyperbaric oxygen for acute References carbon monoxide poisoning. NEnglJMed. 2004;347:1057-1067. 1. Weaver LK. Clinical practice. Carbon monoxide poisoning. 26. Weaver L, Hopkins R, Chan K, Thomas F, Churchill S, Elliot G. N Engl J Med. 2009;360:1217-1225. Carbon monoxide research group, LDS Hospital, Utah in reply 2. Centers for Disease Control and Prevention. Carbon monoxide to Scheinkestel et al and Emerson: the role of hyperbaric oxygen related deathsVUnited States, 1999-2004, Morbidity and in carbon monoxide poisoning. Emerg Med Australas. 2004; Mortality Weekly Report, December 21, 2007. MMWR Morb 16(5-6):394-399. Mortal Wkly Rep. 2007;56(50):1309-1312. 27. Beppu T, Nishimoto H, Ishigaki D, Fujiwara S, Yoshida T, 3. Gulati R, Kwan-Gett T, Hampson N, et al. Carbon monoxide epi- Oikawa H. Assessment of damage to cerebral white matter fiber demic among immigrant populations: King County, Washington, in the subacute phase after carbon monoxide poisoning using frac- 2006. Am J Public Health. 2009;99(9):1687-1692. tional anisotropy in tensor imaging. Neuroradiology. 4. Kao L, Nanagas K. Carbon monoxide poisoning. Emerg Med 2010;52(8):735-743. Clin North Am. 2004;22(4):985-1018. 28. Breimer LH, Mikhailidis DP. Could carbon monoxide and 5. Centers for Disease Control and Prevention. Unintentional bilirubin be friends as well as foes of the body? Scand J Clin nonYfire related carbon monoxide exposuresVUnited States, Lab Investig. 2009;70(1):1-5. 2001-2003, Morbidity and Mortality Weekly Report, January 21, 29. Ide T, Kamijo Y. The early elevation of interleukin 6 concentra- 2005. MMWR Morb Mortal Wkly Rep. 2005;54(2):36-39. tion in cerebrospinal fluid and delayed encephalopathy of carbon 6. Colomb-Lippa D. Acute carbon monoxide exposure: diagno- monoxide poisoning treated with hyperbaric oxygen. Am J sis, evaluation, treatment. JAAPA. 2005;18(1):41-46. Emerg Med. 2009;27(8):992-996. 7. Centers for Disease Control and Prevention. Unintentional 30. Chou Y, Hsiao-Lun K, Kai-Chun Y, Ming-Been L, Ying-Chiao L. Y poisoning deathsVUnited States. MMWR Morb Mortal Wkly Predictors of carbon monoxide poisoning induced delayed neuro- Report. 2007;56:93-96. psychological sequelae. Gen Hosp Psychiatry. 2010;32:310-314. 8. Reinisch C. Carbon monoxide poisoning: implications for patient 31. Yelken B, Tanriverdi B, Cetinbas F, Memis D, Sut N. The and family care in the emergency department. Clin Scholars Rev. assessment of QT intervals in acute carbon monoxide poisoning. 2008;1(1):46-49. Anadolu Kardiyol Derg. 2009;9(5):397-400. 9. Akkose S, Turkmen N, Bulut M, Akgoz S, Iscimen R, Eren B. 32. Tucciaron M, Dileo P, Castro E, Guerrero M. Myocardial in- An analysis of carbon monoxide poisoning cases in Bursa, farction secondary to carbon monoxide poisoning: an uncommon Turkey. East Mediterr Health J. 2010;16(1):101-106. presentation of a common condition. Case report and review of the literature. Am J Ther. 2009;16(5):462-465. 10. Audin C. Carbon monoxide poisoning following a natural disaster: a report on Hurricane Rita. J Emerg Nurs. 2006;32(5):409-411. 33. Ackley BJ, Ladwig GB. Nursing Diagnosis Handbook: A Guide to Planning Care. 8th ed. St Louis, MO: Mosby Elsevier; 2008: 11. Goldstein M. Carbon monoxide poisoning. J Emerg Nurs. 148-155. 2008;34(6):538-542. 12. Kamijo Y. The early elevation of interleukin 6 in cerebrospinal fluid and delayed encephalopathy or carbon ABOUT THE AUTHORS monoxide poisoning. Am J Emerg Med. 2009;27(8):992-996. Lisa A. Ruth-Sahd, DEd, RN, CCRN, CEN, is a tenured associate 13. Carlin BW. Carbon monoxide poisoning: case presentation. professor of nursing at York College of Pennsylvania, York, where she Top Emerg Med. 1999;21(4):84-90. 14. Rosenthal LD. Carbon monoxide poisoning, immediate diag- teaches various courses in the baccalaureate and master’s programs. nosis and treatment are crucial to avoid complications. AJN. Dr Ruth-Sahd was a critical care and emergency room nurse for 25 2006;106(3):40-46. years and serves as a reviewer of manuscripts for DCCN.

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Kristen Zulkosky, PhD, RN, CCRN, is an assistant professor of nursing Fetter worked on a telemetry unit for 3 years and as a at Lancaster General College of Nursing and Health Sciences, Lancaster, cardiothoracic nurse clinician for 9 years. Pennsylvania, where she teaches at the associate and baccalaureate The authors have disclosed that they have no significant relationships level. Dr Zulkosky has been a critical care nurse for 23 years. with, or financial interest in, any commercial companies pertaining Mary E. Fetter, MSN, RN, is an instructor of nursing at Lancaster to this article. General College of Nursing and Health Sciences, Lancaster, Address correspondence and reprint requests to: Lisa A. Ruth-Sahd, DEd, Pennsylvania, where she teaches at the associate level. Nurse RN, CCRN, CEN, 25 Wynwood Dr, Mountville, PA 17554 ([email protected]).

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