C42-23 Pulmonary Embolism and Peripheral Neuropathy Secondary to Inhaled Nitrous Oxide and Vitamin B12 Deficiency

Abstract

Abstract Introduction Chronic use of inhaled nitrous oxide (NO) or “laughing gas” inactivates vitamin B12 causing a functional B12 deficiency. Active B12 is a coenzyme for the conversion of methylmalonic acid to succinyl Co-A and homocysteine to methionine. These molecules are precursors for the synthesis and maintenance of myelin nerve sheaths. Therefore, functional B12 deficiency compromises myelin integrity causing peripheral neuropathy and subacute combined degeneration of the spinal cord. Chronic NO inhalation likely also increases the risk for pulmonary embolism (PE) due to the resultant hyperhomocystenemia, which has been found to be an intermediate risk factor for arterial and venous thrombosis. Hyperhomocystenemia causes endothelium dysfunction, platelet and clotting activation and impaired fibrinolysis. Case Report A 30-year-old man presented to hospital with acute onset dyspnea and left sided chest pain. Incidentally, he reported a 2-week history of altered sensation in his lower limbs bilaterally. He had no contributory medical history. Neurological exam revealed ascending reduced fine sensation in his lower limbs, with preserved power and an ataxic, high-stepping gait. There was loss of proprioception to the medial malleoli bilaterally. The patient was anemic with a borderline macrocytosis. His blood film demonstrated polychromasia and occasional nucleated red blood cells. Hematinics revealed a severe B12 deficiency (active B12 = 24 pmol/L, ref 33-170 pmol/L). Further testing revealed elevated methylmalonic acid (9279 nmol/L , ref 0-280nmol/L) and homocysteine (96.68 umol/L, ref 5.46-16.20 umol/L) levels. On further questioning, the patient reported significant recreational inhaled NO use, using up to 100 NO balloons per week. A CTPA demonstrated a left subsegmental pulmonary embolism. He was initially treated with therapeutic low-molecular-weight heparin, before transitioning to oral anticoagulation. His dyspnea and chest pain improved within days. The patient was investigated for other causes of the PE; a CT abdomen/pelvis, OGD, echocardiogram and colonoscopy were all normal. Screening for antiphospholipid syndrome was normal. A neurology consult service diagnosed the patient with peripheral neuropathy secondary to NO use. His MRI whole spine and brain were unremarkable. He was treated with high-dose intramuscular cobalamin (B12) and had some improvement in his gait within weeks. The importance of abstaining from nitric oxide use was impressed on the patient prior to discharge. Discussion and Conclusion In this case, there was initially no obvious association between the PE and neurological symptoms. However, the pathologies were ultimately both linked to NO inhalation. Further studies are needed to confirm the relationship between chronic NO use and VTE. This abstract is funded by: None