Inhalant Abuse
John Brick in Handbook of the Medical Consequences of Alcohol and Drug Abuse, 2012
Nitrous oxide is an anesthetic agent used by medical practitioners, especially dentists, for pain control during procedures. Transient euphoria and central nervous system (CNS) depression occur when nitrous oxide is inhaled. Excluding intoxication, the acute side effects are minimal. Chronic inhalation of nitrous oxide can cause significant side effects. With chronic abuse, nitrous oxide can produce a demyelinating polyneuropathy and extremity weakness (Layzer, 1987; Pema, Horak, and Wyatt, 1998). The neurologic sequelae associated with chronic abuse occurs secondary to vitamin B12 inactivation (Pema, Horak, and Wyatt, 1998). Nitrous oxide abuse is very common today among younger drug abusers because of its ease of availability. Nitrous oxide abuse is very common at sporting event and rock concert tailgaters parties, where the gas is transferred from large containers into balloons and then inhaled. On a smaller scale, compressed nitrous oxide is present in cartridges for whipped cream dispensers and easily obtained in many supermarkets. Abusers discharge the cartridge into an empty cream dispenser and inhale the nitrous oxide (Lai et al., 1997). The slang term for abuse of nitrous oxide in this fashion is “whippets.” Nitrous oxide–induced peripheral neuropathy is reversible following avoidance.
General Anesthetics
Sahab Uddin, Rashid Mamunur in Advances in Neuropharmacology, 2020
As a weak anesthetic agent, Nitrous oxide shows consistent anesthetic effects during surgery under hyperbaric situation. It produces marked analgesia at 20% concentrations and sedation at 30% and 80% concentrations. It also produces analgesia and sedation in outpatient dentistry at 50% concentration. Nitrous oxide is often used along with other agents like inhalational anesthetics or intravenous anesthetics. In the body cavity having hollow space, nitrous oxide exchange with N2 as it produces different blood: a gas partition coefficient which is consider as one of the disadvantage of nitrous oxide. The formed nitrous oxide enters into body cavity at a faster rate than escape of nitrogen thereby raising the volume and/or pressure inside the body cavity. The increased pressure and/or pressure causes development of pneumothorax which is fundamentally associated with hindered middle ear, embolus ofair, a hindered bowel loop, an air bubble in inner ocular cavity, a pulmonary bulla, and intracranial air (Brunton et al., 2011; Sharma and Sharma, 2017).
Toxins in Neuro-Ophthalmology
Vivek Lal in A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Nitrous oxide is an anesthetic agent and is popular as a recreational drug due to its euphoric properties and availability as a so-called “legal high.” It is usually inhaled from balloons filled from “whippits” (small, pressurized canisters of N2O used in whipped cream dispensers). It irreversibly binds, oxidizes, inactivates and depletes vitamin B12. B12 inactivation further leads to depletion of methionine and accumulation of homocysteine as it is an essential cofactor for methionine synthase. Neurologically, B12 depletion results in demyelination leading to myelopathy, neuropathy, myeloneuropathy, cognitive changes and optic nerve toxicity. Ocular symptoms will be similar to B12 deficiency due to other causes. The visual loss is symmetric, painless and progressive. Central and centrocecal scotomas are the rule, and the optic disc will be normal in the early stages of the condition. Vision recovered usually with intramuscular injections of hydroxocobalamin unless optic atrophy becomes well established.
