Professional Documents
Culture Documents
Atelectasis 2
Atelectasis 2
Atelectasis, adhesive otitis media, and fibroadhesive otitis media are different forms
of a retraction of an intact tympanic membrane, transformed into a very thin epider-
mal membrane, retracted towards the medial wall of the tympanic cavity, as shown
in Fig. 7.1.
In atelectatic ears, the middle ear space is partially or completely obliterated, but
the tympanic membrane is not adherent to the medial wall of the middle ear, and the
mucosal lining of the middle ear is intact.
However, in adhesive otitis media, the tympanic membrane is bound partially or
totally to the medial wall of the middle ear by fibrous adhesions; consequently, there
is no possibility of reversing the retraction by reaerating the middle ear. In cases
with partial adhesions, there may be serous or mucous effusion in the middle ear.
In mild cases, only few adhesions may be present, while in more severely affected
ears, the space area of the ME cavity has vanished and the tympano-ossicular sys-
tem is no longer functional (ossicular ankylosis).
Fibroadhesive otitis media is characterized by the presence of fibrosis filling the
middle ear cavity.
Adhesive otitis accounts for 3–5 % of operated chronic otitis media [1, 2].
Bilateral disease is found in 8–21 % of cases [1]. Adhesive otitis media is frequently
bilateral or associated with a contralateral pre-adhesive process. Sometimes, it is
associated with a contralateral cholesteatoma [3–5]. Cleft palate is associated with
an adhesive process in 20 % of cases [6, 7].
7.1 Pathogenesis
Adhesive otitis media is a sequela of neglected otitis media with effusion (OME)
from long-standing Eustachian tube dysfunction and the subsequent chronic OME
[8–15]. The negative pressure due to malfunction of the middle ear gas exchange,
associated to the lack of rigidity of the tympanic membrane (called “myringomalacia”
a b
c d
Fig. 7.1 (a) Normal ear, (b) fibroadhesive otitis media, (c) atelectasis, and (d) adhesive otitis
media
by Bremond) and the inward traction from granulation tissue, are essential for the
development of adhesive otitis media.
Only some patients with chronic OME develop atelectasis; in most patients with
OME, retraction of the tympanic membrane is limited. In patients with bilateral
OME, very few cases (2–5 %) of untreated ears develop severe atelectasis [3, 16, 17].
Recurrent infection of middle ear fluid leads to a progressive destruction of the
lamina propria of the tympanic membrane rendering it atrophic and prone to retrac-
tion [3, 11]. Middle ear global dysventilation due to Eustachian tube dysfunction
and inflammatory mucosa leads to a retraction of the whole atrophic TM towards
the tympanic cavity with consequent loss of middle ear space, representing
atelectasis.
However, a severe inflammatory process either suppurative or nonsuppurative
(e.g., acute suppurative otitis media, chronic suppurative otitis media, or persistent
mucoid otitis media) provokes mucosal ulcerations, surface breakdown, and bone
exposure that induce osteitis and periostitis. One of the most common reactions of
7.1 Pathogenesis 73
a b
Fig. 7.2 (a) Left partial adhesive otitis media associated with myringo-incudopexy and
myringosclerosis in the anteroinferior quadrant. (b) Left ear with adhesive otitis media
and tympanosclerotic plates covering the stapes and around the malleus
a b
Fig. 7.3 CT scan of a left adhesive otitis media associated with a huge mastoid cholesterol granu-
loma. (a) in transverse plane showing erosion of the posterior dural plate (arrow), A=antrum,
M=Mastoid. (b) In sagittal plane showing tympanic membrane retraction on the promontory
(short arrow) and erosion of the tegmen (long arrow)
middle ear, all middle ear infections should be treated aggressively with full courses
of the appropriate antibiotics. Persistent mucoid effusions should be drained.
The lamina propria is quite atrophic, even completely absent in some areas particu-
larly in the central portion of the pars tensa. Moreover, it is thin, formed of fibrous
remains invaded by inflammatory cells, with disorganized and disoriented fibers of
collagen. The mucous layer of the eardrum disappeared and is replaced by an
inflammatory tissue which induces the adhesion of the epithelial layer to the bone
of the promontory.
Adhesive otitis media is a silent disease and usually pauci-symptomatic. The most
common symptom is ear blockage from middle ear negative pressure. Hearing loss
is usually isolated and of insidious onset and progressively worsening over several
months or even years.
Hearing loss may be due to a blockage of the tympano-ossicular system of the
middle ear by adhesions or secondary to ossicular chain erosion by the adherent
skin. The audiogram could be normal even in the presence of ossicular erosion due
to the pexy of the retracted drum on the remaining ossicles.
The presence of an aural discharge is an important symptom and may indicate
that a retraction pocket with cholesteatoma has developed. However, frequently
otorrhea is due to superimposed infections of the peeled epidermal scales accumu-
lated in the fundus of the ear canal which is poorly ventilated.
