Eustachian Tube Function and Allergy in Otitis Media

(1)

PEDIATRICS FOR THE CLINICIAN

Recurrent otitis media represents the major cause of ear disease in infants, children, and adolescents and is a common problem in any pediatrician’s office. Many times, the recurrent nature of the disease is not apparent until after several months of intermittent acute and episodic care begin to reveal a trend of

persistent and recurring middle ear disease. Even more vexing is the problem of recurrent “ear trouble” where no fever or obvious form of infection is responsible for the persistent serous otitis media. Because of widespread interest in this common problem of pediatric practice and its management, the following four papers were assembled by the Section on Allergy and presented as a Symposium on Eustachian Tube Dysfunction at the annual meeting of the Academy on October 18, 1976.

WILLIAM E. PIxsoN, M.D., Chairman Section on Allergy and Immunology

Eustachian

Tube Function

and Allergy

in Otitis Media

Charles D.

Bluestone, M.D.

From the Department of Owlanjngokgy, Childrens Hospital of Pittsburgh and the University of Pittsburgh School of Medicine

Otitis media with effusion (OME) is one of the

most common diseases of childhood. Acute OME

is

usually of the suppurative type, although it may

be

serous,

while chronic OME has many

synonyms,

including “serous otitis media,”

“mu-coid otitis,” “nonsuppurative otitis media,” “glue

ear,” and “allergic otitis media.” The following

discussion is a review of some of the factors that

influence the etiology and pathogenesis of OME

in general, and more specifically the role of

Eustachian tube (ET) function and allergy in the

disease process of OME.

The pathogenesis of OME appears to be related

to abnormal function of the ET. Investigation into

the exact nature of this dysfunction requires an

understanding of the system constituted by the

palate, nasal cavity, nasopharynx, ET, middle ear,

and

mastoid air cells. Within this system the ET

has at least three physiologic functions with

respect to the middle ear: protection from

naso-pharyngeal sound pressure and secretions,

clear-ance

into the nasopharynx of secretions produced

within the middle ear, and ventilation of the

middle ear to equilibrate air pressure in

the middle ear with atmospheric pressure

and

to replenish oxygen which has been absorbed

(Fig. 1).

ROENTGENOGRAPHIC STUDIES

The protective and clearance functions of the

ET have been assessed by a radiographic

tech-nique.’2 Radiopaque material was instilled

through the nose of patients in order to observe

the retrograde flow of the medium from the

nasopharynx into the ET. Patients were

consid-ered to have normal protective function when

radiopaque material entered only the

nasopha-ryngeal

or isthmic portion of the tube but did not

enter the bony portion of the tube or middle ear

cavity.

The normal ET protected the middle ear

from the contrast material even when the liquid

was under increased nasopharyngeal pressure

during

closed-nose swallowing (Fig. 2). If, during

the retrograde study, contrast medium traversed

the entire ET and refluxed into the middle ear

during

swallowing,

the tube was considered to

have increased distensibility and poor protective

function (Fig. 3). The effectiveness of the ET in

clearing the ra1iopaque medium instilled into the

middle ear was taken as an indication of the

effectiveness of the ET in the clearance of

secre-tions. Rapid and complete clearance of the

medium into the nasopharynx was considered to

indicate normal drainage function, while failure

of the contrast material to drain from the middle

ear

into the nasopharynx indicated mechanical

obstruction of the ET, especially when contrast

material also failed to enter the nasopharyngeal

rt5

of the tube during the retrograde study

(Fig. 4).

FLUID FLOW THROUGH A FLASK

The understanding of these radiographic

stud-Read before the American Academy of Pediatrics Section on Allergy, Chicago, October 18, 1976.

ADDRESS FOR REPRINTS: (C.D.B.) Department of

(2)

PROTECTION

FIG. 1. Three physiologic functions of Eustachian tube in

relation to middle ear. NP

=

nasopharynx; ET

Eusta-chian tube; TYP tensor veli palatini muscle; ME

=

mid-die ear; Mast mastoid; TM

=

tympanic membrane;

EC

=

external canal.

