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Home , Asphyxia, Barotrauma, Hypercapnia, Hypoxia (medical)

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 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 non-specific in mild and severe cases. Delayed neuropsychiatric effects can occur, which are considered a serious . Diagnosis of carbon monoxide poisoning is based upon the patient history and physical examination as well as an elevated level. The etiology, clinical presentation and treatment are discussed, including those for children and special cases such as pregnancy. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1 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 2 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 (CO) exposures and the standard treatments for CO poisoning.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 2 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.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 3 1. Carbon monoxide is produced by:

a. incomplete combustion of carbon-containing fuel b. combustion of -containing materials c. vapors emitted from carbon-containing fuel d. combustion of in organic acids

2. Carbon monoxide can also be produced by:

a. toluene b. methylene chloride c. cyanide d.

3. One of the basic ways by which CO causes harm is:

a. decreased production of b. production of abnormal hemoglobin c. d. pulmonary and coronary

4. One of the basic ways by which CO causes harm is:

a. damage to pulmonary capillaries b. production of c. hemolysis d. direct cellular toxicity

5. Two organs particularly vulnerable to CO poisoning are:

a. the and the heart b. the kidneys and the pancreas c. the thyroid gland and the small bowel d. the and the liver

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 4 Introduction

Carbon monoxide (CO) is sometimes called the silent killer, and aptly so. It is a that is produced by incomplete combustion of carbon- containing material, it is colorless, odorless, and tasteless, and CO can be lethal. Despite large-scale public education and prevention programs, CO exposure is still a serious 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

As mentioned in the introduction, despite increased public awareness of the dangers of CO and widespread public education and prevention measures, CO poisoning is still very common. Many sources consider CO poisoning to be among the leading causes of poisoning in the United States, and CO poisoning is perhaps the number one worldwide cause of by poisoning.1,2,3

Carbon monoxide is produced by the incomplete combustion of carbon-containing material. Automobile exhaust and home heating and/or cooking systems that use oil, gas, coal, or wood are the most common causes of CO poisoning, excluding exposures to fires. Carbon monoxide is also produced when tobacco is burned.

Exposures to carbon monoxide and cases of CO poisoning can happen at any time of the year but are more common during the winter months. If are particularly cold and/or there is a power outage, people may attempt to heat their homes in ways that are

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 5 unsafe. In 2011, in Connecticut, a heavy snowstorm caused a widespread power outage and ambient temperatures at the time were quite cold. Emergency rooms in the state were inundated with cases of carbon monoxide poisoning as people were using gasoline generators and charcoal burning grills inside their homes to try and stay warm.4

Two other sources of carbon monoxide are methylene chloride and methylene iodide. Methylene chloride is a chemical that is often used as a 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 tissues and the metabolizing enzymes are quickly saturated, peak CO levels produced by methylene chloride , ingestion, or dermal absorption are seen 8 hours or longer after an exposure.5 Methylene iodide is used by jewelers to examine gems and, like methylene chloride, it is converted in vivo to CO.6 Carbon monoxide poisoning caused by either of these is very uncommon.

Carbon Monoxide: Pathophysiology

The traditional and commonly understood mechanism of CO poisoning is that CO preferentially binds to hemoglobin, displacing from hemoglobin binding sites and causing cellular and tissue hypoxia. The binding of CO to hemoglobin and the reduced oxygen delivery to tissues and organs is certainly one of the primary ways that CO acts a poison. But research has shown that CO poisoning is much more complex and there are multiple, dynamic processes by which CO causes harm. 7-13 Some of these are known to affect humans and some have only been found in animal models.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 6 Hemoglobin Binding

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 does not bind with oxygen, so most of the hemoglobin is rendered functionally useless.

Oxygen Transfer and the Oxyhemoglobin Dissociation Curve

The oxyhemoglobin dissociation indicates how saturated hemoglobin is at any particular level of oxygen tension of the blood. It also indicates how tightly hemoglobin holds on to oxygen and how easily it releases oxygen for transfer to the tissues. Carbon monoxide shifts the oxyhemoglobin dissociation curve to the left so for any particular level of less oxygen will be transferred to the tissues. This happens for two reasons. First, CO greatly increases the attachment of oxygen to hemoglobin. Second, because there is very little oxygen bound to hemoglobin, the difference between the oxygen level in tissues and the oxygen level of hemoglobin is greatly decreased.

This difference is usually a strong driving for the transfer of oxygen from hemoglobin to the tissues, but it is significantly diminished by the presence of CO. In CO poisoning the oxyhemoglobin dissociation curve shifts to the left and less oxygen reaches the tissues.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 7 Binding to Myoglobin

Myoglobin is an oxygen-transporting and storage pigment that is found inside cells. Carbon monoxide binds to myoglobin - particularly in the myocardium - thus preventing oxygen utilization.

Interference with Oxidative Phosphorylation

Carbon monoxide binds with mitochondrial cytochrome oxidase, an important enzyme that is needed for proper functioning of the electron transport chain in cellular that produces the bulk of the triphosphate (ATP) needed by the body.

Vasodilation

Carbon monoxide increases the formation of cyclic guanosine monophosphate. Cyclic guanosine is second messenger similar to cyclic adenosine monophoshosphate cAMP). Second messengers act to transfer the effects of hormones and other compounds that cannot pass through cell membranes. Cyclic guanosine causes the release of nitric acid from platelets and the vascular endothelium. Cyclic guanosine monophosphate and nitric oxide are potent vasodilators, blood is pooled in the vascular bed, and this decreases oxygen delivery to the tissues.

Free Formation

High levels of nitric oxide initiate the formation of free radicals, and the tissue damage that is caused by poor stimulates an inflammatory response and free radical formation. The result is a reperfusion that can affect the brain and other parts of the central nervous system.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 8 Peroxidation

Carbon monoxide poisoning causes lipid peroxidation. Lipid peroxidation refers to damage caused by free radicals to the that are an integral part of cell membranes. This process is thought to be one of the causes of the neurological effects of CO poisoning.

