CARBON MONOXIDE POISONING

CARBON MONOXIDE POISONING - Felix B. Chang, MD
BASICS
DESCRIPTION
• Carbon Monoxide (CO) is the leading cause of poisoning death in the us CO is an odorless, tasteless, colorless, gas, produced by combustion of carbon-containing compounds.
• CO inhalation leads to displacement of oxygen from binding sites on hemoglobin.
• CO has about 250 times the affinity for hemoglobin that oxygen has.
• Detrimental effects are related to tissue hypoxia from decreased oxygen content and a shift of the oxyhemoglobin dissociation curve to the left.
• CO binds to cytochrome oxidase, impairing mitochondrial function and to cytochrome oxidase, affecting muscle function.
• CO binding to myoglobin affects muscle activity.
• System(s) Affected: Cardiovascular; Musculoskeletal; Nervous
ALERT
Tissue hypoxia includes the fetus. CO poisoning may cause significant fetal abnormalities, depending on the developmental stage. However, adult hemoglobin holds to oxygen less tightly than does fetal hemoglobin. Therefore, a pregnant mother potentially may be unaffected while the fetus is affected.
EPIDEMIOLOGY
• 40,000 emergency department visits annually
• 5,000 to 6,000 deaths annually in the US
• Inadvertent CO poisoning likely causes 500 deaths annually.
• Unintended poisoning is most common during winter month in cold climates.
• 10,000 individuals miss 1 or more days of work due to CO poisoning.
RISK FACTORS
• Cigarette smoking
• Smoke inhalation
• Being in a closed space with a faulty furnace or stove or running engine
• Employment in coal mine, as an auto mechanic, paint stripper, or in the solvent industry
• Improper vented fuel-burning devices
- Kerosene heaters, charcoal grills, camping stoves, gasoline-power generators, wood stoves
- Open air exposure to motorboat exhaust
- Underground utility electrical cable fires
PATHOPHYSIOLOGY
• CO is rapidly absorbed in lungs.
• CO binds to hemoglobin to form carboxyhemoglobin (COHb), resulting in impaired oxygen carrying capacity, utilization, and delivery.
- Leftward shift of the oxyhemoglobin dissociation curve occurs.
- CO interferes with peripheral oxygen utilization by inactivating cytochrome oxidase.
• Delayed neurologic sequelae, probably involves lipid peroxidation by toxic oxygen species generated by xanthine oxidase.
• The half-life of CO while the patient is breathing room air is ~300 minutes, while breathing high-flow oxygen via a nonrebreathing face mask is ~90 minutes, and with 100 % hyperbaric oxygen is ~30 minutes.
ETIOLOGY
• CO inhalation
• Inhaled or ingested methylene chloride (from paint remover) (dichloromethane) is metabolized to CO by the liver, causing CO toxicity in the absence of ambient CO.
ASSOCIATED CONDITIONS
CO and cyanide poisoning can occur simultaneously following smoke inhalation (synergistic effect).

DIAGNOSIS
• Acute CO poisoning is suggestive by history, physical examination, and an elevated COHb
• Chronic CO intoxication is difficult to diagnose.
• Pulse oximetry cannot screen for CO exposure, because it does not differentiate carboxyhemoglobin from oxyhemoglobin.
PRE HOSPITAL
Patients often present in clusters, with similar symptoms and a common environment.
SIGNS AND SYMPTOMS
• Headaches
• Tinnitus
• Nausea
• Dizziness
• Weakness
• Confusion
• Fatigue
• Flushing
• Vomiting
• Central nervous system depression
• Syncope
• Angina
• Tachycardia
• Tachypnea
• Cardiac dysrhythmias
• Nystagmus
• Ataxia
• Seizures
• Coma
• Diarrhea
• Cardiopulmonary arrest
Physical Exam
• A careful neurologic examination is crucial.
• In absence of trauma or burns, look for altered mental status.
• "Cherry red" appearance of the lips and skin
• Impaired judgment, respiratory depression, arrhythmias, hypotension
• Cyanosis
• Visual field defects, blindness, papilledema
TESTS
Lab
• Measurement of COHb.
• Check CO level via co-oximetry of arterial or venous blood.
• Check acid-base status on blood gas.
• EKG in all patients
• Cardiac enzymes in
-  65 years
- Patient with cardiac risk factors
- Younger patients with chest pain or symptoms suggestive of ischemia
Imaging
Head CT scan is helpful to rule out other causes of neurologic decompensation.
