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A. Elhakeem et al.

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Fig. 4.5 Patient with a normal left ear and a right glue ear; Tympanometry showing curve type A in the left ear and type

B in the right ear

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4.7 Treatment

1. Medical treatment:

The use of the topical nasal steroid has shown to speed the clearance of OME and prevents recurrences. However, oral steroids, antibiotics, antihistamine, nasal decongestants, and mucolytics did not show any benet in OME [9].

2. Surgical treatment: The benet of myringotomy and tympa-

nostomy tubes’ (TT) insertion is to improve hearing and decrease rates of recurrent otitis media. TT is inserted in the anteroinferior

Fig. 4.6 Nasopharyngeal mass compressing the left torus

tubarius. (Adapted from Mansour S., Magnan J., Nicolas K., and Haider H. (2018). Middle ear disease)

rent episodes. If effusion persists, then the following pathologies can happen:

1. Tympanosclerosis.

2. Atelectasis, retraction pocket, or adhesive otitis media.

3. Cholesteatoma.

In cases of ventilation tube insertion, if tubes

persisted for more than 36months, then TM perforation can occur.

quadrant of TM; posterior positioning of TT is associated with earlier extrusion.

4.7.1 Indication ofTT Insertion

1. Patient with OME has symptoms like poor school performance, balance disturbance, or behavioral issues [10].

2. Patient with bilateral OME of less than 3 months and documented hearing loss, especially when hearing loss is more than 30dB.

3. Changes to TM-like retraction may mandate TT insertion [10].

4 Otitis Media withEusion (OME)

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Note: Children with chronic OME who do not receive TT insertion should be re-evaluated at 3and 6-month interval until resolution of the effusion [11].

4.7.2 TT Types

1. Short-term tube: Armstrong, Shepard, and

Teon Reuter Bobbin. They last between 6

and 24months.

2. Long-term tubes: Modied Goode T-tubes,

buttery, Triune, and Paparella II.These tubes

can last for years (Fig.4.7).

4.7.3 Role ofAdenoidectomy

Adenoidectomy is offered in children who present with nasal obstruction or recurrent rhinorrhea. Moreover, it is considered in cases where the second trial of TT placement is warranted.

Fig. 4.7 Right ear with T-tube for more than 2 years.

(Adapted from Mansour S., Magnan J., Nicolas K., and Haider H. (2018). Middle ear disease)

4.7.4 The Complications ofTT (See

Table4.2)

Short-Term Complications

1. Otorrhea: it is the most common complica-

tion. In cases of uncomplicated otorrhea, then

topical ear drops can be used.

2. Occlusion of the tube.

3. Premature extrusion.

4. Development of granulation tissue.

5. Intrusion in the middle ear (Fig.4.8).

Table 4.2 Complications of TT

Short-term complication Long-term complication Otorrhea Myringosclerosis Premature extrusion Failure of spontaneous tube

Development of granulation tissue Intrusion in the middle ear

extrusion TM perforation

Development of cholesteatoma

Fig. 4.8 Right ear with the intrusion of the grommet into

the ME and recurrence of effusion. (Adapted from Mansour S., Magnan J., Nicolas K., and Haider H. (2018). Middle ear disease)

Long-Term Complications

1. Myringosclerosis, which is usually related to TM.

2. Failure of spontaneous tube extrusion.

3. TM perforation; it is more likely if TT remain for more than 36months.

4. Development of cholesteatoma.

AL GRAWANY

Take-Home Messages

• Ninety percent of children will have middle ear effusion by the age of 4, but the majority will resolve spontaneously.

• Ex vacuo theory and inammatory theory are the two leading theories that explain the pathogenesis of OME.

• Risk factors of OME are young age, horizontal ET anatomy, craniofacial abnormalities, adenoid hypertrophy, daycare attendance, passive smoking, recurrent middle ear infection, bacterial biolms, allergic rhinitis, gastroesophageal reux, and genetic predisposition.

• Acute symptoms are usually absent in OME, and conductive hearing loss is the main complaint in a symptomatic patient. Otoscopic ndings can show air-uid level, which is the most specic feature, Amber-colored TM, or retracted and dull TM. Tympanometry shows a at curve (type B).

• The use of topical nasal steroids can speed the clearance of the effusion and prevent recurrences.

• TT insertion is indicated in specic situations like children with poor school performance, balance disturbance, or behavioral issues or those with documented hearing loss.

