Relationship between mastoid pneumatization and middle ear barotrauma in divers

OBJECTIVES/HYPOTHESIS: Previous studies have shown a relationship between eustachian tube function and size of mastoid pneumatization, as well as eustachian tube function and middle ear (ME) barotrauma. The purpose of this study is to investigate a possible relationship between size of mastoid pneumatization and ME barotrauma in sports scuba (self-contained underwater breathing apparatus) divers. STUDY DESIGN: Prospective, blinded. MATERIAL AND METHODS: Twenty-four sports scuba divers (48 ears), who were fit to dive in the predive and otolaryngologic examination, were included in the study. Size of mastoid pneumatization was measured by simplified rectangular dimension method on a mastoid x-ray taken at Schüller's view. Divers were counseled to refer to the investigators if any symptoms occurred during and/or after diving. All symptomatic ears were examined within 24 hours of diving by the same investigator, who was blinded to the degree of pneumatization. RESULTS: ME barotrauma occurred in 15 ears (31%) of 11 divers (46%) at one time or another. The median degree of pneumatization in ears with barotrauma (22.9 cm2) was significantly smaller than that in unaffected ears (34.1 cm2; (P <.001). Furthermore, findings showed that with increasing degree of pneumatization, there was a decreasing risk of symptomatic barotrauma (P <.001). No barotrauma occurred in ears with a pneumatization greater than 34.7 cm2. However, barotrauma occurred in all 3 ears with a pneumatization degree smaller than 13.6 cm2. CONCLUSION: Our findings indicate an inverse relationship between size of pneumatization and risk of symptomatic ME barotrauma in sport scuba divers.     

The correlation of middle ear aeration with mastoid pneumatization

Summary Atelectatic 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.     

Relationship between severity of middle ear mucosal lesion and middle ear pneumatic space volume in patients with otitis media with effusion.

If we assume that the state of suppression of pneumatic cells is the result of suppression of pneumatic cell growth by inflammatory stimulation in the middle ear pneumatic space, it is possible to improve the state of suppression by performing sufficient treatment during the growth period of the pneumatic cells. We indwelt a tympanic membrane ventilation tube (hereinafter referred to as tube) for treatment of otitis media with effusion (OME) in child patients aged 3-13 years and investigated the following points: i) relationship between the severity of inflammation of the lamina propria of middle ear mucosal specimens (hereinafter referred to as lamina propria) collected at the time of tube indwelling and the degree of growth of the pneumatic space; and ii) changes in the pneumatic space associated with treatment by tube indwelling, which was studied by comparing the above-described mucosal severity with the pneumatic space area of 2 years after tube indwelling, and with increase in the pneumatic space volume measured periodically after tube indwelling. The results indicated that mastoid cell growth suppression is higher in patients with a higher degree of inflammatory changes in the lamina propria. In association with treatment by tube indwelling, effusion accumulated in the pneumatic space and mucosal swelling disappeared early after the treatment, or 2 months of tube indwelling. After that, in patients with severe mucosal lesion, a long time, 1.5-2 years, was found to be required for repneumatization accompanying regrowth of the temporal bone. We confirmed that the severity of inflammation of the lamina propria is deeply involved in the growth and repneumatization of the pneumatic cells.     

Pseudoepitheliomatous hyperplasia of the external ear,middle ear,and mastoid

A case of pseudoepitheliomatous hyperplasia involving the external, middle ear, and mastoid air cells and labyrinth resulting from long standing irrigations with alcohol is described for the first time.     

