Tympanoplasty techniques were classically outlined by Zollner (1) and Wullstein (2). Subsequent modifications of Wullstein’s classification have been based on the underlying properties of acoustic mechanics associated with each tympanoplasty type as opposed to classification based on underlying tympanic and ossicular pathology. Understanding this classification system is helpful not only for purposes of grasping a global and historical view of tympanic membrane and ossicular chain reconstruction, but also for understanding basic principles of middle ear acoustic mechanics.

The modern view of middle ear acoustic science involves two basic pathways by which sound is able to stimulate the inner ear (3, 4). The first involves transmission of sound pressure through the tympanic membrane and ossicular chain via the oval window. This is known as ossicular coupling. This mechanism is the primary means by which the state of impedance mismatch that exists between the air in the ear canal (low impedance) and the fluid within the cochlea (high impedance) is overcome. In such a state, sound pressure is deflected during passage through the air-fluid interface, resulting in a loss of gain in the realm of 30 dB. The coupling effect of the tympanic membrane and ossicles almost overcomes this loss.

Ossicular coupling has been attributed to the collective effect of three characteristics of the tympanoossicular mechanism traditionally known as the acoustic transformer theory (5). The first and most significant of these characteristics is the hydraulic lever effect that results from the difference between the surface area of the tympanic membrane relative to that of the oval window (usually a ratio of nearly 21:1). This effect results in compression of sound energy and increase in force at the oval window, equating to a theoretic approximate increase in gain of 26 dB. The second characteristic is the malleoincudal lever effect that results from the difference in length between the malleus manubrium relative to that of the long process of the incus along the axis of ossicular rotation (a ratio of 1.3:1). However, this effect only accounts for an additional 2 dB theoretical increase in gain. The final factor is the so-called catenary lever effect that is generated by the elastic stretching of the tympanic membrane from the annulus to the malleus manubrium—somewhat akin to the stretched strings across a tennis racquet. The specific degree of acoustic benefit derived from the catenary effect is not well understood but probably lies within a range similar to that of the malleoincudal lever.

It is important to recognize that, in reality, ossicular coupling is a much more complex phenomenon than what is suggested by these simplified traditional models as they do not account for factors such as variation in efficiency with changes in frequency or inefficiencies in sound transmission through the tympanic membrane and ossicular chain attributed to the inherent tension or laxity of the ossicular ligaments. Thus, it is perhaps not surprising that the 25 to 30 dB of gain that is predicted by the acoustic transformer theory does not equate well with experimental
measurements, which suggest an actual more modest increase in the realm of just over 20 dB (6, 7, 8).

The second pathway of sound stimulation of the inner ear involves direct passage of sound pressure via the oval and round windows without involvement of the tympanic membrane or ossicular chain. This is known as acoustic coupling (4). Given an intact tympanic membrane and functional ossicular chain, this pathway is of only minor importance. However, in the various conditions of a diseased ear, acoustic coupling can be important. This is why, for example, a conductive hearing loss will be greater in the case of ossicular discontinuity and an intact tympanic membrane (60 dB) compared with ossicular discontinuity and an absent tympanic membrane (40 to 50 dB). With the former, the intact tympanic membrane restricts the acoustic coupling pathway by blocking direct access of sound pressure to the oval and round window membranes.

A final relevant consideration in middle ear acoustic mechanics is that of phase. A sound stimulus to the inner ear is detected as the net difference in sound pressures applied to the round and oval windows that results in movement of intracochlear fluids. If these sound pressures are simultaneously applied to the round and oval windows with equal amplitude and phase, they will counteract each other and no resultant intracochlear fluid displacement will occur. In the normal situation, this does not occur due to the unbalanced selective effect of ossicular coupling upon the oval window, the acoustic shielding effect of the tympanic membrane upon the round window, and the uneven anatomical positioning of the round window versus the oval widow relative to incoming sound. However, when the tympano-ossicular mechanism is absent and acoustic coupling is primarily relied upon (as in the case of a type IV or V tympanoplasty), an unshielded round window can yield significant negative acoustic consequences due to phase cancellation (4).

