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Nitrous oxide, or laughing gas, is used as an adjuvant for general anesthesia, an anesthetic and analgesic agent for minor procedures, and a propellant in many commercial products, such as whipped cream and cooking oil spray. (“Whippets” are small cartridges of nitrous oxide that can be purchased at restaurant supply stores, grocery convenience stores, and “head shops.”) Nitrous oxide is used by many US dentists, in some cases without adequate scavenging equipment. Abuse of nitrous oxide is not uncommon in the medical and dental professions.

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  1. Mechanism of toxicity

    1. Acute toxicity after exposure to nitrous oxide is caused mainly by asphyxia if adequate oxygen is not supplied with the gas.

    2. Chronic toxicity to the hematologic and nervous systems results from inactivation of vitamin B12 after irreversible oxidation of its cobalt atom. Vitamin B12 is required for the synthesis of methionine from homocysteine and for the production of tetrahydrofolate. Methionine is essential for myelin production, and tetrahydrofolate is essential for DNA synthesis. Use of nitrous oxide can precipitate neurologic symptoms in patients with subclinical vitamin B12 or folic acid deficiency.

    3. Adverse reproductive outcomes have been reported in workers chronically exposed to nitrous oxide.

  2. Toxic dose. The toxic dose is not established. Chronic occupational exposure to nitrous oxide at 2000 ppm produced asymptomatic but measurable depression of vitamin B12 in dentists. The ACGIH-recommended workplace exposure limit (TLV-TWA) is 50 ppm (90 mg/m3) as an 8-hour time-weighted average.

  3. Clinical presentation

    1. Signs of acute toxicity are related to asphyxia and include headache, dizziness, confusion, syncope, seizures, and cardiac arrhythmias. Interstitial emphysema and pneumomediastinum have been reported after forceful inhalation from a pressurized whipped cream dispenser.

    2. Chronic nitrous oxide abuse may produce megaloblastic anemia, thrombocytopenia, leukopenia, peripheral neuropathy (especially posterior column findings), and myelopathy, similar to the effects of vitamin B12 deficiency.

  4. Diagnosis is based on a history of exposure and clinical presentation (eg, evidence of asphyxia and an empty can or tank). It also should be considered in a patient with manifestations suggesting chronic vitamin B12 deficiency but with normal vitamin B12 levels.

    1. Specific levels. Specific levels are not generally available and are unreliable owing to off-gassing.

    2. Other useful laboratory studies include CBC with manual differential, vitamin B12 , folic acid, nerve conduction studies, and magnetic resonance imaging (MRI) if the patient has neuropathy. Elevated homocysteine and methylmalonic acid levels have been documented in nitrous oxide abusers who had normal vitamin B12 levels.

  5. Treatment

    1. Emergency and supportive measures

      1. Maintain an open airway and assist ventilation if necessary (See Airway and Breathing). Administer high-flow supplemental oxygen.

      2. After significant asphyxia, anticipate and treat coma (See Coma and stupor), seizures (See Seizures), and cardiac arrhythmias (See QRS interval prolongation, Tachycardia, and Ventricular dysrhythmias).

    2. Specific drugs and antidotes. Chronic effects may resolve over 2–3 months after discontinuation of exposure. Vitamin B12 and folic acid supplementation is indicated to correct ...

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