TOC  |  Toxicology

Carbon monoxide               See see also  Carbon Monoxide2009.pdf
is the most frequent cause of asphyxiant poisoning and the most common cause of fatal occupational inhalation in the United States. The incidence of carbon monoxide poisoning is greater during the winter season, because most exposures result from the escape of the chemical from faulty heating systems or in exhaust from combustion-powered vehicles or appliances and because carbon monoxide readily accumulates indoors.  A diagnosis of carbon monoxide poisoning is confirmed by an elevated carboxyhemoglobin level (COHb) for which there is a specific test with rapidly available results. Low carboxyhemoglobin values must be interpreted cautiously, however, because they can be the result of treatment with oxygen or substantial delays between the end of the exposure and the carboxyhemoglobin measurement.

Carbon Monoxide Poisoning                                                                           REF: FirstConsult (MedConsult) 2006

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Description * Carbon monoxide (CO) is an odorless, colorless, tasteless gas produced by incomplete combustion of carbon materials. Potential sources include fires, smoke, wood-burning stoves, gas or kerosene space heaters, and engine exhaust * CO has 200-250 times greater affinity for hemoglobin than oxygen, and competes with oxygen for reversible binding at the iron-porphyrin center of hemoglobin, producing carboxyhemoglobin (COHb) * The presence of COHb shifts the oxyhemoglobin dissociation curve to the left, impairing the release of oxygen to tissues and resulting in tissue hypoxemia * COHb also binds with intracellular proteins, such as myoglobin and cytochrome oxidase, impairing muscular and mitochondrial function, respectively Carboxyhemoglobin Blood  Level Test: Description: Carboxyhemoglobin (COHb) level measured by spectrophotometer not pulse oximetry (the pulse oximeter cannot distinguish between carboxyhemoglobin, oxyhemoglobin, deoxyhemoglobin, and abnormal hemoglobins such as carboxyhemoglobin, methemoglobin, cyanomethemoglobin, and sulfhemoglobin) Advantage: * Used to help evaluate for poisoning and to monitor treatment Disadvantages: * Do not completely rely on carboxyhemoglobin levels because the level may be deceivingly low if the transport time is prolonged or if the patient received supplemental oxygen in the pre-hospital environment (e.g. from ambulance or fire personnel) * The clinical presentation and duration and extent of exposure are better indicators of the severity of poisoning Normal Levels: * Nonsmoker: 0-2.3%;   * Smoker: up to 12% Abnormal Level * Any level above normal (levels greater than 50% can be fatal) * Levels do not necessarily correlate with severity of poisoning, but help confirm the diagnosis if elevated Cause of abnormal result: Exposure to carbon moxide (CO), resulting in elevated concentrations in tissues and in the blood.

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Immediate action !!! Patients suspected of carbon monoxide poisoning should be treated immediately with 100% oxygen either by non-rebreather mask or intubation and mechanical ventilation.

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Cardinal features * There are no pathognomonic features; therefore, the diagnosis of carbon monoxide (CO) poisoning requires a high index of suspicion as the clinical presentation is often confused with other common conditions such as influenza, gastroenteritis, and benign headache syndromes * Acute CO poisoning is defined as a single exposure to CO lasting less than 24h. In chronic CO poisoning, exposure occurs more than once, lasts longer than 24h and usually involves lower CO levels and lower carboxyhemoglobin saturations * The severity of poisoning is the product of the concentration of CO and the length of the exposure. Prolonged exposure to relatively low levels of CO may produce moderate or severe poisoning, while a relatively brief exposure to high levels may produce a similar clinical picture * Central nervous system and cardiovascular signs and symptoms predominate * Symptoms that may be encountered with mild CO poisoning include headaches, dizziness, nausea, and vomiting * With moderate or severe poisoning, the patient may develop chest pain, dyspnea, syncope, severe headache, ataxia, mental confusion, seizures, coma and death * Development of delayed neuropsychiatric sequelae, including dementia, psychosis, parkinsonism, chorea, peripheral neuropathy, and incontinence, are the feared long-term consequences of CO poisoning

