ESTADO DE LA CUESTIÓN: CONTRIBUCIONES TEÓRICAS EN RESPUESTA A LA VIOLENCIA DE GÉNERO ENTRE LA POBLACIÓN ADOLESCENTE
2. El concepto de “violencia de género”
12. Decreased bone conduction: In an audiogram it indicates the involvement of cochlea.
13. Maximum conductive hearing loss: It is approximately 54 dB and is caused by ossicular disruption with intact tympanic membrane. Ossicular disruption with perforated tympanic membrane results in about 38 dB hearing loss.
14. Phonetically balanced words: These are used to measure speech discrimination score. 15. Spondee words: These are used to measure speech reception threshold.
16. Otoacoustic emissions: They arise from outer hair cells.
17. Brainstem evoked response auditory: Interpretation is affected by the age of the child. It tracks electrical conductivity of hearing up to the brain-stem.
18. Tuning fork tests: They should confirm the results of audiometry. Never trust the audiogram alone when surgical intervention is considered. The inconsistency must be resolved with the audiologist.
19. Types of hearing losses: In addition to mixed hearing loss there are two major types of hearing loss: 1) conductive, and 2) sensorineural.
20. Discrimination test: It measures patient’s ability to understand speech.
FURTHER READING
1. Biswas A. Clinical Audiovestibulometry for Otologists and Neurologists, 3rd edition. Mumbai: Bhalani Medical Book House; 2001. 2. Dutta A, Vankatesh MD, Kashyap RC. Study of the effects of chemotherapy on auditory function. Indian J Otolaryngol Head Neck Surg.
2005;57:226-8.
3. Emerson LP, Mathew J, Balraj A, et al. Peripheral auditory assessment in minor head injury: a prospective study in tertiary hospital. India J Otolaryngol Head and Neck Surg 2011;63:45-9.
4. Rao TVK. National programme for prevention and control of deafness. Indian J Otolaryngol Head Neck Surg. 2008;60:293-4. 5. Rupa V. Clinical utility of distortion product otoacoustic emissions. Indian J Otolaryngol Head Neck Surg. 2002;54:87-90.
6. Sharma R, Gupta SC, Tyagi I, et al. Brainstem evoked responses in patients with diabetes mellitus. Indian J Otolaryngol Head Neck Surg. 2000;52:224-9.
7. Sharma R, Sharma ML, Mohan C, et al. Electrocochleography: a comparative study in potential at the ear canal in normal and sensorineural hearing loss. Indian J Otolaryngol Head Neck Surg. 2005;Special Issue-II:369-71.
8. Sinha SK, Basavraj V. Speech Evoked Auditory Brainstem Responses: a New Tool to Study Brainstem Encoding of Speech Sounds. Indian J Otolaryngol Head Neck Surg. 2010;62:395-9.
It is better to do something; never mind even if it proves to be wrong; it is better than doing nothing. Purity, patience, and persever- ance are the three essentials to success, and above all–love.
—Swami Vivekananda
¯ClaSSifiCation of Hearing loSS
Differences between Conductive and Sensorineural hearing losses
¯ConduCtiVe Hearing loSS Etiology
history and physical Examination Treatment ¯otoSCleroSiS pertinent anatomy Etiology Types pathology Clinical features audiometry Differential Diagnoses Treatment ¯StapedeCtomy Selection Criteria Contraindications anesthesia Operative Steps
postoperative Care and follow-up Complications
¯CliniCal HigHligHtS
points of focus
ClaSSifiCation of Hearing loSS
The two broad categories (Box 1) of hearing loss are conduc- tive hearing loss (CHL) and sensorineural hearing loss (SNHL). SNHL is further divided into sensory (cochlear) and neural (CN VIII and central auditory connections).
Sensorineural hearing loss and CHL have their own characteristic features. On the basis of history, examination, tuning fork tests and audiometry, usually they can be easily differentiated from each other (Table 1).
ConduCtiVe Hearing loSS
The disorders of external and middle ear up to stapedioves- tibular joint interfere with the conduction of sound and cause CHL (Table 2).
The ossicular disorders with intact tympanic membrane cause more hearing loss than ossicular diseases with tympanic membrane perforation.
