Secretory Otitis Media

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耳鼻咽喉科学 郑州大学一附院 • 1. Secretory Otitis Media (分泌性中耳炎) • 2. Acute suppurative otitis media • • • •

( 急性化脓性中耳炎) 3. Chronic suppurative otitis media (慢性化脓性中耳炎) 4. The complications of the chronic suppurative otitis media (慢性化脓性中耳炎并发症 ) 5.Idiopathic Facial Paralysis(Bell’ Palsy) (面神经麻痹、面瘫) 6. Otosclerosis (耳硬化症) 1

Secretory Otitis Media (分泌性中耳炎) Outline: The classification of middle ear

conditions connected with effusion varies a great deal and terms such as ‘serous otitis media’, ‘catarrhal otitis media’, ‘secretory otitis media’ and ‘gule ear’ are often used as synonyms. This confusion prevents accurate assessment of clinical and epidemiological studies and restricts the value of comparisons between the clinical and laboratory data.

2

1. Symptoms • There is a felling of pressure and fullness in the

• •

ear often accompanying an infection of the upper airway and a considerable decrease in hearing on one or both sides. Noises are heard in the ear on yawning,swallowing,and sneering. The patients do not have pain .

3

2. Pathogenesis • Tubal incompetence and the resulting reduced

tympanic pressure are preeminent. Obstructive processes of the nasopharynx, disorder of tubalkinetics, especially incompetence of the muscles opening the tube in cleft palate,and virus infections are the most common underlying mechanisms. • Experimental infection of the middle ear of guineapigs produces a section in less than 2 weeks,but in humans the timing of the onset of the disease has not been accurately defined. 4

• The onset may be very insidious and not precipitated by an acute inflammatory attack but the possibility alwayas remains that the middle ear process may have started at some time during antibiotic treatment for an upper respiratory illness during the subclinical stage of acute otitis media.

5

3. Diagnosis • Otoscopy shows a markedly retracted tympanic

• •

membrane with localized protrusion, an exudate in the middle ear,and a dark discoloration behind the tympanic membrane ( the so called “blue drum”) with a blackish fluid level . There is a conductive deafness for the entire frequency range of 40 to 50 dB. A typical impedance curve ( flat curve ) is found.

6

• The primary cause shows chronic inflammation of •

the adenoids, sinusitis, rhinitis,allergy,or tumor. The nasopharygeal cancer is also a cause of the disease,for it can obstruct the Eustachian tube.

7

4.Treatment • 1.Surgical restoration of tubal patency by adenoid• •

ectomy or re-adenoidectomy under direct vision and elimination of infection of sinuses. 2.Paracentesis and drainage of the middle ear. The tympanic membrane is incised in the anteroinferior guadrant,under general anesthesia in children and under local anesthesia in adults. The middle ear effusion is aspirated out and long-term drainage is provided for at least 6 months by introduction of a drainage tube(or “grommet”).

8

• 3.Laser treatment. Using the laser to make a • •

appoprate hole on the tympanic membrane , the hole will heal in one month or more. 4. Using vasoconstrictor nose drops to relieve the troublesome nasal obstruction. 5. Antibiotics shoud be used.

9

Acute suppurative otitis media ( 急性化脓性中耳炎) 一 . Symptoms

1.

In the first phase of exudative inflammation which lasts for 1 to 2 days, there is an increase of temperature to 39° to 40° C, and in severe cases ,rigors, and occasionally meningismus in children. The patient has a severe pulsating pain worse by night than by day. There is a muffled noise in the ear synchronous with the pulse, deafness, and sensitivity of the mastoid process to press. There is often no fever in older patients.

10

• 2. The second phase of resistance and demarcation lasts 3 to 8 days

. The pus and middle ear exuade usually

discharge spontaneously where upon the pain and fever

• •

subside.This phase can be considerably shortened by early application of an appropriate antibiotic, which also prevents spontaneous perforation of the tympanic membrane. 3. In the third healing phase lasting 2 to 4 weeks, the aural discharge dries up and the hearing return to normal. If the disease is not treated in time , it can occure the serious complications.