Leukocyte-Mediated Inflammation

There is evidence that the induced by free radicals causes neutrophils to adhere to cerebral microvasculature. The result is an inflammatory process that may be the cause of the acute and delayed neurological damage that is a common feature of CO poisoning.

Apoptosis

Apoptosis is the process of programmed cell death. Carbon monoxide poisoning is thought to accelerate the process of apoptosis.

Cardiac Stunning

Carbon monoxide is thought to at times produce a catecholamine surge and this can cause what is called myocardial stunning - a temporary, non-ischemic ventricular dysfunction.

Thrombus Formation

Carbon monoxide can inhibit or impair fibrinolysis and increase the amount of thrombin that is formed. Thromboembolic complications caused by CO poisoning have been reported.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 9 The contribution of each of these to CO poisoning is not clearly understood. Carbon monoxide clearly causes tissue hypoxia and decreased oxygen utilization at the cellular level. Those mechanisms are probably responsible for the immediate of CO poisoning that are so familiar to and recognized by health care personnel.

Carboxyhemoglobin levels that reflect tissue hypoxia do not always correlate with the severity of signs and symptoms.14,15 Patients do not always improve as CO is eliminated, and animal experiments have shown that transfused blood with a high level of CO will cause a very high COHb level, but this is less toxic than lower levels of CO that are inhaled.16 Carbon monoxide poisoning then, is probably caused by tissue hypoxia and by direct cellular poisoning. How, why, and when these processes affect a patient who has been exposed to CO is not known.

The mechanisms by which CO poisoning produces signs and symptoms are complex and still not completely understood. Research is ongoing and there are probably other ways that CO causes harm. However, the basic effects of CO poisoning are a) decreased oxygen delivery, b) decreased oxygen utilization, and c) direct toxic to the tissues.

The Endogenous Production Of Carbon Monoxide

Carbon monoxide is an endogenous compound produced by the breakdown of hemoglobin, lipid peroxidation, and the of xenobiotics (substances foreign to the body). The normal level of COHb is approximately 0.1-1%. In the past several decades, many functional roles of CO have been identified. Carbon monoxide acts as a nursece4less.com nursece4less.com nursece4less.com nursece4less.com 10 neural messenger and a vasodilator, it inhibits platelet aggregation, and it appears also to protect against apoptosis, cell proliferation, inflammation, and vasoconstriction.17-19 In vitro and animal studies have shown that CO could be used therapeutically, possibly as a potent anti-inflammatory to treat -, injury, , or pathological processes, such as multiple sclerosis, that are characterized by inflammation.

Caring For A Patient With CO Poisoning

Are you a clinician caring for a patient who has CO poisoning? That may seem like an odd question because the situation and the patient’s complaints quite often make it obvious that a CO exposure has occurred. The patient states that her/his home heating system malfunctioned, the CO detector was alarming, and the patient has common signs and symptoms of CO poisoning.

Remember, CO is called the silent killer. It is colorless, odorless and tasteless, and some exposures to CO can be easily overlooked. Occult CO exposures, poisonings in which CO was not initially identified as the cause of the patient’s complaints, which prompt a patient to seek medical attention, are relatively common; and, CO poisoning frequently produces a clinical picture that is vague and non-specific. Carbon monoxide poisoning can be mistaken for , encephalitis, , influenza, migraine , or other . Aside from knowing the common signs and symptoms of CO poisoning, the health team must also know and be able to recognize the circumstances and situations that are likely to cause exposure to CO.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 11 If CO poisoning is suspected and the attending health team wants to determine if CO poisoning has occurred, the patient(s) and/or their significant other needs to be asked the following questions.

 Where were you when you began to feel sick? If you were at home was the heating system on? If these signs and symptoms have occurred before, do they only happen when you are at home? Do they improve when you are out of the house? Does the patient have a functioning CO detector?

 Who do you live with? Has anyone else been sick? If yes, what are their symptoms? If the patient is living with other people but no one else is sick, CO exposure is unlikely.

 Has your heating system, water heater, etc., and the exhaust systems and chimneys in your house been checked recently?

 Do you get sick when you are driving your car? Do your symptoms improve after you leave the car? Has your car’s exhaust system been inspected recently?

 Do the symptoms happen while you are at work? If so, what does the patient do, and what is happening at work when he/she gets sick? Does the patient work inside? If yes, are there obvious sources of CO? Is the patient a mechanic working in a poorly ventilated garage, or is he/she working in a building where gas- powered or gasoline-powered machinery is operating?

 Has the patient been stripping furniture?

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 12  If there is more than one patient and everyone has essentially the same signs and symptoms, determine if all of the patients got sick at the same time (indicating possible CO poisoning) or did the illness start with one person and seem to spread to the others (indicating a possible infectious illness).

Signs And Symptoms Of Carbon Monoxide Poisoning

Carbon monoxide poisoning can be difficult to detect because the If there is no obvious or symptoms may be mild and even in known exposure to CO, a mild CO exposure can be severe cases they are non-specific. overlooked or misdiagnosed. Also, the number and intensity of the signs and symptoms of CO poisoning is not always related to the COHB level (discussed in more detail later on the learning module).14,15,20 Patients with low levels may be sicker than patients with high levels.