Box 1: Classification of different types of hearing losses
a. Non-organic 1. Malingering 2. psychogenic b. Organic
1. Conductive hearing loss (Chl) 2. Sensorineural hearing loss (SNhl)
a. peripheral
i. Cochlear (Sensory) ii. CN VIII (Neural) b. Central
i. brainstem (medulla, pons, midbrain) ii. Thalamus
iii. Temporal lobe 3. Mixed hearing loss
etiology
The causes may be congenital, traumatic, infectious/inflamma- tory, neoplasms and miscellaneous. They may lie in external ear, tympanic membrane, middle ear space, ossicles or in Eustachian tube (Box 2).
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taBle 1 Differences between conductive hearing loss and sensorineural hearing loss Features Conductive hearing loss Sensorineural hearing loss
Speech understanding Good poor
Intolerance to loud sounds absent present in cochlear lesions Speech of the patient low voice loud voice
paracusis willisii Common absent Common associated symptom Otorrhea/earache Tinnitus profound hearing loss Never Common
Rinne test Negative (bC > aC) positive (aC > bC)
Weber test lateralized toward worst ear lateralized toward better ear absolute bone conduction Normal Reduced
pure Tone audiometry (pTa) air-bone gap present absent
pTa: Recruitment absent present in cochlear lesions pTa: Tone decay absent present in CN VIII lesion pTa: frequencies usually low tones involved usually higher tones involved pTa: Thresholds Never > 60–70 db Can be > 60–70 db
Speech discrimination Not affected poor
Site of lesion External and middle ear Internal ear, CN VIII and central auditory connections
History: Mode and age of onset; duration and progression
of hearing loss; side of ear; associated symptoms of ear fullness, ear pain, otorrhea, tinnitus, vertigo/dizziness; preceding history of upper respiratory tract infection (URI), trauma, medications; visual, speech, or other neurologic deficit; family history.
Physical examination (Fig. 1): Local examination of external
ear, tympanic membrane, middle ear; pneumatic otoscopy; tuning fork tests; complete nose, throat, head and neck examination.
See chapters (1) Otologic Symptoms and Examination; and
(2) Hearing Evaluation.
treatment
Most cases of CHL can be managed by medical and surgical treatment, which depend upon the cause of deafness. The details of the treatment of these conditions are given in their respective chapters but Table 3 briefly provides different modalities and their indications.
Different types of mastoid and tympanoplasty operations are described in chapter Middle Ear and Mastoid Surgeries.
otoSCleroSiS
Otosclerosis is a common disorder of bony labyrinth with normal tympanic membrane. It is characterized by gradually progressive CHL as a result of stapes fixation. Though there is no cure, the treatment of choice is stapedectomy.
pertinent anatomy
Labyrinth consists of three parts: membranous labyrinth, peri- lymphatic labyrinth and bony labyrinth. The bony labyrinth has three layers: endosteal, bony (enchondral) and periosteal (See chapter Anatomy and Physiology of Ear).
1. Membranous labyrinth (Otic labyrinth or endolymphatic
labyrinth): Otic labyrinth consists of utricle, saccule, cochlear
duct (scala media), semicircular ducts and endolymphatic duct and sac. It is filled with endolymph.
Box 2: Causes of conductive hearing loss
• External auditory canal: Wax, foreign bodies, otitis externa, congenital and acquired stenosis, exostoses, osteomas, tumors, cyst
• Tympanic membrane: perforations (traumatic, aSOM, CSOM), tympanosclerosis, retraction
• Ossicles: fixation (otosclerosis, tympanosclerosis, adhesive otitis media, congenital); discontinuity (traumatic, inflammatory, cholesteatoma)
• Middle ear: Otitis media with effusion, hemotympanum, cholesteatoma, tumors (benign and malignant); Eustachian tube dysfunction
Occlusion of external auditory canal (EaC) 30–40 db perforation of tympanic membrane. hearing
loss depends on the size and site of perforation
10–40 db
Ossicular interruption without eardrum perforation (fixity and discontinuity)
54 db
Ossicular interruption with eardrum perforation (fixation and discontinuation)
38 db
Malleus fixation 10-25 db Closure of oval window 60 db pure and complete conductive hearing loss 60–70 db
taBle 2 Common causes of conductive hearing loss and their approximate hearing loss in db
The most common causes include wax, otitis media [acute suppurative otitis media (aSOM) and chronic suppurative otitis media (CSOM)], tympanosclerosis, and otosclerosis. In children, the most common cause is otitis media with effusion.
