CASE PRESENTATION

ACUTE OTITIS MEDIA

Supervised by:

dr. H. Oscar Djauhari, Sp. THT-KL

Presented by:Adrienne Trinovia Sulistyo 2011.061.020Daniela Angelina 2012.061.001

Clinical RotationOtolaryngology, Head and Neck Surgery Department

Medical Faculty of Unika Atma JayaSyamsudin, S.H. Regional General Hospital, Sukabumi

July 8th, 2013 – August 3rd, 2013

1

CASE DISCUSSION

A 7-year-old boy came to ENT clinic with a complaint of right earache since 3 days ago. He

was also having cold, runny nose and fever since 7 days ago.

A. PATIENT’S IDENTITY

Name : R

Gender : Male

Age : 7 years old

Occupation : Primary school student

Address : Cikole

B. HISTORY

Chief Complaint : right earache since 3 days before admission to the hospital

Additional Complaint : cold, runny nose, and fever

History of Present Illness

A 7-years-old boy came to ENT clinic with right earache since 3 before

admission. The earache was felt insidiously and continuously all day long. The pain

was increasing in severity, from mild pain at the beginning and became more severe at

the time of presentation. He also felt fullness inside his right ear. There was a high-

grade fever following this earache. History of ear discharge, tinnitus and hearing loss

was denied.

Seven days before admission, the child suffered from runny nose, cold, and

fever. The nasal discharge was clear, watery, and massive in amount. The boy also had

low-grade fever during the cold.

The boy has not been given any medication.

History of Past Illness

History of previous illness was denied

History of Family Illness

History of family illness was denied

2

C. PHYSICAL EXAMINATION

General condition : Moderately ill

Body weight : 19 kg

Height : 44 cm

Blood pressure : 110/60 mmHg

Pulse : 120 beat per minute

Respiratory rate : 22 times per minute

Temperature : 38, 8oC

ENT Examination

Ear

Right ear

- Auricle : with in normal range

- External auditory canal :

hyperemic (-), edema (-), mass (-), laceration (-) secretion (-) , cerumen (-)

- Tymphanic membrane :

Intact, hyperemic (+), bulging (+), decreased light reflex

Left ear

- Auricle : with in normal range

- External auditory canal :

hyperemic (-), edema (-), mass (-), laceration (-) secretion (-) , cerumen (-)

- Tymphanic membrane:

Intact, bulging (-), retraction (-), light reflex (+)

Nose

Right nose

- Mucous membrane:

hyperemic (+), edema (+), watery and clear discharge (+), mass (-), laceration

(-) , crust (-)

- Inferior conchae : eutrophy

- Septum : no deviation

3

- Air passage : normal

Left nose

- Mucous membrane:

hyperemic (+), edema (+), watery and clear secretion (+), mass (-), laceration

(-), crust (-)

- Inferior conchae : eurtrophy

- Septum : no deviation

- Air passage : normal

Oropharynx

- Posterior pharynx : hyperemic (-)

- Palatine tonsils : T1 / T1, hyperemic (-), detritus (-)

- Uvula : symmetrical

- Dental : no abnormatlities

Maxillofacial : symmetrical, no tenderness

Neck : mass (-), lymphadenopathy (-)

D. WORKING DIAGNOSIS

Acute otitis media dextra, suppurative stage

E. DIFFERENTIAL DIAGNOSIS

-

F. TREATMENT

Outpatient care

Antibiotic : Amoxicilin 3 x 500 mg PO for 7 days

Antipyretic and analgetic : Paracetamol 3 x 250 mg PO for 3 – 5 days

Topical anticholinergic : Ipatropium nasal spray 3 x 2 sprays per nostril for 2 –

4 days

4

ACUTE OTITIS MEDIA

Otitis media (OM) is the most common reason for an illness-related medical visit in

preschool-age children (1). National expenditures for treatment of otitis media in children

younger than 13 years are more than $4 billion per year (2,3). Non-life-threatening

complications such as conductive hearing loss are common, and much controversy exists

about the importance and management of such complications (4). Serious complications still

occur despite the improvements in diagnosis and treatment of OM (4).

Definitions and Terminology

Otitis media represents an inflammatory condition of the middle ear and mastoid

space, without reference to etiology or pathogenesis (5). Numerous terms and classifications

have been used to define the various inflammatory processes related to OM. The current

terminology is based on knowledge of the pathogenesis of OM as well as on the etiology and

clinical course. The presence or absence of middle-ear effusion (MEE) and its duration help

further to define the process. Effusion is the liquid resulting from infection and mucosal

inflammation and can occur in all areas of the pneumatized temporal bone. Effusion may be

serous (thin, watery), mucoid (thick, viscous), or purulent (pus). The temporal sequence of

the process may be described as acute (0 to 3 weeks in duration), subacute (3 to 12 weeks in

duration), or chronic (longer than 12 weeks in duration). However, the duration of the disease

can be very difficult to determine unless the patient's previous middle-ear status is known to

the examiner. Tympanograms and audiograms obtained previously can often help to define

the duration further.

The term recurrent AOM indicates four or more episodes of acute OM in 1 year or

three or more episodes in a 6-month period. Medically refractory AOM has persistent signs

and symptoms of AOM despite appropriate medical therapy (6). Otitis media with effusion

(OME) can occur as a postinflammatory response to AOM, from a viral infection, or because

of Eustachian-tube dysfunction (7). When OME is a persistent fluid collection, it can cause

decreased mobility of the tympanic membrane, serving as a barrier to sound conduction (8).

Many children with OME are asymptomatic. Chronic suppurative otitis media (CSOM) is

characterized by persistence of purulent otorrhea through a tympanic membrane (TM)

perforation or tympanostomy tube (TT) that is unresponsive to medical therapy. Further

5

description of the TM (intact, perforated, TT present, retracted, atelectatic, or presence of

tympanosclerosis) will help more clearly define the examination (5).

Epidemiology

The epidemiology of OM has been well studied (2,5). The onset of AOM during the

first year of life is important because the majority of children with multiple recurrences of

AOM have their first episode before the age of 12 months (5). If a child has not had OM

before the age of 3 years, he is statistically unlikely to develop severe or recurrent OM. In a

study by Bondy et al. (2), the proportion of children with a diagnosis of OM was highest

(42% to 60%) in the 7- to 36-month age range. Other studies have shown the highest

incidence of AOM for both sexes was in the 6- to 11-month age group (4,5).