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Causes Common causes * Exposure may be accidental or intentional (as seen in suicide attempts) * Exposure to incomplete combustion of carbon materials such as fires, smoke, furnaces, charcoal grills, gas or wood-burning stoves, gas or kerosene space heaters, and the exhaust of internal combustion engines Rare causes * Breakdown of anesthetic in desiccated carbon dioxide absorbents during the administration of inhalational anesthesia * Exposure to methylene chloride, a solvent used as a paint-stripping agent Contributory or predisposing factors * Malfunctioning hydrocarbon combustion devices * Exposure in an enclosed or poorly ventilated environment * Certain groups of patients are predisposed to toxicity: infants and children, owing to their high minute ventilation and increased metabolic rates; the elderly and those with comorbid conditions that predispose to poor cardiovascular reserves; and pregnant patients (fetal toxicity)

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Epidemiology * Leading cause of accidental poisoning in US   * Leading cause of death from poisoning in US * Leading cause of fire-related death * More common during the winter months due to faulty central heating * Highest death rates among males, African-Americans, the elderly, and residents of northern states Incidence * 600 accidental deaths per year in US; 57% from automobile exposures * Intentional deaths 5-10 times higher Frequency Number of CO poisonings: * In 1997: 20,930 During the period of 1979-1988 the number of deaths from: * CO poisoning: 56,133 * Suicides: 25,889   * Homicides: 210 * Severe burns or house fires: 15,523

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Symptoms Symptoms of acute carbon monoxide (CO) poisoning are nonspecific. Cardiovascular: * Mild exposure: presyncope, palpitations * Moderate to severe exposure: chest pain, dyspnea on exertion, pink, frothy sputum Central nervous system: * Mild exposure: headache, nausea, vomiting, dizziness, weakness, impaired fine motor skills, tinnitus * Moderate to severe exposure: confusion, ataxia, hypothermia, syncope, hallucinations Ophthalmologic: * Decreased visual acuity * Accommodation changes * Decreased peripheral vision Initial presentation - smoke inhalation presents initially with: * Tachypnea * Cough * Dyspnea * Wheezing * Hoarseness * Stridor Chronic CO poisoning - symptoms include: * Nausea * Vomiting * Headache * Dizziness * Fatigue * Paresthesias * Visual disturbances * Apathy * Reduced libido * Loss of appetite * Sleep disturbances * Memory disturbances * Chest pain * Palpitations Signs The cardiovascular and central nervous systems are affected most frequently; signs range from mild to severe. Cardiovascular: * Arrhythmias * Tachycardia * Hypotension * Myocardial ischemia or infarction * Cardiopulmonary arrest Central nervous system: * Confusion * CNS depression * Coma * Cerebral edema Skin: * Blisters and bullae over pressure points * Cherry red skin and mucous membranes is a post-mortem finding * Facial burns and soot indicate possible smoke inhalation and carbon monoxide poisoning Ophthalmologic: * Venous engorgement with papilledema * Optic atrophy * Visual field defects * Retrobulbar neuritis Associated disorders * Metabolic acidosis due to tissue hypoxemia, anaerobic metabolism, and lactic acidosis * Myoglobinuria due to rhabdomyolysis, which may lead to acute renal failure * Myocardial or cerebral ischemia or infarction