Because CO impairs oxygen delivery and utilization, organs that are very metabolically active, such as the brain and the heart, are most affected by CO. The heart and the brain are also susceptible to direct cellular poisoning as CO has toxic mechanisms that affect those organs. The elderly, children (possibly), people with , cardiovascular disease, or pulmonary disease, and people who have a higher risk of developing CO poisoning than do healthy individuals or those who are neither very young nor very old. The severity of CO poisoning depends on patient risk factors and on the particulars of the exposure: the higher the CO level and the longer the time of exposure, the sicker the patient is likely to be.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 13 CO Symptom Severity

The clinical picture of CO poisoning can be divided into mild, moderate, and severe. Patients with mild CO will have confusion, dizziness, , headache, , and . Patients with moderate CO poisoning will have , chest , dyspnea, , and tachycardia. Patients with severe CO poisoning will have , , , metabolic , and . There can be considerable overlap in the signs and symptoms of the presentation, and it is helpful to think of CO poisoning as a continuum of signs and symptoms, caused by tissue hypoxia and direct cellular toxicity that affect vulnerable organs.

As mentioned previously, the heart is particularly vulnerable to damage from CO because it is so metabolically active and has a very high need for oxygen. The heart is also affected by mechanisms of injury that cause direct cellular damage. Cardiovascular signs and symptoms, from mild to serious, are very common after CO exposure. Patients often have and tachycardia and may develop , arrhythmias, cardiogenic , cardiomyopathy, , non-specific ST segment and T wave changes, , and ST-segment and non-ST-segment myocardial .8,10,11, 21-28 can occur in patients who do not have coronary disease 8,24 and myocardial injury caused by CO poisoning has been associated with an increased risk of short-term and long-term mortality.25,29

Neurologic signs and symptoms are a prominent part of the clinical picture of CO poisoning. Hypoxia increases intracranial and can cause , and these effects, along with direct cellular

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 14 toxicity, is partially the cause of the neurologic signs and symptoms of CO poisoning. Ataxia, dizziness, drowsiness, fatigue, headache, and other neurologic signs and symptoms are common after CO poisoning. More serious effects such as coma, seizures, and syncope can occur after a moderate to severe exposure to CO.3,7,20 Other neurologic effects such as ,30,31 peripheral neuropathy,32 ,33 cataracts,34 chorea,35 tics,36 and monoparesis,37 have been reported.

Perhaps the most studied and most concerning of the neurologic effects of CO poisoning is a phenomenon called delayed neuropsychiatric sequelae (DNS). Some patients who have suffered CO poisoning will develop neurological deficits after a symptom-free period of time. Because of the seriousness of this problem and because the risk of neurological sequelae is one of the primary reasons for the use of hyperbaric oxygen (HBO) therapy to treat patients who have been poisoned with CO, DNS will be discussed separately.

Delayed Neuropsychiatric Sequelae

Delayed neuropsychiatric effects are considered to be one of the most serious complications of CO poisoning. Complete recovery is possible and most patients do recover, but severe and permanent affective, cognitive, and autonomic and motor impairments can also happen.

 Incidence: Delayed neuropsychiatric sequelae appear to be relatively common, but the exact incidence of this complication is not known. Researchers have reported incidences of 2.75%, 14.4%, 30%, 40%, and 47%,38-42 and abnormal EEGs have been reported in 58% of patients who were diagnosed as having

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 15 DNS.43 Different criteria used to evaluate patients, different criteria used to define DNS, and different patient populations probably explain why the reported incidence of DNS varies so widely.

 Onset: The onset of DNS has been reported to be from 7-40 days after exposure,44 6-42 days after exposure,45 and other figures have been cited as well.

 COHb levels and signs/symptoms: There does not seem to be a correlation between COHb levels and the development of DNS. Patients who are comatose often do, but may not develop neuropsychiatric sequelae, and patients who have not lost consciousness may develop serious neurological problems.46,47

Some factors that seem to be consistently associated with an increased risk of developing DNS are age > 36 and a duration of exposure > 24 hours.48 Other researchers noted an association between a duration of exposure > 6 hours, seizures, a Glasgow Coma Score < 9, leukocytosis, and elevated CK, or a systolic < 90 mm Hg and DNS.41 A recent (2014) study found that predictors for the development of delayed were: abnormal CT findings that indicated hypoxic encephalopathy; high ; high creatine- kinase MB; high , and; low Global Assessment Scale score.49

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 16  Recovery: Recovery from DNS is possible.50-52 The rate of recovery from DNS has been estimated to be approximately 75%.42,53

 Signs and Symptoms: The signs and symptoms of neuropsychiatric sequelae can be divided into affective, cognitive, and autonomic and motor impairments. Affective impairments that have been reported include , depression, irritability, mood swings, and . Cognitive effects that have been reported include deficits in attention, , memory, and speech, and dementia. Autonomic and motor impairments that have been reported include chorea, dystonia, incontinence, , and parkinsonism signs such as bradykinesia, mask face rigidity, and shuffling gait.7,44,54-56

The Toxic Dose Of Carbon Monoxide

The toxic dose of CO will depend on the patient characteristics such as age, medical history, metabolic rate, and and the environmental factors of CO concentration in the air and the duration of exposure. The concentration of CO in the inspired air and the duration of exposure are the factors that are most predictive of the seriousness of the exposure. The higher the concentration of CO and the longer the duration of the exposure, the higher the COHb level will be.

The Occupational Safety and Health Administration (OSHA) standard is that workers cannot be exposed in an eight hour work day to an nursece4less.com nursece4less.com nursece4less.com nursece4less.com 17 average of more than 50 parts per million (ppm). Most CO detectors that are installed in homes begin to alarm if the CO concentration in the air averages 70 ppm for an hour or longer. Most people will begin to experience symptoms, e.g., dizziness, headache, when the CO level is 100 ppm, and, a CO level of 5000 ppm is usually lethal within five minutes. Blood levels of CO do not correlate well with symptoms, but higher levels are more likely to cause signs and symptoms, and COHb levels 50% and higher have been associated with coma, seizures, and death.3,57

The Carboxyhemoglobin Level

The carboxyhemoglobin level is a vital piece of information that is needed to assess a patient who has or is suspected to have CO poisoning. In order to use the COHb as an assessment tool you must know: 1) if the patient and if she/he does, how much; 2) the medical problems and clinical conditions that can affect COHb level; 3) how the COHb level was measured; 4) when the COHb level was measured in relation to the time the patient was last exposed, and; 5) what treatment for CO poisoning the patient has received.