History and physical examination
In the evaluation of a CHL, following points should be consid- ered during the history taking and physical examination keeping in mind the various causes of CHL (Box 2):
Chapter 12 w Conductive Hearing loss and o tosclerosis
taBle 3 Different modalities of treatment of conductive hearing loss and their indications Removal of external auditory canal
canal occlusions
Impacted wax, foreign body, osteoma, exostosis, keratosis obturans, tumors, meatal stenosis
Myringotomy acute otitis media Grommet Otitis media with effusion
Stapedectomy Otosclerosis (fixation of stapes footplate)
Tympanoplasty Tympanic membrane perforations and ossicular disruptions Hearing aids When surgery is not possible, refused or failed
fig. 1: flow chart for clinical diagnoses of causes of conductive hearing losses
2. Perilymphatic labyrinth or space (Periotic labyrinth): Periotic labyrinth surrounds the otic labyrinth and filled with peri- lymph. It consists of vestibule, scala tympani, scala vestibuli and perilymphatic spaces of semicircular and endolym- phatic ducts.
3. Bony labyrinth (Otic capsule): It consists of three layers:
endosteal, enchondral and periosteal.
The bony labyrinth ossifies from 14 centers. The first center appears in the cochlea at 16 weeks. The last center appears in the posterolateral part of posterior semicircular canal at 20th week.
I. Endosteal, which is the innermost layer, lines the internal surface of bony labyrinth.
II. Bony (enchondral) layer, which is subject to little change in life, develops from the cartilage.
– Pathogenesis
- Otosclerosis is a primary disease of this enchon-
dral bony labyrinth. In this hard enchondral bone, some islands of cartilage remain unossi- fied. This cartilage rests due to certain nonspe- cific factors, are activated to form new spongy bone (otospongiosis).
- These irregular foci of spongy bone replace
normal dense enchondral bony labyrinth. Therefore, many call this disease as otospongiosis. The otosclerotic focus usually involves the stapes region and results in stapes fixation and conduc- tive deafness. The fissula ante fenestram, which lies in front of the oval window, is the site of predilection for stapedial type of otospongiosis. The otospongiosis process can involve other areas of bony labyrinth and can cause SNHL or remains asymptomatic.
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III. Periosteal, which is the outermost layer, covers the external surface of bony labyrinth that is temporal bone.
etiology
The exact cause of the disease is yet not known. The following factors have been documented in the literature:
Heredity: About 50% of the cases give positive family history.
Remaining cases are sporadic. An autosomal dominant inheritance with penetrance in range of 20–40 has been reported. Other studies report heterogenetic, with more than one gene defect. Some cases have been suggested to be related with COL1A1 gene, which is one of the two genes that code for type I collagen (predominant collagen of bone).
Osteogenesis imperfecta: About 50% cases of type I osteo-
genesis imperfecta develop hearing loss, histological changes and COL1A1 expression that are indistinguishable from otosclerosis. Patients of osteogenesis imperfecta have history of multiple fractures. The van der Hoeve syndrome presents with the triad of osteogenesis imperfecta, otoscle- rosis and blue sclera.
Viral: Many reports suggest that otosclerosis may be related
to a persistent measles virus infection of otic capsule. Perhaps it is similar to Paget’s disease of bone, which is related with defective paramyxovirus.
types
1. Stapedial otosclerosis: Stapedial otosclerosis is the most common variety. It causes stapes fixation and presents with conductive deafness (Figs 2A to E).
a. Anterior focus: The fissula ante fenestram, which lies in front of the oval window, is the site of predilection. b. Posterior focus: Otosclerosis may start behind the oval
window.
c. Circumferential: Disease process spreads around the margin of the stapes footplate.
d. Biscuit type: Disease process involves the footplate but annular ligament is free.
e. Obliterative type: The disease process completely oblit- erates the oval window niche.
2. Cochlear otosclerosis: It involves region of round window and
areas in the bony labyrinth and petrous part of temporal bone. It presents with irreversible SNHL, which is probably caused by toxic materials liberated into the inner ear fluid. 3. Histologic otosclerosis: Histologic otosclerosis is diagnosed
only on histological examination. Patient remains asymp- tomatic.
pathology
1. Gross appearance
a. Otosclerotic lesions appear chalky white, grayish or yellow.
b. The red color lesions indicate increased vascularity, which is the feature of active and rapidly progressive otosclerotic focus.
