Malignant otitis externa is a severe infection of the external auditory canal and skull base .Chandler (1968) 1st adopted this term to describe a severe progressive form of otitis externa usually occurring in elderly diabetic patients. Zaky et al (1976) found 91 % patients were above 55 years and 93% to be diabetic. It is infrequent, occasionally life-threatening infection caused by Pseudomonas aeroginosa. Periosteum and bone are involved in later stages leading to mastoiditis, osteomyelitis of temporal bone and a spreading osteomyelitis of the skull base. It may spread to soft tissue of the neck and parotid region and involve the temporo-mandibular joint. Facial nerve palsy is a bad prognostic sign, spreading osteomyelitis of the skull base results in other cranial nerve palsies and meningitis. Early diagnosis and aggressive treatment are important in terms of reducing risks of dissemination.

Severe otalgia and persistent ottorhea are the symptomatic hallmark of MEO.It is further confirmed by granulation in EAC and isolation of pseudomonas. Elevated erythrocyte sedimentation rate is the only distinctive laboratory abnormality. The diagnosis is mainly clinical and requires high degree of suspicion. Imaging useful in MOE is CT for exact information regarding the bone involvement, and MRI for soft tissue evaluation. The ESR is an excellent method to follow the response to therapy.

The principle of management is control of diabetes, localized surgical debridement supplemented with long term anti-pseudomonal antibiotics. 2% Acetic acid as ear drops or irrigation has an important role in management of pseudomonas. (Household Vinegar is 6%)

Wherever pseudomonas is suspected 2% Acetic acid locally is used as acidic PH lowers pseudomonas multiplication.

X-rays show lytic changes when significant demineralization occurs and are now of little use because of their limited diagnostic efficiency

CT shows the extent of bone erosion but is not useful in the early stages of the disease because at least 30% of the trabecular bone is lost before being detected. Furthermore, the bone does not remineralize with cure and therefore it cannot be used for assessing response to therapy.

MRI has proved superior to all other imaging techniques concerning the soft-tissues in the neck and skull base area because of the inherent superior contrast and the multiplanar capability. It also has ability to detect bone marrow changes and changes in the surrounding soft tissue, the degree of enhancement after contrast medium administration and the degree of response to therapy.

We have had several patients with MOE in the past that were managed by surgical debridement, 30 to 45 days of IV antibiotics and 2% Acetic acid. The following case is highlighted as he presented with a severe MOE and unstable diabetes mellitus.

A 65 year old diabetic male patient presented with left malignant otitis externa with grade V facial palsy and zygomatic abscess.

Pre op MRI showed left zygomatic abscess with otitis externa. Pus C/s grew Pseudomonas which was resistant to all antibiotics available to us.

Undercover of IV Quinolones he underwent cortical Mastoidectomy, zygomatic abscess drainage with laser canalplasty (removing subdermal dense thick fibrosis causing stenosis) with Tympanoplasty (lateralized tympanic annulus). He had a large seqestrum from the medial aspect of Eustachian tube orifice, which was carefully removed without damaging internal carotid artery. Post-op wound healed well and the graft was taken up. Blood sugar was controlled with insulin; parenteral ciprofloxacin was given for 53 days with topical 2 % acetic acid ear drops.

Post op MRI done 40 days later showed minimal collection which resolved with antibiotic treatment. This resulted in complete resolution of the disease with grade III facial palsy (recovery from G-V to G-III) and healed tympanic membrane.

In conclusion MOE can be successfully managed even in drug resistant pseudomonas.