More than 50% of children experience OME in thefirst year of life (9). Although

many episodes resolve spontaneously, 30% to 40% persist, and 5% to 10% of episodes last 1

year or longer (5,10). OME is diagnosed 2.2 million times annually (3). Investigations

involving healthy children have revealed a high incidence of asymptomatic OME (5). The

incidence of OME appears to peak during the second year of life, is most prevalent during the

winter months, and is associated with upper respiratory infections (URIs). Most children have

resolution of asymptomatic MEE within a few months without medical or surgical

intervention (5). Spontaneously, 30% to 40% persist, and 5% to 10% of episodes last 1 year

or longer (5,10). OME is diagnosed 2.2 million times annually (3). Investigations involving

healthy children have revealed a high incidence of asymptomatic OME (5). The incidence of

OME appears to peak during the second year of life, is most prevalent during the winter

months, and is associated with upper respiratory infections (URIs). Most children have

resolution of asymptomatic MEE within a few months without medical or surgical

intervention (5). In some studies, the incidence of AOM is similar between boys and girls.

However, several other studies have shown a higher incidence in boys than in girls (5,9).

Although some studies have shown an increased incidence of OM in American white and

Hispanic children in comparison to American black children, Casselbrant and colleagues (11)

and Paradise et al. (11a) found that black children had at least as much middle-ear disease as

did white children who had received equivalent care. A very high incidence of middle-ear

infections has been reported in Native Americans and Eskimos, despite excellent access to

medical care (5).

Casselbrant and colleagues (11b) showed a strong genetic predisposition to OM, with

a higher incidence of OM in children who have siblings or parents with a significant history

6

of OM. Children who live in crowded households or low socioeconomic conditions or who

have poor medical care or both also have been found to have an increased incidence in both

acute and chronic OM (12). These factors are not definitive in all studies, however, and may

simply reflect increased exposure to many other children with URIs. In addition, the relation

between attending day care and an increased incidence of OM in children younger than 3

years is well established (5,12,13). Contributing factors for this increased incidence include

exposure to large numbers of other children (often with URIs), decreased breast-feeding, and

exposure to second-hand smoke. Seasonal variation in the incidence of OM also has been

reported, most commonly in winter, fall, and spring (5). All studies have shown a correlation

between the frequency of URIs and incidence of OM, and MEE that is associated with URI in

the winter months lasts longer than in the summer (5).

Risk Factors for Middle-Ear Disease

Many medical and or anatomic abnormalities have been noted to increase the risk of

middle-ear disease. Craniofacial anomalies affecting Eustachian tube (ET) function often

increase the risk of OM. Children with a cleft palate or deformity of the midface, skull base,

or nose/paranasal sinuses have a statistically higher incidence of OM at all ages, especially

during the first 2 years of life (5). Although some studies have shown that the incidence of

middle-ear disease decreases after surgical repair of the cleft palate, many children with a

cleft palate continue to have middle-ear problems. Other craniofacial disorders associated

with an increased risk of OM include Down syndrome, Apert syndrome, and the

mucopolysaccharidoses (5).

Children with congenital or acquired immunodeficiency are at a higher risk of many

types of infection, including middle-ear disease. Children with conditions such as

hypogammaglobulinemia, immunoglobulin (Ig)A deficiency, DiGeorge syndrome, human

immunodeficiency virus (HIV) disease, and drug-induced immunodeficiency (chemotherapy,

steroids) often have difficulty fighting and clearing infections. Infants and young children

have immature immune systems, which appear to make them more susceptible to OM.

Other conditions associated with an increased incidence of OM include allergy, nasal

obstruction (sinusitis, adenoid hypertrophy, nasal or nasopharyngeal tumors), ciliary

dysfunction, and prolonged nasal intubation or nasogastric tube placement, and possibly

gastroesophageal reflux (5,14). A role for allergy in the etiology of OM has long been

postulated (Fig. 91.2). The first OME guideline found no data supporting antihistamine-

decongestant combinations in treating OME (12). Meta-analysis of four randomized trials

7

showed no significant benefit for antihistamines or decongestants versus placebo. The second

OME guideline found that no additional studies have been published since 1994 to change

this recommendation (7).

Most children with recurrent or persistent OM have intact immune systems. However,

if the middle-ear infections are especially severe or are associated with recurrent sinusitis,

bronchitis, or gastrointestinal problems, immunologic abnormalities may be present. The

middle-ear mucosa has a secretory immune system similar to the rest of the respiratory tract.

Middle-ear effusions that result from acute or chronic infection contain immunoglobulins

IgA, IgG, IgM, IgD), immune complexes, and chemical mediators involved in the

inflammatory response. Possible humoral immune deficiencies in children with OM include

IgA, IgG (especially of IgG subclasses 2 and 3), and complement deficiency (5,15). Otitis

media also may be one of the multiple infectious complications seen in the presence of

neutropenia or HIV disease. Defects in immune cell function such as problems with

chemotaxis, phagocytosis, and killing can predispose to OM. In comparing otitis-prone

children with those who have only occasional episodes of OM, Prellner and Kalm noted a

decreased ability of the OM-prone children to produce antibodies against AOM-associated

antigens, and these children also may have delayed B-cell maturation.

Pathophysiology

Abnormal function of the ET is the cornerstone of the pathogenesis of OM. The ET in

infants and children is shorter, more horizontal, and functionally less mature compared with

that in adults. Conditions such as URIs lead to edema and congestion of respiratory mucosa

of the ET and middle ear, causing narrowing of the ET lumen. This leads to an increase in

8

negative middle-ear pressure, causing an influx of bacteria and viruses from the nasopharynx

when the ET opens. The bacteria and viruses in the middle ear then elicit an inflammatory

response (5). The acute inflammatory response includes mucosal edema, capillary

engorgement, and infiltration of polymorphonuclear leukocytes into the middle-ear space. As

the inflammatory response becomes chronic, infiltration of lymphocytes, proliferation of the

mucosal lamina propria, enzymatic destruction of bone, and granulation tissue formation

occur, which worsens the obstruction and ventilation of the middle ear and ET (5).

Other confounding variables affecting ET function include patulous or

functionally/anatomically obstructed tubes, and abnormalities of the respiratory mucosa,

including allergy, immunocompromise, and ciliary dysfunction (see Fig. 91.2). Allergy has

long been implicated in the etiology of OM, but the exact mechanism remains elusive.

Possibilities include inflammatory swelling of the middle-ear–mastoid–ET mucosa or

allergic nasal obstruction. However, because large numbers of highly allergic children do not

have significant otitis, and many children with significant otitis do not have documented

allergy, the relation between allergy and OME is clearly not a straightforward one.

