Table 18.1 Nomenclature of bone tumors

• Viral syndromes
• Cyanide
• Hydrogen sulfide
• Methemoglobinemia
• Amphetamines and derivatives
• Cocaine
• Cyclic antidepressants
• Phencyclidine (PCP)
• Phenothiazines
• Theophylline
WORKUP
History of exposure to carbon monoxide, physical examination, laboratory tests
LABORATORY TESTS
• Carboxyhemoglobin level
NOTE: CoHgb level >5% in nonsmoker confirms exposure. Heavy smokers may have levels of 10%.
• Direct measurement of arterial oxygen saturation
NOTE: Pulse oximetry and arterial blood gas may be falsely normal because neither measures oxygen saturation directly. Pulse oximetry is inaccurate because of the similar absorption characteristics of oxyhemoglobin and carboxyhemoglobin. An arterial blood gas is inaccurate because it measures oxygen dissolved in plasma (which is not affected by carbon monoxide) and then calculates oxygen saturation.
• Electrolytes, glucose, BUN, creatinine, CPK, ABG (because lactic acidosis and rhabdomyolysis may develop)
• ECG (rule out ischemia)
• Pregnancy test (fetus at high risk)
TREATMENT
ACUTE GENERAL Rx
• Remove from site of carbon monoxide exposure
• Ensure adequate airway
• Continuous ECG monitor
• 100% oxygen by tight-fitting nonrebreather mask or endotreacheal tube (this decreases the half-life of carboxyhemoglobin from 4 to 6 hours to 60 to 90 minutes)
• Measure carboxyhemoglobin level every 2 to 4 hours
• Continue oxygen until carboxyhemoglobin level is less than 10-12%
Hyperbaric oxygen (3 ATM) decreases half-life of carbon monoxide to 20 to 30 minutes
• Controversial if there is any beneficial effect over regular 100% oxygen
• Recent study suggests patients with acute (<24 hours), symptomatic carbon monoxide poisoning treated with 3 hyperbaric O₂ sessions within 24 hours had lower rates of cognitive sequelae at 6 weeks and 12 months compared with those treated with normobaric O₂.

Carbon monoxide poisoning

BASIC INFORMATION
DEFINITION
Carbon monoxide is a colorless, odorless gas produced by the combustion of carbon-containing materials. Poisoning may occur as a result of suicidal or accidental exposure to automobile exhaust, smoke inhalation in a fire, or accidental exposure to an improperly vented gas heater or other appliance. Carbon monoxide avidly binds to hemoglobin, with an affinity approximately 250 times that of oxygen. This results in reduced oxygen-carrying capacity and altered delivery of oxygen to cells.
EPIDEMIOLOGY & DEMOGRAPHICS
• Carbon monoxide poisoning is seen more frequently during the winter months.
• Most common cause of lethal poisoning in the U.S.
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Symptoms of toxicity and prognosis do not correlate well with carboxyhemoglobin levels.
• Depend on the severity and duration of exposure. The brain and heart are most sensitive to carbon monoxide poisoning.
ETIOLOGY
Carbon monoxide causes tissue hypoxia by a number of mechanisms.
• Carbon monoxide binds to hemoglobin with an affinity 200 to 250 times greater than oxygen, thus displacing oxygen from hemoglobin and decreasing the oxygen-carrying capacity of blood.
• Carbon monoxide shifts the oxyhemoglobin curve to the left, thus decreasing oxygen release to tissue.
• Cellular respiration is depressed by inhibition of the mitochondrial cytochrome oxidase system.
• Cardiac function is depressed by direct binding to cardiac myoglobin.
• Neurologic toxicity is not explained by hypoxia alone and is thought to be related to the intracellular uptake of carbon monoxide, its role as a neural messenger, ischemic reperfusion injury of the brain, and delayed lipid peroxidation of brain tissue.
Carbon monoxide poisoning occurs when individuals are exposed to smoke from fires; motor vehicle exhaust; or the burning of wood, charcoal or natural gas for cooking or heating in poorly ventilated areas.
• Methylene chloride (paint stripper) fumes are converted to carbon monoxide by the liver.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS

• Consider for individuals with:
1. Severe intoxication (carboxyhemoglobin >25%, neurologic symptoms or signs, ischemic ECG changes, severe metabolic acidosis, rhabdomyolysis, pulmonary edema, shock)
2. Those who remain symptomatic after 2 to 4 hours of oxygen at room air
3. Pregnant women with carboxyhemoglobin >15% or signs of fetal distress: lower threshold for treatment suggested given the higher affinity of carbon monoxide for fetal hemoglobin
• Consult local poison control center
• Consider concomitant poisoning with other toxic/irritant gases that may be present in smoke and/or thermal injury to the airway
DISPOSITION
• Depends on severity of exposure
• Survivors of severe poisoning are at 15% to 45% risk for neurologic sequelae ranging from parkinsonism to neuropychiatric symptoms (personality and memory disorders). Neurologic deficits are usually apparent within 3 weeks of poisoning. Brain MRI may show changes in the white matter and basal ganglia.
• High risk of fetal demise
REFERRAL
• Regional poison control center
• +/- Hyperbaric chamber