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  • Title: Recreational nitrous oxide induced subacute combined degeneration of the spinal cord: A case report.
    Author: Simpson K, Mukherji A.
    Journal: Clin Case Rep; 2023 Jan; 11(1):e6770. PubMed ID: 36694646.
    Abstract:
    Nitrous oxide is a gas frequently used in the medical/dental field for anesthesia and analgesic purposes and in the food industry as a spray propellant or foaming agent. Overexposure can lead to subacute combined degeneration (SACD) of the spinal cord through the mechanism of vitamin B12 deficiency. Because this drug is easily accessible, relatively inexpensive, and legal to possess, it has potential to be abused for recreational purposes. The number of published cases of nitrous oxide abuse has been increasing since 2010. Large-scale and long-term use of nitrous oxide have been found to cause nerve damage from vitamin B12 deficiency, thromboembolic phenomenon from elevated homocysteine levels, and even death from hypoxia. A 44-year-old male patient with past medical history of recently diagnosed type 2 diabetes, on Metformin, presented for 1 month of worsening bilateral upper and lower extremity weakness. On initial physical examination, he demonstrated pertinent abnormal findings of 2/5 hand strength bilaterally, 4/5 strength in his left upper extremity and right lower extremity, impaired coordination, ataxic gait, rigidity, and decreased but symmetrical reflexes. He reported using 50-100 canisters of nitrous oxide per day to obtain a feeling of relaxation and euphoria. Blood work revealed vitamin B12 deficiency, and abnormalities were seen on MRI. He was treated with 1000 μg of intramuscular vitamin B12 every other day for 3 doses, followed by 500 μg oral cyanocobalamin daily. He demonstrated a great amount of improvement in his neuropathy during his stay. However, he was still dependent in basic transfers, activities of daily living, and mobility and was discharged to acute rehabilitation. Vitamin B12 deficiency can lead to subacute combined degeneration, which presents with sensory deficits, weakness, ataxia, spasticity, and gait abnormalities. Treatment for SACD should be aggressive and rapid to prevent irreversible neurological deficits. Amid an opioid epidemic, practitioners can easily overlook the use of nitrous oxide and patients may consider this drug to be relatively harmless. This case demonstrates the importance of thorough history taking, patient education, and early recognition and treatment of vitamin B12 deficiency and the deleterious effects that may result without intervention.
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