Tos Surgical Solutions for Conductive Hearing Loss

Vol. 4 of the Manual of Middle Ear Surgery
1. Auflage 2000
ISBN: 978-3-13-258082-4
Verlag: Thieme
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 280 Seiten, ePub

In this book the best surgical solutions for conductive hearing loss due to ossicular fixations are thoroughly described and discussed. The first section covers thympanosclerosis, collating all knowledge on the pathogenesis and pathology of this obscure condition, as well as the surgical methods used in fixation of the ossicular chain, when caused by myringosclerosis and tympanosclerosis. The second section covers postinflammatory, posttraumatic, and postoperative bony fixations of the ossicular chain. In the third section, the voluminous topic of otosclerosis, in particular the evolution of stapes surgery, the various stapedectomy and stapedotomy methods, and the complications of surgery for otosclerosis, are covered in great detail. This section also includes the problems that are encountered in otosclerosis surgery when the ear has been affected with chronic otitis. In the fourth section, congenital ossicular fixations and defects are covered along with some new aspects on the classification and embryology of these problems. For all topics, there is in-depth discussion of the pathogenesis and pathology of the diseases in question. Excellent hand-drawn illustrations provide a level of detail and comprehension not attainable through photography. This book will cover tympanosclerotic, bony, and fibrous fixations, retractions, atelectasis, secretory and adhesive otitis, ventilation problems of the middle ear, cholesteatoma in the tympanic cavity and more!

Mirko Tos

Zielgruppe

Ärzte

Autoren/Hrsg.

Tos, Mirko

Fachgebiete

• Medizin | Veterinärmedizin Medizin | Public Health | Pharmazie | Zahnmedizin Klinische und Innere Medizin HNO-Heilkunde, Phoniatrie, Audiologie

Inhaltsverzeichnis

Chapter 1 Tympanosclerosis
Chapter 2 Surgery of Myringosclerosis
Chapter 3 Surgery of Tympanoscclerosis
Chapter 4 Bony Ossicular Fixation
Chapter 5 Surgery of Bony Fixations
Chapter 6 Bony Fixation of the Grafts
Chapter 7 Otosclerosis
Chapter 8 Stapedectomy Techniques
Chapter 9 Stapes Prostheses in Stapedectomy and Stapedotomy
Chapter 10 Stapedotomy Techniques
Chapter 11 Stapedectomy with Stapes Tendon Preservation
Chapter 12 Lasers in Stapes Surgery
Chapter 13 Complications during Stapedectomy
Chapter 14 Complications after Stapedectomy
Chapter 15 Conductive Hearing Loss after Stapedectomy
Chapter 16 Complications of Stapedotomy
Chapter 17 Otosclerosis Associated with Chronic Otitis Media
Chapter 18 Postoperative Conditions Associated with Otosclerosis
Chapter 19 Congenital Ossicular Fixations and Defects
Chapter 20 Embryology of Stapes Ankylosis
Chapter 21 Osteogenesis Imperfecta

Leseproben

1    Tympanosclerosis

Pathogenesis

Tympanosclerosis may hamper movements of the eardrum and the ossicular chain and can, in severe cases, totally fixate the stapes, malleus, and incus. Tympanosclerotic fixation of the ossicular chain can confidently be differentiated by the surgeon from the other fixations described in the following chapters, such as bony or fibrous fixation of the malleus and incus, otosclerotic fixation of the stapes, and congenital fixations of the ossicular chain.

Definition

Von Tröltsch (1873) first described tympanoscleros is as “a stiffness of the fibrous tissue of the deepest layer of the middle ear mucosa.” Interest in tympanosclerosis, however, became accentuated following the reports of surgery by Zöllner and others (Zöllner and Beck, 1955; Zöllner, 1956, 1963, 1969; Goodhill, 1960; House and Sheehy, 1960; Harris, 1961; Sheehy and House, 1962; Harris and Weiss, 1962). All the authors agreed that tympanosclerosis is an irreversible end product of a chronic infection or inflammation. Tympanosclerosis is commonly found in cul-de-sac areas, with few ciliary and goblet cells, typically the oval window niche (Gibb, 1971). Tympanosclerosis is not an invasive process and it does not destroy the ossicles, even though it may commonly be found along intact or partly resorbed ossicles.

Tympanosclerosis localized to the lamina propria of the pars tensa is, in this book, called myringosclerosis, but in general the term tympanosclerosis is used. There is no tympanoscleros is in Shrapnell’s membrane.

Histopathology

Histologically, the tympanosclerotic mass or plaque reveals an increase in collagen and fibrous fibers with hyaline degeneration within the lamina propria of the middle ear mucosa and the pars tensa of the eardrum. Hyalin masses in the middle ear mucosa form white layers between the bone and the epithelium and may attain a thickness of some millimeters. Secondary ossification occurs in the tympanosclerotic masses or in tympanosclerotic plaques of the eardrum (Igarashi et al., 1970; Friedmann, 1971; Surján and Juhász, 1971; Tos and Bak-Pedersen, 1974a; Ferlito, 1979). Transmission electron microscopy demonstrates a dense network of collagen fibers with interposed calcospherules, which are masses of calcium phosphate, 1–5 µm in diameter (Chang, 1969; Sørensen and True, 1971; Friedmann and Galey, 1980; Friedmann et al., 1980; Mann et al., 1980; Møller 1981, 1984; McKee and Kerr, 1989).

Classification of Tympanosclerosis

The definition of tympanosclerosis as hyaline degeneration of lamina propria demands a quantitative view of the disease. It can be subdivided in to histological (subclinical) (Tos and Bak-Pedersen, 1974), clinical, and surgical forms.

