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Bullet retrieval from the cauda equina after penetrating spinal injury: A case report and review of the literature.

ABSTRACT:

Background

When gunshot injuries occur to the spine, bullet fragments may be retained within the spinal canal. Indications for bullet removal include incomplete spinal cord injury, progressive loss of neurologic function including injury to the cauda equina, and dural leaks with impending risk of meningitis.

Case description

Here, we present a 34-year-old male with a missile penetrating spinal injury to the cauda equina. In addition to the computed tomography scan demonstrating retention of a bullet in the left L1/2 disc space, the scan suggested likely dural injury. The patient underwent a decompression/instrumented fusion with retrieval of the retained bullet fragment. A laminectomy was performed from T12 to L3, and at L1 and L2, a large traumatic durotomy was identified and repaired. The patient, unfortunately, continued to have bilateral lower extremity plegia with neurogenic bladder/bowel dysfunction at 1-year follow-up.

Conclusion

We discuss the operative management and provide an intraoperative video showing the bullet extraction and dural closure.

SUBMITTER: Ojukwu DI

PROVIDER: S-EPMC8088496 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionPersistent neuroinflammatory response after cauda equina injury (CEI) lowers nociceptor firing thresholds, accompanied by pathological pain and decreasing extremity dysfunction. Histone deacetylation has been considered a key regulator of immunity, inflammation, and neurological dysfunction. Our previous study suggested that valproic acid (VPA), a histone deacetylase inhibitor, exhibited neuroprotective effects in rat models of CEI, although the underlying mechanism remains elusive.MethodsThe cauda equina compression surgery was performed to establish the CEI model. The Basso, Beattie, Bresnahan score, and the von Frey filament test were carried out to measure the animal behavior. Immunofluorescence staining of myelin basic protein and GPX4 was carried out. In addition, transmission electron microscope analysis was used to assess the effect of VPA on the morphological changes of mitochondria. RNA-sequencing was conducted to clarify the underlying mechanism of VPA on CEI protection.ResultsIn this current study, we revealed that the expression level of HDAC1 and HDAC2 was elevated after cauda equina compression model but was reversed by VPA treatment. Meanwhile, HDAC2 knockdown resulted in the improvement of motor functions and pathologic pain, similar to treatment with VPA. Histology analysis also showed that knockdown of histone deacetylase (HDAC)-2, but not HDAC1, remarkably alleviated cauda equina injury and demyelinating lesions. The potential mechanism may be related to lowering oxidative stress and inflammatory response in the injured region. Notably, the transcriptome sequencing indicated that the therapeutic effect of VPA may depend on HDAC2-mediated ferroptosis. Ferroptosis-related genes were analyzed in vivo and DRG cells further validated the reliability of RNA-sequencing results, suggesting HDAC2-H4K12ac axis participated in epigenetic modulation of ferroptosis-related genes.ConclusionHDAC2 is critically involved in the ferroptosis and neuroinflammation in cauda equina injury, and VPA ameliorated cauda equina injury by suppressing HDAC2-mediated ferroptosis.