Necrotizing Otitis Media Research Articles

Sulfur hexafluoride therapy.

After almost 40 years of experience with antibiotics, treatment of otitis media (which, in the preantibiotic era, was the most common suppurative head and neck infection) still occupies the single largest time effort of the otorhinolaryngologist.1However, the type of fluid and the nature of the complications have changed substantially. Instead of doing myringotomies and mastoidectomies to drain purulent fluid, we are doing myringotomies and inserting tubes for removal and prevention of serous and mucoid effusions. Ironically, some physicians have postulated that the apparent current increase in the prevalence of secretory otitis media is the result of the widespread use of antibiotics. Thus, in controlling one problem it would seem that we have exacerbated another. Few would argue that society is not better off, however, because death from otitis media is now virtually unknown, and necrotizing otitis media is rarely observed. Nonetheless, it would seem that the proportion of

Some observations on the pathogenesis of middle-ear cholesteatoma.

The widespread use of chemotherapy and antibiotics has modified considerably the general picture of middle-ear cholesteatoma. Cholesteatoma which originates by immigration of epidermis through a marginal or total perforation of pars tensa after necrotizing otitis media, as substantiated by Habermann¹and Polvogt,²has been greatly reduced, while the incidence of attic cholesteatoma has shown no definite decrease. The origin of attic cholesteatoma has not been agreed upon in spite of extensive clinical and histopathologic studies. The evidence presented by various sources supports the theory of several origins. No single explanation has been adequate to account for all types which have been examined histologically or observed clinically. The current theories may be summarized as follows: Epidermoid theory. This theory assumes the inclusion during embryonic life of fetal epidermal cells. McKenzie³argued that all middle-ear cholesteatomas are primarily epidermoids of the same nature as the intracranial cholesteatoma of Johannes

Aural changes in the embryo of diabetic mother.

Discussion on the combination of diabetes with ear disease is 100 years old. In his historical survey Lederer (1926) mentioned Jordão as the first to have published, in 1857, a case history of diabetes accompanied by deafness. Leaving aside considerations as to the eczematous and other skin conditions in the external auditory canal that are frequently found in diabetes, these hundred years have seen great variations in the manner in which the topic has been handled. The first symptoms to attract attention were deafness and dizziness. During the period of great and rapid advance in temporal bone surgery the interest switched to diseases of the middle ear and their complications, and the destructions caused by diabetes were recognized as of a particularly vicious nature (the "diabetic, necrotic otitis media" of the textbooks). Lately, sulfonamides and antibiotics have reduced the destructivity of the inflammatory process, and insulin has taken over control

ACUTE DEAFNESS IN SCARLATINA

IT IS AN old experience that occasionally a child with scarlatina may become acutely deaf and eventually deaf-mute. The acute deafness in these instances is thought to be caused by purulent panotitis or, according to the observations of Wittmaack, 1 by neuritis of the cochlear nerve. Manasse 2 was the first to emphasize that acute deafness in scarlatina may be caused by diffuse purulent labyrinthitis on one side and serous labyrinthitis on the other. In the case of Manasse 2 there was necrotic otitis media on both sides, which had caused diffuse purulent labyrinthitis on the left, and on the right, localized purulent labyrinthitis in the round window; this, in turn, had caused diffuse serous labyrinthitis. This type of serous labyrinthitis has been called secondary by Ruttin 3 because it originates from localized purulent labyrinthitis. It must be distinguished from induced diffuse serous labyrinthitis, in which there is no purulent