• TT placement can cause some complications: some are short-term like otorrhea, premature extrusion, development of granulation tissue, and intrusion in the middle ear, but others are long-term like myringosclerosis, failure of spontaneous tube extrusion, TM perforation, and development of cholesteatoma.

A. Elhakeem et al.

References

1. Tos M.Epidemiology and natural history of secretory otitis. Am J Otol. 1984;5:459.

2. Mansour S, Magnan J, Nicolas K, Haider H.Middle ear disease. Cham: Springer; 2018. p.115–42.

3. Ehrlich GD, Veeh R, Wang X, etal. Mucosal biolm formation on middle-ear mucosa in the chinchilla model of otitis media. JAMA. 2002;287(13):1710–

5. https://doi.org/10.1001/jama.287.13.1710. Preliminary Communication April 3, 2002.

4. Miura MS, Mascaro M, Rosenfeld RM. Association between otitis media and gastroesophageal reux: a systematic review. Otolaryngol Head Neck Surg. 2012;146:345.

5. Casselbrant ML, Mandel EM, Fall PA, et al. The heritability of otitis media: a twin and triplet study. JAMA. 1999;282:2125–30.

6. Fria TJ, Cantekin EI, Eichler JA. Hearing acuity of children with otitis media with effusion. Arch Otolaryngol. 1985;111:10.

7. Roberts JE, Burchinal MR, Zeisel SA. Otitis media in early childhood in relation to children’s schoolage language and academic skills. Pediatrics. 2002;110:696.

8. Shaikh N, Hoberman A, Rockette HE, Kurs-Lasky M.Development of an algorithm for the diagnosis of otitis media. Acad Pediatr. 2012;12:214.

9. Simpson SA, Lewis R, van der Voort J, Butler CC. Oral or topical nasal steroids for hearing loss associated with otitis media with effusion in children. Cochrane Database Syst Rev. 2011;5:CD001935.

10. Rosenfeld RM, Schwartz SR, Pynnonen MA, Tunkel DE, Hussey HM, Fichera JS, Grimes AM, Hackell JM, Farrison MF, Haskell H, Haynes DS, Kim TW, Lafrenierre DC, Netterville JL, Pipan ME, Raol NP, Schellhase KG. Clinical practice guidelines: tympanostomy tubes in children. Otolaryngol Head Neck Surg. 2013;149(s1):1–35.

11. Teele DW, Klein JO, Rosner BA. Epidemiology of otitis media in children. Ann Otol Rhinol Laryngol Suppl. 1980;89:5.

Chronic Suppurative Otitis Media

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

(CSOM)

SalahMansour, Ma’inAliAl Shawabkeh, KarenNicolas, andHassanHaidar

5.1 Introduction

Chronic suppurative otitis media (CSOM) is a chronic inammation of the middle ear and mastoid which presents with otorrhea and tympanic membrane perforation (TM). Basic features are otorrhea, a sign of active disease, TM perforation, and inammatory middle ear mucosa.

TM perforation Can Be

1. Central perforation: in which the annulus is preserved. TM perforation can be anterior, posterior, inferior, or subtotal. Historically, this presentation was called tubotympanic disease. Safe ear is a new nomenclature for a mucosal disease without cholesteatomatous pathology [1] (Fig.5.1).

2. Marginal perforation: a posterior perforation with loss of the annulus or attic perforation with Pars Flaccida defect. Historically, it was

S. Mansour (*) Centre Medical Westmount Square, Otology, Westmount, QC, Canada

M. A. Al Shawabkeh ENT Department, Hamad Medical Corporation, Doha, Qatar

K. Nicolas Radiology Department, Bsalim Hospital, Beirut, Lebanon

H. Haidar Hamad Medical Corporation, Doha, Qatar

Fig. 5.1 Small anterior perforation of the right ear.

(Adapted from cholesteatoma Mansour S., Magnan J., Nicolas K., and Haider H. (2018). Middle ear disease)

named atticoantral disease. Unsafe ear, a new nomenclature, is usually associated with cholesteatoma [1] (Fig.5.2).