FIG. 3. Retrograde reflu.x. Radiograph of 6-year-old boy with otitis media. On open-nose swallowing, contrast material traversed entire Eustachian tube and entered middle ear and

mastoid (arrow).

NP

-P MEVENTILATIONTMEC MAST

ies can be enhanced if a model of the system is

constructed. The ET, middle ear, and mastoid can

be likened to a flask with a long, narrow neck

(Fig. 5), the mouth of the flask representing the

nasopharyngeal end, the narrow neck the isthmus

of the ET, and the bulbous portion the middle ear

and

mastoid air chamber. Figure 5, a, shows that

when a small amount of liquid is instilled into the

mouth of the flask, liquid flow will stop

some-where in the narrow neck, due to capillarity and

FIG. 2. Normal retrograde function. During both open-nose and closed-nose swallowing, radiopaque contrast material filled nasopharyngeal portion of Eustachian tube (arrow) of

child with normal tympanic membranes and negative

otologic history.

the relative positive air pressure that develops in

the chamber of the flask. This basic geometric

design is considered to be critical for the

protec-tive function of the ET-middle ear system. Reflux

of the liquid into the vessel occurs if a hole is

made in the bulbous portion of the flask (Fig. 5, b)

since the pressure in the bottom of the flask

remains unchanged. This is analagous to the

condition in which a perforation of the tympanic

membrane or the presence of a tympanostomy

tube

could allow reflux of nasopharyngeal

secre-tions as a result of loss of the middle ear-mastoid

air cushion. Similarly, following a radical

mas-toidectomy the presence of the patent ET could

cause troublesome otorrhea. Figure 5, c, shows

the effect of the application of a negative pressure

to the bottom of

the

flask: the liquid is aspirated

into the vessel. In the clinical situation

(3)

1

r

Fic. 4. Retrograde obstruction. Radiograph of 5-year-old boy with otitis media. Radiopaque media failed to enter nasopha-ryngeal portion of Eustachian tube during both open- and

closed-nose swallowing. Note enlarged adenoids (arrow).

C

FIG. 5. Fluid flow into flask.

pressure could lead to the aspiration of

nasopha-ryngeal secretions into the middle ear. Figure 5,

d,

shows the effect of applied positive pressure to

the mouth of the flask: the liquid is insufflated

into the vessel. Nose-blowing, crying, or

closed-nose swallowing could create a high positive

nasopharyngeal pressure and result in a similar

condition in the human system.

However, one of the major differences between

a flask with a rigid neck and a biological tube such

as the ET is that the isthmus (neck) of the human

tube is compliant. Application of positive

pres-sure at the mouth of the flask with a compliant

neck would distend the neck, enhancing fluid

flow into the vessel. The effect of applied nega-tive pressure in a flask with a compliant neck is

shown in Figure 6: liquid flow through the neck

would not occur (Fig. 6, a) until a negative

pressure was slowly applied to the bottom of the

flask (Fig. 6, b). In this case fluid flow would occur

even if the neck was collapsed, but if the negative

pressure was applied suddenly temporary locking

of the compliant neck would prevent. flow of the

liquid (Fig. 6, c). Therefore, the speed of the

application of the negative pressure as well as the

compliance in such a system would appear to be

critical factors in the results obtained. Clinically,

aspiration of gas into the middle ear would be

possible, since negative middle ear pressure

would develop slowly as the gas was absorbed

by the middle ear mucous membrane. However,

sudden application of negative middle ear

pres-sure, such as would occur with rapid alterations in

atmospheric pressure (as in an airplane changing

altitude, when diving, or when attempting to test

the ventilatory function of the ET) could lock the

tube, thus preventing the flow of air.