11

二 . Pathogenesis The effects of the acute inflammtion on anatomy and physiology explain the clinical presentation and natural history of the condition.The normal function of the middle ear has an impedance matching mechanism requires it to be filled with air at atmospheric pressure. However, oxygen is being continually absorbed from the middle ear spaces by the blood vessels in its mucosa. To correct this developing negative intratympanic pressure, the Eustachian tube is opened periodically to allow aeration and pressure equalization. The tube is shorter,wider and more horizontal in infant.

12

• A disturbance in the normal aeration of the middle ear

may cause a pathological sequence of events leading to acute suppurative otitis media. • Route of infection: The tubal route is the most common . • Hematogenous infection is unusual and occurs in measles, scarlet fever,typhus,and septicemia. Exogenous infection requires rupture of the tympanic membrane or preceding perforation allowing peneration of bath water or dirt duringirrigation of the ear. Incorrect methods for the removal of a foreign body from the external meatus are also another a cause.

13

三 . Organism • The infecting organisms in decreasing order of frequency are: streptococci in adults,pneumococci in children,Hemophilus influenzae, staphylococci and coliforms.

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四 . Diagnosis • 1. Otoscopy shows hyperemia,then moist infiltration and opacity of • • • •

the surface of the tympantic membrane. The contours of the handl of the malleus and its short process disappear. 2.Hemorrhagic bullae form on the tympanic membrane. The patient has a conductive deafness. The mastoid process is tender to pressure as a result of the accompanying mastoiditis. 3.Before spontaneous rupture,a pinhole-size fistula forms. This discharges a pulsating ,thin,fluid,odorless pus.

15

五 . Differential diagnosis • One must consider otitis externa. In the latter

disease, there is pain on pressure on the tragus,the exudate is not pulsating,is usually fetid,and is never mucoid. There is little or no deafness.

16

六 Treatment • 1.Systemic antibiotics in high dosages are given,not

only until the symptoms abate but for a further 10 days.Penicillin and other broad-spectrum penicillins are indicated; • 2. Nasal drops(1% 麻黄素) are given to decongest the mucosa of the nasopharynx around the opening of the tube; • 3.Culture and sensitivity tests are performed and appropriate antibiotics given if the tympanic membrane perforates.

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• • • •

Paracentesis in the following circumstances: 1.Marked bulging of the tympanic membrane; 2.Persisting high fever and sever pain ; 3.Unsatisfactory spontaneous perforation with incomplete differentiation of the tympanic membrane.

18

Chronic suppurative otitis media (慢性化脓性中耳炎)

• 一、 Chronic mucosal inflammation • 1.Concept: Chronic mucosal inflammation is a form

• •

of chronic otitis media in which the inflammation is mainly confined to the mucosa. It usually does not cause progressive bone destruction and therefore is free of complication,but runs a protracted course. 2.Symptoms: (1) There is a chronic discharge of mucoid, purulent, odorless exudate. The otitis demonstrates periods of complete freedom from symptoms, alternating with acute exacerbation. The exudate may be creamy and purulent in acute phase and then becomes mucoid and 19

• • • •

stringy as the infection resolves.It is, however, always odoreless; (2) Hearing. The patient has a conductive deafness; (3) Pain. The pain is absent,and the general condition is good. 3.Pathgenesis. This is not a disease with a unique cause, but it is the end result of several different primary disease processes. The inflammation remains confined to the mucosa but in certain patients lead in time to a rarifying osteitis,I.e., a chronic inflammatory destruction of the ossicles,e.g., the long process of the incus( 砧骨 ).

20

• In contrast to cholesteatoma, this destructive process of • • • •

bone is unusual and less likely to extentd and progress. 4.Pathogenetic factors. (1) Constitutional reduced mucosal(immunological) competence; (2) Type, pathogenicity,virulence, and resistance of the bacterial organisms; (3) Anatomic conditions of the middle ear such as pneumatization, and the connections between the attic, antrum, middle ear cavity,and eustachiantube;

21

• (4) Disordered function of the eustachian • • • •

tube,I.e., in patients with cleft palate; (5) Generalized diseases such as allergy,immune defects,cachexia,and diabets. 5.Diagnosis (1) The history shows a chronic recurrent aural discharge with reduced hearing; (2) The otoscopic findings include a central defect of the tympanic membrane, scarring of the pars tensa, and occasionally aural polys due to mucosal hyper plasia in acute exacerbations. 22

• •

• • • • •

(3) Radiographs. CT shows either reduced pneumatization or opacity of the cell system,if it is well pneumatized, and occasionally signs of bony destruction .This is regarted as the signs of chronic mastoiditis. (4) Hearing. The audiogram shows a conductive deafness. 6.Differential diagnosis. (1) Acquired cholesteatoma of the middle ear; (2) Aural tuberculosis ; (3) Middle ear carcinoma.

