Non-infectious rhinitis is a chronic inflammatory disease of the nasal mucosa,
characterized by obstruction, sneezing, pruritus and hypersecretion. These clinical
findings are due to hypersensitivity of the immune system and nervous phenomena
occurring in the mucous membrane. The etiology may be allergic or non-allergic,
depending whether the individual has a type I immunologic response or not.
Allergic rhinitis affects a large amount of the population. Recent studies show that
10 to 30% of the American population has allergic rhinitis. According to Vining,
40 to 50 million of Americans have rhinitis. In São Paulo, Brazil, these numbers
are even higher, due to its unique atmospheric conditions and pollution.
In allergic rhinitis, after the contact of the nasal mucosa to a specific antigen,
mediators like histamine, leukotriens, kinines and cytokines are released by
mucosal mast cells increasing vascular permeability, mucosal blood flow and
mucous production. They also contribute to the attraction and activation of
eosinophils, which leads to an inflammatory response (allergic inflammation).
These aspects are responsible for the clinical findings of the disease.
Regarding non-allergic rhinitis, this entity is considered a diagnosis of exclusion,
due to the various etiologies of non-allergic inflammatory mucosa, like non-
allergic rhinitis eosinophilia (NARES), and non-allergic non-infectious perennial
rhinitis (NANIPER). The first is sometimes associated with eosinophilic nasal
poliposis and even asthma, and the latter is a form of persistent rhinitis with no
Otitis media has multifactorial causes. Contributing factors to the genesis of
otitis media are eustachian tube dysfunction, bacterial or viral infections of the
middle ear, nasal inflammation resulting from allergic rhinitis or upper airway
Some risk factors for otitis media (acute or chronic) have been pointed: upper
airways viral infections, allergic rhinitis, Eustachian tube dysfunction, cigarette
smoking, bottle feed, male sex, immunologic deficiency, ciliary dysfunction, cleft
palate disease, genetic predisposition.
The role of rhinitis in middle ear disease is very controversial. The reported inci-
dence of patients with OME and allergy varies from 5 to 80%, usually around
23%. Although there is clinical evidence of nasal inflammatory disease affecting
Eustachian tube function in the middle ear mucosa, there is no scientific evidence
The Role of Rhinitis in Chronic Otitis Media
V IAPO MANUAL OF PEDIATRIC OTORHINOLARYNGOLOGY?
to prove that fact. In 1931, Proetz noted a relationship between patients with aller-
gic and chronic otitis media. Koch’s study of 222 patients was the first to include
observations of eosinophilia in otorrhea “supporting the contention that the middle
ear takes part in allergic reactions similar to those seen in the nose and sinuses”.
Shambaugh suspected allergy as an etiology, reporting empiric data issuing the
following caution: “Surgical mastoidectomy, simple or radical, is not indicated.
With competent allergic diagnosis and management, preferably by an otologist
trained in allergic methods, the otorrhea is finally brought under control”.
Mion et al found about 50% of patients with chronic otitis media presenting
nasal disease and nasal eosinophilia (33,33% of allergic and 15,69% of NARES),
showing a slight increase in nasal pathology compared to other reports. The
conclusion was that nasal disease has an impact on otologic middle ear disease,
considering that the normal nasal mucosa do not have eosinophils.
In the genesis of chronic otitis media, rhinitis can be related by two ways: the
Eustachian tube dysfunction caused by the allergic reaction in the nasal mucosa
and the decrease of the ciliary beat frequency. According to Bernstein, there are
three possibilities leading the inflammatory reaction to block the Eustachian tube.
The dysfunction can represent retrograde extension of nasal mucosal edema and
congestion; the mucociliary activity could cause the secretion to cover the ostium
and lead to intraluminal inflammation. Many of the substances released are known
to cause hypersecretion. They could also stimulate the seromucinous glands of the
Eustachian tube to hypersecrete, obstructing the lumen.
Although protection of the middle ear from nasopharyngeal secretions and muco-
ciliary clearance of the middle ear are known to be two important functions of the
Eustachian tube, perhaps the most critical function of the Eustachian tube is the
replacement of respiratory gases into the middle ear cleft to maintain atmospheric
pressure in the middle ear. Disruption of the mechanism for middle ear pressure
regulation is associated with pathophysiologic changes including the develope-
ment of significant low pressures and, if prolonged, otitis media with effusion.
The Eustachian tube offers a potential pathway for antigen access to the middle
ear. Although most clinical studies did not show elevation of middle ear IgE
levels, Bernstein’s early studies suggested that about 23% of allergic patients
with otitis media with effusion may have had a local allergic reaction within
the middle ear. Most clinical and experimental studies using specific antigen or
inflammatory mediators have failed to demonstrate the development of middle
ear effusion despite the presence of Eustachian tube dysfunction. Therefore,
it is likely that other factors, including bacterial and viral infections involving
the nasopharyngeal area, contribute to the development of middle ear fluid and
middle ear infection.
Forty to fifty percent of the children with otitis media with effusion have allergic
rhinitis diagnosed with positive skin prick test and specific IgE.
High levels of histamine are present in middle ear secretions in allergic patients,
even though the treatment with oral antihistamines has not shown significant
difference when compared allergic and non-allergic patients with otitis media with
effusion. This data confirms once more the complex nature of these diseases.
The level of cellular inflammatory components is also involved. Mast cells
degranulation mainly triptase, is found in higher levels in the middle ear secretions
of allergic children with otitis media with effusion. Eosinophils degranulation
of eosinophilic cationic protein is present in 87% of patients with otitis media
Eosinophils penetrate the nasal mucosa through adhesion and diapedesys.
Respiratory viruses also penetrate the respiratory mucosa the same way. The
expression of the endothelial adhesion molecules, specially ICAM-1, during
allergic rhinitis and NARES, can facilitate viral infections of the upper airway,
including the middle ear.
Tobacco smoking has an important role in chronic otitis media as well as in
allergy. Among the risk factors for upper respiratory tract infections are passive
smoking, low income and child care. Atopy was confirmed in 35% to 38% of the
children with upper respiratory tract infections. Adenoid tissue removed from
tobacco exposed children showed increased thickness in histopathology.
However, authors cited by several investigators found no clinical or pathologic basis
for allergy in the etiology of otitis media with effusion. According to Bernstein,
the relationship between allergy and otitis media with effusion will remain
controversial until well controlled clinical studies are conducted documenting that
in select populations therapy for allergic conditions is efficacious in preventing or
limiting the duration of otitis media with effusion.
Nevertheless, we must always suspect of nasal inflammatory disease in patients
with chronic otitis media who are refractory to treatment or do not respond
accordingly after appropriate surgery.
V IAPO MANUAL OF PEDIATRIC OTORHINOLARYNGOLOGY
1. Fireman, P. Otitis media and Eustachian tube disfunction: conection to allergic
rhinitis. J Allergy Clin Immunol. 1997; 99: S787-797.
2. Mion, O. et al. The Role of Rhinitis in Chronic Otitis Media. Otolaryngol Head
Neck Surg, Volume 128(1): 27-31, January 2003.
3. Bousquet J et al. The Workshop Expert Panel. Allergic rhinitis and its impact
on asthma.In collaboration with the World Health Organization.Executive
Summary of the Workshop Report,7 –10 December 1999, Geneva, Switzerland.
Allergy 2002; 57 :841 –855.