Whipe that B12 out. A case report describing the devastating consequences of a recreational use of nitrous oxide.

Author: Yuliia Varava
Program: Resident/Clinical Fellow
Mentor(s): Rehan Qayyum, MD


Abstract

Introduction:

Nitrous oxide is an increasingly popular inhalant of abuse commonly called "Whip-its". It exhibits euphoric properties via NMDA receptor antagonism. One of the adverse effects include multiple neurologic deficits secondary to the functional vitamin B12 deficiency. Nitrous oxide irreversibly oxides the cobalt ion of cobalamin, inactivating it and resulting in impaired DNA synthesis and myelin production, as well as accumulation of homocysteine.

Case description:

A 25-year-old woman with no known past medical history presented to our emergency department (ED) complaining of six weeks of progressive symptoms of neck pain, weakness, numbness in the bilateral lower extremities and inability to walk. The symptoms started shortly after suffering from a fall in her home and got worse after seeing a chiropractor. Patient went to the ED 2 weeks prior to her current presentation, where an MRI neck and brain were done followed by an outpatient neurologist evaluation. She was prescribed gabapentin for a neuropathic pain and sent home.

On our evaluation patient had unusual distribution of multimodal sensory disturbances notable for absence of vibratory and proprioception in distal extremities but preserved pain and temperature sensations. She had positive Romberg test and unsteadiness when standing. Cervical MRI from her prior ED visit was reviewed and noted to have nonspecific changes in the dorsal column at the level of C3 through C5 consistent with subacute combined degeneration. Her lumbar puncture, complete blood count, complete metabolic panel, HIV, syphilis, serum zinc and copper level, and serum B12 levels were within normal limits. On further interview the patient endorsed a long-term daily use of nitrous oxide and taking vitamin supplement a night prior to her hospitalization. A serum methylmalonic acid was markedly elevated which confirmed the total body B12 deficiency despite the normal serum levels. The patient was given daily intramuscular vitamin B12 during hospitalization and a prescription for oral vitamin B9 and B12 supplementation at discharge.

Discussion:

This case illustrates the importance of awareness of vitamin B12 deficiency with nitrous oxide use. Our patient did not provide a full history on her initial visits to the ED and to neurology and had denied any recreational drug use. This led to the misinterpretation of her cervical spine MRI and delayed the treatment. Furthermore, with this degree of neurological damage one would expect her vitB12 level to be low rather than normal. However, this was again misinterpreted as she took vitamin supplement a night before coming to the hospital.

Educational point:

It is important to recognize subacute combined degeneration of spinal cord in a high-risk patient population with typical symptoms despite normal vitamin B12 level. The high index of suspicion, early recognition, and treatment are the mainstay to prevent irreversible neurological damage.