2. Histology: A wave of abnormal bone remodeling occurs with resorption of enchondral bony labyrinth, which is replaced with hypercellular woven spongy bone that further remodels and results in sclerotic mosaic architecture. a. Immature active lesions: Numerous marrow and
vascular spaces (increased vascularity) with plenty of histiocytes, osteoblasts and osteoblast precursor cells, and mononuclear cells indicate active remodeling phase. A lot of cement substance is present which stains blue with hematoxylin-eosin stain. Acute inflammatory cells are absent.
b. Mature lesions: Less vascular spaces and laying of more bone and fibrillar substance than cementum and stains red with hematoxylin-eosin stain.
Clinical features
Otosclerosis is characterized by gradually progressive CHL with normal tympanic membrane. In most cases, the disease is bilateral.
1. Race: White races are affected more than blacks. It is common in Indians but rare among Chinese and Japa- nese.
2. Age of onset: Patients are usually between 20–30 years of age. Disease is rare before 10 and after 40 years.
3. Hormonal effect: In females, deafness seems to worsen or manifest during pregnancy and menopause.
4. Trauma: Some patients try to correlate deafness with an accident or a major operation.
5. Hearing loss: The presenting feature is painless bilateral gradually progressive CHL.
Paracusis Willisii: In this phenomenon the patient’s
hearing improves in noisy background. It happens because a normal person raises his voice in noisy surroundings and patient takes advantage of that. The speech discrimination is not affected in pure conductive hearing loss.
Tuning fork tests and audiometry They show CHL.
6. Tinnitus: It is usually present in cochlear otosclerosis and active lesions.
7. Vertigo: It is an uncommon symptom. The cause of it is
figs 2a to e: Types of otosclerotic lesions causing fixation of
stapes footplate. (A) Anterior focus, the site of predilection “fissu- la ante fenestram”; (b) posterior focus the lesion begins behind the oval window; (C) Circumferential, lesion begins around the margins of footplate; (D) biscuit type lesion involves only foot- plate sparing the annular ligament; (E) Obliterative lesion com- pletely obliterates the oval window niche
Chapter 12 w Conductive Hearing loss and o tosclerosis audiometry
Conductive hearing loss more for lower frequencies (Fig. 3).
Carhart’s notch: There is a dip (from 500–4,000 Hz) in bone
conduction curve, which is maximum (15 dB) at 2,000 Hz (5 dB at 500 Hz, 10 dB at 1,000Hz, 15 dB at 2,000 Hz and 5 dB at 4,000 Hz). The Carhart’s notch disappears after successful stapedectomy surgery.
Air-bone gap: The degree of footplate fixation is estimated
by the size of air-bone gap. Audiometry does not predict the pattern and extent of oval window involvement. It is determined on exploratory tympanotomy during the stapedectomy surgery.
Mixed hearing loss with SNHL element indicates cochlear
otosclerosis.
differential diagnoses
They include following causes of CHL. They can be differenti- ated with the help of ear microexamination, siegalization, impedance audiometry and exploratory tympanotomy: 1. Serous otitis media
2. Adhesive otitis media 3. Tympanosclerosis
4. Attic fixation of head of malleus 5. Ossicular discontinuity
6. Congenital stapes fixation
treatment
There is no curative treatment. The treatment of choice is stapedectomy. Other modalities of management include
permanent hearing in these cases. Simple mobilization of stapes is not indicated in most of the cases as it commonly results in refixation.
Fenestration operation: In fenestration operation, which is
almost abandoned, an alternative window is created in the lateral semicircular canal. The main disadvantage is a postop- erative mastoid cavity and an inherent hearing loss of 25 dB.
Hearing aid: Hearing aids offer good hearing results and
are indicated in patients who refuse surgery or are unfit for surgery.
• Otosclerosis: fifty percent of patients give positive family history. patient has Chl with normal tympanic membrane and impaired acoustic reflexes. The patients with negative Rinne (bC > aC) are candidate for stapedectomy, which provides very gratifying results.
StapedeCtomy
An ideal case for stapedectomy surgery is also an ideal candi- date for hearing aid. So the patient should be fully informed of the results and risks of the stapedectomy.
Selection Criteria
Firmly fixed stapes is indicated by an air-bone gap of
minimum 30 dB for the speech frequencies and a negative Rinne for 256- and 512-Hz magnesium tuning forks and speech discrimination score of 60% or more.