The normal level of COHb is approximately 0.1-1% in non-smokers. Tobacco combustion produces CO so smokers will have higher CO levels than non-smokers. The typical smoker will have a COHb level of 3-5%.9 Each pack of smoked per day will raise the COHb level approximately 2.6%,58 and heavy smokers who have lung disease may have a COHb level > 10%.9 There are individual variations in COHb level, but if a non-smoker has a COHb level > 4% or a smoker has a COHb level > 10%, CO exposure should be suspected.9

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 18 Patients who have hemolytic anemia, patients who have an elevated serum bilirubin level, patients who have malaria, and patients with sepsis or shock, can have elevated COHb levels.59-61 An elevated COHb level has been reported in a patient who was mechanically ventilated and receiving nitric oxide therapy.62 The accuracy of COHb levels can be affected if the level is < 2-3%, if the blood specimen is lipemic, if the patient has received methylene blue, or in the presence of fetal hemoglobin.63 The issue of fetal hemoglobin and measuring COHb levels in infants will be discussed in a separate section.

Carboxyhemoglobin levels are measured with a co-oximeter, a device that can measure the amount of hemoglobin that is saturated with CO. Either arterial or venous blood can be used to measure COHb.3,9 Some types of oximeters - but not all - can accurately measure COHb, as well. Older models of pulse oximeters were not able to distinguish between hemoglobin saturated with oxygen and COHb. However, there are newer types of pulse oximeters that can make this distinction and prove an accurate measurement of CO.3

Carbon monoxide is rapidly absorbed. Elimination depends on several factors but the rate of dissociation of COHb is directly proportional to the percentage of inhaled oxygen, so the more oxygen that can be delivered the faster COHb will be eliminated. The half-life of CO when someone is room air is approximately 4-6 hours, the half-life of CO is approximately 60 minutes when someone is breathing 100% oxygen, and the half-life of CO is approximately 20 minutes if someone is treated with hyperbaric oxygen.3 When you are interpreting COHb levels, you must always take into account: a) how long the patient has been away from the source, and b) how long the

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 19 patient has been receiving oxygen and how much oxygen he/she has been receiving.

Carboxyhemoglobin levels are needed to confirm the presence of CO poisoning. Carboxyhemoglobin levels are also used to determine what treatment the patient should receive, and to some degree the COHb level may predict the level of severity of CO poisoning. However, there is universal agreement that COHb levels are unreliable for predicting the severity of any particular case of CO poisoning and should not be depended upon to do so.7,14.15 Levels of 47% have been reported in patients who have minimal symptoms, and levels of 10% have been noted in patients who were comatose.64 Also, the level of COHb that is used to determine what treatment the patient needs - specifically whether or not the patient should receive hyperbaric - is not clear or universally agreed upon.

Treatment Of Carbon Monoxide Poisoning

Treating a case of CO poisoning begins by removing the patient from the source, assessing the patient’s airway, breathing, and circulation (ABCs), and assessing the patient’s cardiac and neurological status. If the patient has suffered a , is comatose, or is having a or an , 100% oxygen should be administered and basic, supportive care provided. The best initial treatment for any patient with CO poisoning is high concentration oxygen and basic supportive care. If the patient has chronic obstructive pulmonary disease and retains , high of oxygen should be used with caution.65 Sometime during the initial assessment learning the circumstances of the exposure should be sought out. If

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 20 the fire department responded to the scene, it should be determined whether a measurement of the CO level of the air was obtained.

If the patient has normal ABCs and no serious signs and symptoms, and there is no report of loss of conscious or seizures, the health team should ensure that he/she is receiving 100% oxygen and start continuous cardiac monitoring. An evaluation of the patient’s cardiac and neurologic status should be performed. At a minimum, a 12-lead ECG, a COHb level, and creatine-kinase MB and troponin levels should be obtained. If the patient lost consciousness, had a seizure, or there is other evidence of serious toxicity, an arterial blood gas (ABG), blood urea nitrogen (BUN) and creatinine, serum electrolytes, serum lactate level, serum CK, and urine myoglobin should be obtained. If the CO exposure resulted from intent to cause self-harm, it’s recommended to obtain an acetaminophen level, an ethanol level, and a salicylate level. Computed tomography (CT) scanning or magnetic resonance imaging (MRI) scanning of the head should be performed if the patient has any neurological deficits.

Learning Break: Be very careful to document when the patient was last exposed to CO, when and at what percent/flow oxygen therapy was started, and when the COHb level was obtained. These facts will be very important in terms of assessing the severity of the case, the patient’s response to therapy, and the possible need for more aggressive treatment.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 21 The patient should continue to receive high-concentration oxygen until he/she is asymptomatic, the ECG is normal, myocardial injury has been ruled out, and the COHb level is < 10%.3 If the patient has cardiovascular or pulmonary disease, he/she should be treated until the COHb is 2%.3 The half-life of CO is approximately 60 minutes when a patient is breathing 100% oxygen, so patients with low levels of COHb and mild signs and symptoms on admission to the emergency department can often be discharged after several hours of treatment.

Before the patient is discharged, a Mini Mental Status exam should be The Mini Mental Status exam is performed and a follow-up performed to screen for cognitive impairment, such as appointment for a neurologic exam to patient orientation to time should be arranged. The Mini Mental and place, attentiveness, Status exam is a 30-question exam memory, speech and the ability that is used to detect cognitive to follow commands. impairments. It is popular because it can be used quickly and easily. If cognitive deficits are detected using this test more sophisticated neurologic testing should be done. Additionally, the safety of the environment that the patient is returning to should be ascertained. For example, if the patient is returning home, it should be verified whether there are functioning CO detectors in the residence. The patient should also be informed about how CO is produced, and an effort made to review with the patient what is/is not safe in terms of home heating strategies.

