Case report of high-dose ceftazidime in an 84-year-old man with skull base osteomyelitis and type 1 diabetes

BackgroundSkull base osteomyelitis (SBO) is an uncommon but life-threatening complication of necrotising otitis externa, typically affecting older adults with diabetes. Presentation is often non-specific, and diagnosis is frequently delayed.CaseAn 84-year-old man with type 1 diabetes, vascular comorbidity and advanced frailty presented with a fall preceded by dizziness on standing. He reported a 6-month history of recurrent falls and severe postural light-headedness; persistent right-sided otalgia and offensive otorrhoea had been present for the preceding 3 months, indicating that the ear symptoms followed the orthostatic symptoms. On admission, he had marked postural hypotension despite withdrawal of potentially contributory medication and initiation of fludrocortisone. Initial CT brain imaging was normal, and the sepsis screen was inconclusive. Ten days after admission, he developed a new right-sided facial palsy. Repeat CT head was again unremarkable. Shortly afterwards, he had profuse bleeding from the right ear. Otoscopy, performed for the first time in hospital by an otorhinolaryngology specialist, showed florid otitis externa with a polypoid lesion in the external auditory canal. MRI with skull base sequences revealed extensive necrotising otitis externa with right skull base osteomyelitis extending towards the carotid canal, while CT venography later showed adjacent inflammatory change around the petrous internal carotid artery. Ear swab culture grew Pseudomonas aeruginosa sensitive to gentamicin and intermediately sensitive to ceftazidime. High-dose intravenous ceftazidime (2 g three times daily) was started shortly after diagnostic MRI, microbiological sampling, and infectious diseases review, approximately 10 days after admission, and was continued for approximately 7 weeks. Inflammatory markers normalised, and repeat swab cultures were negative. However, follow-up MRI demonstrated partial resolution of the primary osteomyelitis focus with extension into the temporomandibular fossa. Severe postural hypotension persisted despite withdrawal of potentially contributory medication, together with non-pharmacological measures and fludrocortisone. The patient became increasingly deconditioned and bed-bound, developed prolonged delirium and stage 3 acute kidney injury, and died in hospital.ConclusionThis case highlights skull base osteomyelitis as an important differential diagnosis in older, frail patients with diabetes who present with chronic ear disease, cranial neuropathy and otherwise unexplained refractory orthostatic hypotension. In this patient, inflammation adjacent to the carotid canal/carotid sinus region may have contributed, although causality could not be proven, and alternative contributors to autonomic dysfunction remained possible.