Junior
Surgery Lecture
Common
Ear Disorders
Symptoms of ear disease include hearing loss, tinnitus,
vertigo, aural pressure, otalgia (pain in the ear), otorrhea (drainage from the
ear). In most instances, the symptom
can be localized to a specific anatomic site within the temporal bone. Physical diagnosis of the ear is limited to
external and middle ear diseases. The
inner ear cannot be directly examined, is poorly imaged using contemporary
radiographic techniques, and cannot be biopsied without substantial risk of
causing permanent dysfunction. For
these reasons, the history is crucial in determining the correct diagnosis.
(Slide
2) Examination of the external canal and middle
ear is enhanced through the use of binocular microscopy. The added depth perception allows more
accurate diagnosis. Pneumatic otoscopy
involved application of positive and negative pressure to the ear canal. In response to pressure change, one should
observe wide excursion of the tympanic membrane (TM). Movement will be limited in the presence of middle ear fluid or
mass lesion. Additional information is
gained from audiometric testing. Tuning
forks allow a rapid assessment of auditory acuity by comparing the two ears, or
comparing the patient’s hearing to the physician’s (assuming the physician has
normal hearing). Hearing is assessed at
512, 1024 and 2048 Hz. These
frequencies are important for speech recognition. Two tests allow the classification of the hearing loss as being
either conductive (external and middle ear) or sensorineural (inner ear and 8th
nerve). The first is the Weber
test. Strike the fork and place it
anywhere in the midline of the skull.
Normally, one should perceive the sound equally in both ears. The sound will lateralize to the affected
ear in a conductive loss and to the better ear in a sensorineural loss. The Rinne test is performed by asking the
patient to compare the intensity of the sound when the fork is placed on the
temporal bone to that when the fork is held next to the external meatus. The fork is louder when placed next to the
meatus in normals and those with sensorineural hearing loss. If the fork is louder when placed against
the temporal bone, a conductive loss is present. Tuning forks provide a gross assessment of hearing. In order to assess the magnitude of a
hearing loss, formal audiometric testing is pursued.
(Slide 3) A. External Otitis. The most common disorder of the
outer ear, also know as Swimmer’s ear.
The process develops due to loss of the protective cerumen and excessive
moistures in the ear canal. This leads
to maceration of the canal skin allowing bacterial growth and invasion. Presenting symptoms include otalgia, mild
hearing loss, and scant otorrhea. On
physical exam, marked edema of external canal skin is present, usually
obscuring view of the tympanic membrane.
A conductive hearing loss is present on tuning fork or audiometric
testing.
Treatment
– Avoid moisture and additional trauma.
Clean the ear canal as thoroughly as possible. Acidify ear canal or use topical antibiotics
(aminoglycoside). Analgesics are
prescribed as necessary. Systemic antibiotics are rarely needed. Prompt recovery is expected. Patient education is important in limiting
recurrences. Complications can develop
if bacterial invasion extends to involve the temporal bone. If osteitis is present, pain increases in
severity, drainage is unrelenting, and granulations are found in the
canal. Cranial nerve deficits or signs
of intracranial infection are seen in advanced cases, and may be associated
with a fatal outcome. Patients at
greatest risk for osteitis include diabetics and immunosuppressed (HIV,
malignancy) individuals.
II. Middle
ear
A. Otitis
Media
(Slide 4) Otitis
media (OM) is one of the most common diseases of children. Over 80% of all children will have at least
one episode of otitis media by age 6.
After this age the disease becomes much less common. The decline in incidence parallels facial
growth and development of the eustachian tube.
OM is very rare in adults without long-standing eustachian tube
dysfunction. Anything that would impair
eustachian tube function, such as cleft palate, craniofacial anomalies,
nasopharyngeal mass, or ciliary dysfunction, would increase the incidence of
OM. Certain ethnic groups have a
greater incidence of the disease, including Native Americans and Pacific
Islanders. Otitis media may be
classified according to the duration of symptoms. Acute
OM is < 3 weeks duration, subacute is between 3 weeks and 3
months, and chronic
is > 3 months. An important
distinction in the pediatric age group is recurrent OM vs. persistent effusion.(Slide
4) Obviously, an ear that returns
to normal has a more favorable long-term prognosis.
Presenting
symptoms of acute OM include otalgia, hearing loss, and aural pressure (fever
and irritability in young children). On
physical exam, a middle ear effusion is present. In some cases it is purulent, more commonly it is thick and
mucoid. A mild to moderate conductive
hearing loss is present on tuning fork or audiometric testing. A flat (type B) tympanogram is
recorded. Treatment – Oral
antibiotics directed at most common pathogens (Strep. Pneumoniae, H
influenza, M. catarrhalis). If
treating an initial infection, antibiotics such as ampicillin,
trimethoprim-sulfamethoxazole, and erythromycin-sulfisoxazole are
effective. Persistent effusion and
multiple recurrences suggest resistant organisms, thus extended spectrum agents
are required. Assuming appropriate
antibiotic therapy is prescribed, no other medications are necessary (steroids,
antihistamines). Surgical treatment
(myringotomy and tubes) is indicated for any of the following: persistent
effusion (>3mths), >4 episodes of acute OM in one year, or >30dB
conductive hearing loss. Most children
do not need more than one set of tubes.
Persistent infection can result in permanent structural damage such as
TM atelectasis or perforation, ossicular erosion, or cholesteatoma.
The term
Chronic OM is also
used to describe those ear with the anatomic deformities cited above. These patients typically present with
otorrhea and conductive hearing loss.
The spectrum of infectious organisms is similar to that seen in external
otitis; Pseudomonas aeruginosa and Staphylococcus aureus are most
common. Cholesteatoma (Slide 5 - 7) is a
term for an epidermoid cyst of the middle ear.