If the patient does not respond to normobaric oxygen (oxygen delivered at normal ), or if the patient has

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 22 serious complications, or if the patient is considered to have a serious exposure, two issues must be considered: a) the patient may be suffering from cyanide exposure or (the latter is very uncommon), or; b) the patient may need hyperbaric oxygen (HBO) therapy.

Cyanide can be produced as a by-product of combustion that occurs during house fires.

Patients who have suffered a serious CO poisoning should be admitted to intensive care. There are no universally agreed upon criteria for what constitutes a serious CO poisoning, but most clinicians would consider the exposure to be serious if any of the following were present.  Arrhythmias  Cardiac ischemia  COHb > 25  Loss of consciousness   Persistent depressed level of consciousness  Seizure  Pregnancy

Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy delivers 100% oxygen at atmospheric that are 2 to 3 times above normal, and it greatly increases the amount of oxygen dissolved in the blood. Normally the blood oxygen concentration is 0.3 ml/dl. When a patient is placed in an HBO chamber at 3 times normal atmospheric pressure (3 ATM), the blood nursece4less.com nursece4less.com nursece4less.com nursece4less.com 23 oxygen concentration is 6 ml/dl. The therapeutic mechanisms by which hyperbaric oxygen work include increased dissociation of COHb, increased plasma concentration of oxygen, increased dissociation of CO from cytochrome oxidase, increasing free radical production, and decreased leukocyte-mediated inflammation.23,24

Hyperbaric oxygen is routinely used for patients with serious CO poisoning or patients who do not respond to normobaric oxygen therapy. The goal of hyperbaric oxygen therapy is to prevent the development and/or reduce the severity of neurological sequelae. Hyperbaric oxygen therapy has been used for many years and is commonly prescribed for patients with moderate to severe CO poisoning. However, some basic issues about using it are still controversial.

 The effectiveness of hyperbaric oxygen therapy: There is no doubt that hyperbaric oxygen has many beneficial physiological effects and given the pathological processes of CO poisoning, it makes that hyperbaric oxygen therapy would be an effective treatment for CO poisoning. There is a lot of evidence that hyperbaric therapy does reduce the incidence and severity of neurological sequelae. However, when the evidence for and against the use of HBO is examined, randomized trials do not show that HBO prevents the development of DNS.66

 Patient selection: There are no universally accepted criteria for selecting patients who would benefit from HBO therapy. There is no agreed upon definition of what constitutes a serious CO poisoning, no one

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 24 knows what level of COHb is dangerous, and there are no highly reliable predictors that can identify which patients with CO poisoning are at risk for developing delayed neuropsychiatric sequelae.

The Undersea and Society recommends using CO when: 1) the patient has had a loss of conscious, even a transient loss; 2) there are abnormal neurologic findings; 3) the COHb level is ≥ 25%; 4) the patient is pregnant, or; 5) there is a significant metabolic acidosis.67 These criteria are widely known and cited, but not used by all HBO centers.

In a 2012 survey of 30 HBO treatment facilities, 19 centers used the COHb level as an independent factor for choosing which patients to treat, 10 centers relied solely on symptoms to decide, 4 used the COHb level as the only factor for selecting patients for HBO therapy, and 19 centers did not have a protocol.68 A survey of the directors of HBO treatment facilities showed similar differences, but significant neurologic problems such as coma, abnormal neuropsychiatric test results, and evidence of cardiac ischemia were commonly agreed upon criteria for the use of HBO.3

 The end-point and the duration of HBO therapy: There are no standard protocols for how often someone should receive HBO therapy, and when it should be discontinued. The effectiveness of HBO therapy may decrease if the patient is treated > 6 hours after the exposure69, but it may be effective if it is given 16 hours to 21 day after CO poisoning.70-71 Some

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 25 hyperbaric oxygen centers will use several treatments, some use only one, and different hyperbaric therapy centers have different endpoints for therapy.

Hyperbaric oxygen therapy (often called a dive) is done in a chamber. These can be small mono-place (holding a single person) chambers or a multi-place sealed room that can accommodate one or more patients, a , monitoring equipment, and (occasionally) a nurse. The mono-place chamber is filled with 100% oxygen, which is compressed to the desired atmospheric pressure. In the multi-place chamber, the patient breathes 100% oxygen from an outside source and the ambient air in the chamber is compressed. Most large cities have a hyperbaric oxygen treatment center, but the initial health care facility may be far away from an HBO treatment center. Deciding who is stable enough to be transferred and when he/she should be transferred should be considered very carefully.

Patients who have been intubated may need sedation and occasionally neuromuscular paralysis during hyperbaric oxygen treatment. The cuff of the endotracheal tube should be deflated and refilled with sterile saline before the patient enters the chamber; the high atmospheric pressure can collapse the cuff if it is filled with air. The patient’s pulmonary status and blood pressure must be monitored carefully when he/she is in the chamber. can increase the risk of seizures, so the PACO2 should be maintained at a normal level. Hyperbaric oxygen therapy can lower the blood pressure, so blood pressure should be checked frequently, especially if the patient has cardiovascular disease or is receiving an intravenous vasopressor. The

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 26 duration of most dives is about 2 hours. Some will require multiple dives over the course of several days.

