· Dinitrogen monoxide; Laughing gas; Hyponitrous acid anhy-dride; Factitious air.
· Nitrous oxide is a colourless gas with a slightly sweetish odour and taste.
· May also exist in the form of a liquid or cubic crystals. Nitrous oxide is abundant in the atmosphere as a result of bacterial decomposition of organic nitrogen compounds in soil.
■■As a sole agent, nitrous oxide is used intermittently to provide analgesia for dental and obstetric procedures.
■■In combination with other agents, nitrous oxide is used as a general anaesthetic.
■■It is also used as a foaming agent for whipped cream, to make nitrates from alkali metals, as an oxidant for organic compounds, and in some rocket fuel combinations. Consumer cans of whipped cream have been reported to release up to 1.5 L of nitrous oxide. High concentrations of carbon dioxide and fluorocarbons may also be released.
· Nitrous oxide is a gas that acts as a central nervous system depressant and can cause asphyxiation by oxygen displace-ment.
· It oxidizes cobalt in vitamin B12, rendering it biologically inactive. This produces a deficiency in available active B12 and the results mimic B12 deprivation states.
· Nitrous oxide has been demonstrated to be a partial agonist at mu, kappa, and sigma receptors of the endogenous opioid system. This may explain the emetic and addictive proper- ties of nitrous oxide. Naloxone appears to partially reverse nitrous oxide-induced analgesia.
· Nitrous oxide is 35 times more soluble in blood than nitrogen. When it is inhaled, compliant air-containingnitrogen. When it is inhaled, compliant air-containing spaces such as the bowel will increase in size, while non- compliant spaces such as eustachian tubes will increase in pressure. This can lead to bowel distension, tympanic membrane rupture, etc.
· Nitrous oxide has been reported to cause mild hyperten- sion when used as an anaesthetic. Cardiac arrhythmias may occur, and may be the result of hypoxia. Nausea and vomiting may occur.
· Acute neurologic effects of intoxication are primarily due to asphyxia. Signs and symptoms may include headache, dizziness, and excitation that may progress to CNS depres- sion, seizures, and death. Respiratory irritation may be noted. Interstitial emphysema and pneumomediastinum have been reported following inhalation from whippedcream dispensers.
· Nitrous oxide is thought to be a potential carcinogen based on animal studies.
· Respiratory depression, increased muscle tone, hyperten-sion, mydriasis, cardiovascular failure.
· Chronic use (or abuse, especially by hospital and dental personnel) can lead to bone marrow depression, polyneu-ropathy, megaloblastic changes, and death. Chronic abuse can also cause myeloneuropathy. Findings include ataxia, peripheral sensory neuropathy, and weakness. Impotence has been reported as an early sensory complaint associ-ated with nitrous oxide-induced myeloneuropathy Many of the neurological and haematopoietic effects of nitrous oxide are believed to be due to the selective inactivation of vitamin B12.
· Bone marrow depression with resultant leukopenia, throm-bocytopenia and severe megaloblastic anaemia has been noted following chronic or intermittent inhalation of nitrous oxide.
· Exposure to 50 to 70% nitrous oxide for 3 hours can result n aplastic anaemia and death.
· Inhalation of 40% nitrous oxide in air can cause confusion and sedation, while an 80% level causes unconsciousness in most individuals.
· Removal from source of exposure. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
· Cerebral oedema and elevated intracranial pressure (ICP) may occur. Emergent management includes head eleva-tion and administration of mannitol; hyperventilation should be performed if there is evidence of impending herniation.
· Plasma nitrous oxide levels are not clinically useful.
· Case reports suggest that administration of folate and vitamin B12 supplements may help reverse myeloneurop-athy associated with chronic nitrous oxide abuse, although this has not been well studied.
· Folinic acid, 30 mg, IV, for bone marrow abnormalities.
· Methionine-supplemented diet to minimise neurologic damage.
· Arrhythmias are generally secondary to hypoxia and usually resolve with oxygenation. Therapy with antiarrhythmics should be reserved for patients with arrhythmias that persist after adequate oxygenation.
· Monitor patient for signs of bleeding and infection. Treatment is symptomatic and supportive. Folate supple-mentation may reverse the bone marrow abnormalities associated with nitrous oxide toxicity.
o Treatment of hypoxia.
o Control of seizures.
o Treatment of pulmonary oedema.
o Continuous cardiac monitoring.
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