Certain aspects of fluid flow from the middle

ear into the nasopharynx can be demonstrated by

inverting the flask of the model. Figure 7, a,

shows that a liquid trapped in the bulbous portion

of the flask does not flow out of the vessel as a

result of the relative negative pressure that

develops inside the chamber. However, if a hole is

made in the vessel the liquid drains out of the

flask since the suction is broken (Fig. 7, b).

Clinically these conditions occur in cases of

REFLUX

/\

/‘

a

PERFORATION

b

INSUFFLAT I ON POSITIVE PRESSURE

/\\

(4)

b

PERFORATION

b

a

SLOW NEGATIVE PRESSURE SUDDEN NEGATIVE PRESSURE

DRAINAGE

FIG. 6. Fluid flow through flask with compliant neck.

middle ear effusion in which pressure is relieved

by myringotomy. Insufliation of air into the flask

achieves a release of pressure, which may explain

the frequent success of politzerization or the

Valsalva manuever in clearing a middle ear

effu-sion.

The foregoing description of fluid flow through

a flask only presents some of the mechanical

aspects of the physiology of the human middle ear

system. Other factors which probably affect the

flow of liquid and air through the middle ear in

the physiological state would include (1) the

mucociliary transport system of the ET and

middle ear, (2) contraction of the tensor tympani

muscle and tympanic membrane movement, (3)

active tubal opening mechanisms, and (4) surface

tension factors.

VENTILATORY FUNCTION

Ventilatory function of the ET can be studied

by a modification of a manometric technique

developed by Flisberg et al.3 If a tympanostomy

tube or tympanic membrane perforation is

pres-ent, middle ear air pressure can be directly

inflated or deflated employing a

pump-manom-eter system.48 Figure 8 shows the symbols

employed and examples of results obtained in

ventilation studies. Example A describes the study

of an adult with a traumatic perforation but an

otherwise negative otologic history. After sealing

the external canal with the probe tip, pressure

was applied (inflation) until passive opening of

the tube occurred. This pressure-induced tubal

opening is called the opening pressure, and the residual external canal-middle ear pressure, after

the tube closes, the closing pressure. Active

swal-lowing by the patient completely equilibrated the remaining positive pressure. The external

canal-middle ear pressure was then reduced

(deflation)

Fic. 7. Fluid flow from inverted flask.

to -200 mm H2O. This negative pressure was also

completely equilibrated by the patient’s

swallow-ing activity. Example B describes the study of a

4-year-old boy who had had a persistent middle ear

effusion. The test ear had a functioning

tympanos-tomy tube in place. The ET passively opened and

closed following inflation, but subsequent

swal-lowing failed to equilibrate the residual positive

pressure.

In

the deflation phase of the study, the

child was unable to equilibrate negative pressure.

Inflation to a pressure less than the opening

pressure but greater than the closing pressure

could not be equilibrated by the active

swallow-ing

function.

PATHOGENIC MECHANISMS OF

MIDDLE EAR EFFUSIONS

From these studies of fluid flow through a

vessel and studies in children, the following stages

in the pathogenesis of OME have been postulated

(Fig. 9). The normal ET is functionally obstructed

or collapsed at rest with probably a slight

nega-tive pressure existing in the middle ear (Fig. 9, a).

(5)

+400 -

J/;r\\c_\\._\4_\LS

S

+200

C

-200 -

-SALLON’ .... . S #{149}#{149}#{149}

E

w

U)

C,,

w

a-EXAMPLE A.

+200

...

SRP S..

MAST.

