The middle ear space is connected to the upper part of your throat. The openings are just about three-quarters of an inch behind your upper wisdom teeth. The tubes between the middle ear and the upper throat are called Eustachian tubes, and they are normally closed. They open whenever we swallow or yawn. When you go over a hill in a car, your ears develop pressure and you need to pop them. When you go up a long hill you move from an area of high pressure to an area of low pressure and visa versa down hill. Moving uphill you have developed a partial vacuum in the middle ear which gives you the sensation that you need to “pop” them.  


Eustachian tube dysfunction

Eustachian tube dysfunction, either extrinsic (from the outside) or intrinsic (from the inside), is regarded as the underlying event that leads to most cases of chronic middle ear disease. What is it about the Eustachian tube  that becomes dysfunctional? Certainly ciliary dysmotility, nasopharynx carcinoma, cleft palate, gastro esophageal reflux and adenoid hypertrophy have all been implicated, but for only a small minority of patients. Most of these are permanant, static conditions and other than reflux, only allergy can account for the intermittent nature of ET function and dysfunction as documented in OME patients.

The symptoms of OME are due at least in part to both inflammation of the middle ear mucosa and/or to eustachian tube obstruction (dysfunction) with failure to ventilate the middle ear. This is caused by allergic reactions, and local inflammation associated with persistence of pathogenic bacteria or bacterial components.[83]  Bluestone[24]outlined four hypothetical mechanisms by which allergy could be responsible for the Eustachian tube  dysfunction leading to the production of OME. These included: (1) the middle ear functioning directly as a “shock organ,” (2) Eustachian tube dysfunction due to intrinsic mechanical obstruction from inflammatory swelling of the ET itself, (3) inflammatory obstruction of the nose, or (4) aspiration of bacteria-laden allergic secretions from the nasopharynx into the middle ear. All have been shown to occur as the result of allergy.

Obstruction of the Eustachian tube in humans has been clearly demonstrated to result from antigen challenge.[78,79,80]The ET has been shown to be involved functionally and morphologically in Type I allegic reactions of the nose.[81] Friedman[82] used a double-blind protocol to show that a provocative intranasal pollen challenge of atopic individuals produced allergic rhinitis followed by Eustachian tube  obstruction. Placebo patients did not obstruct. He demonstrated that allergic reactions in the nose and nasopharynx inhibit even transient dilations of the Eustachian tube during  swallowing. Double-blind protocols have shown that provocative intranasal challenges with allergens or histamine produce severe functional obstruction of the Eustachian tube.[30,80,81,83]

All this confirms the hypothesis that the Eustachian tube may become “dysfunctional” due to allergic inflammation causing intrinsic mucosal edema and obstruction. Skoner’s review(2003) states that “much of the research into OM pathophysiology has indicated that there is a pivotal role for allergen-induced dysfunction of the Eustachian tube… Allergen-induced blockage subverts the normal mechanism of gas exchange between the middle ear and the environment, thus setting the stage for development of middle ear underpressured OME.”[43]

The most frequently cited objection of past decades to the allergy hypothesis is that an allergen is unlikely to get into the middle ear itself due to the structural gatekeeper function of the E.T.[83,84]Possible mechanisms of  immune response in the ear have been proposed. Secretory immunity does not rely on the premise of direct allergen transport to the middle ear, but rather are dependent on our newer understanding of both humoral and cell mediated immunology. These concepts are best explained under the heading of the “Unified Airway.”

Evidence based medicine proves that various well established past explanations for chronic OME are myths. It has been shown that “there are no substantial differences in Eustachian tube function between ears that develop OME recurrence and ears that do not.”[85]It is also a commonly held myth that the Eustachian tube will grow to normal size as children mature despite evidence that there is no difference in the size of either the isthmus or pharyngeal portion of the Eustachian tube  in children with OME vs. normals.[86]Sade showed that the Eustachian tube  of otitis patients do not have an “immature morphology.” Parents are also falsely told that their otitis prone child cannot equalize the pressure in his middle ears, yet the fact is that there is no organic obstruction or stenosis of the Eustachian tube  in OME patients. Only 11% of active OME patients have abnormally high opening pressures.[87]Finally, there is the myth of antibiotics. Rosenfeld and Bluestone[88]have shown that meta analysis of all treatment studies demonstrate antibiotics to be no better than placebo in treating chronic OME. Chronic otitis media with effusion is not an infection.

The bottom of the eustachian tube can also be obstgructed by adenoids sitting in the back of the nose. Adenoidectomy must also be considered as a treatment for OME.