5.2 Epidemiology

CSOM is more common in developing countries and less prevalent in developed countries where it is mostly related to tympanostomy tube insertion. Male and female are equally affected [2]. Acute otitis media is a major risk factor for the develop-

https://doi.org/10.1007/978-3-030-54088-3_5

AL GRAWANY

S. Mansour et al.

During otitis media, a large number of inammatory cells and mucosa hyperplasia can lead to hypoxia. ET edema and obstruction can increase hypoxia. Hypoxia leads to overproduction of oxygen radicals, which result in cell damage. The cascade of events presents the following:

• Inammation → hypoxia → edema of the

mucosa → ulcerations → reparative reac-

tion → granulations → polyps → ossicular

lysis [3]

5.4 Molecular Biology ofCSOM

Fig. 5.2 Unsafe CSOM with subtotal and posterosupe-

rior marginal perforation of the left tympanic membrane with keratin debris migrating medially over the incudostapedial joint. (Adapted from Mansour S., Magnan J., Nicolas K., and Haider H. (2018). Middle ear disease)

ment of CSOM.There is still enormous nancial burden associated to acute otitis media, CSOM, and sequelae.

5.3 Etiology

CSOM is a multifactorial disease that results from the host and environmental factors. Risk factors are the same as for acute otitis media. Figure5.3 shows specic factors for CSOM.

Associated Features to CSOM

1. Eustachian tube (ET) dysfunction: Cleft palate, Down’s syndrome, patulous ET.

2. Mucosa immune system disorders.

3. Systemic immune deciency like HIV and hypogammaglobulinemia.

4. Poor mastoid pneumatization.

Healing failure of TM perforation can lead to

CSOM.Many factors lie behind this failure:

1. Persistent infection in the middle ear.

2. ET obstruction.

3. Large size perforation.

4. Mucositis, granulation tissue formation, and polyps.

Bacteria endotoxins can stimulate macrophage to produce TNF-alpha and IL-1 mediators. Immune cells can also produce IL-1 and TNFalpha. These mediators can damage the host cells and have the potential to enhance the chronicity of otitis media development. Also, IL-8 plays a role in the chronicity of CSOM [4]. Other cytokines such IL-6 and INF-gamma have been found in higher levels in the middle ear mucosa of CSOM [3, 5].

It is crucial to know that IgG and IgA are the most important immunoglobulins in the defense mechanism against mucosal infection (like in CSOM) due to their adherence to the bacterial wall, that is, coating [6]. However, Pseudomonas aeruginosa, the main agent of CSOM, lacks effective coating, and that can explain why it is difcult to eradicate this microorganism from the middle ear [7].

5.5 Microbiology ofCSOM

1. Pseudomonas aeruginosa is the most com-

mon microorganism prevalent in CSOM.They

are resistant to macrolides, extended- spectrum

penicillin, and the rst and second-generation

cephalosporins, a condition that complicates

treatment plans, especially in children.

2. Staphylococcus aureus is the second most

common organism. Klebsiella and Proteus are

other microorganisms isolated in CSOM.

Polymicrobial infections are seen in 5–10% of

cases Fig.5.4.

P. aeruginosa

Staphylococcus aureus

5 Chronic Suppurative Otitis Media (CSOM)

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Fig. 5.3 Risks factors

for chronic otitis media. (Adapted from Mansour S., Magnan J., Nicolas K., and Haider H. (2018). Middle ear disease)

Atopy

Young age

Immune

response

Bacterial/ Viral load

Genetic

predisposi

tion

Chronic otitis

media

Siblings

Attending

daycare

60% 50% 40% 30% 20% 10%

Klebsiella

Fig. 5.4 Percentage of different pathogens in CSOM

Proteus

Polymicrobial

other

Biolms formation is commonly seen in CSOM; they are microorganisms that adhere to each other and are embedded in a self-produced matrix that can act as a self-protector, hence its resistance to antibiotics.

Cases of superimposed fungal infections are encountered in excessive usage of antibiotic ear drops.

5.6 Histopathology ofCSOM

Changes observed in the mucosa of the middle ear in CSOM are:

Season

3. Increased number of ciliated cells, goblet cells, increased muco-ciliary clearance, and secretions.

4. Inammatory granulation tissue and oral polyp during the early stages of healing.

5. Fibrosis and tympanosclerosis in late stage which is a special form of the healing process.

5.7 Ossicular Chain Erosion

inCSOM (Fig.

Ossicular erosion is much more common in unsafe CSOM than in safe CSOM.