Histological Tympanosclerosis

In the middle ear mucosa from patients operated on for middle ear tympanosclerosis, histological evidence of tympanosclerosis was found even in areas thought to be free of the condition when examined with the otomicroscope (Sørensen and True, 1971; Tos and Bak-Pedersen, 1974a). Histological tympanosclerosis was also often found in the mucosa of clinical entities other than middle ear tympanosclerosis, such as sequelae to chronic otitis, active chronic otitis, adhesive otitis, and cholesteatoma (Tos and Bak-Pedersen, 1973a and b, 1974b, 1975). Applying the quantitative view, histological tympanosclerosis may be found in any case of chronic middle ear infection—all depending upon the extent of the search and the power of magnification used. The same quantitative view can be applied to myringosclerosis, which appears just 2–4 weeks after experimental tubal occlusion of germ-free rats (van der Beek and Kuijpers, 1984) due to low pressure with an increase of collagen and fibrous fibers (Tos, 1981a; Kuijpers and Van der Beek, 1984) and accumulation of serous effusion material (Wielinga et al., 1988). In secretory otitis the plaques are initially hardly recognizable and therefore subclinical, but can, after a gradual increase in thickness, become visible and clinical. Such “growth” of myringosclerosis from subclinical to clinical forms can often be followed by otomicroscopic examination of children with secretory otitis who have undergone grommet insertion.

Clinical Tympanosclerosis

Clinical myringosclerosis is defined as any visible plaque seen by otoscopy or otomicroscopy of the eardrum or middle ear. The majority of small plaques do not cause any hearing loss. Some produce a very slight, 1 or 2 dB loss in some of the frequencies (Tos and Poulsen, 1976, 1979; Tos and Stangerup, 1989; Tos et al., 1987) (Fig. 1, A, B, and E). Other plaques may cause 5–10 dB hearing loss, which is of less importance in childhood, but may become important in elderly patients, in combination with presbyacusis. Some large plaques may cause 10–15 dB hearing loss, even without any fixation of the malleus handle (Fig. 1, C, D, and F). The term clinical myringosclerosis can be suitably applied in cases following secretory otitis media with an intact drum and relatively good hearing. The myringosclerotic plaques can, however, be heavily calcified or ossified, impeding movements of the eardrum.

Myringosclerosis often appears together with atrophy as a sequelae of secretory otitis, documented by epidemiological studies (Tos et al., 1982, 1984; Holm-Jensen et al., 1982; Tos 1985, 1990; Stangerup et al., 1995) and clinical studies of secretory otitis (Kilby et al., 1971, 1972; Mawson and Fagan, 1972; Bonding and Lorenzen, 1973; Kokko, 1974; Lildholdt, 1979; Al-Sheikhli, 1980; Gibb, 1980, 1985; Tos and Bonding, 1983; Møller 1984; Larsen et al., 1988; Maw, 1991; Maw and Bawden, 1994; Riley et al., 1997; Gaihede et al., 1997). This strange phenomenon of a thin drum (e.g. in the posterosuperior quadrant) and a thickening (e.g. in the anterosuperior quadrant) has never been fully understood. In ears without perforation, tympanosclerotic plaques, also commonly known as “chalk patches” are localized either anteriorly, posteriorly, or circularly (Fig. 1). In circular or “horses hoe” myringosclerosis, the plaque forms a 0.5 to 1.5 mm broad ring stretched along the annulus with a tympanosclerotic free belt close to it, all owing good movements of the drum (Fig. 1, B and F). In diffuse myringosclerosis all parts of the eardrum are involved. If the diffuse myringosclerosis is massive then the entire pars tensa is rigid and the malleus handle fixed (Fig. 1, A and B).

The term clinical myringosclerosis can also be applied in all cases of chronic otitis media with perforation, which is usually located at the site of former atrophy. The tympanosclerotic involvement of the remaining drum varies; sometimes it is not severe at all and sometimes the plaques are thick, impeding the movement of the drum (Fig. 2).

In the middle ear, the term clinical tympanosclerosis can be applied to all evident whitish plaques localized in the mesotympanum, hypotympanum, tubal orifice, or elsewhere, which do not involve the ossicles to such a degree that surgery is necessary.

During surgery for any chronic disease it is not uncommon to see (with the otomicroscope) tympanosclerotic changes affecting ligaments, the fibrous annulus being stiffer than normal.

Fig. 1 Examples of various shapes and localizations of myringosclerotic plaques in an otherwise intact eardrum. A) Anterior. B) Anterior and inferior. C and F) Horseshoe myringosclerosis. D) Anterior and posterior plaques combined with inferior atrophy (thick arrow). E) Anterior, inferior, and posterior plaques. A ring along the fibrous annulus without myringosclerosis is seen in slight and moderate cases (thin arrows).

Fig. 2 Examples of thick myringosclerotic plaques with some fixation of the malleus handle. A) Diffuse massive tympanosclerosis. B) Diffuse massive tympanosclerosis with a partly retracted atrophic area, inferior to the umbo. C) With a small anterior perforation. D) Inferior perforation surrounded by extensive myringosclerosis. E) Anterior atrophy with perforation and thick myringosclerosis posteriorly and inferiorly. F) Subtotal perforation surrounded by thick myringosclerosis.

Surgical Tympanosclerosis

Surgical myringosclerosis is said to be present when there is severe fixation of the malleus handle or when the eardrum movement is impeded to such an extent that surgical removal will improve hearing. There is, of course, a gradual transition from clinical to surgical myringosclerosis. In the clinic, many combinations of the various sizes and locations of perforations and the myringosclerotic plaques of the eardrum remnant may be seen.

The typical cases of middle ear tympanosclerosis are fixation of either the stapes in the oval window niche—stapes tympanosclerosis—or of the malleus head and/or incus body in the attic—attic tympanosclerosis. Seldom are all three...

Über Autor(innen)

Mirko Tos