Jacob Sadé

The metaplastic and congenital origin of cholesteatoma

Nineteen out of 101 biopsies taken from cholesteatomatous ears showed in the subepithelial inflamed connective tissue small or large aggregates of keratin fibres surrounded by special cells. The larger aggregates were similar to epidermoid cysts. All these biopsies also contained mucus glands. The fibres were identified as keratin by their morphological features, birefringence and specific immuno-horseradish peroxidase reaction. The cells surrounding the keratin fibres also stained positive to keratin, suggesting synthesis or phagocytosis. Three ossicles contained the above keratin-containing structures in their vascular spaces. Serial sections excluded any connection of the described keratin and mucus-producing centres with the surface epithelium. We interpret these findings to be an expression of middle ear mucosa metaplasia. Such subsurface squamous and glandular metaplasia does occur frequently on the surface of the middle ear lining, as described previously. Of especial interest is our finding that c...

Secretory otitis media in adults : II. The role of mastoid pneumatization as a prognostic factor

We analyzed clinically 102 ears with secretory otitis media (SOM) belonging to 72 adult patients who during their adult life had not suffered previously from ear disease. As in children, most of the cases (63%) could be traced directly to an upper respiratory tract infection. The most striking finding was the preponderance of poorly pneumatized mastoids—which were measured planimetrically — among our SOM cohort. This was found in adult SOM ears compared to contralateral healthy ears (4.59 versus 7.88 cm2), as well as when all 102 SOM ears were compared with values of the normal population (5.41 versus 12.9 cm2). This study showed that poorly pneumatized mastoids are a significant risk factor as far as adult SOM is concerned.

Atelectatic Tympanic Membrane: Histologic Study

This study aims to elucidate the morphological difference between the noncollapsible physiologic tympanic membrane (TM) and the collapsible atelectatic TM. Histologic examination of atelectatic TMs obtained at surgery from 16 ears revealed inflammatory changes and destruction of the pars tensa collagenous “backbone.” The disappearance of the organized collagenous layer seen in atelectatic TMs explains their conversion from the stiff physiologic membrane to a flexible one. This in turn will convert the middle ear from a noncollapsible gas pocket to a partially collapsible gas pocket, in which minimal pressure of only a few millimeters of water can cause retraction or ballooning of the atrophic TM. These pressure differences are too small to equilibrate automatically the difference created with the atmospheric pressure. Integrity of the pars tensa collagenous layer thus appears to be essential for the proper mechanical functioning of the physiologic TM.

The correlation of middle ear aeration with mastoid pneumatization

SummaryAtelectatic ears, which by definition are poorly aerated, are also usually associated with poor mastoid pneumatization. On the other hand, otosclerotic patients, whose middle ears are usually exceptionally well aerated, also have excellent mastoid pneumatization. Three unusual cases are presented, in which partial atelectasis developed in stapedectomized patients. In each case the mastoid was later found to be nonpneumatized, and further analysis revealed that their stapes fixation had in effect most probably been of non-otosclerotic origin. Thus, although these three cases had at first appeared to represent exceptions to the general rule of otosclerotics having a well-aerated middle ear, in fact they support the association between atelectasis and poor pneumatization. The linkage of good middle ear aeration with large mastoid pneumatization and vice versa may suggest that the mastoid plays a role of a pressure buffer in the middle ear, which is a system of a gas pocket with fluctuating pressures. Also, otosclerosis may be considered to be an unlikely cause of conductive deafness in cases of poor pneumatization.

Dynamic measurement of gas composition in the middle ear. II: Steady state values

On-line measurement of ME gas composition in normal middle ears of 5 anesthetized guinea pigs at an established steady state was performed by mass spectrometry. The mean values for the gas composition of the middle ear were found to be: PN2: 82.4%, PO2: 7.6% and PCO2: 10.0%. This composition is very different from that of atmospheric air, and very similar to the gas composition of mixed venous blood. Our conclusions are that the gas composition is basically controlled by interchange with gases present in the blood and not by introduction of air through the eustachian tube. It is therefore proposed that middle ear gas deficiency is secondary not to eustachian tube input failure but to excess loss of middle ear gas due to enhanced diffusion into the blood. This situation exists especially under inflammatory conditions when there is an enlarged number of blood vessels promoting increased gas diffusion into them. Under ordinary conditions this middle ear gas deficiency will probably cause no significant underpressure because the mastoid pneumatization will act as a pressure buffer. When mastoid pneumatization is lacking, as happens in the otitis media syndrome, a pathological negative pressure will ensue.