Speculation has long occurred regarding food allergy and OME. Although no consensus has

been reached, a study by Aydogan et al. (16) found food allergy in 44% of patients diagnosed

with OME. Conversely, in patients with known food allergy, 25% were found to have OME.

In the control group, 18% were diagnosed with food allergy, and 3% were diagnosed with

OME.

Children with congenital or acquired immunocompromise require special

consideration, because they are often more susceptible to infections, including OM, and to

unusual organisms. Congenital immune abnormalities include B-cell deficiencies, such as

hypogammaglobulinemia and IgA deficiency; T-cell deficiencies, such as DiGeorge

syndrome; combined T- and B-cell deficiencies, including ataxia telangiectasia; phagocyte

defects, including Chediak-Hagashi syndrome; and complement deficiencies. Acquired

abnormalities include those secondary to neoplasms and inflammatory processes such as

acute or chronic infections. Drugs causing immune deficiencies include steroids,

chemotherapeutic agents, and antirejection agents used in transplantation patients. Although

severe forms of immune deficiency are uncommon in children, many of the otherwise normal

otitis-prone children may have immature immune systems, as documented by poor response

to polysaccharide antigen vaccines, including Haemophilus influenzae type B (HIB), tetanus,

and pneumococcal vaccine.

9

Abnormalities, either physiologic or anatomic, of the palate-associated musculature

(especially the tensor veli palatini) may cause or worsen ET dysfunction. For example, many

craniofacial abnormalities, including cleft palate, Crouzon syndrome, Apert syndrome, and

Down syndrome, are associated with abnormal skull base or palate musculature with resultant

ET dysfunction.

Microbiology

The most commonly identified aerobic pathogens associated with AOM are

Streptococcus pneumoniae (30% to 50%), nontypable Haemophilus influenzae (20% to

30%), Moraxella catarrhalis (10% to 20%), and group A streptococci (1% to 5%) (5,6). Other

bacteria, such as Staphylococcus aureus and gram-negative enteric organisms, including

Escherichia coli, Klebsiella species, and Pseudomonas aeruginosa, are consistently isolated in

a small proportion of patients. In neonates and young infants, S. pneumoniae and H.

influenzae are still the most commonly isolated pathogens; however, S. aureus, group B

streptococci, gram-negative enteric pathogens, and other organisms are found up to 20% of

the time. In immunocompromised children or those requiring prolonged hospitalization,

unusual organisms (i.e., Mycobacterium tuberculosis, Mycoplasma pneumoniae, and

Chlamydia trachomatis) have been isolated. M. pneumoniae is an important upper respiratory

pathogen in children and adults. Although it has been infrequently isolated from middle-ear

fluid in immunocompetent children, it is not considered a major pathogen for OM.

Chlamydia trachomatis is associated with pneumonitis in infants and has occasionally been

isolated from the middle ear of infants younger than 6 months.

β-Lactamase–producing bacteria are increasingly causing middle-ear disease. Up to

34% of the H. influenzae and 100% of M. catarrhalis are β-lactamase positive (17). Although

S. pneumoniae does not make beta-lactamase, other resistance factors, including

chromosomal alterations, lead to a decrease in penicillin-binding proteins and an increase in

resistance to sulfa, chloramphenicol, tetracycline, and trimethoprim. The exact percentage of

bacterial resistance for any particular organism varies with the geographic area and the

population studied. Possible clinical factors in the development of bacterial resistance to

antimicrobials include multiple and prolonged courses (including prophylaxis), not taking the

entire prescribed course, and inappropriate administration.

In patients with medically refractory AOM who exhibit signs of toxicity despite

second-phase antibiotics, middle-ear cultures at the time of urgent myringotomy show

primarily gram-positive bacteria (coagulase negative staphylococci, Staphylococcus aureus,

10

and Streptococcus pneumoniae, in decreasing order of incidence) (6). Block et al. (18) looked

at children aged 7 to 24 months who were vaccinated with heptavalent pneumococcal vaccine

and who had severe or refractory AOM and found them to have twofold more gram-negative

bacteria than S. pneumoniae.

In the past, chronic MEE was often thought to be sterile. However, several studies

have isolated S. pneumoniae, H. influenzae, M. catarrhalis, and group A streptococci in 30%

to 50% of children with chronic MEE (5,19). In 1995, Post et al. reported on the usefulness of

the polymerase chain reaction (PCR) in the detection of bacterial DNA in pediatric MEE

samples that were sterile by standard culture techniques. In this study, 77.3% of patients

tested PCR positive for one or more of the standard organisms (M. catarrhalis, S.

pneumoniae, H. influenzae), whereas only 28.9% were both PCR and culture positive for one

or more of these organisms. No samples were culture positive and PCR negative. Although

these results are not proof of an active bacterial infections process, they suggest that bacteria

may be present in a higher percentage of OME specimens than was previously thought. A

positive PCR result may indicate the presence of viable, although nonculturable, bacteria

(20). The role of anaerobic bacteria in chronic MEE remains unclear; they have been isolated

in up to 10% of chronic MEE samples (19). Anaerobic bacteria play a minor role in the

pathogenesis of AOM. In chronic OME, anaerobic organisms such as Peptostreptococcus

spp., Prevotella spp., and Propionibacterium acnes have been isolated (19).

The role of viruses as primary or copathogenic organisms in OM has gained

increasing attention. Viruses such as respiratory syncytial virus, rhinovirus, influenza virus,

adenovirus, enterovirus, and parainfluenza viruses have been isolated from middle-ear fluid.

Cytomegalovirus and herpes simplex viruses also have been isolated in a smaller number of

cases. Respiratory viruses may potentiate the possibility of nasopharyngeal colonization with

bacteria, further increasing the incidence of OM. OM also is known to accompany viral

exanthems, including measles and the Epstein Barr virus.

Evaluation

History

The diagnosis of OM is based on history and physical examination. AOM is

characterized by acute onset of signs and symptoms of middle-ear inflammation with MEE

seen on physical examination. Symptoms are variable but commonly include fever,

irritability, otalgia, and hearing loss. Other symptoms include anorexia, nausea, vomiting, and

headache.

11

Children themselves may complain of hearing loss, dizziness, and tinnitus. Fever is

present in up to two-thirds of children with AOM, but fever over 40°C is uncommon and may

represent bacteremia or other complications. Other symptoms associated with AOM include

anorexia, nausea, vomiting, and headache. Children may complain of hearing loss, dizziness,

and tinnitus. Parents and caretakers of infants and younger children may notice hearing loss

or loss of balance. Because the ET is less functional when the child is lying down, symptoms

often appear worse at night or during naps. In children with OME, hearing loss may be the

only symptom. Children with draining ears (especially if chronic) may have little or no pain

and may sleep well, but may still complain of hearing loss and occasional low-grade fevers.

