The basic pathophysiologic mechanism of otitis media with effusion (OME) or chronic otitis media (COM) is impaired ventilation of the middle ear cavity and mastoid air cells usually caused by Eustachian tube dysfunction secondary to swelling of the nasal mucosa or mucous stasis around the pharyngeal orifice of the Eustachian tube (1). Conventional treatments for OME or COM include myringotomy, insertion of a tympanostomy tube, administration of antibiotics or ear surgery in advanced cases (2).

Eosinophilic otitis media is characterized by extreme viscous mucoid effusion containing eosinophils and is associated with a history of adult bronchial asthma and nasal allergies (3). EOM is typically intractable to conventional treatments for OME or COM, and there is no effective treatment except for systemic administration of steroids in cases of EOM. However, most patients with EOM are treated for COM for a prolonged period of time by therapies such as tympanoplasty or mastoidectomy for EOM, usually induce deterioration of hearing symptoms (2). Therefore, accurate diagnosis and treatment are necessary in order to avoid inadequate treatment and severe complications such as deafness.

To our knowledge, the imaging findings of EOM of the temporal bone have rarely been reported in the literature (4). We present imaging findings of pathologically confirmed EOM in two patients and review this recently described disease entity.

EOM is a relatively rare, intractable disease characterized by the presence of a highly viscous yellow effusion with extensive accumulation of eosinophils in the middle ear (5). The mechanism underlying ear damage caused by eosinophilic inflammation is still unclear. On physical examination, most EOM patients show a patulous Eustachian tube rather than tubal stenosis, which is different from OME or COM. Iino et al. suggested that in patients with T helper type 2-dominant predisposition, such as bronchial asthma, an antigenic material may easily invade via a patulous Eustachian tube and stimulate inflammatory cells, thus resulting in the accumulation of eosinophils and further inducing fibroblasts or endothelial cells to produce eosinophil chemoattractants (2). The cytotoxic proteins and active oxygen species generated by eosinophils may damage the epithelial layer, including the round window membrane, and lipid mediators released from eosinophils render the membrane permeable. These events allow inflammatory substances such as bacterial toxins and inflammatory cytokines to enter into the middle and inner ear, thus resulting in ear damage. Therefore the systemic or topical glucocorticoid is believed to be the most effective treatment for EOM (2).

Nagamine et al. (5) revealed that the pharyngeal orifice of the Eustachian tubes was not markedly edematous and that the Eustachian tube dysfunction was not always obstructive but sometimes patulous in EOM patients. A middle-ear condition for EOM could be an eosinophilic inflammation of the middle ear, itself, rather than that caused by secondary allergic inflammation of the nose. Based on these observations, Iino et al. (6) proposed the diagnostic criteria of EOM in 2011; a patient who shows OME or COM with eosinophil-dominant effusion (major criterion) and with two or more among the highest four items (minor criteria): highly viscous middle ear effusion; resistance to conventional treatment for OME association with bronchial asthma; and association with nasal polyposis.

In our two cases, the symptoms, including persistent otorrhea and progressive hearing disturbance, were initially misdiagnosed as COM. However, the histopathological findings of these lesions showed chronic inflammatory infiltration with numerous eosinophils. They also had bronchial asthma and chronic recurrent sinusitis. From a retrospective review of TBCT in the present cases, we could see an unusual large polypoid mass bulging from the inflamed middle-ear cavities, similar to that seen in the sinonasal cavities. Furthermore, in the second case, we could see that the lumina of the bilateral Eustachian tubes were clearly traced on serial images, which are not commonly observed findings in usual OME or COM patients with paranasal sinus inflammation.

The prospective radiologic diagnosis of the eosinophilic otitis media is nonetheless difficult, probably because of the rarity of this lesion and the few cases studied with CT or MR imaging described in the literature, which may lead to an erroneous preoperative diagnosis of EOM. On a CT scan, image findings of EOM might be similar to COM, with heterogeneous soft tissue within the middle ear and mastoid, with or without minimal erosion of the ossicles. However, there are some findings providing clues for differentiating EOM from COM on CT and MR images. EOM shows higher incidences of bilaterality and chronic rhinosinusitis. Also, it can be accompanied by the patulous Eustachian tubes distinctively. We consider these collective findings as helpful imaging criteria to suggest a diagnosis of EOM on TBCT, but these findings should be verified in a larger study. Although cholesteatoma, keratosis obturans, or medial canal fibrosis involving the external auditory canal could be considered as part of the differential diagnoses, they can be differentiated from EOM by the presence of bony erosion or predominant involvement of external auditory canal.

Iwasaki et al. (4) reported an EOM patient who had noted sudden bilateral deafness and vertigo. In that case, TBCT performed after the systemic steroid demonstrated ossification of the cochlea at the symptomatic side. They speculated that the accumulation of activated eosinophils induced by mastoid surgery may increase the susceptibility of the infiltration of protein associated with tissue damage to the round window membrane. Therefore, they suggested that tympanoplasty and mastoidectomy should be contraindicated for eosinopilic otitis media.

In the EOM patient who suffered from severe chronic recurrent otitis media with eardrum damage, even tympanoplasty can make the disease worse. Although the exact mechanism has not yet been elucidated, Tomioka et al. reported a patient who finally became deaf in both ears several years after ear surgery. A multi-institutional study showed a significantly higher ratio of deafness among patients s compared to those without tympanoplasty (17% vs. 4%, p < 0.05) (4). Therefore, adequate diagnosis and treatment are necessary in order to avoid severe complications such as deafness.