The diagnosis of MEO is based on clinical and laboratory evidence along with heightened suspicion of the physician. But there is no absolute diagnostic criteria. However, cohen and Friedman 6 proposed diagnostic criteria by developing obligatory and occasional caregories. The major obligatory criteria includes pain, exudate, oedema, granulation tissue, microabscess, positive technitium-99 scan or the failure of local treatment after more than 1 week and the presence of Pseudomonas auregenosa. The minor occasional criteria includes positive CTscan tomography, oldage,cranial nerve palsy, diabetes mellitus or other debilitating conditions. In the absence of otologic complaints and findings SBO may be difficult to diagnose. Isolated case reports have been published that review SBO without any history of ear infection. The clinician must be aware of any prior history of MEO despite having received successsful treatment as the classic presentation in these cases is that patient leaves the hospital completely asymptomatic only to return 4 to 7 weeks later with the onset of low grade fever, malaise and a unilateral unremitting headache that requires narcotic analgesic. It has also been reported that SBO can develop nearly one year after resolution of MEO 1. MEO s not unique to elderly diabetic patients alone but few cases are reported in paediatric population also with Pseudomonas aeurogenosa 13 and Proteus mirabilis 7 infection. Disorders other than DM associated with MEO in children are anemia, malnutrition, S.J. Syndrome, lG deficiency 8 and agranulocytosis. It is proposed that the medial location 12 of the bony cartilagenous Junction in infants and children account for earlier compromise of Facial nerve and mastoid.
The importance of staging for OSB is to alert the clinician that certain diagnostic tests are necessary to determine the presence and extent of the disease. Baseline CT and radionucleide scans will attempt to differentiate NOE from MEO and SBO. Gallium-67 scanning identifies inflammation if immunocompetent white cells are present and functioning. The technitium – 99 bone scan reflects the increased osteoblastic activity which is indicative of Osteitis and osteomyelitis. A three level staging is proposed by Benecke 3. Stage I or NOE is limited disease in the soft tissue without bone involvement where as Stage II describes MEO in which the disease is limited to the mastoid and is the earliest form of SBO with positive gallium and technitium scan. Finally State III is extensive SBO with markedly positive gallium and technitium scan. Another staging system is proposed by Davis 9 based on clinical criteria and prognosis in three stages. A third staging system was proposed by Krum, Rehm and Kenny 16 which describe Stage – I MEO limited to the EAC and mastoid aircells, Stage – II SBO with cranial nerve palsy and Stage – III extension to the brain and meninges. Radiographic and radionucleide including Indium-III play an important role in evaluating, staging and managing MEO and SBO. Sequential imaging is critical in establishing diagnosis, demonstrating extent of the disease, monitoring the efficacy of treatment and determining the duration and end point of therapy.
The complex management of MEO and SBO consists of establishing the diagnosis, determining the extent of the disease, operating when indicated and providing appropriate antimicrobial therapy along with adjuvant therapy till the resolution of the infective process. It is also necessary to correct any metabolic abnormality and maintain glucose levels. The role of surgery is not very well defined except taking biopsy and local debridement of necrotic tissue and drianage of abscess or formal tympanomastoid procedures like MRM or Radical mastoidectomy with partial petrous apicectomy and embolectomy for Jugular vein thrombosis. Farrier 10 proposed planned surgical debridement for persistant pain or failure of the granulation tissue to heal after 2 weeks of I.V. antibiotics. Raines and schindler 26 advocated radical surgery on new onset of cranial neuropathies directly in recalcitrant MEO. Concern exists that surgery may enhance MEO and SBO by opening up facial spaces and new tissue plane with spreading infection. Prolonged anibiotic therapy with third generation cephalosporins has been the principal mean of therapy. Management of MEO and SBO significantly changed in the last decade with the availability of oral fluro-Quinolones like Ciprofloxacin and ofloxacin 29. In a report by Rubinetal 27 patients were cured of MEO with the combination of ciprolfloxacin and rifampicin for 6 to 12 weeks. Oral ciprofloxacin alone in 750 mg BID dose cured 21 out of 23 patients treated by lang 18. Ciprofloxacin given orally for a minimum of 6 weeks to 6 months was successful in patients who failed in conventional combination intravenous therapy Similar efficacy with ofloxacin (200mg) BD given to 17 patients with MEO achieved subjective improvement in all patients with in 6 days and objective improvement within 12 days of treatment 19 20 Despite the reported efficacy of prolonged systemic antibiotic therapy, treatment failure do occur due to tissue hypoperfusion and hypoxia where the use of hyperbaric oxygen (BHO) increases wound PO2 levels, enhances phagocytic oxidative killing of aerobic micro-organisms, promotes angioneogenesis and osteoneogenesis. Treatment consists of 100% O2 given for 90 minutes at 2.5 atm absolute pressure five days a week for 4 weeks as an adjuvant therapy 23.