Spinal Epidural Abscess: Raising the Index of Suspicion

A spinal epidural abscess is an uncommon but life-threatening infection. Typically, it arises secondary to an insult that provides bacterial entry into the bloodstream. Often, spinal epidural abscesses are managed with a combination of surgical intervention and systemic antibiotics in order to minimize the risk of antibiotic resistance and recurrence. The standard of diagnosis for spinal epidural abscesses is through contrast-enhanced magnetic resonance imaging (MRI), which has high sensitivity and specificity. This particular case describes an indolent course of a spinal epidural abscess that presented with neurological deficits unaccounted for by preliminary spinal imaging, underscoring the value of clinical reasoning in patient assessment. An 81-year-old Caucasian female was brought to the emergency department by her daughter with concern of low back pain and a 12-hour history of weakness in the bilateral lower extremities. Her lumbar pain worsened with spinal extension and improved with spinal flexion. She denied any injury, fever, or bowel and bladder incontinence. A review of her past surgical history revealed a recent left shoulder arthroplasty complicated by postoperative cellulitis. She denied any alcohol, tobacco, or drug use. At presentation, her respiratory rate was 28 breaths/minute, and all other vital signs were within normal limits. A physical exam demonstrated bilateral lower extremity strength 3/5, straight leg raising test positive on the right, and the remainder of the exam was unremarkable. To investigate mechanical spinal cord compression, an MRI without contrast of the lumbar spine was obtained. This revealed chronic degenerative changes and failed to explain her acute onset of weakness. Complete blood count revealed a white blood cell count of 16.0 x10³/µL (reference range: 4.5-11.5 x10³/µL), and in correlation with her tachypnea, bacteremia was now suspected. Empiric antibiotic treatment was promptly started; however, despite intervention, she failed to show signs of improvement, and blood cultures were inconclusive. Finally, on day three of admission, re-evaluation of her neurological deficits demonstrated +1 patellar reflexes in both legs. Given her bilateral lower extremity weakness, leukocytosis, and low back pain, the index of suspicion for a spinal epidural abscess increased, and she underwent a contrast-enhanced MRI of the lumbar spine. The imaging revealed a 17.1 mm abscess. Intravenous nafcillin was started, and she was transferred to a higher level of care for neurosurgical evaluation. There, she underwent emergent surgical debridement of the abscess and was discharged with a six-week course of outpatient intravenous oxacillin infusions. In summary, by assessing the entire clinical picture and not dismissing her persistent symptoms in spite of equivocal MRI findings, the abscess was correctly identified. Delays in the diagnosis of spinal epidural abscesses occur far too frequently in clinical practice. Therefore, this case reflects on the importance of systematic clinical reasoning, a thorough neurological exam, vigilance against anchoring bias, and considering a broad differential to minimize diagnostic delay and improve patient outcomes.