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• 7.Treatment • • • • •

1.Conservative measures to dry up the middle ear. The external meatus is cleaned periodically. Pus is taken for culture and sensitivity tests,and the appropriate systemic and local antibiotics(3% hydrogen peroxide solution;0.3% ofloxacim, 氧氟沙星 ) are given, One must take car not to use ototoxic drugs(gentamycin solution). Aural polys shoud be removed. Chronic infections of the nasopharynx and paranasal sinuses must be looked for.

24

• 2. Mastoidectomy may be carried out to •

eliminate the foci of infection in the temporal bone and the middle ear cavity. A tympanoplasty may be carried out to reconstruct the sound –conducting apparatus,i.e., the tympanic membrane and the ossicular chain.

25

Acquired cholesteatoma of the middle ear (胆脂瘤性中耳炎) • 1. Symptoms. • (1) Fetid otorrhea which is sometimes minimal or • •

completely absent,when present always purulent,and never mucoid; (2) Progressive deafness, possibly dizziness; (3) Otalgia and fever in acute exacerbations;

26

(4) Dull headaches or a felling of pressure in the head. 2. Pathogenesis An acquired middle ear cholesteatoma is not a tumor but a chronic inflammation which, unlike chronic mucosal inflammation,causes progressive destruction of the bony structures. 3.Promoting factors. • 1. Disordered ventilation and drainabe of the middle ear(chronic reduction of pressure) with • hypopneumatization; 2. Displaced squamous epithelium as a result of the capacity for growth of the meatal skin in • the upper

• • •

to be continued • – capacity for growth of the meatal skin in the upper part of the anulus tympanicus ( the papillary ingrowths form the later matrix either as a result of invagination of the pars flaccida or by formation of a retention pocket in the pars tensa); – 3. An increased proliferative tendency of the stratum germinativum caused by the stimulus of inflammation; – 4. Incompletely resolved embryonal hyperplastic mesenchymal remnaats n the submucosa of the middle ear which later form the perimatrix.

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• part of the anulus tympanicus (the papillary

• •

ingrowths form the later matrix either as a result of invagination of the pars flaccida or by formation of a retention pocket in the pars tensa); 3. An increased proliferative tendency of the stratum germinativum caused by the stimulus of inflammation; 4. Incompletely resolved embryonal hyperplastic mesenchymal remnants the submucosa of the middle ear which later form the perimatrix. 28

• 4. Histopathgenesis • A cholesteatoma may form a compact sac of

desquamated lamellae arranged like the layers of an onion and connected with a fairly thick pedicle to its site of origin from the tympanic membrane. Alternatively,it consists of a widely fanned-out cholesteatoma matrix lining the antrum and mastoid cavity and sending off shoots into the furthest bony niches of the bony process. The bone destruction is caused first by enzymes (e.g., collagenase ) formed in the perimatrix and second by osteoclastic destruction of bony tissue,I.e., a chronic osteomyelitis.

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• 5. Diagnosis

(1) Fetid otorrhea; (2) Radiography: The CT of the temporal bone is now recognized as the most useful and versatil procedure for demonstrating bone destruction in the petrous pyramid, soft-tissue abnormalities in the middle ear, and extention of the cholesteatoma into the cranial cavity; (3) Audiometry: The audiogram shows a conductive deafness possibly combined with sensorineural deafness;

(4) Facial nerve: The disease may cause facial paralysis.

30

• 6. Treatment • The disease should be treated by surgery as soon as possible , because the disease may at any time develop the lifethreatening complications. • Perpose of the operation: • 1.Radical removal of the cholesteatoma with its matrix and perimatrix; • 2.Reconstruction of the sound pressure protection of the round window and of the sound pressure transformation between the tympanic membrane and the oval window by means of:

31

(1) Closure of the perforation of the tympanic membrane with fascia or perichondrium; (2) Reconstruction of the direct connection between the tympanic membrane and stapes footplate if the ossicular chain is defective, i. e.,construction of acolumella to bridge the defect using a bone, cartilage,or synthetic prosthesis; (3) Separation of the middle ear cavity from the external meatus by reconstruction of the posterior meatal and lateral attic walls by bony or cartilaginous graft or preservation of the intact bony meatal wall.

