Abstract

Skull base osteomyelitis may develop as a complication of paranasal sinusitis or other regional infectious process or as an unfortunate sequelae of iatrogenic injury or trauma. Afflicted patients generally have some form of systemic immunocompromise, most often diabetes, or a history of external beam radiotherapy for a head and neck malignancy with the radiation portal encompassing the area of the skull base.¹ Before the era of systemic antimicrobial therapy, skull base osteomyelitis was almost universally fatal. Acute osteomyelitis often results in rapid lytic destruction of the skull base bone commonly associated with cranial nerve palsy/paralysis, and rarely, with craniovertebral instability and intracranial abscess formation.² It may or may not be associated with a deep fascial, orbital or intracranial soft tissue component. Chronic osteomyelitis, as seen in granulomatous conditions, is often much more indolent and slowly progressive. Patients may still exhibit cranial nerve palsies, albeit usually more slowly. As such, they are often able to compensate for these losses over time and hence often delay their clinical presentation.