A simplified chart depicting the theoretic ideal acoustic effects of various tympano-ossicular scenarios is shown in Table 153.1.

When a patient is considered for tympanoplasty or ossiculoplasty, a thorough history, examination, and audiometric evaluation should be performed on both ears. Otoscopy and pneumatic insufflation under the binocular microscope, following careful removal of debris, provide a wealth of information. The results of the audiogram should always be correlated with the physical exam, including Weber and Rinne tuning fork tests, especially when a masking dilemma is present. If the audiogram and tuning fork exam do not agree, surgery should not be performed until this is reconciled.

A preoperative audiogram can be helpful in suggesting underlying pathology. Generally, a perforation will cause a conductive hearing loss between 5 and 40 dB depending on its characteristics (9). Controversy exists as to whether or not the location of a perforation impacts the degree of hearing loss, yet perforation size and underlying middle ear volume do matter (an ear with a smaller volume tends to have worse hearing than one with a larger volume, even given identical perforations).

When the tympanic membrane is intact, a conductive hearing loss greater than 35 to 40 dB strongly suggests the possibility of ossicular chain dysfunction. Furthermore, the pattern of hearing loss may be typical of particular scenarios; for example, ossicular fixation generally causes a low-tone conductive hearing loss, the degree of which is related to the extent and location of the fixation. With malleus head fixation, the low-tone air-bone gap generally closes at the higher frequencies, whereas stapes fixation tends to affect the middle and high frequencies to a relatively greater degree (10).

The status of the eustachian tube will impact surgical outcomes, yet there is no consensus on the optimal way to reliably assess its function (11). Auto-inflation using the Valsalva or Toyenbee maneuver is helpful, albeit a nonphysiologic test of tubal patency. The clinical status of the contralateral ear likewise can provide insight into tubal maturity and function in the diseased ear (12). As part of the eustachian tube evaluation, the nose should be examined so that allergy, adenoiditis, and rhinosinusitis can be treated in an effort to promote optimized tubal function (13). Furthermore, aggressive medical treatment of infection involving the ear itself should be undertaken prior to surgery, including aural toilet and ototopical agent application. When an ear will not dry with medical therapy, culture acquisition may be useful in helping to identify antimicrobial-resistant pathogens.

Once patient assessment is complete, a few general rules should be applied to surgical candidacy. First, one should avoid elective surgery on an only-hearing ear as much as is reasonably possible. Exceptions to this would be situations where surgery is primarily confined to the tympanic membrane, and drilling or significant ossicular manipulation is unlikely, or when a perforation is contributing to difficulty with hearing aid usage. Also, cases that involve disease processes that impart risk of hearing loss, such as cholesteatoma, will generally warrant intervention. Second, when bilateral disease is present, surgery should be undertaken on the worse-hearing ear in the absence of any other compelling reason to do otherwise on account of underlying disease. Finally, special consideration should be given to the timing of surgery in the pediatric patient.

Age as a prognostic factor in tympanoplasty is controversial, with contradicting reports present in the literature (14, 15). The authors’ approach to pediatric patients is to avoid repairing the tympanic membrane during the otitis-prone years (≤3 years). If the contralateral ear is normal, routine tympanoplasty is considered at age 4 for an ear that is dry or only occasionally drains with water

contamination (16). However, if the contralateral ear is abnormal at this time, adenoidectomy is considered and tympanoplasty is deferred until the contralateral ear reaches stable quiescence or the patient reaches age 7. If contralateral disease is still present at this time, a more aggressive technique, such as cartilage tympanoplasty, is performed on the worse-hearing ear. The second ear is repaired several months later, but only after the first ear is documented to have a stable satisfactory outcome and is not expected to require further surgery.