(b)

(C)

(d) -200

S1’ALLOW

EXAMPLE B

Fic. 8. Symbols and examples of results of inflation-deflation ventilation studies. A, Normal adult with traumatic perforation. B, 4-year-old boy with functioning tympanostomy tube who had had persistent middle ear effusion. 0

=

opening pressure; C

=

closing pressure; S

=

pressure after

swallow; RI’ residual pressure. Dots indicate swallows.

tensor veli palatini muscle.9 In normal tubal

function, intermittent opening of the tube

main-tains near-ambient pressures in the middle ear

cavity

(Fig. 9, b). It is suspected that in cases in

which active forces alone are inadequate to

overcome tubal resistance, the interval between

openings also depends on the establishment of a

pressure gradient between the middle ear cavity

and the nasopharynx which passively assists tubal

function. Physiologically this gradient is achieved

by

the absorption of middle ear gas, which results

in progressive negative middle ear pressure.

This

type of ventilation appears to be quite common in

children, as moderate-to-high negative middle ear

pressures have been identified by tympanometry

in many who are apparently normal.1#{176}However,

periodic or persistent high negative pressure can

be pathologic and has been associated with

abnormal function of the ET.4 Persistent high

negative middle ear pressure in this stage

has

been termed atelectasv of the tympanic

mem-brane-middle ear (Fig. 9, c). If ventilation occurs

when there is high negative middle ear pressure,

nasopharyngeal

secretions could be aspirated into

the middle ear and result in an acute OME (Fig. 9,

d). To test this hypothesis in the experimental

animal,

a

pilot investigation in the

Rhesus

monkey was and it

was

found that

unilateral transection of the tensor veli palatini

muscle posterior to the hamulus of the pterygoid

bone resulted in persistent high negative middle

ear

pressure without effusion while in the

oppo-site, unoperated side, middle ear pressure

remained normal. Tympanometry documented

the middle ear status. Forty-eight hours after

instillation of type 18

Streptococcus

pneumoniae

NORMAL

EAR EFFUSION

Fic. 9. Proposed pathogenic mechanisms of middle ear

effusion. N-P

=

nasopharynx; ET Eustachian tube; PIP

= tensor veli palatini muscle; ME middle ear;

mast

=

mastoid; TM tympanic membrane; EC

(6)

NASAL

NASAL

OBSTRUCTION

I

u\

I 1+)

PRESSURE

///‘

\

MIDDLE #{163}A

MIDDLE EAR

FIG. 10. “Toynbee phenomenon.”

into the nasopharynx of each monkey, acute OME

developed in the ear with high negative pressure

but not in the unoperated side. Tympanocentesis

revealed purulent material, and type 18

pneumo-coccus was cultured from both the nasopharynx

and the middle ear effusion.

Figure 9, e, shows that if ventilation does not

occur, persistent ET obstruction could result in an

OME. The occurrence of an OME at this stage

might be dependent on the degree and duration

of the negative pressure as well as middle ear

hypoxia or hypercarbia. Since tubal opening

could be possible in a middle ear with an effusion,

aspiration of nasopharyngeal secretions might

occur, thus creating the clinical condition in

which persistent OME and recurrent acute

bacte-rial OME occur together (Fig. 9, f). In this

situation, the presence of a tympanostomy tube

could maintain ambient middle ear pressures and

prevent aspiration of nasopharyngeal secretions

but would not prevent reflux.

There appear to be

two

types of ET obstruction

which

would

result

in an OME: mechanical

and

functional. Intrinsic mechanical obstruction may

result from infiammation,12 whereas extrinsic

obstruction could be from obstructive adenoids.’3

OME

has

been produced in animal models when

the ET was mechanically obstructed.’

Function-al obstruction could result from persistent

collapse of the tube due to increased tubal

compliance, or an inadequate active opening

mechanism, or both. Animal models of functional

ET obstruction have also been developed.h1.15

Functional obstruction of the ET appears to be

the most common

type

of obstruction found in

children

with

OME.8

Nasal obstruction may also be involved in the

pathogenesis of OME. Swallowing when the nose

is obstructed (due to inflammation or obstructive

adenoids) results in an initial positive

nasopharyn-geal

air

pressure, followed by a negative pressure

phase. Figure 10 shows that the possible effect of

these pressures on a pliant tube could be the

following: with positive nasopharyngeal pressure,

secretions might be insufflated into the middle

ear, especially when the middle ear

has

a

high

negative pressure; or with negative

nasopharyn-geal pressures, such a tube could be prevented

from opening

and

be further obstructed

function-ally (the “Toynbee phenomenon”’ 13).

