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

Research output: Contribution to journalArticle

Abstract

Objective: Vitamin B12 deficiency can lead to subacute combined degeneration (SCD). Nitrous oxide (N2O) 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 39 cases of nitrous oxide-induced SCD, were included through the screening process. These cases included 22 male patients and 17 female patients, with an average age of 51.3 years (SD 17.6). An etiology for subclinical B12 deficiency was determined in 31 reports; of these, 26 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 = 0.41), sex (p = 0.48), positive MRI findings (p = 0.42), post-operative serum B12 (p = 0.96), post-operative hemoglobin (p = 0.17), type of surgery (p = 0.58), or post-operative high mean corpuscular volume (p = 0.14). 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.

Original languageEnglish (US)
Pages (from-to)163-168
Number of pages6
JournalClinical Neurology and Neurosurgery
Volume173
DOIs
StatePublished - Oct 1 2018

Fingerprint

Subacute Combined Degeneration
Nitrous Oxide
Spinal Cord
Anesthesia
Vitamin B 12 Deficiency
Erythrocyte Indices
Spinal Cord Diseases
Coenzymes
Vitamin B 12
Cobalt
Vitamins
Anesthetics
Comorbidity
Hemoglobins
Databases
Ions
Therapeutics
Serum

Keywords

  • Anesthesia
  • Cobalamin
  • Myelopathy
  • Nitrous oxide
  • Spinal cord
  • Subacute combined degeneration
  • Vitamin B12

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology

Cite this

Subacute combined degeneration of the spinal cord following nitrous oxide anesthesia : A systematic review of cases. / Patel, Kishan K.; Mejia Munne, Juan Carlos; Gunness, Vimal Raj Nitish; Hersey, Denise; Alshafai, Nabeel; Sciubba, Daniel; Nasser, Rani; Gimbel, David; Cheng, Joseph; Nouri, Aria.

In: Clinical Neurology and Neurosurgery, Vol. 173, 01.10.2018, p. 163-168.

Research output: Contribution to journalArticle

Patel, KK, Mejia Munne, JC, Gunness, VRN, Hersey, D, Alshafai, N, Sciubba, D, Nasser, R, Gimbel, D, Cheng, J & Nouri, A 2018, 'Subacute combined degeneration of the spinal cord following nitrous oxide anesthesia: A systematic review of cases', Clinical Neurology and Neurosurgery, vol. 173, pp. 163-168. https://doi.org/10.1016/j.clineuro.2018.08.016
Patel, Kishan K. ; Mejia Munne, Juan Carlos ; Gunness, Vimal Raj Nitish ; Hersey, Denise ; Alshafai, Nabeel ; Sciubba, Daniel ; Nasser, Rani ; Gimbel, David ; Cheng, Joseph ; Nouri, Aria. / Subacute combined degeneration of the spinal cord following nitrous oxide anesthesia : A systematic review of cases. In: Clinical Neurology and Neurosurgery. 2018 ; Vol. 173. pp. 163-168.
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abstract = "Objective: Vitamin B12 deficiency can lead to subacute combined degeneration (SCD). Nitrous oxide (N2O) 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 39 cases of nitrous oxide-induced SCD, were included through the screening process. These cases included 22 male patients and 17 female patients, with an average age of 51.3 years (SD 17.6). An etiology for subclinical B12 deficiency was determined in 31 reports; of these, 26 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 = 0.41), sex (p = 0.48), positive MRI findings (p = 0.42), post-operative serum B12 (p = 0.96), post-operative hemoglobin (p = 0.17), type of surgery (p = 0.58), or post-operative high mean corpuscular volume (p = 0.14). 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.",
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AU - Patel, Kishan K.

AU - Mejia Munne, Juan Carlos

AU - Gunness, Vimal Raj Nitish

AU - Hersey, Denise

AU - Alshafai, Nabeel

AU - Sciubba, Daniel

AU - Nasser, Rani

AU - Gimbel, David

AU - Cheng, Joseph

AU - Nouri, Aria

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N2 - Objective: Vitamin B12 deficiency can lead to subacute combined degeneration (SCD). Nitrous oxide (N2O) 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 39 cases of nitrous oxide-induced SCD, were included through the screening process. These cases included 22 male patients and 17 female patients, with an average age of 51.3 years (SD 17.6). An etiology for subclinical B12 deficiency was determined in 31 reports; of these, 26 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 = 0.41), sex (p = 0.48), positive MRI findings (p = 0.42), post-operative serum B12 (p = 0.96), post-operative hemoglobin (p = 0.17), type of surgery (p = 0.58), or post-operative high mean corpuscular volume (p = 0.14). 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.

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KW - Subacute combined degeneration

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