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Differential diagnosis Symptoms often vague and nonspecific; therefore CO poisoning requires a high index of suspicion. Influenza Influenza has vague symptoms and a higher occurrence rate in winter and during epidemics. Features: * Headache * Dizziness * Fever * Chills * Cough * Runny nose * Nausea * Vomiting * Myalgias Gastroenteritis Viruses are a common cause of gastroenteritis. Foodborne illness often has a bacterial etiology. Features: * Fever may be present * Nausea * Vomiting * Diarrhea * Abdominal cramping or bloating * History of exposure to contaminated food or other sick contacts Ethanol intoxication Ethanol intoxication may occur with binge drinking or in chronic alcoholism. Features: * Nausea * Vomiting * Gastritis * Altered mentation * Impaired judgment * Aspiration  * Coma * Seizure * Death Drug overdose Presentation of drug overdose varies with the specific drug used. Can mimic central nervous system symptoms of CO poisoning. Features: * Decreased level of consciousness * Confusion * Coma * History of drug exposure Migraine headache A relatively common form of headache with specific criteria. The key features of migraine headache are as follows. Features: * Moderate to severe headache * Usually unilateral * Pulsating or throbbing in nature * Aggravated by movement * Nausea * Vomiting * Visual symptoms - photophobia, scotomata * Auditory symptoms - phonophobia * Lasts between 4h and 72h Hydrogen cyanide poisoning Hydrogen cyanide poisoning may be seen with exposure to burning plastic compounds or 'smoke inhalation' in structure fires. Hydrogen cyanide is also generated by the breakdown of nitroprusside. Hydrogen cyanide poisoning can accompany CO poisoning, worsening the toxicity and the prognosis. Features: * Nausea * Vomiting * Headache * Weakness * Dizziness * Almond-like odor on the patient's breath or emesis * Syncope * Hyperventilation * Pulmonary edema * Arrhythmias * Shock * Seizures * Coma * Death Cerebrovascular accident CO poisoning generally lacks focal central nervous system findings. The key features of cerebrovascular accident are as follows. Features: * Headache is uncommon * Possible decreased level of consciousness * Confusion * Aphasia * Hemiparesis * Coma Hypoxic encephalopathy Brain injury due to lack of oxygen. The key features of hypoxic encephalopathy headache are as follows. Features: * History of hypoxic event * Weakness * Confusion * Coma * Seizures * Cardiopulmonary arrest Trauma Presentation varies with mechanism. May be associated with CO poisoning as cause or effect. The key features of trauma are as follows. Features: * Decreased level of consciousness * Headache * Confusion * Coma * Unstable vital signs * History of trauma Methemoglobinemia Methemoglobin is formed from exposure to chemicals that oxidize iron in hemoglobin from ferrous (Fe2+) to ferric (Fe3+) state. Ferric hemoglobin cannot carry oxygen, causing symptoms due to tissue hypoxemia with subsequent anaerobic metabolism. Methemoglobinemia may occur secondary to exposure to drugs, such as benzocaine, nitrates, dapsone, and Pyridium (phenazopyridine hydrochloride). Features: * Fatigue * Nausea * Vomiting * Headache * Dizziness * Weakness * Cyanosis * Blood may appear 'chocolate brown' in color * Dyspnea * Arrhythmias * Coma * Seizures * Death Depression Depression is a persistent low mood over a period of at least 2 weeks.