1
In his comment to the question about Histopathology of Adhesive Otitis Media, Professor Jacques
Magnan wrote:
Regarding Adhesive Otitis Media, actually there is no specific histological picture, except
that it is represented by a keratinizing squamous epithelium lying on a more or less thick
layer of connective inflammatory tissue. The mucosa has disappeared secondary to the adhe-
sion of the tympanic membrane on the denuded bone of the floor of the tympanic cavity.
While speaking about histopathology of adhesive otitis media, the only interest to keep
in mind is historical: in the past when otologists practiced a biopsy on the adhesive tissue
on the floor of the tympanic cavity, they generated the hypothesis of metaplasia of the tym-
panic mucosa to become of squamous type!!
In fact before the operative microscope era, otologists used to think that they were doing
a biopsy from the middle ear region, this is why pathologists described the presence of epi-
dermis in the middle ear; consequently a concept of metaplasia of the mucosa was formu-
lated in pathology, missing the fact that the skin canal is capable of migration into the middle
ear cavity even better the epithelial layer of the tympanic membrane could inhabit the mid-
dle ear floor!
Thanks to otomicroscopy and modern endoscopy, the theory of metaplasia has been
abandoned. In fact the clinicians themselves were behind this advance in pathology.
7.2 Clinical Manifestations 75
incudostapedial joint which is usually lysed (Fig. 7.5). The lysis interests mostly
the descending branch of the incus, and the eardrum lines the stapes (Fig. 7.6). If the
stapes is eroded, the eardrum covers directly the footplate (Fig. 7.7).
Attempts to mobilize the eardrum using speculum of Siegle or Valsalva maneu-
ver are always negative. Pure tone audiometry shows the degree of hearing loss. It
is generally a conductive hearing loss, with an average air–bone gap of 25–50 dB.
Mixed hearing loss can be present in advanced cases of adhesive otitis media and
reflects the beginning of labyrinthization process.
The impedance, which is of no interest, shows a flat tympanometric curve.
7.5 Treatment 77
7.3 Complications
Adhesion of the retracted tympanic membrane to the ossicles may lead to their
resorption which is virtually constant in adhesive otitis media. It is found in about
60–80 % of cases [3, 19, 20]. This lysis is easily recognized in the otoscopic exami-
nation through an atrophic eardrum, molding the ossicular elements.
The most common is the erosion of the long process of the incus due to its tenu-
ous blood supply with the result of a natural myringostapediopexy (Figs. 7.5 and
7.6). The stapes is eroded in 25 % of cases [19–21].
The malleus handle is driven medially by the retracted tympanic membrane to
the medial wall of the middle ear cavity, due to the unopposed tensor tympani mus-
cle contraction. The otoscopic examination revealed a handle in a horizontal posi-
tion, pressed against the promontory (Figs. 7.5, 7.6 and 7.7).
7.3.2 Cholesteatoma
Adhesive otitis media with epithelialization of the middle ear cavity wall makes a
scarred middle ear cover, which is almost stable but must be distinguished from
active lesions evolving readily to cholesteatoma. In such cases, continuous retrac-
tion of the tympanic membrane into the attic or the retrotympanum may lead to deep
retraction pockets in which desquamated keratin debris would not be cleared into
the ear canal. This leads to cholesteatoma development which manifests by recur-
rent otorrhea.
Association of adhesive otitis media and cholesteatoma is not exceptional (25 %
of cases Bremond and Magnan) [1, 22] (Fig. 7.8).
Cholesteatoma must be distinguished from secondary superinfections of peeled
epidermal debris accumulated in the fundus of the ear canal which is poorly venti-
lated (Fig. 7.9).
7.4 Imaging
7.5 Treatment
Once adhesion has occurred between TM and middle ear mucosa and ossicles,
treatment becomes quite difficult.
a b
Fig. 7.10 (a) Right ear showing atelectasis. (b) The same ear after nitrous oxide inhalation during
anesthesia which brings the majority of the tympanic membrane into its normal position. This
makes grommet insertion possible and it is a good prognostic sign.
Once adhesions between the TM and middle ear mucosa and ossicles have formed,
treatment is quite difficult.
There is no consensus in literature as to the best treatment strategy of adhesive
otitis media.
Medical treatment is ineffective, and its side effects outweigh any benefit.
Surgical treatment in adhesive otitis media is controversial. It consists of lifting
of the adherent skin from the medial wall of the middle ear and reinforcing the ear-
drum by cartilage after reconstructing the ossicular chain aiming to maintain an
air-filled tympanic cavity.
This procedure carries high risk of inducing iatrogenic cholesteatoma and hear-
ing loss and carries a high rate of failure and it is not advised by most otologists. The
improvement of the hearing function is not easy to achieve; therefore, the surgery is
not indicated in asymptomatic adhesive otitis with normal hearing. Some clinicians
prefer watchful waiting, with their rationale to avoid the potential risk of iatrogenic
hearing loss or cholesteatoma in an ear that is often otherwise relatively asymptom-
atic. Others prefer early intervention in order to limit the risk of ossicular erosion or
progression of disease towards cholesteatoma [35–46].
