Case Presentation: A 50-year-old previously healthy man presented with three weeks of progressive low back pain following a recent tooth extraction. Symptoms progressed to bilateral lower extremity weakness, perineal numbness, and night sweats. He was afebrile and normotensive. Examination revealed lumbar midline and paraspinal tenderness, bilateral proximal 4/5 lower extremity strength, and positive straight-leg-raise test bilaterally. Initial labs showed WBC 11.4 cells/µL, Hgb 11.6 g/dL, CRP 78.7 mg/L (< 1 mg/L), and ESR 21 mm/hr (0-15 mm/hr). Blood cultures were negative. Empiric vancomycin and ceftriaxone were initiated for suspected spinal epidural abscess (SEA).MRI of the lumbar spine revealed diffuse inflammatory enhancement, microabscesses, and involvement of the thecal sac consistent with arachnoiditis secondary to SEA. Multiple lumbar puncture attempts were unsuccessful, and the patient underwent a C1–C2 puncture. CSF analysis showed WBC 114 cells/μL (0-5 cells/μL), protein 79.5 mg/dL (15-45 mg/dL), and glucose 32 mg/dL (50-80 mg/dL). CSF gram stain and culture were negative. Cytology was positive for myeloma cells, raising concern for plasma cell neoplasm. Serum and urine electrophoresis, immunofixation, serum free light chains, flow cytometry, PET-CT, and bone marrow biopsy revealed no evidence of a clonal plasma cell disorder. The patient completed a six-week course of intravenous daptomycin for bacterial SEA. He demonstrated neurological improvement at four-week neurology follow-up.
Discussion: SEA is an uncommon but potentially life-threatening infection. Classic findings of fever, back pain, and neurologic deficits occur together in less than 10% of cases at presentation, contributing to frequent diagnostic delays. Arachnoiditis, particularly the adhesive subtype, is even rarer, with fewer than 1,000 cases reported in the literature. Its presentation may mimic infectious, autoimmune, or neoplastic disease. In this case, repeated failed lumbar punctures provided an early clue to dense arachnoid adhesions, which can hinder lumbar access.The presence of plasma cells in the CSF raised initial concern for leptomeningeal myeloma, a rare plasma cell malignancy involving the CNS. However, plasma cells in CSF can also occur in reactive inflammatory conditions, including chronic meningitis, autoimmune processes, and post-infectious arachnoiditis. Distinguishing reactive from malignant plasma cells requires integration of imaging, clinical course, immunophenotyping studies and bone marrow biopsy. The absence of monoclonal protein, clonal plasma cells, or systemic lesions, combined with improvement on antibiotics, strongly supported a reactive inflammatory process rather than myeloma.Management of arachnoiditis depends on its underlying cause. Noninfectious forms are treated with supportive care, pain control, and occasionally immunomodulatory therapy. Arachnoiditis secondary to SEA mandates antimicrobial therapy to prevent permanent neurologic compromise. Differentiating between these etiologies is critical as immunosuppression may be appropriate in noninfectious cases but is harmful in infectious arachnoiditis.
Conclusions: SEA-associated arachnoiditis can masquerade as neoplastic disease, particularly when plasma cells appear in the CSF. Hospitalists should recognize this and rely on clinical context, imaging, and systemic evaluation to distinguish reactive inflammation from malignancy and initiate prompt antimicrobial therapy.