Subacute combined degeneration of the spinal cord following nitrous oxide anesthesia: A systematic review of cases.

Kishan K Patel, Juan Carlos Mejia Munne, Vimal Raj Nitish Gunness, Denise Hersey, Nabeel Alshafai, Daniel Sciubba, Rani Nasser, David Gimbel, Joseph Cheng, Aria Nouri

Journal: Clinical neurology and neurosurgery 2019;173():163-168

PMID: 30144777

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Abstract

OBJECTIVE

Vitamin B12 deficiency can lead to subacute combined degeneration (SCD). Nitrous oxide (NO) is an anesthetic which oxidizes the cobalt ion of vitamin B12, interfering with its function as a coenzyme. In this study, we conduct a systematic review of reported cases of SCD following nitrous oxide anesthesia.

PATIENTS AND METHODS

A comprehensive search of multiple databases was conducted, and information about patient characteristics, symptomatology, clinical work-up, and treatment was extracted from eligible articles. Univariate analyses were performed to identify predictors of poor neurological recovery following SCD.

RESULTS

32 studies, reporting 37 cases of nitrous oxide-induced SCD, were included through the screening process. These cases included 21 male patients and 16 female patients, with an average age of 50.4 years (SD 17.6). An etiology for subclinical B12 deficiency was determined in 30 reports; of these, 25 were due to vitamin malabsorption secondary to a gastrointestinal disorder. Duration of nitrous oxide exposure was described in 19 reports, and ranged from 30 min to 11 h. Univariate analysis failed to find an association between post-operative recovery and age (p = 0.60), sex (p = 0.46), positive MRI findings (p = 0.47), post-operative serum B12 (p = 1.00), post-operative hemoglobin (p = 0.18), type of surgery (p = 0.58), or post-operative high mean corpuscular volume (p = 0.13).

CONCLUSION

In patients with postsurgical myelopathy, surgeons should evaluate B12 status and consider the possibility that nitrous oxide could cause a subclinical B12 deficiency to become overt, particularly in patients with malabsorptive GI comorbidities. Treatment with B12 in this population can result in significant improvement of neurological function.

Address: Department of Neurosurgery, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, 06510, USA. Electronic address: [email protected].; Department of Neurosurgery, University of Cincinnati College of Medicine, PO Box 670515, Cincinnati, OH, 45267, USA. Electronic address: [email protected].; Department of Neurosurgery, University of Toronto, 1 King's College Cir, Toronto, ON, M5S 1A8, Canada. Electronic address: [email protected].; Cushing/Whitney Medical Library, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, 06510, USA. Electronic address: [email protected].; Alshafai Neurosurgical Academy, Toronto, ON, M5J 2S2, Canada. Electronic address: [email protected].; Department of Neurosurgery, Johns Hopkins School of Medicine, 733 N Broadway, Baltimore, MD, 21205, USA. Electronic address: [email protected].; Department of Neurosurgery, University of Cincinnati College of Medicine, PO Box 670515, Cincinnati, OH, 45267, USA. Electronic address: [email protected].; Department of Neurosurgery, University of Cincinnati College of Medicine, PO Box 670515, Cincinnati, OH, 45267, USA. Electronic address: [email protected].; Department of Neurosurgery, University of Cincinnati College of Medicine, PO Box 670515, Cincinnati, OH, 45267, USA. Electronic address: [email protected].; Department of Neurosurgery, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, 06510, USA; Department of Neurosurgery, University of Cincinnati College of Medicine, PO Box 670515, Cincinnati, OH, 45267, USA. Electronic address: [email protected].

DOI: 10.1016/j.clineuro.2018.08.016

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MeSH Terms: Adult, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Nitrous Oxide, Spinal Cord, Spinal Cord Diseases, Subacute Combined Degeneration, Vitamin B 12, Vitamin B 12 Deficiency