32

The complications of the chronic suppurative otitis media (慢性化脓性中耳炎并发症 ) • 一 .Labyrinthitis • 1. Symptoms: Dizziness,nausea,vomiting,whistling

noises in the ears,and deafness develop within a brief period. The patient has no fever and no pain. • 2.Treatment: Intravenous antibiotics are administered in high doses by continuous infusion. The middle ear should be drained ,and a mastoidecomy may need to be carried out immediately.

33

• • • • •

二 .Epidural empyema( 硬膜外脓肿 ) 1.Symptoms: Dull pulsating pain in the head, otorrhea ,and subfebrile temperature occur. There is no completely characteristic pattern of symptoms. 2.Treatment: Immediate mastoidectomy with wide exposure of the dura,drainage,and antibiotics are indicated.

34

• 三 .Otogenic meningitis( 耳源性脑膜炎 ) • 1. Symptoms: • Headaches,stiffness of the neck,scaphoid • • •

abdomen, increasing loss consciousness, photophobia, restlessness,tonicclonic convulsions,and facial paralysis. Typically there is bounding pulse,irregular breathing,and a fever of 39 º to 40º C. 2.Treatment: Antibiotics are given intravenously in high dosages determined by sensitivity tests, Immediate mastoidectomy 35

• shoud be carried out immediately.

36

四 Otogenic sinus thrombosis( 乙状窦血栓性静脉炎) 1.Symptoms: Chills, a spiking temperature chart,with several peaks on the same day, increased pulse rate, headaches, vomiting,somnolence,neck stiffness,dyspnea due to septic lung metastases or pneumonia. • 2.Treatment: • Immediate surgical excision of the primary inflammatory focus in the mastoid and sigmoid sinus by cortical or by mastoidecomy for cholesteatoma is performed.

• • •

37

• 五 Otitic hydrocephalus( 耳源性脑积 水)

• 1.Symptoms: • Failing vision,vomiting, double vision, jacksonian epilepsy, pareses and disorders of sensation. • 2.Treatment: • Mastoidectomy and antibiotics are given intravenously in high dosages determined by sensitivity tests .

38

• •

六 Otogenic brain abscess (耳源性脑脓肿)

• 1.Symptoms: • (1) Initial stage: • • • •

Meningismus,nausea,headache,psychological changes,fever; (2)Latent stage: Epileptiform attacke,neurologic signs; (3)Manifest stage: Papilledema,psychological changes,focal signs of aphasia,

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• alexia,agraphia,hemiplegia,epileptic attacks,and ataxia in

• • • •

cerebellar abscess. Symptoms due to spread to neighboring organs include cranial nerve paralysis,visual field defects,disorders of the oculomotor system and of posture. (4) Terminal stage: Stupor,coma,conjugated deviation to the side of the lesion, bradycardia,and Cheyne-Stokes respiration (潮式呼吸) . 2.Treatment: Mastoidectomy,removal of the brain abscess,antibiotic.

40

• In a word,the complications of

the chronic suppurative otitis media was usual before,but nowdays,it is usually controlled by antibiotics and has therefore become rare.

41

Idiopathic Facial Paralysis(Bell’ Palsy) (面神经麻痹、面瘫) • The incidence of the most common form of

intratemporal facial palsy,i.e. Bell’ palsy ,varies in

• • • • • •

Europe between 11.5 and 18.8 patients per 100000 per year.Higher figures are reported from countries like Egypt,Columbia and India. In order of frequency the most common forms of intratemporal facial palsy are: (1) idiopathic or Bell’ palsy (39.7%); (2) trauma (24.7%); (3) tumours (12.5 %); (4) herpes zoster oticus (6.8%)( 耳带状疱疹 ); (5) acute and chronic otitis media (5.5%). 42



• •

Bell’ palsy are evenly distributed in children and adults.Palsies due to acute middle ear infections predominate in children,whereas herpetis lesions characteristically occur in the adult. Tumours originating from the facial nerve (neurinomas,haemangiomas) or involving the seventh nerve (glomus jugulare tumours,meningiomas, epidermoids) are mostly found in adults. 1.Cause: It may be a disturbance of the microscirculation leading to a serous inflammation with the formation of edema.