Most side effects of HBO therapy are mild and temporary. Middle such as bleeding, pain, and perforation of the is very common72,73 with an incidence as high as 35.8% reported.72 Barotrauma to the lung and air embolization are rare adverse effects.74,75 Seizures are possible, but they do not cause residual damage. The incidence of seizures during hyperbaric oxygen therapy is very low, typically < 1%.76 The presence of anxiety, fever, hypothermia, prior seizure, and a high HBO pressure may increase the risk of seizure occurrence during HBO therapy.76

Children And Carbon Monoxide Poisoning

There is a relative lack about CO poisoning in the pediatric population. Children have a higher metabolic rate and a developing nervous system, so it seems intuitive that they would be more susceptible to the effects of CO poisoning at lower levels of CO. However, the published literature that discusses pediatric CO poisoning either does not mention the issue or simply offers speculation about it. It does appear that central nervous system effects such as lethargy and syncope are more common in children who have CO poisoning than in adults,77-79 and the incidence of DNS is lower for children than adults.44,80

Significant cardiac damage in pediatric patients with CO poisoning has been reported,81 and a 2010 study found that 16 of 107 pediatric patients with CO poisoning had cardiac biomarkers, and nursece4less.com nursece4less.com nursece4less.com nursece4less.com 27 revealed some that had a low ejection fraction and left ventricular dysfunction.82

The other issue specific to the pediatric patient and CO poisoning is interference with measurement of the COHb level by the presence of fetal hemoglobin. Fetal hemoglobin is a form of hemoglobin that has a greater affinity for oxygen than adult hemoglobin. At birth infants have a fetal hemoglobin concentration of approximately 70%. By age 6 months the fetal hemoglobin concentration is typically 1-2%,83 although children with or thalassemia can have higher levels. Certain methods of measuring COHb will also measure fetal hemoglobin as COHb. The higher the level of fetal hemoglobin the greater the degree of interference and false COHb levels as high as 7- 8% have been reported.3,84

Carbon Monoxide Poisoning In The Pregnant Patient

Carbon monoxide can be very dangerous to a because even a relatively small decrease in maternal oxygen saturation can cause a sharp drop in fetal oxygen saturation. In addition, fetal hemoglobin has a higher affinity for binding to CO than maternal hemoglobin, COHb levels in the fetus can be 10-15% higher than in the mother, and fetal elimination of COHb is much slower than the maternal elimination rate.85

Severe maternal carbon monoxide poisoning has been associated with high fetal mortality rates, and serious complications such as , limb deformities, microcephaly, motor and neurological disabilities, and mental retardation are possible.57,85,86 Fetal death and

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 28 fetal injury can also occur even if the mother is relatively asymptomatic.87

The recommendations for treating the pregnant patient who has CO poisoning are essentially the same as for any other patient, but there are several important differences. A medical toxicologist or a hyperbaric medicine physician should be consulted in all such cases. Administration of 100% oxygen may need to be continued for much longer than it would normally be needed because of the COHb-fetal hemoglobin binding and the higher fetal COHb levels. Additionally, as pregnancy is considered to be one of the indications for the use of HBO therapy in cases of CO poisoning, early notification of the local HBO treatment facility would be prudent.

What If The Patient Does Not Respond To Treatment?

There are several reasons why a patient who has been poisoned with CO does not respond to treatment, but perhaps the most common cause of a lack of response would be . Cyanide is a highly toxic gas that is produced when there is incomplete combustion of nitrogen-containing material. It is a chemical asphyxiant, which interferes with aerobic production of ATP by binding to cytochrome oxidase and preventing the use of oxygen by the electron transport chain, and it is a very dangerous gas.

The exact incidence of cyanide poisoning caused by fire and smoke inhalation is not known, but it is thought to be common.88 Since these situations (house fires, etc.) very often cause CO poisoning as well, the patient is at great risk for hypoxic injury and there may be a

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 29 synergistic effect between CO and cyanide that increases the toxicity of each one.

Determining if a patient who has CO poisoning also has been poisoned by cyanide is not simple. Cyanide poisoning should be suspected if: 1) The patient with CO poisoning caused by a fire does not respond to oxygen therapy as expected; 2) The patient was involved in an enclosed space fire; 3) The patient has an altered level of consciousness; 4) The patient has an elevated plasma lactate level, and; 5) The patient has hypotension that cannot be explained by the CO poisoning or by another pathologic mechanism.88

Cyanide poisoning will not respond to oxygen therapy; the pathologic mechanism of cyanide poisoning and CO poising are distinctly different. Patients with cyanide poisoning must be given the cyanide antidote kit or hydroxocobalamin (an injectable form of vitamin B-12).

Patients with combined CO and cyanide poisoning may also benefit from hyperbaric oxygen therapy but there is no evidence that proves it is effective for cyanide poisoning. Some toxicologists and emergency department physicians feel that hydroxocobalamin should be given empirically to most fire victims; these patients should be evaluated on a case-by-case basis for the use of this antidotal therapy.

Is Ambient Levels Of CO Harmful?

Carbon monoxide is a by-product of the combustion of fossil fuels and the combustion of carbon-containing material for fuel, and it is a common air pollutant. The ambient levels of CO in urban areas have nursece4less.com nursece4less.com nursece4less.com nursece4less.com 30 been found to range from 2-40 ppm, but in areas of heavy automobile traffic the ambient level can reach an average of 500 ppm.89 Second- hand smoke can also be a significant source of ambient CO.90

The harm that can be caused by second-hand smoke is well documented. There is also strong evidence that chronic exposure to ambient CO as part of air pollution increases cardiovascular morbidity and mortality.89,91-95 The studies that have examined the health effects of chronic exposure to CO as an air pollutant are in part confounded by the presence of other air pollutants and varying study group population, and the contribution of ambient CO to cardiovascular morbidity and mortality has not yet been determined.