Effect of middle ear infection upon the pneumatization of the mastoid: An experimental study in pigs

The suppression of the temporal bone's pneumatized cavities is commonly observed in chronic middle ear inflammatory disease, but this fact has not been explained in respect to its etiology, i.e., whether the poorly pneumatized cavity induces chronic middle ear infection or middle ear inflammatory condition suppresses the pneumatization of cellulae. We studied the effect of middle ear infection and eustachian tubal dysfunction in the early stage of life upon the development of pneumatization of the mastoid using 13 pigs, whose mastoid is comparable to that of man. We used two methods, the eustachian tube stenosis test and the tympanic membrane paraffin infusion test. The present study indicated that in six pigs infection of the middle ear in the early stage of life suppressed the normal development of pneumatization of the mastoid bone in pigs.     

Effect of middle ear infection on pneumatization and growth of the mastoid process. An experimental study in pigs

The intention of this experiment was to investigate whether anatomical variations of the temporal bone such as low middle fossa dura, anterior position of the sigmoid sinus or small mastoid process, which are often seen at surgery in cholesteatoma patients, are caused by inflammation in early childhood. In 7 pigs, 1.5 ml paraffin liquid were instilled into the left tympanic cavity 2 or 7 days after birth in order to produce inflammation of the middle ear and tubal dysfunction. After six and a half months the length and area of the mastoid process were significantly smaller on the left instilled side than on the right, normal side. In all cases there was remarkable hypocellularity and increased thickness of the cortical bone strongly supporting the environmental theory of pneumatization that inflammation suppresses the pneumatization process and growth of the mastoid process.     

Adenomatous tumors of the middle ear and mastoid

Three cases of middle ear and mastoid neoplasms are reported as “adenomatous tumors” since in their search of the literature the authors did not find any previously described lesions with a similar histologic appearance and benign biologic behavior. Microscopically, all three tumors are similarly composed of solid cords and nests of closely-packed small cells having an epithelial appearance. Two distinct cell types are present: cuboidal cells, arranged in a rudimentary gland-like pattern, and angular cells forming irregular nests with no distinct pattern. All three tumors developed in patients in their 20′s, over a period of months with minimal symptoms; yet in all of the lesions the tympanic membrane was intact at the time of initial examination. None of the neoplasms was diagnosed preoperatively, and, once removed, all three tumors were pathologic enigmas and therapeutic problems in view of the initial and subsequent consultant pathologic opinions; nevertheless, total local excision with preservation of the tympanic membrane would appear to be safe treatment in these cases. The term “adenomatous tumor” is applied to these three neoplasms because: 1. a true glandular epithelial origin warranting the term adenoma or adenocarcinoma cannot be proven; and 2. the biologic behavior and prognosis is not necessarily reflected by the histologic appearance. A more specific term reflecting the origin and behavior of these tumors does not appear possible without the study of further cases.     

Adenomatous tumors of the middle ear and mastoid

Adenomatous tumors of the middle ear and mastoid have been called adenoma or adenocarcinoma. The clinical and pathologic distinction between the two has been difficult. The resultant pathologic ambiguity makes it difficult to decide whether conservative or radical management is appropriate. The Otologic Medical Group's (OMG) experience with glandular tumors of the middle ear and mastoid over the past 27 years was reviewed. Thirteen cases were found and analyzed with respect to signs and symptoms at presentation. Extensive histopathologic review with light and electron microscopy was performed on tumor specimens. Two distinctive histopathologic and clinical patterns were identified. The mixed type of tumor was always confined to the middle ear and mastoid, was commonly misdiagnosed as chronic otitis media, and rarely demonstrated otic capsule or facial nerve involvement. The papillary pattern always had extension to the petrous apex and frequently involved the middle and/or posterior cranial fossa. Papillary tumors were more frequent in females and usually involved the facial nerve. On the basis of the findings in this review as well as information from the literature, we have come to the following conclusions: 1. The correct general pathologic heading be Adenomatous Tumors of the Middle ear and Mastoid with each tumor then being subclassified into Mixed or Papillary tumor and adenocarcinoma when warranted by histology. 2. There is a high rate of local recurrence. 3. Long-term follow-up (at least 10 years) for all adenomatous tumors is necessary. 4. Primary surgical treatment is required.