BACTERIA ISOLATED FROM CmsoNlc MIDDLE E.ii EnusIoNs#{176}

Organism Type of Effusion Total

‘4

,-

-,

(No.=102)

Leukocytic

(No.

=

20) Serous

(No.

=

35)

Mucoid (No.

=

47)

Haemophilus influenwe 5 3 8 16

Streptococcus pneumoniae 0 2 0 2

Group A streptococcus 2 2 1 5

Staphylococcus aureus Diphtheroids

Staphylococcus epidermidis

0 4 7

2 5 2

1 1 3

3 10 12

Pseudomonas aeruginosa 2 1 0 3

Neisseria catarrhalLs 3 1 0 4

Group D streptococcus 1 1 0 2

Kiebsiella pneumoniae 0 1 0 1

Haemophilus ducreyi 1 0 0 1

Total organisms 25 20 14 59

Total positive effusions 22 17 14 53

Percent positive effusions 63 36 70 52

(7)

NASAL OBSTRUCTION (TOYNBEE

PHENOMENON)

ETIOLOGY Infection

Acute OME is usually bacterial in origin.’6

Streptococcus pneumoniae accounts for about

40%

of the isolates and is the most common

etiologic agent in all age groups. Haemophilus

influenwe causes approximately 20% of cases.

Streptococcus pyogenes accounts for 5% and

Staphylococcus aureus for only 1%. The effusions

from 25% of cases are usually sterile for bacteria,

and it has been assumed that chronic effusions are

sterile, especially after apparently adequate

antimicrobial therapy. However, Senturia et al.’7

demonstrated that 30% of the effusions they

studied contained bacteria. In a study by Liu et

al.,18 approximately half of the effusions had

positive cultures for bacteria and, furthermore,

half

of the positive isolates were common

patho-gens (Table). According to Lim,19 the growth of

these organisms may have been restrained by

immunoglobulins and bactericidal enzymes.

When the bacterial recovery rate from the middle

ear effusions

was

compared with immunoglobulin

and lysozyme levels on an age scale, there was an

inverse relationship: the bacterial recovery rate

declined with an increase in age, whereas the

immunoglobulins and lysozymes in the effusions

rapidly increased with the age of the children.

This raises the possibility that many middle ear

effusions may be of bacterial origin but that the

infection is limited by the immunologic and

enzymatic defense systems of the middle ear.

Early treatment of acute bacterial OME with

antimicrobials may impede the natural

develop-ment of antibodies in the middle ear and thus may

result in a low-grade infection. The same

condi-tion might occur if antibiotics had not been

administered in sufficient amounts or not taken as

directed. It has been suggested that viruses may

be a significant factor in otitis media, but this

has

not been demonstrated.’#{176} It is apparent that the

only definitive method to determine if bacteria

are

present in the middle ear effusion is to culture

the middle ear aspirate.

Allergy

Allergy

is thought to be one of the etiologic

factors in OME because OME

occurs

frequently

in allergic individuals2’ and because favorable

responses of OME to allergic management have

been reported. The majority of allergic

individ-uals with OME have nasal allergies with

demon-strable hypersensitivity to a mixed variety of

inhalants,

especially dust, molds, and pollen. Only

a very small percentage of allergic patients with

ASPIRATION, REFLUX OR INSUFFLATION

OF NASOPHARYNGEAL SECRETIONS INTO MIDDLE EAR VIA EUSTACHIAN

TUBE

EUSTACHIAN TUBE INTRINSIC

OBSTRUCTION

EAR- ‘SHOCK

ORGAN’

Fic. 11. Four possible mechanisms by which allergy may be involved in etiology and pathogenesis of OME.