However, the presence of recurrent otorrhea (a sign of developing cholestea-
toma) is an absolute indication for intervention. Important conductive hearing loss
is a relative indication for surgery as hearing can be restored by a hearing aid better
than by surgery. The risks and benefit of surgery and hearing aid should be dis-
cussed with the patient.
The surgical treatment of severe cases of end-stage adhesive otitis media is gen-
erally unrewarding, and the use of a hearing aid in those patients with extensive
ossicular fixation remains the most practical form of therapy.
Nevertheless, in cases of advesive otitis media associated with cholesteatoma, sur-
gery is necessarily indicated.
References
1. Bremond G, Magnan J, Bonnaud G. L’otite adhésive. Otorhinolaryngologie. Encycl Méd Chir,
20-182-G-30. Paris: Elsevier SAS; 1985. p. 8.
2. Dommerby H, Tos M. Sensorineural hearing loss in chronic adhesive otitis. Arch Otolaryngol
Head Neck Surg. 1986;112:628–34.
3. Sadé J, Berco E. Atelectasis and secretory otitis media. Ann Otol Rhinol Laryngol. 1976;85(2
Suppl 25 Pt 2):66–72.
4. Moller P, Dingsor G, Breck P, Thomassen R. Tympanic membrane changes and retraction
pockets after secretory otitis media. In: Tos M, Thomsen J, Peitersen E, editors. Cholesteatoma
and mastoid surgery. Amsterdam: Kugler and Ghedini Publications; 1989. p. 351–5.
5. Fujita A, Sato H, Nakamura H, Yagi N, Honjo I. The etiological role of the retraction pocket
in cholesteatoma. In: Tos M, Thomsen J, Peitersen E, editors. Cholesteatoma and mastoid
surgery. Amsterdam: Kugler and Ghedini Publications; 1989. p. 421–4.
6. Guerrier Y, Charachon R, Dejean Y, et al. Pathologie fonctionnelle du voile du palais et sa
réhabilitation. Rapport Société Française d’ORL et pathologie cervicofaciale. Paris: Arnette;
1978. p. 154–65.
References 81
31. Low WK, Wilatt DJ. The relationship between middle ear pressure and deviated nasal septum.
Clin Otolaryngol. 1993;18:308–10.
32. Hashimoto S. A guinea pig model of adhesive otitis media and the effect of tympanostomy.
Auris Nasus Larynx. 2000;27:39–43.
33. Buckingham RA, Ferrer JL. Reversibility of chronic adhesive otitis media with polyethylene
tube, middle ear air-vent, kodachrome time lapse study. Laryngoscope. 1966;76(6):993–1014.
34. Valtonen H, Qvarnberg Y, Nuutinen J. Tympanostomy in young children with recurrent otitis
media. A long-term follow-up study. J Laryngol Otol. 1999;113:207–11.
35. Dogru H, Tuz M, Uygur K, Candir O, Yariktas M. Tympanostomy preceding tympanoplasty:
could it be a new approach for the management of adhesive otitis media. J Otolaryngol.
2003;32:411–4.
36. Tos M. Tympanoplasty in chronic adhesive otitis media. Acta Otolaryngol. 1972;73(1):53–60.
37. Vartiainen E, Härmä R, Karjalainen S. Surgery of chronic adhesive otitis media. Clin
Otolaryngol Allied Sci. 1985;10(3):163–4.
38. Nielsen KO, Bak-Pedersen K. Otosurgery of incipient adhesive otitis media in children.
J Laryngol Otol. 1984;98(4):341–5.
39. Li-Sheng YU. QI Zhen-min operative therapy of the adhesive otitis media. Chin
J Otorhinolaryngol. 2004;39(1):40–3.
40. Politzer A. Traite des maladies de l’oreille. Paris: Doin; 1884.
41. Palva T. Surgical treatment of adhesive tympanum. Acta Otolaryngol Suppl. 1964;188 suppl
188:70–4.
42. Siirala U. Pathogenesis and treatment of adhesive otitis. Acta Otolaryngol Suppl. 1964;188
suppl 188:9–18.
43. Sade J, Avraham S, Brown M. Dynamics of atelectasis and retraction pockets. In: Sade J, edi-
tor. Cholesteatoma and mastoid surgery. Amsterdam: Kugler Publ; 1982.
44. Charachon R, Gratacap B, Vuarnet J. Classification and surgical treatment of fibroadhesive
otitis. Am J Otol. 1985;6(4):305–10.
45. Tos M. Obliterative otitis media. J Laryngol Otol. 1979;93(6):569–73.
46. Bremond G, Magnan J. L’otite adhesive. Ann Otolaryngol (Paris). 1977;94:73–82.