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Internal Medicine
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Abstract
Background: Nitrous oxide also known as “laughing gas” is a naturally occurring gas that is colorless, odorless, nonflammable, and nontoxic. It has been used as an inhalant anesthetic in the medical field for more than 150 years for dental and surgical procedures. Due to its wide availability and ability to cause euphoria, recreational use is on the rise.1 Here, I will present a case of subacute combined degeneration in the setting of nitrous oxide induced vitamin B-12 deficiency.
Case presentation: 23-year-old right-handed gentleman with no past medical history presented to the ED complaining of 1 week of bilateral lower extremity symmetric paresthesia, weakness, and difficulty with ambulation. He initially experienced paresthesia in the lower extremities. Two days later, he experienced difficulty ambulating which led to multiple falls at home. The patient stated sensation in both legs was reduced in addition to experiencing difficulty with positioning during movement and balance difficulty. Strength in bilateral lower extremities was also markedly reduced as he eventually noticed he was unable to stand by himself and after his most recent fall which prompted his visit to the emergency department. The patient denied trauma, fever, chills, fatigue, weight loss, nausea, vomiting, diarrhea, dizziness, vision changes. He denied alcohol use, tobacco use, or drug use.
On neurological examination, the patient was alert and oriented to place, time, and situation, normal 5-minute recollection, normal mood, no aphasia, cranial nerves II-XII intact. Motor strength was 4/5 hip flexion bilaterally with eyes open, decreased to 3/5 with eyes closed. Dorsiflexion 4/5 bilaterally with eyes open, decreased to 3/5 with eyes closed. Deep tendon reflexes were 2+ in bicep reflex bilaterally, 3+ in patellar reflex with cross adductor response bilaterally, 3+ in achilles reflex. No clonus. Absent Babinski. On sensory exam, there was profound impairment in proprioception and vibration in bilateral lower extremities and decreased sensation to vibration in bilateral upper extremities. Proprioception preserved in upper extremities. Finger to nose, normal heal to the shin, normal rapid alternating movements. The patient had no tremor, and he was found to have an ataxic gait.
Laboratory studies including complete blood count, complete metabolic panel, thyroid-stimulating hormone, creatine kinase, lactate dehydrogenase, folate levels were within normal limits. Serum vitamin B-12 was low at 78 pg/mL and vitamin D was low at 13.9 ng/mL. MRI of the cervical spine showed an abnormal T2 signal within the cervical spinal cord extending from the level of C2-C6, which appears to be centered posteriorly, without associated abnormal enhancement, potentially indicating evidence of myelopathy. In order to rule out Neuromyelitis Optica Spectrum Disorders, aquaporin 4 antibody and anti-myelin oligodendrocyte antibody were ordered. HIV type 1 and 2 antibodies revealed no reactivity. Immunologic workup with ANA, dsDNA, SSA/Ro Ab, SS-B/La Ab, gastric parietal cell Ab was negative. Lumbar puncture was performed with CSF studies showing normal opening pressure, glucose, and white blood cell count, however, CSF protein was elevated at 243 mg/dL. Infectious workup with CSF culture, CSF acid-fast bacilli, CSF VDRL, CSF West Nile virus was negative. CSF oligoclonal revealed no bands. CSF cytology was negative for malignant cells. Aquaporin 4 antibody and anti-myelin oligodendrocyte glycoprotein antibody were negative. Workup revealed no evidence of infectious or immunologic underlying disease. While waiting for additional laboratory results, the patient was started on IVIG. On day 5 of hospitalization patient reported that he has been inhaling nitric oxide from whipped cream cans for recreational use for approximately a year. The patient was started on vitamin B-12 and vitamin D supplementation. He was also started on methylprednisolone IV 1000mg for 5 days. The patient’s condition improved progressively with vitamin B-12 supplementation and physical therapy enabling him to be transferred to inpatient rehabilitation to continue recovering.
Conclusion: Patients presenting with neurological symptoms like paresthesia, numbness, weakness, and ataxic gait along with laboratory studies indicating vitamin B-12 deficiency should be questioned about nitrous oxide recreational use. Unfortunately, there is no test to screen for nitrous oxide use so this shows how essential it is to obtain a thorough complete history in regard to recreational drug use. Nitrous oxide inactivates vitamin B-12 making it unable to function as a cofactor for methionine synthase which normally converts homocysteine to methionine.2 Methionine is a precursor of S-adenosyl methionine which is used as a methyl donor required for the maintenance of the integrity of the neuron sheath. This will result in damaged myelin sheath by impairing the methylation of myelin basic proteins and lipids.3 Treatment consists of cessation of nitrous oxide use and vitamin B 12 supplementation. Vitamin B-12 supplementation should be started immediately upon suspected diagnosis since the response to treatment is associated with severity and duration of symptoms. Patients should be educated on the importance of the cessation of nitrous oxide for recreational use.