Follow-Up After CO Poisoning

People who have had CO poisoning should be followed closely after discharge. People who survive CO poisoning appear to have a significantly higher rate of death than the general population: one study found the increase in deaths in this population to be twice what would be expected.96 The onset of delayed neuropsychiatric sequelae can occur weeks after an exposure to CO, so the patient and the physician who is providing follow-up care must be aware of this. If these complications do occur, there are no treatments that have been evaluated with clinical trials.

Symptomatic and supportive care should be provided, and this can include (when appropriate) , physical therapy, and speech therapy. Cognitive symptoms from DNS have been treated with donepezil (a drug used for the treatment of mild to moderate dementia), but this is an unlabeled use of the drug, there is very little nursece4less.com nursece4less.com nursece4less.com nursece4less.com 31 experience using donepezil for this purpose, and the results have been equivocal.97-99 Hyperbaric oxygen therapy has also been used for this purpose but again, the clinical experience is limited.100-101

Stimulant drugs such as dextroamphetamine, methylphenidate, and modafanil might be helpful to treat attention and memory deficits, but there is no clinical experience with them as yet. If the patient has signs and symptoms of Parkinsonism, standard therapy with anticholinergics and levodopa can be used, but as with the other pharmacological therapies mentioned, there is very little clinical experience and the results have been equivocal.102

Summary

Carbon monoxide is a dangerous gas that is produced by the incomplete combustion of fossil fuels such as gasoline and kerosene, and by the combustion of carbon-containing materials like coal and wood. Carbon monoxide is also produced endogenously and by burning of tobacco. The normal COHb level for a non-smoker is usually ≤ 1% and for a smoker it is 3-5%. Poisoning with CO occurs when the gas is inhaled, and CO causes harm by two basic mechanisms: 1) preferentially binding hemoglobin, thus causing tissue hypoxia, and; 2) direct cellular toxic mechanisms. The result of CO poisoning is decreased oxygen delivery and disruption of cellular metabolism.

The signs and symptoms of CO poisoning are vague and non-specific. However, CO has the strongest effect on the organs that are the most metabolically active and have high oxygen demands, so the brain and the heart are the most vulnerable to CO. Cardiac and neurologic signs and symptoms predominate in cases of CO poisoning. These can be

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 32 mild and self-limiting or quite serious. Most patients will complain of headache, dizziness, and palpitations, but coma, myocardial infarction, permanent neurological deficits, seizures and death are possible. A particularly concerning effect of CO poisoning is delayed neuropsychiatric sequelae (DNS). Some patients who have suffered CO poisoning will have an asymptomatic period of days to weeks and then will develop debilitating affective, cognitive, and autonomic/motor deficits.

Treating CO poisoning begins with understanding the circumstances and situations in which CO poisoning is likely. These may not always be obvious or reported by the patient, and studies have shown that occult CO poisonings, poisonings in which CO was not initially identified as the cause of the patient’s complaints, are relatively common.103-104 Treatment of confirmed cases of CO poisoning always begins with assessment and stabilization of the ABCs, administration of 100% oxygen, and continuous cardiac monitoring.

Diagnostic and laboratory test should include a COHb level, creatine kinase MB and troponin levels, and a 12-lead ECG. Other tests that may be needed will depend on the patient’s condition and may include an ABG, BUN and creatinine, serum electrolytes, serum CK, serum lactate level, urine myoglobin level, and CT or other scanning of the head. A thorough assessment of the patient’s neurological and cardiovascular status should be done as well. The COHb level is a vital part of the assessment, but COHb levels do not accurately predict the seriousness of the exposure.

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 33 Patients should receive supplemental oxygen and be observed for at least four to six hours, and most patients can be discharged when the COHb level is < 10and the signs and symptoms have resolved. A Mini Mental Status exam should be performed before the patient leaves the emergency department. In addition, the health team should make sure that the patient understands how CO poisoning happens and, if he/she is returning home, that there are functioning CO detectors at the residence. A follow-up appointment for a neurologic exam should be arranged.

If the patient has had serious signs of symptom of CO poisoning, normobaric oxygen may not be sufficient and HBO may be indicated. There are no universally accepted criteria for when to use HBO and for whom, but the commonly cited indications for HBO are: 1) the patient has had a loss of conscious, even a transient loss; 2) there are abnormal neurologic findings; 3) the COHb level is ≥ 25%; 4) the patient is pregnant, or; 5) there is a significant metabolic acidosis. Hyperbaric oxygen therapy is primarily used to prevent the development of DNS. However, despite many years of clinical experience and much study, the clinical benefits of HBO therapy for the prevention of DNS are still unproven.

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nursece4less.com nursece4less.com nursece4less.com nursece4less.com 34 1. Carbon monoxide is produced by:

a. incomplete combustion of carbon-containing fuel b. combustion of nitrogen-containing materials c. vapors emitted from carbon-containing fuel d. combustion of in organic acids

2. Carbon monoxide can also be produced by:

a. toluene b. methylene chloride c. cyanide d. cadmium

3. One of the basic ways by which CO causes harm is:

a. decreased production of hemoglobin b. production of abnormal hemoglobin c. tissue hypoxia d. pulmonary and coronary vasoconstriction

4. One of the basic ways by which CO causes harm is:

a. damage to pulmonary capillaries 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

6. True or false: COHb level is a good predictor of the seriousness of the CO exposure.

a. True b. False

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 35 7. The primary treatment for CO poisoning is:

a. hydroxocobalamin b. 100% oxygen c. endotracheal intubation d. methylene blue

8. Patients who have had CO poisoning are at risk for:

a. delayed neuropsychiatric sequelae b. increased risk of developing metabolic syndrome c. delayed onset of liver damage d. increased risk of developing Alzheimer’s

9. Which of the following are indications for the use of HBO?

a. Age < 5 years, COHb level > 10% b. Pregnancy, COHb level ≥ 25% c. Age > 55 years, headache d. Female gender, metabolic acidosis

10. The primary use of HBO is to prevent:

a. the development of delayed myocardial ischemia b. the development of shock to the liver c. the development of rhabdomyolysis d. the development of delayed neuropsychiatric sequelae

Correct Answers:

1. A 2. B 3. C 4. D 5. A 6. B 7. B 8. A 9. B 10. D

nursece4less.com nursece4less.com nursece4less.com nursece4less.com 36 References Section

The References below include published works and in-text citations of published works that are intended as helpful material for your further reading.