1. The long duration of the inammatory process is the most harmful factor for the ossicles [8].

2. Incudal necrosis is the most common ossicular pathology seen [8].

3. The stapes lysis is uncommon in a safe ear [8].

4. The malleus is the most resilient middle ear ossicles. In cases of subtotal perforation, the malleus is medialized due to the unopposed action of tensor tympani [8].

5.5)

1. Chronic inammatory inltrates associated with mucosal edema.

2. Middle ear epithelium metaplasia to respiratory type.

Note: TM perforation can lead to a decrease of the sound pressure difference between the external ear and middle ear, leading to hearing loss (HL). HL is dependent on the size of perforation,

AL GRAWANY

Fig. 5.5 Right chronic ear showing erosion of the lentic-

ular process of the incus with a residual brous band (black arrow) connecting incus and stapes [3]

S. Mansour et al.

not its location. Also, in the presence of a perforation, HL varies inversely with the volume of the air in the middle ear and mastoid [9].

5.8 Tympanosclerosis inCSOM

Long-standing inammatory inltrate may end up with abnormal healing process leaving mostly tympanosclerosis which is a hyaline calcareous deposits found on the tympanic membrane (myringosclerosis) (Fig. 5.6) or the tympanic cavity, ossicular chain, ligaments, or the mastoid with a secondary conductive hearing loss (CHL) (Fig.5.7) [3].

5.9 Cholesterol Granuloma

The etiology of this entity is still unclear, but it is believed to arise from the same factors leading to CSOM.Negative middle ear pressure can lead to hemorrhage into the ears, the membrane of erythrocytes ruptures releasing the cholesterol inside the ears, and that will act as a nidus for crystal formation and subsequent inammatory reaction. This can explain the microscopic appearance of cholesterol granuloma as cholesterol crystals sur-

Fig. 5.6 Tympanosclerosis (TS) limited to the tympanic

membrane in the right ear

rounded by multinucleated giant cells. Inammation can lead to the growth of that lesion in size.

Cholesterol granuloma can occur in any part of a pneumatized temporal bone. However, the petrous apex is the most common location. It can be asymptomatic, but in some patients, it can cause mass effect manifested by hearing loss, vertigo, tinnitus, and facial twitching. CT scan can demonstrate an isodense, smooth border mass that does not enhance with contrast. MRI can show a hyperintense mass in both T1 and T2, but it does not enhance with contrast due to its avascularity. In fact, it has a unique feature of hyperintensity on T1 due to its composition of protein, crystal, and hemorrhage, and this feature can distinguish it from cholesteatoma.

Treatment is based on its location and patients’ hearing status. Considering the fact that recurrence of cholesterol granuloma after surgical excision is not uncommon, then conservative treatment is advised in asymptomatic patients, and they are followed by serial MRI and CT. Drainage and ventilation are the primary goals of surgical management (see Fig.5.8).

5 Chronic Suppurative Otitis Media (CSOM)

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Fig. 5.7 (a) Reformatted coronal CT image showing a

large tympanic perforation (empty arrow), a large calcied medial attical band (short black arrow), that attaches the malleus head (long black arrow) to the tegmen. Thickened brous band along the incus (white arrow). (b)

Fig. 5.8 Cholesterol granuloma: hyper T1, hyper T2 of a

left ear. (a) Coronal T1-weighted image showing a round mass predominantly hyperintense (arrow), containing

Axial CT cut at the level of the attic: thickened bands around the incus (white arrows). Dense and thickened stapes crura (thick black arrow). Thickened stapes tendon (thin black arrow)

some central hypointense structures and (b) coronal T2-weighted image showing the same hyperintense aspect of the mass lesion (arrow)

5.10 Clinical Features

2. Hearing Loss (HL): it can be conductive hear-

ing loss (CHL), caused by TM perforation and/

The two classic symptoms are otorrhea and hearing loss.

or ossicular erosion. HL caused by TM perfora-

tion only is larger at low frequencies and

decreases with increasing frequencies; it is not

1. Otorrhea: moderate to profuse, continuous or intermittent, serous or mucoid, and sometimes purulent.

related to the location of the perforation [8] and varies inversely to middle ear and mastoid air volume.

AL GRAWANY

S. Mansour et al.

5.10.1 Otoscopy

1. TM perforation: can vary in size and location (central or marginal). Note: multiple TM perforations associated with pale granulation tissue and facial palsy can indicate tuberculosis.

