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Nitrous Oxide Toxicity

Key Recommendations
Consider nitrous oxide as a potential cause for unexplained neurological abnormalities.
Systems should allow for homocysteine and methylmalonic acid testing in the Emergency Department.
Results may take several days; local protocols should manage delayed results.

Key Recommendations
Emergency clinicians should promote early consideration of nitrous oxide toxicity.
Focus investigations on excluding other causes of neuropathy.
Initiate treatment before definitive diagnostic results if nitrous oxide toxicity is suspected.

Scope of the Guideline
Limited to unregulated nitrous oxide use.
Does not apply to medical use (e.g., Entonox or anesthesia).
Applicable only in Emergency Department settings.

Background on Nitrous Oxide Use
Nitrous oxide has a history of recreational use predating its medical applications.
In the UK, 2.4% of adults aged 16–59 used nitrous oxide in the last year (data from March 2020).
Higher rates observed in younger users (8.7% of adults aged 16–24).

Risks of Nitrous Oxide Use
Responsible for 56 deaths in England and Wales over the past 20 years.
Low risk compared to other substances (3060 drug misuse deaths recorded in 2021 alone).
Male-to-female user ratio approximately 3:2.

Acute Toxicity Effects
Injuries from intoxication or syncope.
Hypoxia and asphyxiation leading to arrhythmias, seizures, or brain injury.
Barotrauma (e.g., pneumothorax, pneumomediastinum).
Confusion, hallucinations, vomiting with aspiration.

Chronic Toxicity Effects
Neurological deficits: sensory, motor, or coordination issues.
Haematological abnormalities: megaloblastic anemia, macrocytosis.
Mechanism involves oxidation of cobalt in vitamin B12, reducing its functionality.

Signs and Symptoms (Neurological)
Sensory deficits: numbness, paraesthesia, or peripheral neuropathy.
Motor deficits: lower limb weakness or fine motor control issues.
Ataxia, urinary retention, erectile dysfunction.

Signs and Symptoms (Haematological)
Anaemia, macrocytosis, agranulocytosis, or pancytopaenia.
Non-specific symptoms: confusion, mood changes, irritability.

Diagnostic Approach
Perform full neurological examination.
Order baseline tests: Full Blood Count (FBC), renal function, thyroid function, vitamin B12, folic acid, ECG.
Vitamin B12 levels may appear normal even if cobalamin is non-functional.

Diagnostic Approach
Test for homocysteine and methylmalonic acid levels (indicators of poor cobalamin function).
Imaging (CT head, MRI brain/spine) may be needed but is not always required.
Consult biochemistry lab for specific sampling procedures.

Management Strategies
Start treatment before diagnostic confirmation if nitrous oxide toxicity is suspected.
Suggested regimen:
Vitamin B12: 1 mg intramuscularly once daily.
Folic acid: 5 mg orally once daily.

Outpatient Management
Provide urgent follow-up within 7 days.
Advise patients to stop nitrous oxide use immediately.
Offer training for self-administration of vitamin B12 injections.
Supply medication to cover out-of-hours periods.

Patient Education and Harm Reduction
Use a balloon as the safest method to inhale nitrous oxide.
Avoid using nitrous oxide in enclosed spaces to prevent oxygen starvation.
Sit down away from hard edges to reduce fall-related injuries.

Subacute Combined Degeneration (SCD)
Definition: Neurological condition caused by vitamin B12 deficiency.
Key Cause: Degeneration of white matter in the spinal cord.
Emerging Cause: Nitrous oxide (N₂O) toxicity, especially in recreational users.
Mechanism: N₂O oxidizes active vitamin B12, causing functional deficiency despite normal serum levels.

Neurological Symptoms
Progressive numbness and weakness.
Spastic paresis (stiffness and weakness in limbs).
Ataxia (loss of coordination).
Loss of vibratory and proprioceptive sensation.
Confusion, irritability, cognitive changes.

Unique Features in N₂O Toxicity:
History of recreational N₂O use (e.g., "whippets") or occupational exposure.
Rapid onset of symptoms after heavy N₂O use.

Diagnosis: History and NE
Detailed history of N₂O use (recreational or occupational).
Hyperreflexia, spasticity, and sensory deficits are common findings.

Diagnosis: Laboratory Tests
Elevated homocysteine and methylmalonic acid levels indicate functional B12 deficiency.
Test for intrinsic factor-blocking antibodies to rule out pernicious anemia.
MRI shows hyperintensities in dorsal columns and lateral corticospinal tracts.

Treatment of SCD
Immediate discontinuation of N2O use to prevent further progression.
Vitamin B12 Supplementation:
High-dose intramuscular injections (e.g., 1,000 µg daily for a week).
Oral supplementation for long-term management.