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Diagnostic decision * The diagnosis is made by a combination of the history of exposure, clinical presentation, and laboratory testing (elevated carboxyhemoglobin level) * If the diagnosis is in doubt, do not rely on any one test (e.g. carboxyhemoglobin levels) because levels may have decreased owing to prolonged transport time and treatment with oxygen in the pre-hospital environment * If the diagnosis is suspected, begin treatment with 100% oxygen before initiating the diagnostic evaluation Questions to ask Presenting condition * Have you been exposed at home or work to devices that burn hydrocarbons, such as wood- or gas-burning stoves, gasoline engines, or gas or kerosene heaters? Patients are often not aware of CO poisoning and its causes * Is anyone else at home or work having similar symptoms? If others are suffering the same symptoms, the cause is more likely external to the patient; this is important for identifying others at risk and for preventing re-exposure * Do your symptoms change when you're at home or in your car? This kind of questioning can help identify the cause and the source Contributory or predisposing factors Acute CO poisoning: * Have you had your household heating devices serviced recently? Malfunctioning hydrocarbon combustion devices may result in carbon monoxide poisoning * Do you keep your home well ventilated? Fires, gasoline engines, barbecue grills, and home furnaces used in poorly ventilated environment (seen especially during the winter) can result in exposure to CO Chronic CO poisoning: * What is your home like? Elevated CO concentrations are more likely in small, multiunit dwellings, households using gas ranges for cooking, and dwellings heated by gas wall furnaces. Conversely, lower CO concentrations are more likely in single family dwelling, homes with forced-air furnaces, and residences with electric cooking appliances Examination * Evaluate the airway, breathing, and circulation (ABC's) * Monitor vital signs frequently * Examine the cardiovascular system for abnormalities (e.g. myocardial ischemia, pulmonary edema, arrhythmias) * Examine the CNS for mental status and any focal or general neurologic findings * Examine the optic fundi for venous dilatation, optic atrophy, and papilledema * Examine the skin for pressure sores Summary of tests * The carboxyhemoglobin level helps evaluate the severity of exposure and monitors treatment * An ECG establishes a baseline and helps evaluate for acute cardiac ischemia and arrhythmias * A chest radiograph is useful to evaluate for pulmonary edema and aspiration pneumonitis * A fingerstick glucose level helps to exclude hypoglycemia as the etiology of the clinical presentation * A measured (not calculated) arterial oxygen saturation determines whether tissue hypoxemia is present * An arterial blood gas and serum electrolytes indicate acid-base status * Cardiac enzymes help to evaluate for acute myocardial infarction * A total creatine kinase level and urine for myoglobin will be useful to evaluate for rhabdomyolysis, a complication of CO toxicity. Additionally, a urinalysis that is 'heme' positive in the absence of RBCs seen on microscopic examination suggests myoglobinuria (or hemolysis) * Other tests to consider include ethanol, methemoglobin, acetaminophen, and salicylate levels and a toxicologic screen (the latter three tests are especially helpful in cases of attempted suicide)

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Clinical pearls * Consider CO poisoning in the differential diagnosis of headache, gastroenteritis, and viral illnesses such as influenza * Pulse oximetry is unreliable in CO poisoning. The oximeter cannot differentiate between oxyhemoglobin and carboxyhemoglobin (COHb); therefore, the reported oxygen saturation will be falsely elevated and a measured oxygen saturation should be obtained instead * The PaO2 obtained on an arterial blood gas measures only oxygen dissolved in the blood and will be normal in CO poisoning * The severity of poisoning is the product of the concentration of CO and the length of the exposure. Prolonged exposure to relatively low levels of CO may produce moderate or severe poisoning, while a relatively brief exposure to high levels may produce a similar clinical picture * COHb levels may not correlate with the severity of poisoning * Check a fingerstick blood glucose level in all patients presenting with altered mental status to rule out hypoglycemia * Screen for co-ingestants (such as acetaminophen, salicylates, and tricyclic antidepressants) in cases of known or suspected suicide attempt * An arterial blood gas and serum electrolytes indicate acid-base status

