High thoracic spinal cord compression due to retained ballistic fragment with delayed presentation and suspected lead poisoning: a case report

Abstract

Case Presentation: A 45-year-old female with a prior history of a gunshot wound to the thoracic spine, initially managed non-surgically, evolved with a retained intrarachidian metallic fragment. At first, she presented with preserved gait, no motor deficits, and mild chronic dorsal pain. Years after the initial trauma, she developed progressive paraparesis (grade 4), a sensory level at T1, and contralateral loss of pain and temperature sensation, associated with dorsal neuropathic pain. This clinical picture was consistent with an incomplete spinal cord syndrome, predominantly affecting the spinothalamic tract. Deep tendon reflexes were globally decreased. Computed tomography revealed an intracanal metallic fragment in the upper thoracic region causing dural sac compression, without spinal instability. MRI was not performed due to the metallic fragment. Plain radiography confirmed the findings. Blood lead levels showed mild elevation (7.5 µg/dL; approximately 1.5 times the upper normal limit), without systemic manifestations of lead poisoning. Due to neurological deterioration, the patient underwent T1 laminectomy, spinal cord decompression, fragment removal, canal irrigation, and external lumbar drainage. She showed significant improvement by postoperative day 5 and achieved complete neurological recovery within 30 days, remaining asymptomatic during follow-up. Discussion: Retained intrarachidian ballistic fragments may remain asymptomatic for long periods; however, delayed complications include progressive spinal cord compression and incomplete spinal cord syndromes. Mechanisms include local inflammatory response, fragment migration, and direct compressive effects. Lead poisoning, although rare, should be considered when fragments are in contact with cerebrospinal fluid, allowing gradual metal leaching. In this case, mild serum elevation without systemic manifestations suggests subclinical exposure. Surgical intervention is indicated in cases of progressive neurological deficit, spinal cord compression, or suspected toxicity. Decompression combined with fragment removal proved effective, leading to complete neurological recovery. Final Comments: This case highlights a delayed complication of a retained intrarachidian ballistic fragment, presenting as an incomplete spinal cord syndrome with mild elevation of blood lead levels. Timely surgical intervention in the setting of neurological deterioration was crucial for full recovery, emphasizing the importance of long-term follow-up in such patients.