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• The bony canal is unyielding( 不易扩张 ) ,and

compression of the nerve leads to ischemia and venous congestion so that a vicious circle is set up. A virus infection may also be responsible. • 2. Clinical picture • Idiopathic palsy is the most common form of isolated facial palsy. It is of sudden onset and occurs at any age,particularly in healthy adults of 20-35 years and children of 6-12years of age. Exposure to cold, emotional stress, and pain over the mastoid may precede the onset of the lesion.

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• Bilateral idiopathic facial palsy has been noted to

• •



occur in 1.5-2% of all Bell’s palsies and must be differentiated from alternating or recurrent Bell’s palsy which are more common. 3 Diagnosis: In a peripheral paralysis all three branches are affected. The secretion of tears and the sensitivity for taste are affected, and hyperacusis may occur due to disruption of the stapedius reflex. The topographical diagnosis of peripheral lesions of the facial nerve should be made.

45

• (1) Taste test: The anterior two-thirds of the tongue



• •

is innervated by the chorda tympani. The test stimulus is 20% sugar,10% saline, or 5% citric acid solution; (2) Schirmer’s test: The reduction of the secretion of tears due to interruption of the lacrimal anastomosis in the greater superfical petrosal nerve is measured on the paralyzed side; (3) The stapedius reflex test: is measured by impedance audiometry; (4) the severity and prognosis of a paralysis can only be determined by electrodiagnosis. 46

• 4.Treatment • The treatment includes injection of steroids, •



stellate ganglion block, and low-molecular-weight intravenous infusion of dextran. Schedule for prednisone in the treatment of idiopathic facial paralysis: 60 mg for 4 days reducing by 5 mg daily to 5 mg on the 15th day,followed by intermittent dosage of 5 mg for 10 days. Immediate decompression of the nerve should be undertaken for progressive denervation after careful assessment of the indication. 47



The principle of treatment is to decompress the nerve fibers by exposure of the nerve and slitting of its sheath.

48

Otosclerosis (耳硬化症)

• • • • •

Otosclerosis is a localized disease of the bony labyrinthine capsule,the cause of which has still not been explained. 1.Symptoms: Depending on the site of the otosclerotic focus,the symptoms include: (1) Conductive deafness of the middle ear type in about 80% of patients; (2) Mixed conductive and sensorineural deafness in about 15% of patients; (3) Pure sensorineural deafness in about 5% of patients. 49

• • • • • •

The disease declares itself subjectively by: (1) A slowly progressive hearing loss which initially usually affects one ear, but later affects both ears in most patients; (2) Constant, progressive tinnitus. The disease never causes otalgia, otorrhea,dizzness, or disorders of balance. 2. Pathogenesis: The disease appears to have a multifactorial cause,which the following being the most important:

50

• (1) Heredity and Constitution; • (2) Disorders of hormone and bone metabolism; • Otosclerosis is due to an extremely localized disorder of

mineral or bone metabolism with an abnomal increase of enzyme activity of the mesenchymal cells of the labyrinthine capsule mainly by genetics but also by hormonal disturbances. The newly reformed bone fixed the stapes footplate in the oval window.

• 3.Diagnosis • •

There is often a positive family history. Otoscopy occasionally shows hyperemia of the promontory shining through the tympanic membrane

51

• (Schwartze’s sign). • Functional symptoms include middle ear deafness, • • • •

occasionally with an inner ear companent. Gelle’s test is abnormal. A pure-tone audiogram usually shows a pure middle ear deafness, occasionaly a mixed deafness, and exceptionally a pure sensorineural deafness with positive recruitment. There is often a characteristic notch of the bone conduction curve at 2,000 Hz (the carhart notch). Impedence audiometry usually shows a normal curve at

52

• normal pressure. However ,the stapedius reflex is • • •

often suppresed due to otosclerosic fixation of the footplate. Radiography usually shows very good pneumatization of the temporal bone 4.Treatment: Stapedectomy is performed.

53

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be to continued • 6. Differential diagnosis: • (1) Carcinoma of the middle ear or external •

meatus; (2) Tuberculosis of the middle ear.

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