Beyond the Ear: Otogenic Skull-Base Osteomyelitis With Central and Intracranial Extension in a Nondiabetic Older Adult

Introduction

Skull-base osteomyelitis (SBO) is a rare, potentially life-threatening infection classically associated with necrotizing otitis externa in older adults with diabetes or immunocompromise. Typical SBO originates in the external auditory canal and temporal bone, whereas central SBO involves the clivus and sphenoid without an obvious otologic source. Otogenic infection may extend centrally to the clivus, petrous apex, prevertebral tissues, dura, meninges, and adjacent neurovascular structures. Diagnosis can be delayed because otalgia and headache are nonspecific, while fever, leukocytosis, and striking otoscopic findings may be absent. We report extensive otogenic SBO with central and intracranial extension in a nondiabetic, afebrile older adult with normal leukocyte count and a relatively benign ear examination.

Case Presentation

An older man with no history of diabetes presented with four months of progressive right otalgia, headache, dizziness, and generalized weakness despite multiple courses of outpatient antibiotics and recent myringotomy with tympanostomy tube placement. He was afebrile, neurologically intact, and had a normal leukocyte count, but inflammatory markers were markedly elevated. MRI demonstrated extensive right otomastoiditis and skull-base osteomyelitis involving the clivus and right petrous apex, with prevertebral extension to the upper cervical spine, dural and meningeal enhancement, and probable epidural phlegmon at the right cerebellopontine angle. CT demonstrated anterior clival cortical erosion with adjacent phlegmonous tissue and extensive middle-ear and mastoid opacification. Blood cultures were negative. Otolaryngologic examination showed only mild external auditory canal edema and dry debris without purulent drainage or necrosis. Multidisciplinary evaluation identified no surgically drainable collection. The patient was treated with broad-spectrum intravenous antimicrobial therapy, including antipseudomonal coverage, with clinical improvement and transition to prolonged outpatient therapy.

Discussion

This case demonstrates that otogenic SBO may extend centrally and intracranially despite the absence of diabetes, fever, leukocytosis, cranial neuropathy, or significant otoscopic abnormalities. Markedly elevated inflammatory markers may provide an important diagnostic clue when systemic signs are absent. SBO may mimic skull-base malignancy, making complementary CT and MRI essential. CT is particularly useful for demonstrating cortical bone destruction, while MRI better delineates marrow, soft-tissue, and intracranial involvement. Pseudomonas aeruginosa is a common pathogen, although microbiologic confirmation may be absent, particularly after prior antimicrobial exposure. Prolonged antimicrobial therapy remains the cornerstone of treatment, with duration individualized according to clinical response and serial inflammatory markers.

Conclusion

Persistent otalgia or headache with markedly elevated inflammatory markers should prompt consideration of SBO even in nondiabetic, afebrile patients with normal leukocyte counts and relatively benign ear examinations. Early CT and MRI, combined with multidisciplinary evaluation, are critical for identifying central and intracranial extension and guiding treatment before neurologic complications develop