OME have a food allergy of significance to the

etiology of OME,22 but when a food allergy is

present, the results of treatment of the food

allergy appear to be more successful for

resolu-lion of the OME than does treatment of allergy

due to an inhalant.’3

The

mechanism

by which allergy might cause

OME remains hypothetical and controversial.

Some have assumed that mucosal swelling

asso-ciated

with

nasal

allergy extends to the ET and

causes intrinsic mechanical obstruction.’4

How-ever, even though this seems logical, there are no

data

available to support this contention. Other

investigators are of the opinion that OME

asso-ciated with nasal allergy is a disease per se of the

middle ear, but studies to substantiate this claim

are contradictory. Aspirates of middle ear

effu-sions have either failed to demonstrate the

presence of eosinophils or have shown them to be

present in insignificant numbers to cause OME.’5

The concentration of IgE in effusions

has

been

investigated: Reisman and Bernstein’6 and Mogi’T

have shown that IgE levels in the effusions of

allergic individuals were lower than the levels in

their sera. They concluded that allergy is not a

major cause of OME. In contrast, Phillips et al.’8

demonstrated that the majority of their patients

had higher levels of IgE in effusions than in the

corresponding serum samples and therefore

concluded that allergy is a major cause of chronic

OME.

Lim

et al.’9 examined middle ear effusions

(8)

with OME who were between the ages of 5 and

15 years. They found a fivefold increase in the

level of IgE in the effusions as compared with the

serum in 14% of the subjects. Middle ear biopsy

specimens from the same group showed mast cells

but only two specimens from the same group

demonstrated eosinophils. Mucoid effusions had

higher IgE levels

than

serous effusions or the

corresponding sera. However, none of the

chil-dren who had elevated IgE levels had a history of

allergy.

In conclusion, the role of allergy in the etiology

and pathogenesis of acute and chronic OME may

be by one or more of the following mechanisms

(Fig. 11): (1) middle ear functioning as a “shock

organ,” (2) inflammatory swelling of the ET, (3)

inflammatory obstruction of the nose, or (4)

aspiration of bacteria-laden allergic

nasopharyn-geal secretions into the middle ear cavity. The

latter three mechanisms would be associated with

abnormal function of the ET. It is obvious that

further research is required to establish the rela-tionship of allergy to OME.

REFERENCES

1. Bluestone CD: Eustachian tube obstruction in the infant with cleft palate. Ann Otol Rhinol Laryngol 80(suppl 2):1, 1971.

2. Bluestone CD, Paradise JL, Beery QC: Physiology of the Eustachian tube in the pathogenesis and

manage-ment of middle ear effusions. Larygoscope 82:1654, 1972.

3. Flisberg K, Ingelstedt S, Ortegren U: Controlled “ear aspiration” of air: A “physiological” test of the tubal function. Acta Otolaryngol 82(suppl):35, 1963.

4. Bluestone CD, Beery QC, Andrus WS: Mechanics of the Eustachian tube as it influences susceptibility to and persistence of middle ear effusions in children. Ann Otol Rhinol Laryngol 83(suppl 11):27, 1974.

5. Bluestone CD: Assessment of Eustachian tube function, in Jerger J (ed): Manual of Clinical Impedance Audiometry. Dobbs Ferry, NY, American Electro-medics Corp, 1975, p 127.

6. Bluestone CD, Cantekin EL, Beery QC, Paradise JL:

Eustachian tube ventilatory function in relation to cleft palate. Ann Otol Rhinol Laryngol 84:333, 1975.

7. Bluestone CD, Paradise JL, Beery QC, Wittel RA:

Certain effects of cleft palate repair on Eustachian tube function. Cleft Palate 9:183, 1972.

8. Cantekin El, Bluestone CD, Parkin LP: Eustachian tube ventilatory function in children. Ann Otol Rhinol Laryngol 85(suppl 25):171, 1976.