A cholesteatoma develops when the squamous epithelium on the surface of
the TM grows inward into the middle ear space.
There are several mechanisms by which this could occur. The most likely is that the TM is retracted
inward by chronic negative middle ear pressure. Squamous epithelium then becomes trapped underneath the boney
ledges of the tympanic cavity. Chronic
inflammation serves to stimulate epithelial cell growth, resulting in large
amounts of desquamating cellular debris from the surface epithelium. The debris cannot migrate out of the ear
canal in the usual manner, thus a cyst develops and expands throughout the
aerated spaced of the middle ear and mastoid.
Chronic
OM and cholesteatoma are treated with local debridement, topical antibiotics,
and in most cases, surgery. The goals
of the operation are to eliminate infection (usually requiring dissection of an
infected mastoid bone) and restore function by repairing the TM and replacing
missing ossicles.
Rarely,
an otitic infection may extend beyond the confines of the temporal bone,
producing a serious CNS infection.
Meningitis, brain abscess, venous sinus thrombosis, and epidural abscess
are most commonly seen. Intracranial
complications are most commonly seen in neglected cholesteatomas, often because
the patient has not sought medical advice.
The usual symptoms are headache, fever, and otorrhea. Be aware that fever and headache are very
uncommon in chronic ear disease.
Meningeal signs and mental status changes are signs of advanced
intracranial infection. Prompt
antibiotic treatment, surgical drainage, and control of intracranial pressure
are necessary to minimize morbidity.
B. Conductive
hearing loss
Other
disorders which alter structure and function of the TM and ossicles can cause
conductive hearing loss. Examples
include: otosclerosis, trauma, and congenital anomalies.
Otosclerosis is a
bone disease that causes progressive fixation of the stapes. Conductive hearing loss results and
increases with advanced fixation. It is
most common in Caucasians, females, and ages 20-40. The disease is familial in 60% of cases, and bilateral in
50%. On physical exam the middle ear is
normal, but a conductive hearing loss is present. Hering can be improved with surgery or hearing aids. The surgical procedure, stapedotomy, (Slide 8 - 9)
bypasses the fixed stapes by removing the supra structure, drilling a hole in
the footplate and placing a prosthesis between the incus and footplate.
III. Facial nerve
From the patient’s
perspective, facial paralysis is a severe problem. It is an obvious deformity that s not easily hidden from public
view. The differential diagnosis is
long but the most important distinction is to separate acute onset paralysis
from progressive paralysis. Acute
paralysis usually implies an infectious etiology while progressive paralysis
typically indicates a neoplasm.
A. Acute facial paralysis Onset
< 72 hours.
In some
cases, the cause of paralysis is easily determined. Traumatic injuries and otitis media are in this category. The associated signs of soft tissue injury,
temporal bone fracture, or middle ear effusion are absent in viral medicated
paralysis.
The most
common cause of acute facial paralysis is Bell’s Palsy (Herpes simplex virus
monoeuropathy). Reactivation of latent
virus in the geniculate ganglion produces neural edema and inflammation. The facial nerve passes through a boney
(fallopian) canal, thus, there is a limit to the amount of swelling that can
occur before an entrapment syndrome develops.
The narrowest portion of the fallopian canal is called the meatal
foramen. Maximal neural damage occurs
at this site. The onset and recovery of
the paralysis is very predictable.
Paralysis develops very rapidly, often in less than 24 hours. Likewise, some return of motion is seen in
nearly all patients i one month. Cases
of incomplete paralysis carry the best prognosis, with over 95% attaining
normal or near normal facial function.
If a complete paralysis occurs, only about 70% will recover
completely. Thus, therapy is intended
to limit progression of paralysis.
Steroids and acyclovir, if given within the first three days, improve
prognosis by preventing neural degeneration.
The
varicella zoster virus (VZV) also produces a syndrome of acute facial
paralysis, named Ramsay Huntt syndrome.
Important distinguishing features are the presence of vesicles around
the ear or in the ear canal, and hearing or vestibular symptoms in about
one-third of patients. While the
treatment is the same as in Bell’s palsy, the prognosis is much poorer. Only 50% of Ramsay Huntt patients attain a
normal recovery.
B. Progressive
facial paralysis
A
paralysis that develops over weeks to months is not Bell’s palsy. The two most common diagnoses are neoplasm
and degenerative neurological disease.
In the latter, there are usually other nerves involved. Tumors may involve the nerve anywhere along
its course, but those distal to the temporal bone are the most common. The presence of facial paralysis and upper
neck mass usually indicates an advanced parotid malignancy. Prompt referral and management is necessary. Intra-temporal tumors causing facial
paralysis are likely to cause hearing loss and have an abnormal appearance on
otoscopy. When an intracranial tumor
pushes against the facial nerve, paralysis is uncommon, but hemifacial spasm
may occur.
C. Treatment
The
goals of treatment are: prevention of complications, restoration of facial
function, and cosmesis. Follow-up is
necessary to confirm the original diagnosis.
Acute facial paralysis that does not recover according to the expected
schedule warrants further evaluation.
The most important complication is corneal drying due to inability to
close the eyelid. Ulceration and
infection of the cornea could result with deterioration of vision. This can be prevented with topical
lubricants. If the nerve has been cut
due to trauma or tumor, the recovery will never by normal. It is important to restore some motor
function with a nerve graft, but this can only be accomplished within 2 years
of the injury. Procedures for chronic
facial paralysis attempt to restore oral sphincter competence and eye closure,
and re-suspend facial musculature to improve appearance.
Posted 6/28/2001