Nitrous oxide misuse reported to two United States data systems during 2000–2019
Published in Journal of Addictive Diseases, 2020
Mathias B. Forrester
Nitrous oxide (N2O), commonly known as laughing gas or nitrous, is a colorless, non-flammable gas used as an anesthetic and analgesic, as an aerosol propellant (particularly as a whipping agent for cream), and in the automotive industry.1,2 Individuals may inhale nitrous oxide as a recreational intoxicant due to its euphoric, dissociative, and sometimes hallucinogenic effects. These effects are rapidly induced, within ten seconds of inhalation.3 Within years after its discovery by Joseph Priestly in the late 1700s, nitrous oxide had been misused for recreational purposes, and reports of nitrous oxide misuse have been reported in the published literature for decades.4–6 The National Survey on Drug Use and Health (NSDUH) in the United States (US) found that past year use of nitrous oxide among past year inhalant initiates age 12-17 years declined from 31.6% in 2002 to 16.3% in 2007.7 A 2014 Global Drug Survey (GDS) found a 29.4% lifetime prevalence of nitrous oxide use among US respondents.8 Among all intentional abuse by inhalation exposures reported to US poison centers during 1993-2008, 902 (2.5%) were due to nitrous oxide.9 It has been reported that nitrous oxide misuse is increasing.1,10
Plasma corticosterone, epinephrine, and norepinephrine levels increase during administration of nitrous oxide in rats
Published in Stress, 2018
Salwa Al-Noori, Andreas Cimpan, Zoe Maltzer, Karl J. Kaiyala, Douglas S. Ramsay
Nitrous oxide (N2O) is a gaseous drug with a long history of clinical use in medicine and dentistry (Becker & Rosenburg, 2008; Sun et al., 2015). N2O’s low anesthetic potency limits its use as a sole anesthetic agent, although it is often administered in combination with other drugs as part of a balanced anesthetic approach (Sun et al., 2015). It is also administered in clinical situations where achieving anesthesia is not the goal. The anxiolytic and modest analgesic effects of subanesthetic N2O concentrations, when administered as “N2O - oxygen sedation,” can benefit many conscious patients undergoing painful or anxiety-provoking medical and dental procedures (Donaldson, Donaldson, & Quarnstrom, 2012). N2O is also an inhalant drug of abuse (Balster, 1998; Cousaert, Heylens, & Audenaert, 2013; Kaar et al., 2016; Layzer, 1985; van Amsterdam, Nabben, & van den Brink, 2015). N2O has positively reinforcing effects for some humans (Kangas & Walker, 2008; Walker & Zacny, 2001, 2002); is self-administered by monkeys (Grubman & Woods, 1981; Wood, Grubman, & Weiss, 1977) and rats (Ramsay Watson, Leroux, Prall & Kaiyala, 2003; Ramsay et al., 2015); and increases dopamine in the nucleus accumbens of rats (Sakamoto et al., 2006). The adverse consequences from chronic N2O abuse were recently reviewed (Garakani et al., 2016). Reviews of N2O’s pharmacological mechanisms of action are also available (Emmanouil & Quock, 2007; Sanders, Weimann, & Maze, 2008).
Nitrous oxide abuse induced subacute combined degeneration despite patient initiated B12 supplementation
Published in Clinical Toxicology, 2022
Courtney Temple, B. Zane Horowitz
Nitrous oxide (N2O) is a colorless inhalational anesthetic gas and legal to purchase as a food additive used in whipped cream dispensers. N2O causes a functional vitamin B12 (cobalamin) deficiency by irreversibly oxidizing the central cobalt ion from its monovalent to divalent state [1]. This inactivates B12, disrupting the function of methionine synthase that is critical for nucleic acid synthesis and myelin production [2]. Methylmalonic acid (MMA) and homocysteine accumulate (Figure 1) which leads to neuronal demyelination and subacute combined spinal cord degeneration (SCD). MMA elevation is more specific for B12 deficiency because homocysteine may be elevated with folate deficiency as well [3]. We present four patients who developed N2O-induced SCD despite self-medicating with B12 supplements with normal serum B12 concentrations on presentation.
Related Knowledge Centers
- Anesthesia
- Chemical Compound
- Dentistry
- Nitrogen Oxide
- Nitrous Oxide
- Oxidizing Agent
- Surgery
- Euphoria
- Analgesic
- Chemical Formula