The successful stapedectomy and stapes mobilization correct the Chl, remove Carhart’s notch and often lead to over-closure of air-bone gap.
fig. 3: audiogram otosclerosis. bilateral predominantly low-frequency conductive hearing loss.
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Mixed profound hearing loss with sufficient speech discrimi-
nation: Stapedectomy improves hearing aid use.
Contraindications
The only hearing ear: There are about 1% chances of devel-
oping dead ear.
Vertigo: History of vertigo in recent months is usually asso-
ciated with Meniere’s disease. There is heightened risk of postoperative SNHL.
Young children: Recurrent Eustachian tube dysfunction
commonly causes AOM in children and can displace the prosthesis. The otosclerotic focus is usually active and progresses rapidly in children and can close the oval window.
Certain occupations:
a. Postoperative vertigo can interfere the working in some professions such as athletes and high construction workers.
b. In divers and frequent fliers, air pressure changes can damage the hearing and induce severe vertigo. c. Industrial workers who work in noisy surroundings are
more vulnerable to occupational SNHL.
Local diseases: Otitis externa, tympanic membrane perfora-
tion and exostosis should be treated before the stapedec- tomy.
Pregnancy: Stapedectomy is avoided.
anesthesia
Surgery is preferably done under local anesthesia so that hearing can be tested on the table.
operative Steps
1. Infiltration of ear canal with lidocaine and epinephrine. 2. Obtaining of the tissue graft to cover oval window: vein,
temporalis fascia, perichondrium or fat. 3. Endomeatal curved or triangular skin incision.
4. Elevation of the posterior deep meatal skin and fibrous annulus from sulcus tympanicus.
5. Removal of 2–4 mm posterosuperior bony overhang (Fig. 4) of the canal rim for an adequate exposure of oval window, stapes, facial nerve canal and pyramid. 6. Removal of stapes superstructure.
7. Making a hole in the stapes footplate (stepedotomy) or remove a part of footplate (stapedectomy).
8. Tissue seal of oval window.
9. Placement of prosthesis between the long process of incus and oval window (Figs 5 and 6): Shea platinum Teflon cup piston, Robinson stainless steel prosthesis, Shea Teflon piston, McGee piston, Fisch platinum Teflon piston and House wire prosthesis.
10. Repositioning the tympanomeatal flap.
postoperative Care and follow-up
Analgesics and antibiotics if needed. Avoid straining and blowing of nose.
Outpatient surgery and discharged after several hours. First follow-up the day after surgery.
fig. 4: Stapedectomy. After elevating the tympanomeatal flap,
posterosuperior bony canal wall is removed to get better view of stapes
fig. 5: Stapedectomy piston. after creating a fenestra in the sta-
pes footplate, piston is placed from long process of incus to the footplate fenestra. Note stapes superstructure is removed
Chapter 12 w Conductive Hearing loss and o tosclerosis
1. otosclerosis: patients present with gradually progressive bilateral conductive hearing loss (Chl), which increases during
pregnancy. Tympanic membrane and Eustachian tube are normal. Rinne’s test is negative. a. prevalence: The prevalence of clinical otosclerosis is highest in Caucasians.
b. inheritance: Otosclerosis has autosomal dominant inheritance.
c. pathogenesis: The disease process starts in bone of otic capsule which develops from cartilage.
d. fissula ante fenestram: This is the most common site of stapedial otosclerosis and is located at the anterior edge of
oval window.
e. Schwartz sign: This sign of active otosclerosis (such as during pregnancy) is seen as a pink reflex (reddish hue seen
over the promontory) through intact tympanic membrane in the area of oval window.
f. Carhart’s notch: This characteristic feature of otosclerosis is seen in the audiograms. bone conduction (sensorineural
hearing loss) dips maximum at 2000 hz (2 khz).
g. impedance audiometry (tympanogram): Otosclerosis patients show ‘A’ type of curve with absent acoustic reflex.
h. treatment: Treatment of otosclerosis includes hearing aid, stapedectomy, and sodium fluoride therapy. Treatment of choice for a young stapedial otosclerosis office going patient is stapedectomy. Sodium fluoride (NaF) is being used in the treatment of cochlear otosclerosis.
2. Habenula perforata: The openings, through which branches of cochlear nerves enter the cochlea. If wide, they can lead
to a perilymph gusher in stapes surgery. This X-linked disease can be diagnosed on CT. It is associated with congenitally