Simpson Kaitlyn, Mukherji Amit
Family Medicine Residency Garnet Health Medical Center Middletown New York USA.
Clin Case Rep. 2023 Jan 16;11(1):e6770. doi: 10.1002/ccr3.6770. eCollection 2023 Jan.
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.
一氧化二氮是一种常用于医疗/牙科领域的麻醉和镇痛气体，在食品工业中用作喷雾推进剂或发泡剂。过度接触可通过维生素B12缺乏的机制导致脊髓亚急性联合变性（SACD）。因为这种药物容易获得、相对便宜且拥有合法，所以它有被滥用用于娱乐目的的可能性。自2010年以来，已发表的一氧化二氮滥用病例数量一直在增加。已发现长期大量使用一氧化二氮会因维生素B12缺乏导致神经损伤，因同型半胱氨酸水平升高导致血栓栓塞现象，甚至因缺氧导致死亡。一名44岁男性患者，既往有近期诊断的2型糖尿病病史，正在服用二甲双胍，因双侧上下肢无力加重1个月前来就诊。初次体格检查时，他表现出相关异常体征，双侧手部力量为2/5，左上肢和右下肢力量为4/5，协调性受损，共济失调步态，僵硬，反射减弱但对称。他报告每天使用一氧化二氮50 - 10个罐以获得放松和欣快感。血液检查显示维生素B12缺乏，MRI检查有异常。他接受了每两天一次、每次1000μg的肌肉注射维生素B12，共3剂，随后每天口服500μg氰钴胺素。住院期间他的神经病变有了很大改善。然而，他在基本转移、日常生活活动和移动方面仍有依赖，随后出院接受急性康复治疗。维生素B12缺乏可导致亚急性联合变性，表现为感觉障碍、无力、共济失调、痉挛和步态异常。对SACD的治疗应积极迅速，以防止不可逆转的神经功能缺损。在阿片类药物流行期间，从业者可能很容易忽视一氧化二氮的使用，而患者可能认为这种药物相对无害。本病例说明了全面病史采集、患者教育以及早期识别和治疗维生素B12缺乏及其可能导致的有害影响（如不干预可能产生的后果）的重要性。
