1

Introduction

NOE may present with a variety of clinical findings. The most common symptoms are purulent otorrhea and exquisite otalgia resistant to analgesics . Cranial nerve palsies can occur if the infection spreads to the skull base . Diabetics are susceptible to microangiopathy that dulls pain perception thus predisposing them to “silent” disease. We present a case of aggressive NOE complicated by otomastoiditis, dural sinus thrombosis, and Bezold’s abscess in a nontoxic appearing diabetic patient initially diagnosed with otitis media and a unilateral facial nerve palsy.

2

Case report

A 74-year-old man was transferred to our facility with left facial paralysis and a painful, draining left ear. He presented to his PCP with otalgia and facial droop six weeks prior and was treated with systemic and topical antibiotics, antivirals, and steroids for suspected otitis media and Bell’s palsy. Despite treatment, his pain progressed to involve the left post auricular area and neck. He also developed decreased hearing on the left. He denied changes in vision or facial numbness. His past medical history is significant for poorly controlled diabetes mellitus type II with a HbA1c of 9.4% and a 30 pack year history with cessation 30 years prior.

On presentation, he was afebrile and nontoxic appearing. WBC count was 14.4×10 ⁹ /L. Physical exam revealed moderate tenderness with manipulation of external ear and palpation of mastoid bone, though the patient had received morphine which could confound the degree of tenderness. He had House–Brackmann grade 6/6 left facial nerve palsy in all branches. Remainder of exam was within normal limits.

Contrast enhanced CT (CECT) scan of the temporal bones revealed complete opacification of the left external auditory canal, middle ear cavity, and mastoid air cells ( Fig. 1 ). There were associated extensive osseous erosion and sclerosis of the middle ear cavity and the mastoid compatible with otomastoiditis and superimposed osteomyelitis resulting in dehiscence of the tympanic and mastoid segments of the left facial nerve ( Fig. 2 ). An adjacent subperiosteal fluid collection extending from the mastoid tip to the sternocleidomastoid muscle was identified, consistent with a Bezold’s abscess ( Fig. 3 ). There were also marked soft tissue edema and fat stranding narrowing the distal cervical and proximal petrous segments of the left internal carotid artery. Acute venous thrombosis of the lateral left transverse and sigmoid sinuses and left jugular bulb was also identified ( Fig. 4 ).

Axial CT in bone window demonstrates complete opacification of the left external auditory canal and the left middle ear cavity.

Coronal CT in bone window demonstrates marked erosion along the left stylomastoid foramen, along the course of the facial nerve. The normal right stylomastoid foramen is shown for comparison.

CECT of the temporal bone demonstrates a peripherally enhancing hypodense fluid collection inferior to the left mastoid tip extending into the sternocleidomastoid. On the axial image, the fluid collection, soft tissue edema, and fat stranding extend into the carotid space.

Axial CECT demonstrates a filling defect without opacification in the expected location of the left sigmoid sinus and jugular bulb.

He was taken to the operating room for a left tympanomastoidectomy, drainage of mastoid tip abscess, and decompression of the facial nerve, which showed no evidence of stimulation up to rates of 2 mA. The facial nerve appeared to be atrophied at the time of decompression. Gross examination revealed inflamed granulation tissue filling the middle ear, facial recess, and around the mastoid tip. Histopathology of scrapings from the mastoid and external auditory canal demonstrated fragments of bone with extensive acute inflammation, fibrinous exudate, and micro abscess formation.

Final pre-operative and intra-operative cultures of the aural discharge revealed Pseudomonas aeruginosa sensitive to ciprofloxacin. He was placed on six weeks of oral ciprofloxacin and three months of anticoagulation. Follow-up EMG and physical exam one month later demonstrated persistent severe left facial nerve weakness with left eye ectropion, and the patient subsequently underwent a left lateral tarsal strip procedure.

The patient presented again with increasing left ear, posterior neck, and shoulder pain despite completing the antibiotic course. CT of the temporal bones demonstrated new, frank osseous destruction of the left clivus, jugular tubercle, and surrounding the hypoglossal canal, consistent with central skull base osteomyelitis ( Fig. 5 ). There were also phlegmonous changes of the retropharyngeal and parapharyngeal deep neck spaces without a drainable abscess. Additional imaging did not identify abnormal intracranial, dural, or parenchymal enhancement. Given a lack of systemic infectious findings and normal serum inflammatory markers, the presentation was most consistent with chronic skull base osteomyelitis and neuropathic pain. The patient was started on Neurontin and planned for close follow-up with repeat lab work and CT temporal bones.

CECT of temporal bone shows abnormal enhancing soft tissue within the left parapharyngeal and retropharyngeal spaces which also extends into the left hypoglossal canal and marginates the left aspect of the central skull base.

Two weeks later, the patient presented back with increasing pain. A repeat CT scan now showed a fluid collection in the nasopharynx. The patient was taken to the operating room for a transnasal drainage of the abscess. This abscess also grew out Pseudomonas . The patient was continued on intravenous antibiotics per the infectious disease service, and remains stable with less pain.