2. Status of the mucosa of the middle ear: Swollen and edematous. Aural polyps may be present.

3. Ossicular status: the most common abnor- mality is the disruption of the incudostapedial joint, necrosis of incus long process, and medialization and shortening of the handle of malleus.

4. Secondary otitis externa.

5. ET function assessment through nasal mucosa evaluation is highly valuable for the diagnosis and prognosis.

5.10.2 Audiology

Hearing assessment by using 512-tuning fork and audiogram. Depending on the mucosal edema and granulation tissue, TM perforation can lead to CHL between 5 and 40dB.CSOM can cause sensorineural hearing loss (SNHL) due to the effect of toxins and inammatory mediators on the inner ear hair cells, mostly on the basal turn. This explains why CSOM patients may be associated with high-frequency SNHL [10].

5.11 Imaging Studies

For patients with CSOM, high-resolution temporal bone CT scan may provide additional information, especially when clinical ndings are in favor of a safe ear but with complex clinical presentations as in:

• A long-standing disease with recurrent episodes of active inammation.

• Cases unresponsive to medical treatment.

• Suspicion of complications.

Preoperative clinico-radiological correlations

may orient the surgical strategy.

1. When TM perforation is central and CT shows that AER, Attic and Antrum (AAA spaces) are well aerated: simple condition—safe ear.

2. When TM perforation is central, but CT shows extended condensations of AAA spaces or condensation of the AER alone, with the scutum, tegmen, cog, and other bony frontiers of the cavity are intact (image of lysis of the long process of the incus could be associated): this is a presentation of the extensive inammatory process—safe ear [3] Fig.5.9

3. When TM perforation (not typically central) with condensation images in the ME cavity is associated to any sign of bony lesion (scutum, tegmen, cog, and bony limits of the mastoid

ab c

Fig. 5.9 (a) Axial CT image showing central perforation

(between two small arrows). Condensation images in the ME cavity (asterisk). (b) Axial CT showing condensation of the entire attic (external attic: black empty arrow, AER:

empty white arrow) A antrum. (c) Lyses of the incudostapedial joint (long arrow). The scutum is intact! (short arrow). There is extended inammation, but it is still a

safe ear

5 Chronic Suppurative Otitis Media (CSOM)

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abc

Fig. 5.10 CT of an 88-year-old man with chronic otor-

rhea and otalgia. (a) Coronal CT showing posterosuperior tympanic perforation. (b) Coronal CT showing intact scutum (short arrow). Condensation images (long arrow) along the ossicular chain start to erode the malleus. (c)

cavity), these features are in favor of an unsafe ear—cholesteatoma [3] (Fig.5.10).

In this context, any lyses of the ossicular chain, incus, and especially of malleus or stapes are in favor of such unsafe ear [3].

5.12 Complications andSequelae

Nowadays, complications of CSOM are decreasing because of early and better control of the infectious process; nevertheless, they remain of serious concern since they still are life- threatening in unfavorable socioeconomic regions [3] (see Chap. 6).

Complications are due to hematogenic or contiguous spread of the infection [3] and could be:

1. Intratemporal: labyrinthine stula, VII

palsy, Mastoid abscess, petrositis, and

labyrinthitis.

2. Extratemporal:

(a) Intracranial such lateral sinus thrombo-

phlebitis, meningitis, and intracerebral access.

(b) Extracranial such as subperiosteal abscess

or Bezold’s.

Axial CT showing complete condensation of the AER with bone lysis of the anterior bony border (empty arrow) and absence of the cog (should be seen between the black arrows). These are signs in favor of cholesteatoma: unsafe ear

5.13 Treatment ofCSOM

5.13.1 Medical Treatment

The main goal of medical treatment is to obtain dry ear as early as possible before surgical treatment. Medical treatment depends on the following steps:

1. Aural toilet: regular in-ofce toilet clearance and placement of ear wick in case of edematous external skin canal.

2. Ototopical ear drops: Including: (a) Quinolones: they have a low incidence of

ototoxicity and vestibulotoxicity.

(b) Aminoglycosides: they have signicant

potential of inducing ototoxicity and vestibulotoxicity despite the protective edematous mucosa of the round window membrane in CSOM.

20% of gram-negative remain sensitive to neomycin, while polymyxin B is still effective.

3. Control of granulation tissue: as these tissues can block the antibiotics from reaching the infected site. Steroid may help in the resolution of the granulation tissues.

AL GRAWANY

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