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Treatment Goals * Reduce levels of carboxyhemoglobin in the patient (and fetus if pregnant) * Reduce immediate symptoms and return patient to premorbid state * Reduce the risk of long-term sequelae * Treatment of any complications (e.g. pulmonary edema, myocardial infarction, acute renal failure, seizures) Immediate treatment action * Immediate removal from the toxic environment * Treat with 100% oxygen by a non-rebreather mask * Obtunded or comatose patients should receive 100% oxygen via endotracheal tube * Hyperbaric oxygen (HBO) if indicated * Intravenous access and cardiac monitoring * Correct tissue hypoxemia and hypovolemia * Manage complications (e.g. pulmonary edema, myocardial infarction, acute renal failure, seizures) 1. Inhalation of 100% O2 is preferred treatment a. This therapy decreases the half-life of Hb-CO by >50% b. Must follow arterial blood glass O2 saturation and Hb-CO level c. Intubation and placement of arterial blood catheter usually required 2. Hyperbaric O2 at 3 Atmospheres (Atm) is very effective a. Normal half life of Hb-CO in room air oxygen is 5-6 hours b. Treatments for carbon monixde poisoning should last ~45 minutes c. Three hyperbaric treatments within 24 hour period reduced risk of cognitive sequellae at 12 months 3. Indications for Hyperbaric Oxygen a. Hb-CO >20-40% b. Any symptomatic carbon monoxide poisoning [4] c. Pregnancy and Hb-CO level >15% d. History of coronary artery disease and Hb-CO level >20% 4. For smoke inhalation, consider concomitant cyanide poisoning 5. Supportive therapy, vasopressors, anti-ischemics, blood transfusions REF: Outlines in Clinical Medicine 2006   Therapeutic options Summary of therapies * All patients with carbon monoxide (CO) poisoning should be treated with 100% oxygen by non-rebreather mask or by intubation and mechanical ventilation * Hypotension and tissue hypoxemia enhance CO binding and should, therefore, be corrected aggressively * Cardiac and respiratory status should be monitored * Obtain a baseline ECG * Determine whether hyperbaric oxygen (HBO) is required. The specific indications for HBO therapy are controversial. Consultation with a toxicologist is recommended * Obtain serial ECGs and serial cardiac enzymes if myocardial ischemia is suspected * Monitor closely for decreased hypoxic respiratory drive in patients with chronic obstructive pulmonary disease (COPD) * Metabolic acidosis should not be treated. Acidosis increases the unloading of oxygen to tissues (by shifting the oxyhemoglobin dissociation curve to the right); this is a theoretical advantage in CO poisoning, in which the oxyhemoglobin dissociation curve is shifted leftward * Monitor the fetus if the patient is pregnant * Patients with CO poisoning secondary to methylene chloride exposure require a longer duration of treatment, as peak levels are delayed up to 8h, due to continued hepatic metabolism of methylene chloride to CO * Treat complications (e.g. pulmonary edema, myocardial infarction, acute renal failure, seizures ) Medications and other therapies 100% Oxygen 100% oxygen using a tight-fitting nonrebreather mask Endotracheal intubation and mechanical ventilation may be necessary Specialist involvement often required for intubation and ventilator management Efficacy: This treatment will decrease the carboxyhemoglobin half-life from 4-6h to approximately 90min. Risks of 100% Oxygen Rx: Patients with COPD may lose their hypoxic respiratory drive when treated with high concentrations of oxygen; this is not a contraindication to treatment, but recognize that mechanical ventilation may be required Do not use near an open flame Use of respiratory suppressants and sedatives should be avoided Benefit of 100% Oxygen Rx: Effective in reducing carboxyhemoglobin levels Follow-up plan Patients with COPD should be monitored closely for loss of their hypoxic respiratory drive, which may result in hypoventilation. Hyperbaric oxygen [EBM] Efficacy of therapies Hyperbaric oxygen (HBO) enhances elimination of carboxyhemoglobin (COHb) and increases amount of dissolved oxygen in plasma The half-life of COHb is: 4-6h on room air; 90min on 100% oxygen; or 30min on 100% oxygen at 3 atmospheres of pressure HBO may reduce toxicity by reducing CO elimination time HBO hastens the resolution of symptoms The specific indications for hyperbaric oxygen (HBO) therapy include the following, but consultation with a toxicologist is recommended: Coma on presentation or a history of syncope Altered mental status Focal neurologic findings Seizures Symptoms persisting beyond 4-6h despite treatment with normobaric oxygen Patients with a carboxyhemoglobin (COHb) level >40% (some centers use a more conservative level of >25%) Pregnant patients with a COHb level >15% Cardiovascular toxicity (chest pain, ECG changes, arrhythmias); however, patients with acute myocardial infarction are probably better served with traditional myocardial salvage techniques Patients with recurrent symptoms up to 3 weeks after exposure Risks of Hyperbaric oxygen: Decompression sickness resulting from intravascular and intracellular expansion of dissolved nitrogen bubbles Rupture