9. Rich AR: Physiological study of Eustachian tube and its related muscles. Bull Johns Hopkins Hosp 31:206,

1920.

10. Bluestone CD, Beery QC, Paradise JL: Audiometry and tympanometry in relation to middle ear effusions in children. Lanjngoscope 83:594, 1973.

11. Cantekin El, Bluestone CD, Saez CA, et al: Normal and abnormal middle ear ventilation. Ann Otol Rhinol Laryngol 86(suppl 41):!, 1977.

12. Bluestone CD, Cantekin El, Beery QC: Effect of inflam-mation on the ventilatory function of the Eusta-chian tube. Lanjrigoscope 87:493, 1977.

13. Bluestone CD, Cantekin El, Beery QC: Certain effects of adenoidectomy on Eustachian tube ventilatory function. Laryngoscope 85:1 13, 1975.

14. Paparella MM, Hiraida F, Juhn SK, et al: Cellular events involved in middle ear fluid production. Ann Owl

Rhinol Laryngol 79:766, 1970.

15. Odoi H, Proud GO, Toledo PS: Effects of pterygoid

hamulotomy upon Eustachian tube function.

Laryngoscope 81:1242, 1971.

16. Bluestone CD, Shurin PA: Middle ear disease in chil-dren. Pediatr Clin North Am 21:379, 1974.

17. Senturia BH, Gessert DF, Carr CD, Baumann ES:

Studies concerned with tubotympanitis. Ann Owl Rhinol Laryngol 67:440, 1958.

18. Liu YS, Lim DJ, Lang R, Birck HG: Microorganisms in chronic otitis media with effusion. Ann Owl Rhinol Laryngol 85(suppl 25):245, 1976.

19. Lim DJ: Infectious and inflammatory auditory disorder, in Tower DB (ed): The Nervous System: Human Communication and Its Disorders. New York, Raven Press, 1975, vol 3, p 263.

20. Klein JO: Teele DW: Isolation of viruses and mycoplas-mas from middle ear effusions: A review. Ann Owl Rhinol liiryngol 85(suppl 25:):140, 1976:

21. Draper WL: Secretory otitis media. Laryngoscope 78:636, 1967.

22. McGovern JP, Haywood TJ, Fernandes A: Allergy and

secretory otitis media. JAMA 200:134, 1967. 23. Clemis JD: Identification of allergic factors in middle

ear effusions. Ann Owl Rhinol Laryngol 85(suppl 25):234, 1976.

24. Paparella MH, Dickson RI: The recurrent middle ear

effusions. Owl Clin North Am, February 1969, p

53.

25. Senturia BH: Allergic manifestations in otologic disease. Laryngoscope 70:287, 1960.

26. Reisman ER, Bernstein J: Allergy and secretory otitis media. Pediatr Clin North Am 22:251, 1975. 27. Mogi G: Secretory IgA and antibody activities in middle

ear effusions. Ann Owl Rhinol Laryngol 85(suppl 25):97, 1976.

28. Phillips MJ, Knight NJ, Manning H, et al: IgE and

secretory otitis media. Lancet 2: 1 176, 1974. 29. Lim DJ, Liu YS, Schram J,Birck HG: Immunoglobulin E

in chronic middle ear effusions. Ann Owl Rhinol Laryngol 85(suppl 25): 1 19, 1976.

ACKNOWLEDGMENT

(9)

1978;61;753

Pediatrics

Charles D. Bluestone

Eustachian Tube Function and Allergy in Otitis Media

Services

Updated Information &

http://pediatrics.aappublications.org/content/61/5/753

including high resolution figures, can be found at:

Permissions & Licensing

http://www.aappublications.org/site/misc/Permissions.xhtml

entirety can be found online at:

Information about reproducing this article in parts (figures, tables) or in its

Reprints

http://www.aappublications.org/site/misc/reprints.xhtml

(10)