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The Journal of Bone and Joint Surgery (American) 83:884-890 (2001)
© 2001 The Journal of Bone and Joint Surgery, Inc.

The Effect of Surgically Implanted Bullet Fragments on the Spinal Cord in a Rabbit Model

Nathaniel L. Tindel, MD, Alexander E. Marcillo, MD, Bobby K.-B. Tay, MD, Richard P. Bunge, MD and Frank J. Eismont, MD

Investigation performed at the Department of Orthopaedics and Rehabilitation, University of Miami School of Medicine, and The Miami Project to Cure Paralysis, Miami, Florida
Nathaniel L. Tindel, MD
North Shore Orthopaedics, St. Johns Episcopal Hospital Medical Office Building, Suite 106, 48 Route 25A, Smithtown, NY 11787

Alexander E. Marcillo, MD
The Miami Project to Cure Paralysis, University of Miami School of Medicine, 1600 NW 10th Avenue (R-48), Miami, FL 33136

Bobby K.-B. Tay, MD
Department of Orthopaedic Surgery, University of California at San Francisco, San Francisco General Hospital, 1001 Potrero Avenue, 3A-36, San Francisco, CA 94110

Richard P. Bunge, MD
Deceased

Frank J. Eismont, MD
Department of Orthopaedics and Rehabilitation (D-27), University of Miami School of Medicine, P.O. Box 016960, Miami, FL 33136

In support of their research or preparation of this manuscript, one or more of the authors received grants or outside funding from the Miami Center for Orthopaedic Research and Education at the University of Miami School of Medicine and a grant to the Miami Project NIH/NINDS NS28059-05. None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

Background: Whether or not to remove bullets or bullet fragments from the spinal column of a neurologically intact patient has been a subject of continual debate. The controversy is due in part to a lack of information about the long-term effects of bullet fragments on spinal cord tissue. Although many studies have demonstrated the toxic effects of metal fragments on brain tissue, to our knowledge no one has evaluated the effects of the metals contained in commercially available bullets on spinal cord tissue.

Methods: Copper, aluminum, and lead fragments from three commercially available bullet cartridges were implanted in intradural and extradural locations in seventeen New Zealand White rabbits. At an average of 9.8 months, the metal content of specimens of blood, cerebrospinal fluid, and liver were determined. The spinal cords were harvested and examined histologically.

Results: There was a significant increase in the copper level of blood from the rabbits with an implanted copper fragment compared with that of the control animals (p = 0.007). Concentrations of copper and lead were not elevated, compared with the control values, in the serum or liver. Histological examination of the spinal cords revealed major destruction of both the axons and the myelin of the dorsal column adjacent to the intradural copper fragments. Intradural fragments of lead caused similar destruction of myelin and axons in the dorsal column, but to a lesser degree. Minimal spinal cord or meningeal histological changes were noted around the aluminum intradural fragments, and no pathological changes were found near any fragments placed in an extradural location.

Conclusions: The results of this study show that certain metals contained in commercially available bullets can cause varying degrees of neural destruction independent of the initial mechanical injury caused by implantation. Of the three metals tested, copper fragments consistently caused a substantial localized area of neural injury within the spinal cord.

Clinical Relevance: In our study, copper fragments caused local neural toxicity involving as much as 10% of the spinal cord area, suggesting that there may be a scientific basis for removal of copper fragments lodged in the spinal cord, even in the absence of a neurological deficit.


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