of tympanic membranes Damaged sinuses Cerebral gas embolism Oxygen toxicity (convulsions and pulmonary edema) Pneumothorax (untreated pneumothorax is the only contraindication to HBO therapy) Complications during transport to a facility with HBO capability (e.g. cardiac arrhythmias and hypotension may make transport hazardous) Physician risk: some physicians feel patients with serious CO poisoning should be transferred to a facility with HBO capability because of published case reports attesting to effectiveness of HBO and the resultant medicolegal risk. Benefits of Hyperbaric oxygen: Decreased COHb elimination half-life Increased rate of symptom resolution Increased tissue clearance of residual CO, reduced cerebral edema, and reduced cytochrome oxidase inhibition Possible reduced incidence of long-term neuropsychiatric sequelae Monitor Patients should be evaluated for the development of delayed neuropsychiatric sequelae. Efficacy Hyperbaric oxygen (HBO) enhances the elimination of CO and increases the amount of oxygen dissolved in plasma The half-life of carboxyhemoglobin (COHb) is: 4-6h on room air; 90min on 100% oxygen; or 30min on 100% oxygen at 3 atmospheres of pressure HBO may reduce toxicity by reducing CO elimination time HBO hastens resolution of symptoms Additional possible benefits of HBO are increased tissue clearance of residual CO, reduced cerebral edema, and reduced cytochrome oxidase inhibition HBO therapy may reduce incidence of long-term neuropsychiatric sequelae (this is very controversial and the evidence is conflicting) HBO is generally considered standard of care for treating CO poisoned patients with coma and altered mental status Ideally, HBO therapy should be initiated within 6h of the exposure, but it may be of benefit up to 21 days later Clinical pearls Correction of hypotension and tissue hypoxemia, if present, help to decrease CO binding Aggressive correction of acidemia is not necessary and may be harmful Monitor COPD patients closely for respiratory depression secondary to high-flow oxygen therapy Untreated pneumothorax is the only absolute contraindication to hyperbaric oxygen therapy A common mistake is to base decision for hyperbaric oxygen therapy solely on CO level rather than on the patient's condition or history Management in special circumstances Coexisting disease Patients with the following conditions are at higher risk for complications: Myocardial ischemia (carboxyhemoglobin levels as low as 2-4% are associated with decreased exercise performance and exacerbation of angina) Heart failure Cerebral ischemia Diabetes Thyrotoxicosis Anemia Fever Hypovolemia Other comorbid conditions Coexisting medication Compounds that may increase the toxicity of CO poisoning: Cyanide increases toxicity in a synergistic fashion Nitrous oxide irritates respiratory surfaces and binds to hemoglobin Hydrogen sulfide causes toxicity and is a respiratory irritant Ethanol, marijuana, etc., may lull, slow, and immobilize user Cocaine may worsen toxicity by increasing the metabolic rate Special patient groups Pregnant patients: Carboxyhemoglobin concentrates in fetus, causes tissue hypoxemia, and may be directly teratogenic Consider early consultation with a toxicologist and treatment with hyperbaric oxygen. If normobaric oxygen is used, the patient should be treated for several hours after carboxyhemoglobin normalizes, and the fetus should be monitored Other considerations: Low oxygen/high altitude exposure increases CO uptake and shortens time to incapacitation Exposure during exercise, work, or other states of increased metabolic demand may worsen toxicity Increased ambient temperature increases the rate of CO uptake Cigarette smoking causes increased baseline levels of CO (up to 12%) Simultaneous exposure to other toxic agents (cyanide, ethanol, etc.) may worsen toxicity The very young, very old, and patients with comorbid conditions are at an increased risk for harm from CO exposure Suicidal patients: Need psychiatry evaluation if suicidal ideation is suspected Patient and caregiver issues Questions patients ask * Will I suffer from any long-term problems? Long-term neuropsychiatric sequelae have been noted to occur up to 8 months and longer after recovery in 10-30% of patients * What are the effects on an unborn child? The fetus is at risk for central nervous system anatomic defects, learning and memory deficits, behavioral deficits, neurochemical changes, skeletal defects, teratologic abnormalities, and death Follow-up Plan for review * Follow-up should be arranged in all patients with a history consistent with CO poisoning, regardless of condition on arrival at the hospital * Patients with suicidal ideation require psychiatric evaluation * Identify the source of exposure, warn others at risk, and prevent re- exposure * Delayed neurologic sequelae can develop several months after exposure; patients should be referred for neuropsychiatric evaluation Information for patient or caregiver * Evaluate the safety of the home and work environment to avoid CO exposure * Consider the use of home CO monitors * Do not use barbecue grills indoors * Fireplaces and wood-burning stoves should be well vented