Pathological Findings
Hemorrhagic infarction of the globus pallidus and deep white matter have been reported (rare).
DIFFERENTIAL DIAGNOSIS
• Cyanide toxicity
• Acute viral syndrome
• Other causes of mental status changes: Metabolic, drugs, infectious, trauma
TREATMENT
STABILIZATION
• ED for mild poisoning
• Inpatient treatment for moderate or severe poisoning
GENERAL MEASURES
• Removal from offending source
• Rapid reduction in tissue hypoxia with 100% oxygen to reduce the half-time of elimination of CO to 40 minutes
• Supportive care as necessary
• Intubation and mechanical ventilation may be necessary for severe intoxication.
• Volume resuscitation
Activity
Rest until carboxyhemoglobin reduced and symptoms abate
SPECIAL THERAPY
• 100% oxygen by tight-fitting nonrebreathing mask
• Hyperbaric oxygen for severe poisoning
• For mild poisoning (carboxyhemoglobin levels 30%); no signs or symptoms of cardiovascular or neurologic dysfunction
- Treatment: Admission if carboxyhemoglobin >25%
- Symptomatic medication for headache
- 100% oxygen by nonrebreathing mask until carboxyhemoglobin 5%
- Patients with underlying heart disease should be admitted regardless of level of carboxyhemoglobin.
• For moderate poisoning (carboxyhemoglobin 30-40%); no signs or symptoms of cardiovascular or neurologic dysfunction
- Treatment: Admission
- Cardiovascular status should be followed closely, even in the absence of clear cardiac effects.
- Determination of acid-base status: Corrected by oxygen
- 100% oxygen by nonrebreathing mask until carboxyhemoglobin 5%
• For severe poisoning (carboxyhemoglobin >40%); cardiovascular or neurologic functional impairment at any carboxyhemoglobin level
- Treatment: Admission
- Cardiovascular function monitoring
- Acid-base status monitoring
- 100% oxygen by nonrebreathing mask until carboxyhemoglobin 5%
- Hyperbaric oxygen immediately if available; if unavailable, treat as in moderate poisoning
- If no improvement occurs in cardiovascular or neurologic function within 4 hours, transport the patient to the nearest facility with hyperbaric oxygen, regardless of distance.
MEDICATION (DRUGS)
First Line
• Institution of 100% oxygen by high-flow mask or endotracheal tube
• 100% normobaric oxygen for all suspected victims of CO poisoning, regardless of pulse oximetry or arterial PO2 (1)[B].
FOLLOW-UP
DISPOSITION
Admission Criteria
Patients whose symptoms do not resolve, who demonstrate ECG or laboratory evidence of severe poisoning, or who have other medical or social cause of concern should be hospitalized.
Discharge Criteria
Patient with mild symptoms from accidental poisoning can be managed in the ED and safely discharged.
PROGNOSIS
Most survivors recover completely, with only a minority developing chronic neuropsychiatric impairment.
COMPLICATIONS
• Myocardial infarction
• Pulmonary edema (CHF)
• Pneumonia (aspiration)
• Anoxic encephalopathy
• Long-term neuropsychiatric complications
- Intellectual deterioration
- Memory impairment
• Dysrhythmia
• Shock
• Rhabdomyolysis, personality changes
- Irritability
- Aggressiveness
- Violence
- Moodiness
ALERT
Geriatric Considerations
• Higher incidence of cardiovascular and neurologic disease, increasing complications.
• Atherosclerosis with chronic exposure
PATIENT MONITORING
• Measurement of carboxyhemoglobin levels
• Arterial blood gases
• Psychiatric evaluation and follow-up for intentional exposure
REFERENCES
1. Hampson NB, Scott KL, Zmaeff JL. Carboxyhemoglobin measurement by hospitals: Implications for the diagnosis of carbon monoxide poisoning. J Emerg Med. 2006;31:13.
2. Kao LW, Nanagas KA. Carbon monoxide poisoning. Emerg Med Clin North Am. 2004;22:985.
3. Satran D, Henry CR, Adkinson C, et al. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol. 2005;45:1513.
ADDITIONAL READING
• Internet resources available at: www.cpsc.gov.
• Insufficient evidence to establish usefulness of hyperbaric oxygen for carbon monoxide poisoning. Cochrane Library 2005;1:CD002041.
• Juurlink D, Buckley N, Stanbrook M, et al. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev 2005;CD002041.