Children with dry TM perforations are usually asymptomatic except for hearing loss.

Children with TM perforations who get water in their ears may experience significant

discomfort. Finally, children with atelectasis of the TM also are usually asymptomatic,

although many of these children experience hearing loss as well. Physical

Examination

Although pneumatic otoscopy is the most important part of the physical examination

for OM, complete evaluation of the head and neck is essential. The pinnae, external auditory

canal, TM, and middle-ear landmarks should be evaluated. If the ear is rotated forward with

edema or erythema of the posterior auricular sulcus, acute mastoiditis may be present.

Pneumatic otoscopy requires the child to be immobile but not uncomfortable. If the child is

extremely uncooperative or cannot be immobilized safely, sedation or general anesthesia may

be needed if the examination is thought to be very important for the diagnosis and treatment

of the ear disease.

The normal TM is gray and translucent with normal mobility on pneumatic otoscopy.

Middle-ear landmarks that may be seen through a normal TM include the short process of the

malleus, the incudostapedial joint, and occasionally the chorda tympani. The position of the

TM can be neutral, bulging, retracted, or full. The color of an abnormal TM is frequently

opaque and may appear yellow or blue (indicating MEE), dark red (trauma, hemorrhage), or

red (AOM or hyperemia due to crying or coughing). The mobility of the TM should be

assessed on both positive and negative pressure. Decreased mobility of the TM on both

positive and negative pressure often indicates MEE, whereas movement only with negative

pressure suggests ET dysfunction. In the case of a patent TT or TM perforation, no mobility

of the TM is found. Middle-ear effusion can be described as serous (thin, watery), mucoid

(thick, viscous), purulent, or clear (which may indicate inflammation or a cerebrospinal fluid

12

leak). Air-fluid levels or bubbles may be seen, indicating intermittent aeration of the middle

ear through the ET.

The location and size of a TM perforation should be noted; it can be of any size, and

occasionally more than one may be seen. An acutely perforated TM is often erythematous

and thickened, with otorrhea discharging through the perforation. Perforations in the posterior

superior quadrant can be difficult to visualize and are often associated with cholesteatoma.

Evaluation of the TM may reveal other pathology, including tympanosclerosis, retraction

pockets, or areas of atelectasis. Tympanosclerosis appears as white and thickened areas of the

TM that must be distinguished from cholesteatoma. Retraction pockets can be located

anywhere in the TM and may represent areas of atelectasis, healed TT or perforation sites, or

the effect of persistent negative middle-ear pressure. Retraction pockets, especially if filled

with debris or associated with otorrhea, may indicate a cholesteatoma.

Hearing Evaluation

Evaluation of hearing is an essential part of the workup in every patient with a history

of middle-ear disease. The method of audiologic workup can be divided into two groups: (a)

audiometric evaluation, to test the peripheral hearing; and (b) immitance audiometry to

evaluate the stiffness of the TM and middle-ear system. Conductive hearing loss is the most

common finding with a history of OM. The type of audiometric evaluation varies based on

the age of the patient, level of cooperation, and maturity. Otoacoustic emissions are one of

the techniques of choice for hearing screening in the newborn nursery. Middle-ear effusion is

one of the main causes of otoacoustic emission (OAE) failure; therefore OAE should not be

used for evaluation of hearing related to middle-ear disease. Auditory brainstem response is

the method of choice to distinguish conductive from sensorineural hearing loss in infants

younger than 6 months. Auditory brainstem response also is recommended in children who

are unable to participate in other audiometric evaluations because of lack of cooperation or

maturity regardless of the age, or if ear-specific information is needed. Behavioral

observation audiometry (BOA) is recommended for infants aged 6 months to 1 year, and

visual reinforcement audiometry (VRA) is used for toddlers aged 1 to 2 years. The accuracy

of BOA and VRA relies on the level of experience of the audiologist and the developmental

level of the child. BOA and VRA do not accurately differentiate between conductive hearing

loss and sensorineural hearing loss and do not generally provide ear-specific information.

Play audiometry is recommended in a cooperative child older than 2 years and is not only ear

13

specific but also distinguishes the type of hearing loss (conductive or sensorineural).

Conventional audiometry can be used in a cooperative child older than 5 years.

Tympanometry is a measure of sound reflected by the TM and middle-ear structures.

This provides a graphic representation of compliance changes as the ear-canal pressure is

varied. Different tympanometric patterns are associated with middle-ear and TM pathology.

Measurement of ear-canal volume can be undertaken to assess further the status of the middle

ear and specifically the TM. Children with a perforated TM or patent TT will have a larger

ear-canal volume. Different immitance audiometry techniques are available to evaluate the

middle ear further if needed.

Acoustic reflectometry is used to measure the total level of the reflected and

transmitted sound. A hand-held instrument is placed in the external auditory canal to provide

an 80-dB sound source that varies from 2,000 to 4,500 Hz in a 100-ms period. The sensitivity

and specificity of this method is operator dependent and varies from fair to excellent (5).

Although acoustic reflectometry is not widely used for the diagnosis of middle-ear disease, it

can be a useful adjunct to otoscopy and impedance audiometry.

Treatment and Prevention

The rationale for treating OM includes avoidance of complications and treatment of

symptomatic disease. Secondary reasons include buying time until the child's ET function

and immune system have matured, and in many cases, waiting for the end of the URI season.

Management is usually medical, with surgical intervention reserved for failures of medical

therapy (Tables 91.3 and 91.4). AOM has a spontaneous resolution rate of 60% within 24

hours and 80% within 2 to 3 days (21). Reasons for spontaneous resolution may include

drainage of MEE down the ET or through a perforated TM, efficacy of local or systemic

immunity, or AOM that has resulted from a virus or some noninfectious process. Sometimes

the diagnosis is in error, especially in a crying child with red eardrums. The most recent

guidelines regarding diagnosis and management of AOM come from an evidence-based

clinical practice guideline for children aged 2 months through 12 years with uncomplicated

AOM. The American Academy of Pediatrics and American Academy of Family Physicians

convened a committee composed of primary care physicians and experts in the fields of

otolaryngology, epidemiology, and infectious disease to review the literature and make the

guidelines (22). These are guidelines only, and each patient should be managed by taking into

account the age and illness severity in the child, as well as any underlying illness or disease

14

process that may make the OM more difficult to manage or less likely to resolve

spontaneously.

