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Abstract
The goal of this article is to review a series of patients with persistent
unilateral middle ear effusion (MEE) and to suggest a more contemporary
diagnostic algorithm. The author conducted a retrospective chart review
of adults with persistent unilateral MEE and normal findings on physical
and nasopharyngoscopic examinations whose MEE was eventually found
to be caused by a variety of occult skull base lesions. The study
population was made up of 79 patients-52 women and 27 men, aged 21 to
83 (mean: 54.8) at presentation-who had been referred to an academic
tertiary care medical center between July 1, 1988, and June 30, 2008.
Follow-up ranged from 9 months to 19.5 years (mean: 8.7 yr). Of this
group, 50 patients (63.3%) had a malignant tumor, 26 (32.9%) had a
benign tumor, and 3 (3.8%) had an internal carotid artery aneurysm.
Eustachian tube occlusion had been caused by diffuse invasion in 33
patients (41.8%), by intracranial pathology in 24 (30.4%), and by
extracranial-infratemporal lesions in 22 (27.8%). Nasopharyngoscopy
cannot identify a variety of rare skull base lesions that cause eustachian
tube compression or tissue invasion that ultimately leads to MEE.
Therefore, patients with unexplained persistent unilateral MEE should
undergo coronal magnetic resonance imaging or computed tomography to
look for any intra- or extracranial lesions before undergoing ventilation
tube placement.
Introduction
Secretory otitis media is a common cause of aural fullness and hearing
loss secondary to eustachian tube inflammation, edema, or
obstruction.1 Some cases of middle ear effusion (MEE) are self-limited
while others require medical management in the form of a topical steroid
nasal spray, an oral steroid, a decongestant, an antihistamine, an
antibiotic, or allergy therapy.2-4
In addition to a complete head and neck examination, all patients who
present with persistent unilateral MEE should undergo nasopharyngoscopy
to look for congenital narrowing, acquired stenosis, or neoplastic
obstruction of the eustachian tube orifice.5 When findings on both
examinations are normal, many adult patients undergo additional medical
management or ventilation tube insertion for presumed MEE induced by
eustachian tube dysfunction.6 Although such a treatment strategy is safe
and successful in patients with typical recurrent MEE, it might not detect
occult skull base lesions that compress or invade the eustachian tube.7
In this article, the author describes his review of a series of MEE patients
with occult skull base lesions.
Results
Presenting symptoms and signs. All 79 patients had complained of
aural fullness and hearing loss. Other presenting otologic symptoms
included tinnitus, otalgia, and dizziness (table 1).
Table 1. Presenting symptoms and signs (N = 79)
Finding
n (%)
Symptoms
Aural fullness
79 (100)
Hearing loss
79 (100)
Tinnitus
37 (46.8)
Otalgia
24 (30.4)
Dizziness
5 (6.3)
Signs
Middle ear fluid
79 (100)
26 (32.9)
Trismus
19 (24.1)
Finding
n (%)
Facial hypoesthesia
12 (15.2)
3 (3.8)
1 (1.3)
All patients had presented with serous MEE, and almost one-third of them
demonstrated a pars tensa retraction. Other presenting signs included
trismus, facial hypoesthesia, cranial nerve VI palsy, and vocal fold
paralysis (table 1).
History. Of the 79 patients, 61 (77.2%) had undergone at least one
myringotomy with ventilation tube insertion, which had delayed their
diagnosis by a mean of more than 3 years; roughly half of these patients
had undergone more than one such procedure. Only 23 of the 79 patients
(29.1%) had undergone any radiographic studies prior to referral. These
investigations included CT of the sinuses in 6 patients, CT of the temporal
bones in 5, CT of the temporomandibular joint in 5, MRI of the head in 4,
and a panoramic x-ray of the mandible in 3.
Site of Origin. Of the 79 previously undetected skull base lesions, 42
were located on the right and 37 on the left. The most common sites of
origin were the infratemporal fossa and the middle cranial fossa. The site
of origin could not be determined in 19 patients because of the extent of
the lesion (table 2).
Table 2. Site of lesion origin (N = 79)
Site of origin
n (%)
Infratemporal fossa
21 (26.6)
19 (24.1)
Clivus
12 (15.2)
Petrous apex
8 (10.1)
19 (24.1)
Site of origin
n (%)
Total
79 (100)
Approach
n (%)
37 (46.8)
Orbitocranial zygomatic
22 (27.8)
Pterional
12 (15.2)
5 (6.3)
Endovascular
Angiography w/ stenting
3 (3.8)
Approach
Total
n (%)
79 (100)
All 3 patients with an internal carotid artery aneurysm were managed with
cerebral angiography and endovascular stenting.
n (%)
Type of lesion
Alive
w/o
disease
Alive
with
disease
Died of
disease
Died
other
causes
Total
2 (2.5)
17
(21.5)
1 (1.3)
20
(25.3
)
Key: Ca = carcinoma;
ICA = internal carotid
artery.
Malignant tumors (n =
50)
Undifferentiated Ca
n (%)
Type of lesion
Alive
w/o
disease
Alive
with
disease
Died of
disease
Died
other
causes
Total
Metastasis
1 (1.3)
11
(13.9)
12
(15.2
)
Adenoid cystic Ca
4 (5.1)
3 (3.8)
2 (2.5)
9
(11.4
)
Mucoepidermoid Ca
1 (1.3)
4 (5.1)
2 (2.5)
7
(8.9)
Osteosarcoma
2 (2.5)
0 2 (2.5)
Trigeminal neuroma
8 (10.1)
2 (2.5)
1 (1.3)
11
(13.9
)
Meningioma
3 (3.8)
4 (5.1)
1 (1.3)
8
(10.1
)
Chordoma
1 (1.3)
1 (1.3)
2
(2.5)
Cholesterol granuloma
2 (2.5)
2
(2.5)
Pleomorphic adenoma
2 (2.5)
2
(2.5)
Benign tumors (n =
26)
n (%)
Type of lesion
Alive
w/o
disease
Alive
with
disease
Died of
disease
Died
other
causes
Total
Cholesteatoma
1 (1.3)
1
(1.3)
ICA aneurysm (n = 3)
3 (3.8)
3
(3.8)
Total
25
(31.6)
17
(21.5)
34
(43.0)
3 (3.8)
79
(100)
Discussion
Aural fullness secondary to MEE is most often associated with eustachian
tube dysfunction.1 Long-term eustachian tube failure may lead to
negative middle ear pressure, tympanic membrane atelectasis, adhesive
middle ear disease, or cholesteatoma.8 In the adult population, unilateral
MEE may result from eustachian tube compression or invasion rather than
from physiologic dysfunction. Gacek identified the four levels of potential
eustachian tube compromise as being (1) the lumen of the eustachian
tube, (2) the nasopharynx, (3) the infratemporal fossa, and (4) the petrous
apex.9 Of these four locations, only the nasopharynx is accessible to
physical examination.
The initial evaluation of any patient with MEE begins with a complete
history of symptoms, including the duration of aural fullness, similar
episodes in the past, recent airplane travel or other causes of barotrauma,
blunt temporal bone injury, sinus disease or surgery, radiotherapy to the
head and neck, tobacco use, cleft palate, gastroesophageal reflux, or
sinonasal allergic disease.5
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