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Prognosis * Prognosis after severe carbon monoxide (CO) poisoning is variable and correlates with extent and duration of insult * Delayed neuropsychiatric sequelae occur in about 10% of patients with serious insult * Risk factors for delayed neuropsychiatric sequelae include age greater than 40 years, prolonged exposure, and the presence of abnormalities on computed tomography (CT) of the brain * Hyperbaric oxygen therapy may decrease the incidence of delayed neuropsychiatric sequelae, but this is controversial Clinical pearls * If in doubt regarding the need for hyperbaric oxygen (HBO) therapy, consult a toxicologist * The reported incidence of delayed neuropsychiatric sequelae varies with the sensitivity of the particular neuropsychiatric test utilized * Improvement in symptoms with a change in environment may suggest a source of exposure (e.g. symptoms from home exposure improve when the patient leaves the house) * A history of sick contacts with similar symptoms may provide a clue to the source of the exposure. Once the source is identified, take the appropriate steps to warn others at risk and to prevent re-exposure * Counsel patients not to use barbecue grills indoors and to ensure that indoor fireplaces and wood-burning stoves are properly vented * Cherry red skin or mucous membranes, when these occur, are post-mortem findings only Progression of disease Clinical complications:  Long-term central nervous system sequelae are possible. Neurologic: * Cerebral edema and hemorrhages * Necrotic lesions in basal ganglia, hippocampus, cerebellum, and peripheral demyelination * Degradation of fine motor skills and coordination: hands, fingers, feet * Dysphagia Psychiatric: * Apathy   * Disorientation   * Amnesia   * Hypokinesia   * Mutism   * Irritability, distractibility   * Apraxia * Bizarre behaviors: silly smiles or frowning   * Manneristic behavior   * Irrational confabulatory talking * Insomnia   * Depressed mood   * Delusions   * Echolalia   * Elated mood Cardiorespiratory: * Myocardial necrosis * Cardiomyopathy * Pulmonary edema * Aspiration pneumonia in comatose patients Hepatic: * Lobar necrosis with chronic repeated exposure Renal: * Acute renal failure; parenchymatous degeneration leading to necrosis Hematologic: * Bone marrow hypertrophy in chronic CO hypoxia Skin:   * Erythema, blisters, and gangrene Ophthalmologic: * Retinal hemorrhages (usually flame-shaped) * Decreased light sensitivity   * Decreased visual acuity   * Cortical blindness * Retrobulbar neuritis   * Papilledema   * Pancentral scotomata   * Loss of peripheral vision * Nystagmus   * Saccades   * Accommodation changes   * Floaters   * Myopia Musculoskeletal: * Rhabdomyolysis   * Myonecrosis * Compartment syndrome   * Gross muscular weakness/fatigue in the arms and legs, unilateral or bilateral

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Primary prevention Modifiable risk factors Tobacco:  Stop or reduce smoking. Environment * Assess functioning of all devices that produce CO at home and work * The local utility and fire departments may be available to check CO levels and provide tips on reducing risk * Consider the use of CO detectors. They are reported to be effective in alerting potential victims, thereby reducing potential CO poisoning * The actual sensitivity of CO detectors varies with the particular model Secondary prevention * Identify and correct the source of CO exposure * Consider the use of home CO detectors * Do not use barbecue grills indoors and ensure that indoor fireplaces and wood-burning stoves are properly vented

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REF: FirstConsult (MedConsult) 2006