AOM Diagnosis and Management Guidelines

The following recommendations were made in the AOM guidelines (22):

1. Confirm a history of acute onset, identify signs of middle-ear effusion (MEE), and

evaluate for the presence of signs and symptoms of middle-ear inflammation.

2. An assessment for pain should be completed and, if pain is present, the clinician

should recommend treatment to reduce pain.

3. Observation without use of antibacterial agents in a child with uncomplicated AOM is

an option for selected children based on diagnostic certainty, age, illness severity, and

assurance of follow-up. �4. If a decision is made to treat with an antibacterial agent, the clinician should prescribe

amoxicillin for most children. When amoxicillin is used, the dose should be 80 to 90

mg/kg/day. �5. If the patient fails to respond to the initial management option within 48 to 72 hours,

the clinician must reassess the patient to confirm AOM and exclude other causes of

illness. If AOM is confirmed in the patient initially managed with observation, the

clinician should begin antibacterial therapy. If the patient was initially managed with

an antibacterial agent, the clinician should change the antibacterial agent.

A definite diagnosis of AOM should meet the following criteria: rapid onset,

presence of MEE, and signs and symptoms of ME inflammation. The position of the

TM can be neutral, bulging, retracted, or full. The color of an abnormal TM is

frequently opaque and may appear yellow or blue (indicating MEE), dark red (trauma,

hemorrhage), or red (AOM or hyperemia due to crying or coughing). When combined

with color and mobility, bulging is the best predictor of AOM. If pain is not

adequately managed with appropriate doses of acetaminophen or ibuprofen or topical

otic analgesics, or if significant pain lasts longer than 24 hours, further medical

evaluation should be undertaken. If the child has a TT or suspected or confirmed TM

perforation, topical analgesics should be avoided. If otorrhea is seen through a TT or

TM perforation, the use of topical antimicrobial otic drops that have been approved

for use in the presence of a nonintact TM can be considered. Because no particular

15

pain-management strategy has been well studied in this setting, the clinician should

use his or her judgment in choosing medication for otalgia.

The observation option includes watchful waiting for 48 to 72 hours in

selected children, with pain management only. Appropriate patients for this option

may include healthy children aged 6 months to 2 years with nonsevere symptoms and

an uncertain diagnosis of AOM or children aged 2 to 12 years who have nonsevere

symptoms or an uncertain diagnosis. If this option is chosen, the patient and family

should have reliable access to a clinician if reevaluation or medication is needed. If

complications are present, if the child has an underlying medical condition that would

make this option potentially problematic, if the family does not have ready access to

follow-up medical care, or if the clinician or family is not comfortable with the

option, then this may not be an appropriate management strategy for the child.

The recommendation for amoxicillin use was made because of its safety and

general efficacy profile. However, if the child is immunocompromised, if unusual or

resistant organisms are suspected, or if the patient is allergic to amoxicillin, other

antibacterial agents should be considered. The AOM guidelines further state: When

antibacterial agents are prescribed for AOM, the time course of clinical response

should be 48 to 72 hours. When observation has been the chosen management and

spontaneous improvement has not been noted by 48 to 72 hours, antibacterial therapy

is indicated to limit the duration of further illness†(7). They recommend amoxicillin�

clavulanate for patients with severe illness, if additional coverage for beta-lactamase

positive H. influenzae and M. catarrhalis is indicated and if those patients initially

treated with amoxicillin did not improve. As always, the clinician should use his or

her judgment for each patient, based on the physical examination, prior or recent use

of antibacterial agents, severity of illness, and medication allergy profile.

6. During infancy and early childhood, reducing the incidence of respiratory tract

infections by altering child-care-center attendance patterns can reduce the incidence

of recurrent AOM significantly. The implementation of breastfeeding for at least the

first 6 months also seems to be helpful against the development of early episodes of

AOM.

7. No recommendations were made regarding the use of complementary or alternative

medicine. This was based on the lack of evidence of the efficacy or effectiveness of

any complementary and alternative medicine (CAM) therapy in comparison to the

natural history of AOM.

16

Prevention

Several measures have been suggested to prevent OM, including antimicrobial

prophylaxis, allergy control, tonsillectomy or adenoidectomy or both, vaccination, the

administration of immunoglobulins, and changing possible environmental contributors.

Allergy management may help if a specific allergen can be identified. Intravenous γ-globulin

may occasionally be recommended for proven or suspected immunoglobulin deficiency.

However, as in the case of allergies, specific medical or surgical management of the otitis

may be needed while waiting for the allergies to become more controlled and for the immune

system to mature. Changes in environmental factors that may help decrease OM include

removing possible allergens, prolonging breastfeeding, removing the child from day care (or

moving the child from a large day-care situation to a small home-care situation), and

preventing exposure to second-hand cigarette smoke (5).

Vaccines directed against the bacteria and viruses that are associated with OM

provide an intriguing method for possible prevention. Most of the vaccine research has been

aimed at S. pneumoniae and nontypable H. influenzae, which is important now that these

bacteria have developed significant antimicrobial resistance patterns. The older 23-valent S.

pneumoniae vaccine has not proven very immunogenic in children younger than 6 years.

However, the new heptavalent S. pneumoniae appears to be very effective against invasive

pneumococcal disease. Use of the heptavalent pneumococcal conjugate vaccine has led to a

major decline in the prevalence of invasive pneumococcal disease (bacteremia, meningitis)

and a more modest decrease in respiratory tract infections (AOM, pneumonia) (24). Recent

studies looking at vaccinated children revealed an increase of infections with serotypes not

included in the vaccine (24,25,26). Several studies have shown only a small effect on

prevention of AOM with pneumococcal conjugate vaccination in children younger than 2

years (26,27,28).

Vaccination against the viruses that are associated with OM has potential for great

benefit. Clements et al. reported that children aged 6 to 30 months who had received the

influenza vaccine had 32% fewer episodes of AOM than did those who did not. In a

randomized controlled trial, Hoberman et al. (29) found influenza vaccination to be no more

effective than placebo in children aged 6 to 24 months. No consensus exists regarding

influenza vaccination and prevention of AOM in children younger than 2 years. Children

younger than 2 years continue to experience the greatest number of AOM episodes but do not

appear to develop the strong immune response from vaccinations that older children display.

