Concerning clinical findings,severe otalgia was seen in all patients whereas otorrhea in 90%, trismus in 6,4%, peripheral facial palsy in 6,4%, abducens palsy in 1 case (3,2%).

For imaging findings in our study, external auditory canal filling was the most frequent lesion (96%), then, bony tympanal and mastoid destruction in 30,7%, temporo mandibular articulation extension (11,5%), deep face spaces extension (15,5%), retropharyngeal abscess (3,8%), skull base osteitis (19,4%), third portion of the facial nerve canal destruction(3,8%), vascular thrombosis (15,2%).

Scintigraphy was positive in all cases. It shows increased uptakein the mastoid and temporal bone.

P. aeruginosa is by far the most common cause of necrotizing otitis externa, especially in patients with diabetes. Microbiology test isolated it in 77,4% of cases.

Discussion:

Typical patients suffering from necrotizing otitis externa are elderly who have diabetes and severe unremitting otalgia, aural fullness, otorrhea, and hearingloss.

Physical examination reveals purulent otorrhea with a swollen, tender external auditorycanal. Skin of the concha may be erythematous and tender. Granulation tissue orexposed bone is frequently seen on the floorof the canal at the bony–cartilaginousjunction.

The initial manifestations of necrotizing otitis externa can mimic those of otitis externa, and clinicians must be aware of this possibility in the high-risk host.

The diagnosis of necrotizing otitis externa relies on specific elements of the history and physical examination, laboratory tests and imaging studies.

Imaging studies include computed tomography (CT), magnetic resonance imaging (MRI) and bone scans.

CT is sensitive in diagnosing bone erosion and decreased skull base density, a later finding in necrotizing otitis externa. It is also sensitive in diagnosing abscess formation, and involvement of the mastoid, temporomandibular joint, infratemporal fossa, nasopharynx, petrous apex, and carotid canal.

The earliest finding is nonspecific soft tissue swelling within and around the EAC. In the next stage of the disease, bone will be demineralized at the petrotympanic fissure, correlating with the clinical tendency for granulation tissue to accumulate at the bony cartilaginous junction and then infiltrate medially along the tympanic bone to its juncture with the petrous portion. Erosion along the walls of the EAC and into the mastoid air cells is a relatively less common initial spread pattern. Later-stage disease will spread along the periosteal surfaces of the mastoid and petrous portions of the temporal bone, usually following the eustachian tube, to the petrous apex and posterior skull base, frequently reaching the clivus and at times crossing to the other side. Frank subperiosteal or other abscess formation is possible but only rarely presents. When present, it may suggest an etiology other than pseudomonas or a superimposed second bacterial infection with a more pyogenic organism. The surrounding cellulitis at the skull base may be very extensive.

Intracranial spread is a very late stage of the disease and not commonly encountered, as antibiotics effective against pseudomonas have been introduced.

MRI better shows changes in soft tissue, particularly dural enhancementand involvement of medullary bone spaces.

Tc 99m scintigraphyallows earlier diagnosisof osteomyelitis than CT.

Complications result from contiguous spread to nearby structures. Spread to the stylomastoid foramen results in facial nerve palsy. Less commonly, the involvement of the jugular foramen results in palsies of the glossopharyngeal, vagus, and accessory nerves. Septic thrombophlebitis of the internal jugular vein and of the sigmoid sinus may occur. Intra­cranial extension can result in meningitis, cerebral abscess, or dural sinus thrombosis, all of which presuming a poor prognosis