Presentation Type
Poster
Recommended Citation
Nadal, Jorge; Hernandez, Daniela; and Cantazaro, Brandon, "Subacute combined degeneration due to nitrous oxide-induced vitamin B-12 deficiency" (2023). Research Colloquium. 20.
https://scholarworks.utrgv.edu/colloquium/2022/posters/20
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Nervous System Diseases Commons, Pathological Conditions, Signs and Symptoms Commons, Substance Abuse and Addiction Commons
Subacute combined degeneration due to nitrous oxide-induced vitamin B-12 deficiency
Background: Nitrous oxide also known as “laughing gas” is a naturally occurring gas that is colorless, odorless, nonflammable, and nontoxic. It has been used as an inhalant anesthetic in the medical field for more than 150 years for dental and surgical procedures. Due to its wide availability and ability to cause euphoria, recreational use is on the rise.1 Here, I will present a case of subacute combined degeneration in the setting of nitrous oxide induced vitamin B-12 deficiency.
Case presentation: 23-year-old right-handed gentleman with no past medical history presented to the ED complaining of 1 week of bilateral lower extremity symmetric paresthesia, weakness, and difficulty with ambulation. He initially experienced paresthesia in the lower extremities. Two days later, he experienced difficulty ambulating which led to multiple falls at home. The patient stated sensation in both legs was reduced in addition to experiencing difficulty with positioning during movement and balance difficulty. Strength in bilateral lower extremities was also markedly reduced as he eventually noticed he was unable to stand by himself and after his most recent fall which prompted his visit to the emergency department. The patient denied trauma, fever, chills, fatigue, weight loss, nausea, vomiting, diarrhea, dizziness, vision changes. He denied alcohol use, tobacco use, or drug use.
On neurological examination, the patient was alert and oriented to place, time, and situation, normal 5-minute recollection, normal mood, no aphasia, cranial nerves II-XII intact. Motor strength was 4/5 hip flexion bilaterally with eyes open, decreased to 3/5 with eyes closed. Dorsiflexion 4/5 bilaterally with eyes open, decreased to 3/5 with eyes closed. Deep tendon reflexes were 2+ in bicep reflex bilaterally, 3+ in patellar reflex with cross adductor response bilaterally, 3+ in achilles reflex. No clonus. Absent Babinski. On sensory exam, there was profound impairment in proprioception and vibration in bilateral lower extremities and decreased sensation to vibration in bilateral upper extremities. Proprioception preserved in upper extremities. Finger to nose, normal heal to the shin, normal rapid alternating movements. The patient had no tremor, and he was found to have an ataxic gait.
Laboratory studies including complete blood count, complete metabolic panel, thyroid-stimulating hormone, creatine kinase, lactate dehydrogenase, folate levels were within normal limits. Serum vitamin B-12 was low at 78 pg/mL and vitamin D was low at 13.9 ng/mL. MRI of the cervical spine showed an abnormal T2 signal within the cervical spinal cord extending from the level of C2-C6, which appears to be centered posteriorly, without associated abnormal enhancement, potentially indicating evidence of myelopathy. In order to rule out Neuromyelitis Optica Spectrum Disorders, aquaporin 4 antibody and anti-myelin oligodendrocyte antibody were ordered. HIV type 1 and 2 antibodies revealed no reactivity. Immunologic workup with ANA, dsDNA, SSA/Ro Ab, SS-B/La Ab, gastric parietal cell Ab was negative. Lumbar puncture was performed with CSF studies showing normal opening pressure, glucose, and white blood cell count, however, CSF protein was elevated at 243 mg/dL. Infectious workup with CSF culture, CSF acid-fast bacilli, CSF VDRL, CSF West Nile virus was negative. CSF oligoclonal revealed no bands. CSF cytology was negative for malignant cells. Aquaporin 4 antibody and anti-myelin oligodendrocyte glycoprotein antibody were negative. Workup revealed no evidence of infectious or immunologic underlying disease. While waiting for additional laboratory results, the patient was started on IVIG. On day 5 of hospitalization patient reported that he has been inhaling nitric oxide from whipped cream cans for recreational use for approximately a year. The patient was started on vitamin B-12 and vitamin D supplementation. He was also started on methylprednisolone IV 1000mg for 5 days. The patient’s condition improved progressively with vitamin B-12 supplementation and physical therapy enabling him to be transferred to inpatient rehabilitation to continue recovering.
Conclusion: Patients presenting with neurological symptoms like paresthesia, numbness, weakness, and ataxic gait along with laboratory studies indicating vitamin B-12 deficiency should be questioned about nitrous oxide recreational use. Unfortunately, there is no test to screen for nitrous oxide use so this shows how essential it is to obtain a thorough complete history in regard to recreational drug use. Nitrous oxide inactivates vitamin B-12 making it unable to function as a cofactor for methionine synthase which normally converts homocysteine to methionine.2 Methionine is a precursor of S-adenosyl methionine which is used as a methyl donor required for the maintenance of the integrity of the neuron sheath. This will result in damaged myelin sheath by impairing the methylation of myelin basic proteins and lipids.3 Treatment consists of cessation of nitrous oxide use and vitamin B 12 supplementation. Vitamin B-12 supplementation should be started immediately upon suspected diagnosis since the response to treatment is associated with severity and duration of symptoms. Patients should be educated on the importance of the cessation of nitrous oxide for recreational use.