17

Surgical Therapy: Myringotomy and Tube Insertion

The use of ventilation tubes has become the treatment of choice for (a) recurrent

AOM unresponsive to medical therapy, (b) chronic OM with persistent effusion for 3 months

and conductive hearing loss, (c) negative middle-ear pressure with impending cholesteatoma,

and (d) intervention in the presence of complications of OM. Insertion of ventilation tubes

not only normalizes the middle-ear pressure, but it also decreases the frequency and severity

of AOM and generally resolves the conductive hearing loss associated with persistent

effusion (5). For children with very severe recurrent AOM, both ventilation tubes and

prophylactic antibiotics may be necessary. Children requiring both tubes and antibiotics to

manage their otitis effectively often have mild immune dysfunction that improves with time.

The average time that TTs remain in place and functional is 6 to 12 months after insertion.

Complications of ear tubes include otorrhea, persistent TM perforation when the tube

has extruded, scarring or tympanosclerosis involving the TM, plugging of the tube, formation

of granulation tissue around the tube, atrophic or thinned areas of the TM (where the tube

was), early extrusion or extrusion into the middle ear, and cholesteatoma. Otorrhea is

relatively common, occurring 12% to 30% of the time right after tube insertion, especially if

the MEE was purulent or mucoid, and in up to 50% of children at some point during the time

the tubes are in place. Otorrhea often occur secondary to a URI. Tympanic membrane

perforations that do not close spontaneously occur in up to 2% to 3% of ears with TTs,

although this number is higher (17%) with long-term tubes (30). Factors that may be related

to a higher persistent perforation rate include tube retention beyond 36 months and multiple

sets of tubes (5).

Adenoidectomy and Tonsillectomy

Historically, adenoidectomy has been recommended as an adjunctive treatment in the

management of chronic OM. The results of studies evaluating the efficacy of adenoidectomy

in preventing or decreasing middle-ear disease vary widely. Some fundamental differences

are found in these studies with regard to (a) definition of OM, (b) presence or absence of

environmental allergy, (c) adenoid size, (d) status of the ET, and (e) concurrent surgeries (i.e.,

tonsillectomy). Several studies have shown that time to recurrence of effusion, duration of

effusion, and the need for further surgery were reduced in the adenoidectomy group (5).

Paradise and colleagues also evaluated the usefulness of adenoidectomy in the management

of recurrent AOM and determined that the number of episodes of AOM was 35% in the

adenoidectomy group versus 28% in the control group (TTs without adenoidectomy); see

18

reference 30a. Gates and colleagues evaluated various combinations of myringotomy,

adenoidectomy, and TT placement for OME. They found that time with recurrent MEE was

decreased by 29% (tube only), 38% (adenoidectomy and myringotomy), and 47%

(adenoidectomy and tubes). Infor-mation about adenoidectomy in children younger than 4

years remains limited (7). Approximately eight adenoidectomies are needed to avoid a single

instance of tube reinsertion (however, this probably represents a larger reduction of

AOM/OME, including those that did not require additional surgery) (31).

Although anecdotal evidence suggests that tonsillectomy is helpful, no study

demonstrates significant efficacy of tonsillectomy and adenoidectomy over adenoidectomy

alone in prevention of OM.

Complications

Since the introduction of antimicrobials, the incidence of both suppurative

intratemporal and intracranial complications associated with OM has plummeted. However,

complications still occur, and vigilance is needed to prevent the potential morbidity and

mortality that can be associated with them (4). Complications can be divided into

intratemporal and intracranial groups (Table 91.5). By far the most common complication is

conductive hearing loss (CHL), usually due to the presence of MEE. Within the past decade,

significant interest has been expressed in the long-term effect of persistent MEE on speech,

language, and cognitive development of the child. Although many studies have been done,

the results remain controversial. Possible reasons for discrepancies in these types of studies

include (a) proper documentation of history of OM, (b) timing of audiologic workup, (c)

otologic status at the time of cognitive evaluation, and (d) varying study populations. Roberts

et al. (32) showed that the care-giving environment is more strongly related to school

outcome than was OME or hearing loss. This is a difficult problem to study well because of

many confounding factors; however, the current recommendation remains for surgical

intervention when children have hearing loss, speech delay, poor performance in school (or a

combination of these) in the setting of OME for longer than 3 months (7).

Fortunately, given the high incidence of OM, infrequent emergency situations occur.

Table 91.6 briefly outlines some of the warning signs for potentially complicated OM. If the

patient continues to be febrile, to have severe pain, or to exhibit any of the complications

listed in Table 91.5, immediate intervention should be considered. A high index of suspicion

should be used in evaluating neonates and immunocompromised hosts because of the

presence of possible unusual organisms. Initial studies include physical examination and

19

tympanocentesis to obtain an organism for culture and susceptibility testing; wide-field

myringotomy with insertion of a TT should also be considered at this time. Computed

tomographic (CT) scanning and magnetic resonance imaging can help to identify intracranial

and intratemporal complications. If the patient does not respond promptly to intravenous

antimicrobials and tympanocentesis/myringotomy, tympanomastoidectomy should be

considered. If intracranial complications are suspected or confirmed, neurosurgical

consultation should be obtained.

EUSTACHIAN TUBE SYSTEM

Anatomy and Physiology of the Eustachian Tube System

20

An understanding of the anatomy and physiology of the Eustachian tube is important

for all who are involved in the management of patients who have diseases and disorders of

the middle-ear cleft and its adjacent anatomic structures. This chapter describes not only the

anatomy and physiology of the tube but also information about how dysfunction of the

Eustachian tube and related structures might result in abnormalities of the middle ear and

mastoid.

The Eustachian tube should not be thought of as a separate entity from the structures

that surround it. The Eustachian tube is part of a system of contiguous organs that includes

the nose, palate, and nasopharynx proximal to the Eustachian tube, and the middle ear and

mastoid at its distal end. In reality, the Eustachian tube is not a tube but an organ consisting

of a lumen with its mucosa, cartilage, surrounding soft tissue, peritubal muscles (i.e., tensor

veli palatini, levator veli palatini, salpingopharyngeus, and tensor tympani), and its superior

bony support, the sphenoid sulcus (2).

Anatomy of the Eustachian Tube System

The Eustachian tube lumen is wider at both the proximal (nasopharyngeal) and distal

(middle ear) ends than in the midportion. The isthmus is the narrowest. A recent three-

dimensional study of nine human temporal bone specimens by Sudo and associates (3)

21

demonstrated the isthmus portion of the lumen to be near the distal end of the cartilaginous

portion and not at the junction of the cartilaginous and osseous portions. They named the

segment where the cartilaginous and osseous portions connect the junctional portion, which

was determined to be 3 mm in length in the adult (3). On the lateral wall of the nasopharynx,

a prominence, the torus tubarius, protrudes into the nasopharynx. This prominence is formed

by the abundant soft tissue overlying the cartilage of the Eustachian tube. Anterior to this is

the triangular nasopharyngeal orifice of the tube. From the torus, a raised ridge of mucous

membrane, the salpingopharyngeal fold, descends vertically. On the posterior wall of the

nasopharynx lie the adenoids, or pharyngeal tonsil, composed of abundant lymphoid tissue.

