A 45-year-old male with no significant past medical or psychiatric history presented with sudden onset of numbness below the umbilicus and unsteady gait. At the time of admission, the patient also had cognitive impairment with a Montreal cognitive assessment (MoCA) score of 22/30. There was no associated phonophobia or photophobia. During the hospital stay, the patient had experienced urinary retention with subsequent Foley catheterization. On physical examination, he had no vibratory sensation or proprioception in bilateral (B/L) lower extremities with cold temperature and spared pinprick. Reflexes were 2+ in B/L knees and ankle (left) with non-sustained clonus on left ankle, big toes were down going, with diminished sensation around T10, increased muscle tone in B/L lower extremities, and no obvious muscle weakness in lower extremities. He had a normal anal tone and post-void residual. Findings were suggestive of a spinal cord lesion mainly affecting the posterior column.\nAll laboratory findings were unremarkable except mean corpuscular volume of 111 fl (80-100 fl), B12 level of 311 pg/mL (160-950 pg/ml), methylmalonic acid (MMA) level of 7397 nmol/L (< 370 nmol/L), and a homocysteine level of 89.7 umol/L (< 15 umol/L). He had a recent history of abuse of nitrous oxide due to recreational usage. Magnetic resonance imaging (MRI) C spine (with and without contrast), T spine (with and without contrast), L spine (with and without contrast), and MRI brain (with and without contrast) were unremarkable. Cerebrospinal fluid (CSF) analysis revealed the presence of immunoglobulin G (IgG) oligoclonal bands. Electromyography showed left non-localizable peroneal neuropathy with a small peroneal compound muscle action potential (CMAP) and small superficial peroneal CMAP with no evidence of polyneuropathy. Based on all these findings, the final diagnosis of “myelopathy secondary to vitamin B12 deficiency induced by nitrous oxide abuse” was made.\nLater, the patient was treated with intramuscular vitamin B12 followed by oral formulation, and discharged to a rehabilitation center. Upon follow-up after 16 weeks, the patient's memory loss and confusion had improved with repeat B12 and MMA values of 1409 pg/mL and 139 nmol/L, respectively. The patient was able to ambulate without the assistance of a walking device and was able to perform all other activities of daily living. The patient's only remaining symptom was mild vibratory sensation deficits below the knees B/L, which was no longer noted at his 24-week follow-up.
Sudden-onset chest pain for 1 d.\nA 29-year-old man complained of sudden precordial pain with no remission for 1 d prior to hospital admission but denied hemoptysis, dyspnea, or syncope. He sought evaluation and was admitted for the purpose of intensive examination and treatment.\nThe patient had been addicted to N2O for 1 year; as a result, peripheral neuropathy had occurred and was treated with vitamin B12 (Vit B12). His medical history included poor blood glucose control and anxiety. However, he had no history of thrombosis, malignant tumor, recent trauma, or prolonged air travel.\nThe patient has smoked over 13 pack-years and did not have alcoholism or a positive family history.\nThe initial assessment revealed that the patient was overweight and fragile, with a body mass index of 31.12 kg/m2, temperature of 36.3 °C, blood pressure of 110-120/70-80 mmHg, heart rate over 110 beats/min, respiratory rate over 30 breaths/min, and pulse oximetry of 93% when the fraction of inspired oxygen was 49%. Moreover, the physical examination indicated diminished breath sounds on both sides and the accentuation of pulmonic second sounds.\nLaboratory data showed a high leukocyte count and an increased hemoglobin level, suggested abnormal liver biochemistry and hyperlipidemia, and revealed HHcy (24.12 µmol/L), high Vit B12 (734 µmol/L), and normal folate (14.39 nmol/L). The results of the protein S, protein C, anti-thrombin III antibody, anti-cardiolipin antibody, lupus anticoagulant, anti-β2gp1 autoantibody, and other autoantibodies were within normal limits. The clotting profile was normal, other than the D-dimer value (1.13 mg/L), and thrombophilia screening was negative. As markers in the risk stratification of PE, the levels of brain natriuretic peptide (BNP) and cardiac troponin I (CTnI) were 533 pg/mL and 0.334 ng/mL, respectively. Arterial blood gas levels measured with an oxygen concentration of 49% showed the following: pH, 7.44; PaCO2, 30 mmHg; and PaO2, 74 mmHg.\nAn electrocardiogram (ECG, Figure ) showed sinus tachycardia with typical changes on SIQIIITIII (S wave in the aVL lead, Q wave and T wave in the III lead). Ultrasonic cardiogram demonstrated right ventricular enlargement with left ventricular compression. Color Doppler scans were used to explore femoral, popliteal, and calf muscular venous thrombosis in the right extremity. Computed tomographic pulmonary angiography (CTPA) revealed occlusion of the pulmonary artery trunk, lobar artery, and arterial branches on both sides and signs of increased right heart load (Figure and ).