Middle Ear Gas Composition and Middle Ear Aeration

Partial pressures of the gases in the middle ears of 14 guinea pigs were measured continuously on-line with a specially designed mass spectrometer. The average values were carbon dioxide 67.55 mm Hg, oxygen 48.91 mm Hg, and nitrogen 596.54 mm Hg. These values confirm earlier measurements and show that the gas composition of the middle ear differs basically from that of air and resembles that of venous blood. These findings are indicative of bilateral diffusion between the middle ear cavity and the blood. We propose that under physiologic as well as under pathologic (ie, atelectatic) conditions, the gas content of the middle ear is also controlled by diffusion. This mechanism fits well with the fluctuating character of atelectatic ears. Thus, a negative middle ear pressure could be secondary to excessive loss of gases through increased and excessive diffusion, although additional mechanisms are probably also involved. A likely contributing factor is poor pneumatization of the mastoid, with consequent absence of a physiologic pressure regulation mechanism by its pneumatic system.

Cellular Differentiation of the Middle Ear Lining

Mucus and keratin, two completely different proteins, are frequently synthesized in the middle ear cleft under pathologic conditions of inflammatory character. Indeed, mucus is found in small amounts in normal ears 14 ,18 but originates in great excess from a larger and new mucus-producing cell population in pathologic ears. 2,5,9 ,19 Stratified squamous epithelium-? (SSE) and keratinized epithelium are the consequence of pathologic phenomena in the middle ear.

Eustachian Tube Lumen: Comparison between Normal and Inflamed Specimens

This study presents measurements of the cross-sectional luminal area of the eustachian tube. Comparisons are made between the lumens of eustachian tubes obtained from temporal bones presenting acute or secretory otitis media and those from noninflamed temporal bones. The material consisted of 71 temporal bones obtained postmortem from individuals up to 2 years of age. Forty-six of these showed no middle ear inflammation, while 25 presented either acute or secretory otitis media. In both groups the lumens of all the eustachian tubes were patent, presenting no obstruction. The mean cross-sectional area of the lumens of inflamed temporal bones was smaller than that of the noninflamed ones. This difference was not found to be statistically significant in the cartilaginous regions and was found to be statistically significant or borderline significant in the bony parts of the eustachian tube.

Gaseous pathways in atelectatic ears.

Thirteen atelectatic ears were politzerized with CO2, O2, air, and N2. In consequence, the atelectasis in these ears disappeared, only to reappear again slowly. The reappearance of retraction corresponded in speed to the diffusion coefficient of the gases, indicating a regular diffusion process. At the same time, four of these politzerized patients were able to collapse the tympanic membrane of their air-filled middle ears abruptly through sniffing or swallowing. At least three patients could introduce air actively and voluntarily into their ears. These observations indicate that in atelectatic ears, as in normal ears, air can enter and leave the middle ear through one of two routes. One is the eustachian tube, through which air can pass both ways as a bolus. The second route is through the bloodstream, which gases enter and leave according to the rules of biologic diffusion. While the origin of negative pressure in atelectatic ears is unknown, this study shows that it may be a complex process stemming from a quantitative imbalance of loss versus gain of gas entry through either of the two routes.

Adenoidectomy in otitis media : a review

For many years adenoids were thought to affect adversely middle ear (ME) aeration by obstructing the eustachian tube opening, leading to ME infections and effusions. Consequently, the adenoids have often been removed in children suffering from ME diseases; indeed, adenoidectomy is still performed around the globe on millions of children annually. Opinions vary, however, on the usefulness of the operation in various ME diseases. The purpose of this study is to review the available studies concerning the relationship of adenoids to the ME as well as the effect and benefit of adenoidectomy on ME effusions and ME infections.