Above the tonsil is a variable depression within the mucous membrane called the pharyngeal

bursa. Behind the torus lies a deep pocket, extending to the nasopharynx posteriorly along the

medial border of the Eustachian tube. This pocket, the fossa of Rosenmüller, varies in

height from 8 to 10 mm and in depth from 3 to 10 mm (4). Adenoid tissue usually extends

into this pocket, giving soft-tissue support to the tube.

In the adult, the Eustachian tube is longer than that in the infant and young child.

Most of the increase in length takes place before age 6 years (5). The Eustachian tube has

been reported to be as short as 30 mm and as long as 40 mm, but the usual range of length

reported in the literature is 31 to 38 mm (4,6,7). It is generally accepted that the posterior

third (11 to 14 mm) of the adult tube is osseous, and the anterior two-thirds (20 to 25 mm) is

composed of membrane and cartilage (4,8). In adults, the Eustachian tube lies at an angle of

45 degrees in relation to the horizontal plane. In infants, this inclination is only 10 degrees

(4). The anatomy of the cranial base may be related to the length of the Eustachian tube,

which may be related to susceptibility for middle-ear disease (9). The anatomic configuration

of the Eustachian tube and its relation to other structures are presented in Figure 90.2A. The

osseous Eustachian tube (protympanum) lies completely within the petrous portion of the

temporal bone and is directly continuous with the anterior wall of the superior portion of the

middle ear. The juncture of the osseous tube and the epitympanum lies 4 mm above the floor

of the tympanic cavity (8). This relation, although valid, is misrepresented in the more

popular descriptions and depictions of the Eustachian tube middle ear juncture and is of some

importance in the functional clearance of middle-ear liquids.

The osseous (protympanic or middle-ear) portion of the tube has a course that is linear

anteromedially, following the petrous apex and deviating little from the horizontal plane. The

lumen is roughly triangular, measuring 2 to 3 mm vertically and 3 to 4 mm along the

22

horizontal base. The healthy osseous portion is open at all times, in contrast to the

fibrocartilaginous portion, which is closed at rest and opens during swallowing or when

forced open, such as during the Valsalva maneuver. The osseous and cartilaginous portions of

the Eustachian tube meet at an irregular bony surface and form an angle of about 160 degrees

with each other. The medial wall of the bony portion of the Eustachian tube consists of two

parts—posterolateral (labyrinthine) and anteromedial (carotid)—whose size, shape, and

relation depend on the position of the internal carotid artery. The average thickness of the

anteromedial portion is 1.5 to 3 mm, and in 2% of persons, the wall is absent, exposing the

carotid artery.

The cartilaginous tube then courses anteromedially and inferiorly, angled in most

cases 30 to 40 degrees to the transverse plane and 45 degrees to the sagittal plane (8). The

tube is applied closely to the basal aspect of the skull and fitted to the sulcus tubae between

the greater wing of the sphenoid bone and the petrous portion of the temporal bone. The

cartilaginous tube is attached firmly at its posterior end to the osseous orifice by fibrous

bands and usually extends some distance (3 mm) into the osseous portion of the tube. At its

inferomedial end, it is attached to a tubercle on the posterior edge of the medial pterygoid

lamina (4,6,10).

The tube in its cartilaginous portion has a crook-shaped mediolateral superior wall

(Fig. 90.2B). It is completed laterally and inferiorly by a veiled membrane that serves as the

site of attachment of the fibers of the dilator tubae, or tensor veli palatini muscle (4,6,11). The

tubal lumen is shaped like two cones joined at their apexes. The juncture of the cones is the

narrowest point of the lumen and has been called the isthmus. Its position is usually described

as at or near the juncture of the osseous and cartilaginous portions of the tube. The lumen at

this point is about 2 mm high and 1 mm wide (4). From the isthmus, the lumen expands to

about 8 to 10 mm in height and 1 to 2 mm in diameter at the pharyngeal orifice. Tubal

cartilage increases in mass from birth to puberty, and this development has physiologic

implications (12,13). The cartilaginous Eustachian tube does not follow a straight course in

the adult but extends along a curve from the junction of the osseous and cartilaginous

portions to the medial pterygoid plate, approximating the cranial base for the greater part of

its course. The Eustachian tube crosses the superior border of the superior constrictor muscle

immediately posterior to its terminus within the nasopharynx. The thickened anterior fibrous

investment of the medial cartilage of the tube presses against the pharyngeal wall to form a

prominent fold, the torus tubarius, which measures 10 to 15 mm thick (4). The torus is the

site of origin of the salpingopalatine muscle and is the point of origin of the

23

salpingopharyngeal muscle, which lies within the inferoposteriorly directed

salpingopharyngeal fold (14).

The mucosal lining of the Eustachian tube is conti-nuous with that of the nasopharynx

and middle ear andis characterized as respiratory epithelium. Structural dif-ferentiation of this

mucosal lining is evident: mucousglands predominate at the nasopharyngeal orifice, and

graded change occurs to a mixture of goblet, columnar, and ciliated cells near the tympanum

(15). The lining is folded, which provides greater surface area (16). Mucosa-associated

lymphoid tissue also is present.

Infant versus Adult Anatomy

It is likely that differences in the anatomy of the infant compared with the adult are

related, in part, to the increased incidence of otitis media in the pediatric age group. These

anatomic differences have been described only recently. The Eustachian tube in the infant is

about 50% as long as that in the adult; its length averages about 18 mm. The cartilaginous

tube represents somewhat less than two thirds of this distance, whereas the osseous portion is

relatively longer and wider in diameter than that in the adult. The height of the pharyngeal

orifice of the infant Eustachian tube is about half that of the adult, but the width is similar.

The ostium of the tube is more exposed in the infant than it is in the adult because it lies

lower in the shallower nasopharyngeal vault. The direction of the tube varies from horizontal

to an angle of about 10 degrees to the horizontal, and the tube is not angulated at the isthmus

but merely narrows (8). Holborow (26) demonstrated that in infants, the medial cartilaginous

lamina is relatively shorter because less tubal mass and stiffness is found in the infant tube

than in that of the older child and adult. The tensor veli palatini muscle is less efficient in the

infant.

