Pathological findings associated with AOM demonstrate inflammatory changes in the lining of the middle ear as well as suppurative exudates in the middle-ear cleft. The quantity of the exudate increases with time and exerts pressure on the tympanic membrane. The bulging tympanic membrane may rupture spontaneously in the central or marginal portions. Marginal perforations are more likely to lead to ingrowth of skin and the formation of a secondary acquired cholesteatoma. Primary acquired cholesteatomas arise in retraction pockets of the tympanic membrane that are induced by eustachian tube dysfunction. Cholesteatoma can also arise from congenital or traumatic implantation of skin into the middle ear as well as from abnormal changes in the middle-ear mucosal lining in response to inflammation.

Suppurative AOM persisting beyond 2 weeks can initiate the development of acute coalescent mastoiditis. The progressive thickening of the mucosa of the middle ear begins to obstruct the drainage of mucopus through the eustachian tube. Stoppage of blood in the veins and the high acidity of that blood promote demineralization and the loss of bony partitions. As a consequence, separate air cells of the mastoid coalesce into large cavities filled with mucopurulent secretions and thickened mucosal granulations. The erosion of bone, however, may not be confined to the air cell partitions within the mastoid bone. Other portions of the temporal bone including the posterior wall of the external canal, the mastoid cortex, and the thin, bony plates separating air cells from the sigmoid sinus and dura may likewise be eroded. Extension of the infection beyond the mucosal lining of the middle ear and mastoid air cells may produce an intracranial complication, generally by passage of the infection along preformed bony pathways or through inflamed veins in intact bone.

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