A Case of Spinal Epidural Abscess Presenting with Horner Syndrome.

Abstract

A spinal epidural abscess (SEA) is an uncommon disease, but it is associated with significant morbidity. SEA can be promoted by multiple risk factors. Moreover, the diagnosis of SEA usually requires the presence of a classic triad of back pain, fever, and neurological deficit, hence, the difficulty in making the diagnosis if presented otherwise. Horner syndrome (HS) is an uncommon presentation in association with SEA. Even though nonsurgical versus surgical management of SEA is still controversial, the literature review indicates a preference for surgical decompression as a treatment for SEA presenting with neurological compromise, followed by long-term antimicrobial therapy. The rapidity of making the diagnosis and the initiation of appropriate treatment determine the outcome.We present a case of a 23-year-old male with no past medical history. The patient arrived at the Hamad General Hospital emergency department (ED) with severe upper back pain radiating to his left shoulder, which progressed to numbness and weakness of the left upper limb and spastic paraplegia. A left HS was revealed in a further neurological examination. However, the diagnosis of a spinal epidural abscess (SEA) was made after a left posterolateral epidural abscess extending from C5/6-T2/3 with associated cord compression and edema was revealed on an MRI scan. The patient then underwent a left C7, T1 hemilaminectomy and received antibiotics followed by admission to the rehabilitation unit. Staph. aureus was reported in culture microbiology results. Unfortunately, motor power recovery after the surgery was not significant.Although it is difficult to diagnose SEA, it is crucial to suspect it in the presence of a neurological deficit regardless of the presence or absence of predisposing factors. Nevertheless, HS is not a relatively common finding in association with SEA. In this case report, we have a young patient with SEA who presented with left HS, upper back pain, and progressive neurological deficit in the absence of identifiable risk factors.