The Eustachian tube lengthens rapidly during early childhood, essentially reaching its

adult size by age 7 years (27). Ishijima and colleagues (28) found the length of the lumen of

the infant tube to be 21 mm compared with the 37 mm average length in an adult. The effect

of these changes on efficiency of Eustachian-tube function has yet to be determined, but age-

related changes in Eustachian-tube function suggest more efficient muscular activity and a

system that is less likely to act as a passive conduit for nasal secretions. Cartilage mass

increases from birth to puberty (12). The density of elastin in the cartilage is less in the infant

(29), but the cartilage cell density is greater (30). The volume of the Ostmann fat pad is less

in the infant, but the width is similar in the two age groups (31). The angular relation between

24

the tensor veli palatini muscle and the cartilage varies in the infant but is relatively stable in

the adult (32). Table 90.1 summarizes the differences between the anatomy of the Eustachian

tube in the infant and that of the adult.

Some or possibly all these developmental differences between the infant and the adult

are related to the relatively less efficient active tubal-opening mechanism in the infant and

young child, which would make this age group susceptible to middle-ear disease. Because the

infant (and young child) has a shorter Eustachian tube than the older child and adult,

nasopharyngeal secretions can reflux more readily into the middle ear through the shorter

tube and result in otitis media.

Physiology of the Eustachian Tube

The Eustachian tube has at least three physiologic functions with respect to the middle ear

(Fig. 90.4): (a) pressure regulation (ventilation) of the middle ear to equilibrate gas pressure

in the middle ear with atmospheric pressure; (b) protection from nasopharyngeal sound

pressure and secretions; and (c) clearance of secretions produced within the middle ear into

the nasopharynx. Even though the pressure-regulation function is the most important of these

functions, the protective, drainage, and clearance functions are reviewed so that the reader

will be better able to visualize and understand the pressure-regulation function. The term

pressure regulation is more accurate than ventilation, because the middle ear is a pressure-

25

regulated cavity and not continuously ventilated. In the following discussion, fluid flow

through the tube includes both gas (airflow) and liquid flow.

Clearance of secretions from the middle ear is provided by the mucociliary system of the

Eustachian tube and some of the middle-ear mucous membrane. In ideal tubal function,

intermittent active opening of the Eustachian tube, which results only from contraction of the

tensor veli palatini muscle during swallowing, maintains nearly ambient pressures in the

middle ear (19,20). Assessment of these functions has been helpful in understanding the

physiology and pathophysiology of Eustachian-tube function as well as in the diagnosis and

management of patients with middle-ear disease (36).

Protective and Clearance Functions

In the past, clearance and drainage functions of the Eustachian tube have been

assessed by a variety of methods. Radiographic techniques have been used to assess

the flow of contrast media from the middle ear (tympanic membrane not intact) into

the nasopharynx (37,38,39,40,41,42). Bauer (43) assessed clearance by observing

methylene blue in the pharynx after it had been instilled into the middle ear. Elbrond

and Larsen (44) assessed middle ear Eustachian-tube mucociliary flow by determining

the time that elapsed after saccharin had been placed on the mucous membrane of the

middle ear until the subject reported tasting it. Unfortunately, all these methods are

qualitative and actually test Eustachian-tube patency rather than measuring the

clearance function of the tube quantitatively. Even though abnormalities of the

protective function are directly related to the pathogenesis of otitis media, this

26

function has been assessed only by radiographic techniques with a test that was a

modification of a tubal patency test described by Wittenborg and Neuhauser

(39,40,41,45).

Pressure-Regulation Function

From studies in children, the function of the Eustachian tube has been postulated (49).

The normal Eustachian tube is functionally obstructed or collapsed at rest; probably a

slight negative pressure develops in the middle ear. When the Eustachian tube

functions ideally, intermittent active dilatation (opening) of the tube maintains near-

ambient pressures in the middle ear. Under physiologic conditions, the fluctuations in

ambient pressure are bidirectional (i.e., either to or from the middle ear), relatively

small in magnitude, and not readily appreciated (58). These fluctuations reflect the

increase and decrease in barometric pressures associated with changing weather

conditions and elevation or both. However, the changes in middle-ear pressure show

mass directionality, can achieve appreciable magnitudes, and can result in pathologic

changes. A major reason for these conditions is that the middle ear is a relatively rigid

(noncollapsible) gas pocket surrounded by mucous membrane in which gases are

exchanged between the middle-ear space and the mucosa (59). Differential pressure

exceeds 54 mm Hg between the middle-ear space at atmospheric pressure and the

microcirculation in the mucous membrane. This represents a diffusion-driven gradient

from the middle-ear cavity to the mucosa that can produce an underpressure (relative

to ambient pressure) in the middle ear of more than 600 mm H2O during equilibration.

Doyle and co-workers (60), in experiments in primates, demonstrated that oxygen

(O2) and carbon dioxide (CO2) exchange is diffusion limited, whereas nitrogen (N2) is

perfusion limited. Some investigators have postulated that gases can pass to and from

the middle ear through the tympanic membrane, but Doyle and co-investigators (61)

showed in animal experiments that no O2 and CO2 transtympanic membrane exchange

exists from the external ear canal into the middle ear; exchange of N2 occurs, but not

at physiologic rates.

Children have less efficient Eustachian-tube ventila-tory function than do

adults. Bylander (63) comparedthe Eustachian-tube function of 53 children with that

of55 adults, all of whom had intact tympanic membranes and who were apparently

otologically healthy. By using a pressure chamber, Bylander and Tjernstrom (64)

reported that 35.8% of the children could not equilibrate applied negative

27

intratympanic pressure (-100 mm H2O) by swallowing, whereas only 5% of the adults

were unable to perform this function. Children aged 3 to 6 years had worse function

than those aged 7 to 12 years. In this study and a subsequent one conducted by the

same research group, children who had tympanometric evidence of negative pressure

within the middle ear had poor Eustachian-tube function (64). From these two studies,

it can be concluded that even in apparently otologically normal children, Eustachian-

tube function is not as good as that in adults; therefore the higher incidence of middle-

ear disease in children can be attributed to this finding.

Many children without apparent middle-ear disease have high negative

middle-ear pressure. In children, however, Eustachian-tube function does improve

with advancing age, which is consistent with the decreasing incidence of otitis media

from infancy to adolescence. Another explanation for the finding of high negative

middle-ear pressure in children is the possibility that some people who are habitual

actually create underpressure within the middle ear by this act (65). This mechanism

is uncommon in children, however.

28