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nursece4less.com nursece4less.com nursece4less.com nursece4less.com 37 12. Ryoo SM, Sohn CH, Kim HJ, Kwak MK, Oh BJ, Lim KS. Intracardiac thrombus formation induced by carbon monoxide poisoning. Human & Experimental Toxicology. 2013;32:1193- 1196. 13. Gawlikowski T, Gomolka E, Piekoszewski W, Jawień W, Undas A. Acute Co poisoning is associated with impaired fibrinolysis and increased thrombin formation. Basic & Clinical Pharmacology & Toxicology. 2013;112:352-356. 14. Hampson NB, Dunn SL. Symptoms of carbon monoxide poisoning do not correlate with the initial carboxyhemoglobin level. Undersea & Hyperbaric Medicine. 2012;39:657-665. 15. Hampson NB, Hauff MN. Carboxyhemoglobin levels in carbon monoxide poisoning: do they correlate with the clinical picture? American Journal of Emergency Medicine. 2008;26:665-669. 16. Goldbaum LR, Orellano T, Dergal E. Mechanism of the toxic action of carbon monoxide. Annals of Clinical and Laboratory Science. 1976;6:372-376. 17. Foresti R, Bani-Hani MG, Motterlini R. Use of carbon monoxide as a therapeutic agent: promises and challenges. . 2008;34:649-658. 18. Fagone P, Mangano K, Coco M, et al. Therapeutic potential of carbon monoxide in multiple sclerosis. Clinical and Experimental Immunology. 2012;167:179-187. 19. Ryter SW, Choi AM. Carbon monoxide: present and future indications for a medical gas. Korean Journal of Internal Medicine. 2013;28:123-140. 20. Olson KR. Carbon monoxide. In: Olson KR, Anderson IB, Benowitz NL, et al., eds. Poisoning & Drug Overdose. 5th ed. New York, NY: Lange Medical Books/McGraw-Hill;2007. 21. Lippi G, Rastelli G, Meschi T, Borghi L, Cervellin G. Pathophysiology, clinics, diagnosis, and treatment of heart involvement in carbon monoxide poisoning. Clinical Biochemistry. 2012;45:1278-1285. 22. Yanir Y, Shupak A, Abramovich A, Reisner SA, Lorber A. complicating acute carbon monoxide poisoning despite neurologic and metabolic recovery. Annals of Emergency Medicine. 2002;20:420-424. 23. Kim S, Lim JH, Kim Y, Oh S, Choi WG. A case of acute carbon monoxide poisoning resulting in an ST segment elevation myocardial infarction. Korean Circulation Journal. 2012;42:133- 135. 24. Tucciarone M, Dileo PA, Castro ER, Guerrero M. Myocardial infarction secondary to carbon monoxide poisoning: an uncommon presentation of a common condition. Case report and nursece4less.com nursece4less.com nursece4less.com nursece4less.com 38 review of the literature. American Journal of Therapeutics. 2009;16:462-465. 25. Henry CR, Satran D, Lingren B, Adkinson C, Nicholson CI, Henry TD. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. Journal of the American Medical Association. 2006;295:398-402. 26. Salih SB, Alenezi H, Alghamdi A. A case of first degree AV block in carbon monoxide poisoning patient. Journal of the Saudi Heart Association. 2013;25:255-259. 27. Satran D, Henry CR, Adkinson C, et al. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. Journal of the American College of Cardiology. 2005;45:1513-1516. 28. Cetin M, Ornek E, Murat SN, Cetin ZG, Oksuz F, Gokcen E. A case of carbon monoxide poisoning presenting with supraventricular tachycardia. Internal Medicine. 2011;50:2607- 2609. 29. Garg J, Krishnamoorthy P, Palaniswamy C, et al. Cardiovascular abnormalities in carbon monoxide poisoning. American Journal of Therapeutics. 2014; Feb 10. [Epub ahead of print] 30. Pillion JP. Sensorineural hearing loss following carbon monoxide poisoning Case Reports in Pediatrics. 2012;May 7. [Epub ahead of print]. 31. Mehrparvar AH, Davari MH, Mollasadeghi A, et al. Hearing loss due to carbon monoxide poisoning. Case Reports in Otolaryngology. 2013;May 13. [Epub ahead of print] 32. Rahmani M, Belaidi H, Benabdeljlil M, et al. Bilateral brachial plexus injury follwing acute carbon monoxide poisoning. BMC Pharmacology & Toxicology. 2013;14:61-64. 33. Mahmoud O, Mestour M, Loualidi M. Carbon monoxide intoxication and anterograde amnesia. Encehphale. 2009;35:281-285. 34. Kasbekar S, Gonzalez-Martin JA. Chronic carbon monoxide poisoning resulting in bilateral cataracts and a cystic globus pallidus lesion. BMJ Case Reports. 2011;July 15. 35. Park S, Choi IS. Chorea following acute carbon monoxide poisoning. Yonsei Medical Journal. 2004;45:363-366. 36. Alioglu Z, Boz C, Sari A, Aynaci M. Transient tic disorder following carbon monoxide poisoning. Journal of Neuroradiology. 2004;31:231-233. 37. Tajima Y, Satoh C, Yaguchi H, Mito Y. Pure motor monoparesis of the leg after carbon monoxide poisoning. Journal of Neurology, Neurosurgery & Psychiatry. 2014;Mar 3. [Epub ahead of print]

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